Avoiding Common Anesthesia Errors [2nd Edition] 9781496355171, 9781496355188

Table of contents :
Cover......Page 1
Cover......Page 2
Title Page......Page 4
Copyright......Page 6
Dedication......Page 7
Preface......Page 8
Foreword......Page 11
Acknowledgments......Page 12
Contributors......Page 13
Contents......Page 51
VENTILATION AND AIRWAY......Page 79
1 Introduction......Page 80
2 Basics of Airway Management ⠀倀愀爀琀 䤀)Always Keep in Mind Complications That Can Occur With Existing Endotracheal Tubes and Tracheal Extubation......Page 81
3 Basics of Airway ManagementPart II ⠀䴀漀爀攀 吀椀瀀猀 愀渀搀 吀椀搀戀椀琀猀 琀漀 刀攀愀搀 漀渀 琀栀攀 吀爀愀椀渀)......Page 90
4 Optimize the Airway: BagMask Ventilation......Page 97
5 Optimize the Airway: Direct Laryngoscopy......Page 102
6 Oxygen Is a Drug......Page 107
7 Advantages and Disadvantages of the Laryngeal Mask Airway ⠀䰀䴀䄀)......Page 115
8 Avoiding Challenges With Video Laryngoscopy......Page 121
9 Do Not Overinflate the Cuff of the Endotracheal Tube......Page 126
10 Consider the Use of Lidocaine in the Cuff of the Endotracheal Tube, but Be Aware of the Risks and Alternatives......Page 130
11 An Easy Intubation Does Not Guarantee an Easy ReintubationEspecially After a Carotid Endarterectomy or Cervical Spine Surgery......Page 137
12 Plan for an Airway Fire With Every Head and Neck Case......Page 141
13 There Are Special Considerations Involved With Both Intubation and Chronic Airway Management of Burn Patients......Page 146
14 To PEEP or Not to PEEPThat Is the Question......Page 152
15 This Is No Time for Wishful Thinking: Always Troubleshoot an Increase in Peak Airway Pressure......Page 158
16 The Key to the Smooth and Skilled Placement and Use of Double-Lumen Endotracheal Tubes Is to Take It One Step at a Time......Page 164
17 Avoid Common Airway and Ventilation Errors in Morbidly Obese Patients......Page 171
18 Anesthesia for Awake Intubations......Page 179
19 Awake IntubationsBeing Able to Do Them Comfortably and Safely for the Patient Is the Benchmark for the Airway Expert......Page 186
20 Airway Management in the ICU, Including the Dreaded Leaking CuffHow to Bring Your Best Game......Page 193
21 Ludwigs Angina......Page 201
22 Jet VentilationHow to Adequately Handle This Exotic Ventilation Technique and Earn the Admiration of Your Spectators......Page 206
23 High-Frequency Jet VentilationThe View From Philadelphia......Page 210
24 Know How to Perform a Cricothyroidotomy......Page 215
25 Dont Make the Mistake of Thinking That a Tracheostomy Is a Guaranteed Airway......Page 219
26 Helium for the Compromised AirwayYou Have to Understand the Principles and Properties but Weve Seen Some Amazing Saves......Page 225
LINES AND ACCESS......Page 233
27 Introduction......Page 234
28 Remember That the IV Start Is Your First Chance to Make a Favorable Impression on the Patient......Page 236
29 Never Use an Intravenous Line Without Palpating and Inspecting It Visually......Page 242
30 Intraosseous Access......Page 246
31 Central Line Placement: Never Neglect the Basics......Page 253
32 Avoid Technique-Related Central Venous Catheter Complications by Using Modern Tools......Page 256
33 Pulmonary Artery CathetersStill Relevant and Still Worthy of a Cautious Approach......Page 260
34 Dont Overflush Lines......Page 269
35 Inadvertent Intra-Arterial Injection Can Result in Severe Patient Injury......Page 273
36 Do Not Use the Subclavian Vein for Central Access of Any Type in a Patient Who Is On or Planned for Dialysis......Page 282
37 Consult the Surgeons Immediately if Your Patient Loses a Patent Hemodialysis FistulaThis Is a Serious Complication for the Patient......Page 285
FLUIDS AND RESUSCITATION......Page 290
38 Introduction......Page 291
39 Crystalloid Fluids: More Than Just a Dash of Salt......Page 292
40 Hypertonic Saline: Still the Solution to the Solution Problem?......Page 297
41 Synthetic Colloid Solutions Have Distinct Properties and Risk/Benefit Ratios That Require Your Attention!......Page 301
42 Do Not Use CVP to Guide Fluid Resuscitation......Page 311
TRANSFUSION MEDICINE......Page 316
43 Introduction......Page 317
44 Know What Screening Tests Are Performed on Volunteer Donor Blood......Page 319
45 Red Blood Cell Primer......Page 324
46 Type and Screen or Type and Cross-Match?......Page 329
47 Special Circumstances: Patients With Antibodies......Page 334
48 PlasmaIts Not Just to Fix an Abnormal INR......Page 339
49 Plasma Part II: Is This Plasma or Pea Soup?......Page 348
50 Remember That the Universal Donor Is Different for Red Cell and Plasma Products......Page 353
51 PlateletsOften a Mystery!......Page 357
52 CryoprecipitateThe Most Misunderstood Product in the Blood Bank......Page 361
53 Washed Blood Products Are a Source of ConfusionHeres Some Help......Page 368
54 This TEG Tracing Looks Like a Rorschach Blot Is It Time for a Transfusapalooza?......Page 372
55 Transfusion Reactions......Page 381
56 Transfusion Outcomes......Page 388
57 Directed Donation Is Generally Not a Good Idea......Page 396
58 Not All Acute Lung Injury After a Transfusion Is Transfusion-Related Acute Lung Injury......Page 400
59 Jehovahs Witnesses and Bloodless Medicine......Page 403
60 The Ethics of Jehovahs Witnesses and Transfusion......Page 408
MEDICATIONS......Page 413
61 Introduction......Page 414
62 What Just Happened! What You Need to Know About Medication Errors......Page 416
63 Make Sure You Understand the Complex Medical and Legal Issues Surrounding Off-Label Drug Use......Page 428
64 Perioperative Beta-Blocker Therapy for High-Risk Patients Having Noncardiac SurgeryNew Data, New Recommendations......Page 433
65 Should I Withhold or Continue Angiotensin Receptor Blockers in the Perioperative Period?......Page 439
66 Stop Metformin Before Elective Surgery or Intravascular Contrast Dye Study to Decrease the Risk of Lactic Acidosis......Page 445
67 Should I Administer Steroids in the Perioperative Period?......Page 448
68 Beware of the Bowel Prep......Page 452
69 What Drugs Require Slow Administration?......Page 456
70 KetamineUse It Well......Page 461
71 TIVAWhat You Need to Understand to Do It Well......Page 467
72 Dexmedetomidine: Is There Such a Thing as a Free Lunch?......Page 476
73 Consider Chloroprocaine in Emergency SituationsIt Is a Rapid-Onset Local Anesthetic With Low Systemic Toxicity......Page 481
74 Use Bicarbonate as a Buffer to Local AnestheticsEspecially for Skin Infiltration......Page 485
75 The Hows, Whys, Ins, and Outs of Succinylcholine or SuccinylcholineStill a Useful Anesthesia Adjunct......Page 490
76 Dont Get Burned by Incomplete Reversal of Neuromuscular Blockade......Page 500
77 Opioid ConversionsIts Not Only About the Table......Page 511
78 Not All Patients Are NaiveManagement of Perioperative Pain in Opioid-Dependent Patients......Page 519
79 The Basal Infusion Mode in Patient-Controlled Analgesia Is Both Friend and Foe......Page 526
80 Keep Discussing the Use of Ketorolac ⠀吀漀爀愀搀漀氀) With Your Surgical Team Before the Need Arises and Keep Your Eye on the Literature......Page 533
81 Special Topic I: Do Patient With Congenital Insensitivity to Pain Need Anesthetics and Postoperative Opioids?......Page 540
82 Special Topic II: Can Your Patients Eat Their Way Out of Chronic Pain? Some Common Sense Advice......Page 545
83 Attacking Acute Perioperative Hypertension The Cleveland Group Shares Their Battle Plan......Page 551
84 Cardiovascular Vasoactive Drugs That Pump You Up......Page 562
85 MilrinoneThe Not-So-Kidney-Friendly Intraaortic Balloon Pump in a Bottle......Page 572
86 Amiodarone and Alternative Antiarrhythmics Double-Edge Swords for the Treatment of Atrial and Ventricular Fibrillation......Page 578
87 Ondansetron Is a Great Drug, We ALL Use It, But Watch for Headache and QT Prolongation......Page 586
88 A Word About Haloperidol in the Perioperative Period......Page 590
89 Remember That Not All Blue-Colored Compounds Are the Same......Page 595
90 Clonidine Considerations......Page 600
91 A Primer on the Psych Syndromes: Serotonin Syndrome Versus Neuroleptic Malignant Syndrome......Page 607
92 Drug-Drug Interactions Are Now Necessary Knowledge for the Anesthesia Provider and We Can Help......Page 618
93 The Six Patterns of Cytochrome P450 Drug-Drug Interactions Relevant to the Perioperative Clinician......Page 620
94 Dont Spend Time Rereading Tom Clancy Novels Until You Have Mastered These Basic Drug-Drug Interactions......Page 626
95 Drug-Drug Interactions and the P-glycoprotein PumpBe Vigilant With Patients on Digoxin......Page 633
96 Can You Name Six Perioperative Drug-Drug Interactions That Involve Oral Contraceptives? Okay, You Can Now!......Page 636
97 Wish We Knew Then What We Know Now A Case of Serotonin Syndrome in the Operating Room......Page 642
EQUIPMENT......Page 647
98 Introduction......Page 648
99 Pulse Oximetry: Perhaps You Need a Refresher?......Page 650
100 The End-Tidal CO2 Monitor Is More Than Just a Device to Tell You That the Tube in the Airway......Page 655
101 Noninvasive Blood Pressure Management Its Not Just a Piece of Nylon Around the Arm......Page 663
102 Avoid Errors in Invasive Blood Pressure Measurement......Page 667
103 How, Why, and When to Use Brain Function Monitors......Page 675
104 Do Not Improvise Techniques to Warm PatientsUse Warming Devices Only as Per Manufacturers Recommendations......Page 681
105 Transesophageal Echocardiography: Contraindications, Complications, and Misinterpretations......Page 685
106 Scavenging Waste Gases Is Perhaps the Only Action We Take That Benefits Us but Not the Patient......Page 689
107 Carbon Dioxide Absorbers Save Gas and Moisture but Create the Potential for Mechanical Hazards, Chemical Soup, or a Thermal Disaster......Page 694
108 Infusion Pumps: Get Them Going and Keep Them Going!......Page 698
109 Dont Bring the Fiberoptic Scope Into the MRI Scanner!......Page 705
110 Understanding the Operating Room Circuit and the Line Isolation MonitorIts Really Pretty Simple......Page 709
111 Cell Phones in the Operating RoomHere Are the Issues......Page 715
112 Dont Let the Tourniquet Cause Extra Pain or Complications......Page 720
PERIOPERATIVE......Page 724
113 Introduction......Page 725
114 Hurdles of the Electronic Health Record......Page 727
115 Hand Hygiene! History, Human Factors, and Helping Your Patients......Page 732
116 Remember That the Same Simple Mistakes at Induction ⠀愀渀搀 䔀洀攀爀最攀渀挀攀) Happen Over and Over Again!......Page 743
117 Smoking Cessation Part IANYTIME Is a Good Time to Quit......Page 747
118 Smoking Cessation Part 2So Good for the Patient as Long as You Understand the Effects on CYP1A2 Drug Metabolism ⠀䔀猀瀀攀挀椀愀氀氀礀 刀ⴀ圀愀爀昀愀爀椀渀)......Page 751
119 Flying to the Mayo Clinic for Surgery? The Clot Thickens......Page 756
120 Dont Let Your Understanding of the Utility of Preoperative Stress Testing in Suspected Heart Disease Lapse......Page 762
121 A Positive Troponin Does Not Always Mean a Myocardial InfarctionWill the New High-Sensitive Assays Help Sort It Out?......Page 765
122 Preoperative Anxiolysis: Its Not Just Two of Midaz......Page 769
123 Schizophrenia Is a Devastating Mental and Medical Illnessand These Patients Have Significantly Greater Perioperative Risks Than Age-Matched Controls......Page 774
124 What to Do About the Tattoos and Body Jewelry......Page 778
125 We Now Know That Obstructive Sleep Apnea Is More Common Than We ThoughtManage These Patients Carefully and Conservatively......Page 784
126 Dont be Shy About Borrowing ICU Equipment, Medications, and Personnel for the Critically Ill Patient Going to the Operating Room......Page 796
127 The Dao of Positioning......Page 801
128 The Supine PositionComplications Can Still Arise!......Page 808
129 Thinking LaterallyHow to Safely Position a Patient in the Sideways Position for Surgery......Page 815
130 Positioning Patients for Spine Surgery......Page 820
131 Sit Back and Relax? Implications of the Sitting Position in Shoulder and Brain Surgery......Page 825
132 Individuals With Cerebral Palsy and Other Spastic Disorders Need Your Best Positioning Prowess......Page 829
133 Use Extra Care in Positioning Patients Who Have Had Amputations......Page 833
134 Never, Ever Fire......Page 836
135 Malignant Hyperthermia: If You Get to the Point Where You See an Elevated Temperature, Its Already Happening......Page 842
136 Good Old-Fashioned Basic Perioperative Blood Pressure Control......Page 847
137 Some Additional Thoughts on Blood Pressure Management TechniquesWhat We Believe, How We Do It, and Where We Think the Science Is Going......Page 851
138 Protect the Kidneys, Not the UOP......Page 856
139 Avoid a 70% Mortality Rate: Do Everything You Can to Prevent Perioperative Renal Failure......Page 859
140 Do Not Use Urine Output as an Indicator of Volume Status in Hypothermic Patients......Page 862
141 Perioperative Hyperglycemia Is Associated With Poorer Clinical Outcomes so Consider Insulin Therapy for Both Diabetic and Nondiabetic Patients With Elevated Blood Glucose......Page 865
142 Seven Ways to Treat Hyperkalemia in the Perioperative Period......Page 868
143 Laparoscopic Procedures: Managing the Risks and Physiologic Effects During Camera Placement, CO2 Insufflation, and Vertical Positioning......Page 873
144 Could This Be Methemoglobinemia, Maybe?......Page 878
145 The Eye RoomIs It the Easiest of Days? Or the Hardest of Days? Regardless, Vigilance Is Key!......Page 883
146 My Eye Hurts! Prevention, Diagnosis, and Treatment of Corneal Injuries After Anesthesia......Page 890
147 Never Forget That Patient Transport Within the Hospital Is One of the Most Dangerous Intervals in the Perioperative Period......Page 897
148 Seek Out Hypercapnia in the PACU and Remember That an Acceptable Pulse Oximeter Reading Is Not Assurance of Adequate Ventilation......Page 902
149 Lets Go Over It Again: Avoid Residual Neuromuscular Blockade in the PACU!......Page 906
150 Give the Intensivist the Best Handover to Improve Patient Outcomes......Page 912
151 Dont Miss Out on UltrasoundWhich ICU Techniques Are Helpful for the Anesthesiologist?......Page 915
152 Dont Overlook the Potential of Perioperative Acupuncture......Page 921
153 Consider Acupuncture as an Adjunct for the Prophylaxis and Treatment of Postoperative Nausea and Vomiting......Page 928
154 Dont Warm Up a Cardiac Arrest Patient Unless They Are Dying of Hemorrhage!......Page 935
155 What to Do If You Get a Needlestick Injury......Page 940
REGIONAL ANESTHESIA......Page 952
156 Introduction......Page 953
157 Complications of Regional Anesthesia: Dont Touch the Needle Before You Know Them......Page 954
158 Make Time for a Timeout Before Placing a Blockthe Preprocedure Check......Page 962
159 Chlorhexidine: Killing Bacteria and Allergic Patients?......Page 966
160 What Is the Correct Brachial Plexus Block to Perform?......Page 971
161 Getting the Right Ultrasound Image......Page 977
162 Interscalene BlocksPreventing the Blues!......Page 982
163 The Old-Fashioned Bier Block Is Still RelevantThe Trick Is to Not Let the Surgeons Get Ahead of You......Page 988
164 Remember the Low-Risk/High-Yield Blocks......Page 993
165 Preparing to Fail: The Dynamics of a Failed Block......Page 998
166 Salvage Techniques for Incomplete Upper-Extremity Blocks......Page 1002
167 Salvage Blocks for Incomplete Lower Extremity Blocks......Page 1006
168 More Than a Stick and a Burn: Local Anesthetic Systemic Toxicity......Page 1010
169 Lipid RescueWhere Are We Now?......Page 1018
170 A Patient Who Is Planned for Spinal Anesthesia Asks Can This Paralyze Me? What Are the Facts and What Do You Say?......Page 1023
171 Spinals in the Lateral Position......Page 1031
172 Consider the Paramedian Approach for Spinal Anesthesia in the Hip Fracture Patient......Page 1034
173 When Is a Whisper a Cry for Help? When the Patient Has a High Block......Page 1038
174 Issues Related to Discharging the Postspinal Patient......Page 1044
175 Epidural or Truncal Block? Sorting It Out......Page 1049
176 Dang It! Wet Tap......Page 1054
177 Consider Continuous Paravertebral Block as Your Primary Analgesic Technique......Page 1061
178 Pneumothorax After Paravertebral, Supraclavicular, or Interscalene Block......Page 1067
179 Epidural Anesthesia for Mastectomy......Page 1070
180 What Is the Right Level for Postoperative Epidural Catheter Insertions Based on Type of Surgery?......Page 1073
181 Know the Complications of Epidural Corticosteroid Injections......Page 1077
182 If You Are New to Neuraxial and Peripheral Nerve Block Infusionsa View From Both Academia and Private Practice......Page 1083
183 What to Do With a Prolonged Block......Page 1091
184 Regional Anesthesia in the ICUWhat Should We Use and When Should We Use It?......Page 1097
PEDIATRIC ANESTHESIA......Page 1106
185 Introduction......Page 1107
186 Assent, Consent, and Refusal: Informed Consent and Decision-Making for Adult and Pediatric Patients......Page 1109
187 NPO Guidelines Made EasyAlways Maintain a Firm Hold on Current Principles, Best Practices, and Your Own Common Sense......Page 1116
188 Aspiration and Food InjuryOr When Not to Extubate Deep......Page 1121
189 Dont Underestimate the Power of Distraction During Separation and Induction of Anesthesia in Kids......Page 1125
190 Parental Presence on InductionIts Your Call and How to Do It......Page 1128
191 The Child With a URI......Page 1132
192 Accept That You Will Have to Meet the Clinical Challenges of Obesity and Obstructive Sleep Apnea in Your Pediatric Patient Cohort......Page 1136
193 Neuromuscular Disease in Kids Can Be Very Challenging Because You Dont Always Have a Definitive DiagnosisHeres How to Approach the Clinical Situations......Page 1144
194 Pediatric Patients With Epilepsy: Considerations for Patients on a Ketogenic Diet and for Cortical Mapping......Page 1151
195 Neonates Deserve Perioperative Analgesia, Too......Page 1155
196 Anesthetic Considerations in Patients With Fontan Physiology Who Present for Noncardiac Surgery......Page 1165
197 Anesthesia for Kids and Neurotoxicity: You Are Going to Be Asked, So Dont Be Surprised and Dont Act Uninformed......Page 1169
198 Double Down on Pediatric Airway Equipment......Page 1173
199 Optimizing Bag Mask Ventilation and Direct Laryngoscopy in Children......Page 1178
200 Why You Should Expect Hypoxemia During Induction and Emergence of the Pediatric Patient and What to Do About It......Page 1182
201 Why Air Bubbles and Air Emboli Can Be So Serious in Pediatric Patients and How to Safeguard Your Patients......Page 1186
202 Pediatric Fluid Management......Page 1190
203 Keeping Babies Warm in the Perioperative Period Is Important, Challenging, and at Times Dangerous!......Page 1194
204 Pediatric Arterial AccessAnd the Beat Goes On......Page 1198
205 Pediatric Regional AnesthesiaThe Karma of Caudals......Page 1202
206 Avoiding the One-Hour Wake Up or How to Save the Sanity of the Parents and Your Own Reputation at the Same Time......Page 1207
207 When Not to Extubate Deep! And if the Patient Is Already Coughing or Swallowing, Its Too Late Anyway......Page 1211
208 Emergence DeliriumDont Overcall It, Dont Undercall It, and Dont Let It Happen......Page 1216
209 Too Much, Too Little, Just Right: Avoiding Opioid Withdrawal in Pediatric Patients on Chronic Opioids......Page 1223
210 Careful and Conservative Clinical Judgment Is Required Before Discharging a Pediatric Patient to Home......Page 1228
211 Chronic Pediatric Pain: Theres Always More Than Enough Pain for Everybody Involved and Its Not About the Blocks!......Page 1232
212 But, Its Just an Herb! Avoiding Problems Resulting From Nontraditional Pain Medications in the Pediatric Population......Page 1240
213 Okay, There Are Herbals, but What About Those Other Herbals?......Page 1247
214 Pitfalls in Pediatric Sedation......Page 1249
215 Pitfalls of Pediatric Anesthesia for International Service Missions......Page 1255
216 Pediatric Cardiac Arrest Under AnesthesiaPredicting and Preventing the Most Devastating Event of All......Page 1262
NEUROANESTHESIA......Page 1269
217 Introduction......Page 1270
218 The Neurophysiology You Learned in Medical School Is Always RelevantGet a Grip on It and Dont Let Go......Page 1271
219 Cerebral Aneurysm Versus Routine CraniotomyThe Anesthetic Goals Are Not the Same......Page 1276
220 Perioperative Visual Loss Is One of the Most Feared and Devastating Complications of Spine Surgery......Page 1280
221 Being Maximally Prepared for Minimally Invasive Pituitary Surgery......Page 1287
222 Evoked Potentials: Dont Approach the Surgeon or Neurophysiologist Until You Know These Principles......Page 1292
223 Awake Craniotomy......Page 1298
224 Anesthesia for the Pregnant Patient With Neurosurgical Disorder: These Cases Actually Do Happen in Real Life .. and on the Oral Boards......Page 1307
225 Dont Forget Theres No Such Thing as a Brain Transplant: Preventing Perioperative Stroke......Page 1315
226 Anesthesia for Emergent Neurointerventional Procedures: Neurology Just Called, They Have a Stroke Patient for Thrombectomy Down in Neuroradiology, Start Time is 2 AM......Page 1320
227 Encephalopathy and Intracranial Hypertension in the Acute Liver Failure Patient Are Not the Same Thing!......Page 1326
CARDIAC ANESTHESIA......Page 1330
228 Introduction......Page 1331
229 Cardiac Surgical CoagulopathyYoull Need the Blood Bank and a Genie in a Bottle......Page 1334
230 A Is for Aortic, C Is for Cannulation, B Is for Be Careful!......Page 1339
231 Transesophageal Echocardiography in the Cardiac Surgery SuiteStrategies to Stay Out of Trouble......Page 1344
232 Myocardial Protection Strategies During Cardiopulmonary BypassDo Everything You Can but Realize That Some Ischemic Damage Is Inevitable......Page 1349
233 The Heartbreak of Left-Sided Valvular Dysfunction......Page 1354
234 Anesthesia for the Descending Thoracic AortaInitiate Damage Control Measures......Page 1361
235 Buckle Your Seat Belt: Taking Care of the Patient With Ascending Aortic Dissection......Page 1366
236 Rolling in the Deep Hypothermic Circulatory Arrest......Page 1374
237 Anesthesia for Left Ventricular Assist Device Surgery: Essentials to Bear in Mind......Page 1380
238 Off-Pump Coronary Artery Grafting Is Like Working on an Engine ⠀圀栀椀氀攀 䤀琀 䤀猀 匀琀椀氀氀 刀甀渀渀椀渀最)......Page 1387
239 What to Do and What Not to Do for Your Patients With Hypertrophic Obstructive Cardiomyopathy......Page 1393
240 Cardiac TransplantGotta Get This One Right......Page 1397
241 The Right Heart Should Never Play Second Fiddle to the Left HeartWhat to Do When the Right Heart Just Really Aint Right at All......Page 1403
OBSTETRIC ANESTHESIA......Page 1410
242 Introduction......Page 1411
243 Be Prepared for the Presence of a Doula in Both the Labor and Delivery Rooms......Page 1412
244 Guests on the Labor Deck and in the Delivery RoomHow to Manage It and Keep Your Professional Demeanor......Page 1415
245 Alternatives to Epidural Analgesia for Labor PainWhat to Consider, What You Might Be Asked......Page 1420
246 Epidural Labor Analgesia: Does It Prolong Labor?......Page 1426
247 We Were Taught Once a C-section, Always a C-Section What to Do When Your Hospital Now Wants to Provide Trial of Labor After Cesarean ⠀吀伀䰀䄀䌀) Services......Page 1431
248 Should We Place a Spinal for a Version? Anesthesia for External Cephalic Version......Page 1435
249 Management of an Accidental Dural Puncture in the Laboring Patient When the Hanging Drop Becomes a Flowing River......Page 1439
250 We Have an Urgent C-Section! The Pitfalls of Intrapartum Monitoring of the Fetus......Page 1443
251 Stat C-SectionThe 30-Minute Rule and Beyond......Page 1449
252 Postpartum Hemorrhage: Dont Forget That Having a Baby Is Major Surgery......Page 1456
253 From Glad to Sad ⠀倀愀爀琀 ㄀): Pain Control After Cesarean Section......Page 1462
254 From Glad to Sad ⠀倀愀爀琀 ㈀): Postpartum Neuropathy of the Lower Extremity......Page 1470
255 Obstetric Anesthesia/Analgesia Can Work in a Small Hospital: The Key Principles Are Commitment, Flexibility, and Planning......Page 1477
256 Resuscitation of the Pregnant Cardiopulmonary Arrest Patient: Not Just Standard ACLS......Page 1482
257 The Pregnant Anesthesia Provider ⠀倀愀爀琀 ㄀)Managing the Occupational Exposures......Page 1488
258 The Pregnant Anesthesia Provider ⠀愀渀搀 一攀眀 䄀搀漀瀀琀椀瘀攀 倀愀爀攀渀琀)Part 2......Page 1494
HUMAN FACTORS......Page 1497
259 Introduction......Page 1498
260 Understanding the Human Factor......Page 1499
261 Minimize Errors in Anesthesia: Lessons Learned From Aviation......Page 1502
262 Eliminate Communication Errors by Using a Spelling Alphabet and Spoken Digits......Page 1506
263 Dont Ignore Your Intuition......Page 1510
264 Ethics in Anesthesiology Practice......Page 1513
265 Know When to StopAnesthesia Providers Have Got to Know Their Limitations......Page 1520
266 Before You Press Play, Lets Talk About Music in the OR......Page 1523
267 Never Rush Through a Signout......Page 1527
268 Dont Ignore the FolkloreIt Can Be a Powerful Ally in Your Clinical Practice......Page 1532
269 Dont Underestimate the Role of Spirituality in Patients Perceptions of Disease and Healing, and Remember to Uphold the Right to Self-Determination......Page 1537
270 Whats in a Name?......Page 1547
271 We Are Not the Only People Who Care About the Patients......Page 1550
272 Working in the ORSometimes the Staff Gets Sick or Injured, Too......Page 1554
273 The Physician as PatientWhat I Learned During the Last Five Times I Went to the OR on the Stretcher Instead of Pushing It......Page 1560
274 A Primer on Simulation in Anesthesiology Definitions and Concepts......Page 1564
275 What Makes a Great Anesthesia Resident?......Page 1569
LEGAL......Page 1575
276 Introduction......Page 1576
277 A Brief on the Legal Process......Page 1577
278 How Not to End Up in a Closed Claims FileLessons Learned From the ASA Closed Claims Project......Page 1582
279 The Anesthesia Closed Claims Project Whats Trending Now?......Page 1591
280 A Careful and Complete Anesthesia Record Is the Best Defense Against a Lawsuit......Page 1594
281 Documentation Disputes in the Medical RecordHow to Avoid a Chart War and How to Survive One......Page 1601
282 Reading in the Operating Room: Is It Worth the Risk?......Page 1604
283 Going to the Operating Room With a Do-Not-Resuscitate Patient......Page 1608
284 Refusal to Do a Case on Moral or Ethical Grounds: More Practical Navigation Through Choppy Waters......Page 1613
285 Dental InjuriesDocument Carefully and Do Not Overpromise......Page 1618
286 Apologizing to Patients After an Adverse Event Is the Ethical Thing to Do and Just Might Keep You Out of Court......Page 1623
PROFESSIONAL PRACTICE......Page 1628
287 Introduction......Page 1629
288 Marketing 101: Know Your Customers and What They Need!......Page 1630
289 Improving OR Throughput: Dont Say No......Page 1634
290 Cost Analysis: You Always Want to Be at the Table......Page 1638
291 Strategic Planning: Failing to Prepare Is Preparing to Fail......Page 1643
292 Business Plan 101: Where You Want to Go and How You Are Going to Get There......Page 1648
293 Avoid Being Labeled Simply a Gas-Passer: An Overview of the Perioperative Surgical Home......Page 1652
294 The Curriculum Vitae: Know Your Audience......Page 1658
295 Your Career: Interviewing......Page 1663
296 Your Career: Understanding the Basics of Ownership Jobs......Page 1669
297 Your Career: Employee Jobs......Page 1675
298 Your Career: Understanding the Basics of Locum Tenens Jobs......Page 1681
299 Your CareerUnderstanding Solo Practice and the Basics of Medical Practice Finance and Legal Organization......Page 1686
300 Your Career: Make Sure You Understand the Compliance Plan......Page 1691
301 Your CareerKnow the Risk-Management Strategies of the Practice......Page 1696
302 Avoiding Bad Employment Contracts: Due Diligence, Termination, and Restrictive Covenants......Page 1698
303 Avoiding Bad Employment Contracts: Duties, Compensation, and Benefits......Page 1702
304 MACRARobbing Peter to Pay Val ⠀甀攀)......Page 1706
CONCLUSION......Page 1713
305 Sage Advice to Close This Book: Anesthesiology and the Aphorisms of B. Franklin, Printer......Page 1714
Index......Page 1719
Index......Page 1797

Citation preview

ASSOCIATE EDITOR Raymond G. Graber, MD Associate Professor, Department of Anesthesiology and Perioperative Medicine, University Hospitals Cleveland Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio SECTION EDITORS Steven L. Orebaugh, MD – Section I Ventilation and Airway Brian T. Gierl, MD and Catherine Marcucci, MD – Section II Lines and Access Brian T. Gierl, MD and Catherine Marcucci, MD – Section III Fluids and Resuscitation Melissa R. George, DO – Section IV Transfusion Medicine Wayne T. Nicholson, MD PharmD – Section V Medications Brian Mitchell, MD – Section VI Equipment Ryan J. Fink, MD – Section VII Perioperative Raymond G. Graber, MD – Section VIII Regional Anesthesia Kirk Lalwani, MD – Section IX Pediatric Anesthesia Laurel E. Moore, MD – Section X Neuroanesthesia Edwin G. Avery IV, MD – Section XI Cardiac Anesthesia Christopher E. Swide, MD – Section XII Obstetrical Anesthesia Brian T. Gierl, MD and Catherine Marcucci, MD – Section XIII Human Factors Cobin Soelberg, MD JD – Section XIV Legal Amr E. Abouleish, MD – Section XV Professional Practice David A. Zvara, MD – Section XVI Conclusion CONTRIBUTING EDITORS Ryan Anderson, MD PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Matthias J. Merkel, MD PhD Professor and Vice Chair Department of Anesthesiology and Perioperative Medicine Knight Cardiovascular Institute Oregon Health & Science University Portland, Oregon Richard W. Rosenquist, MD Chairman Pain Management Department Anesthesiology Institute

Cleveland Clinic Cleveland, Ohio

AVOIDING COMMON ANESTHESIA ERRORS EDITORS

CATHERINE MARCUCCI, MD Senior Research Anesthesiologist Corporal Michael J. Crescenz Veterans Affairs Medical Center Philadelphia, Pennsylvania

BRIAN T. GIERL, MD Section Chief of Neuroanesthesiology Director, Neuroanesthesia and Supportive Care, UPMC Presbyterian Director, Neuroanesthesiology Fellowship Program University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

JEFFREY R. KIRSCH, MD FASA Professor Associate Dean for Faculty Affairs Senior Medical Director, Perioperative Services Vice Chair, Faculty Development; Anesthesiology Medical College of Wisconsin/Froedtert Hospital Milwaukee, Wisconsin Chair Emeritus, Anesthesiology & Perioperative Medicine Oregon Health & Science University Portland, Oregon

Acquisitions Editor: Keith Donnellan Development Editor: Ashley Fischer Editorial Coordinator: Dave Murphy Senior Production Project Manager: Alicia Jackson Team Lead, Design: Stephen Druding Senior Manufacturing Coordinator: Beth Welsh Prepress Vendor: Aptara, Inc. 2nd edition Copyright © 2020 Wolters Kluwer. 1st Edition Copyright © 2008 Lippincott Williams & Wilkins, a Wolters Kluwer business. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at [email protected], or via our website at shop.lww.com (products and services). 9 8 7 6 5 4 3 2 1 Printed in China 978-1-4963-5518-8 Library of Congress Cataloging-in-Publication Data available upon request This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency of the content of this work. This work is no substitute for individual patient assessment based upon healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data and other factors unique to the patient. The publisher does not provide medical advice or guidance and this work is merely a reference tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources. When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings and side effects and identify any changes in dosage schedule or contraindications, particularly if the medication to be administered is new, infrequently used or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work. shop.lww.com

To Charlie and Lisa Sandson, and Neil too, of course—this book would never have happened without your love and patience; many thanks also and always to the people who extended their unwavering support during the past few hectic years. Catherine Marcucci, MD To my family, who continue to inspire, and all of the other individuals who have taught me, challenged me, and encouraged my lifetime of learning. Brian T. Gierl, MD To Robin, my life-long source of inspiration; and to our granddaughters, Noa and Romi, my source of energy for the future. Jeffrey R. Kirsch, MD The editors also wish to dedicate this book to the following individuals for their love and/or steadfast support: Ray Graber: To my lovely wife, Mary; and our kids—Luke, Colin, and Aubrie Steve Orebaugh: To my wife, Jennifer; and my daughter, Olivia Melissa George: To my parents, Melanie and Joseph Smola; and my husband, Joe George Nick Nicholson: To my wife, Jo Ann Nicholson Brian Mitchell: To my wife, Katherine Mitchell Ryan Fink: To Derek Applewhite, PhD for constant inspiration and support; and to Miko Enomoto, MD and Jeffrey Kirsch, MD for their mentorship and guidance Ryan Anderson: To Lisa Matthias J. Merkel: To my wife, Jennifer; and my daughters, Rebecca, Katharina, and Annika Merkel Rick Rosenquist: To my wife, Ellen; and my children, Anders, Taryn, Leif, and Karl Kirk Lalwani: To my wife, Seema Lalwani, who has dedicated her career to our family; and to my children, Nikita and Rohan, who inspire me to do the best I can Laurel Moore: To Dr. Charles R. Moore, my father and favorite anesthesiologist Ed Avery: To my wife, Lauren Avery; and our children, Sophia and Edwin Avery V Chris Swide: To my wife, Sharon Kenny; and Joseph, Erin, and Thomas Swide Cobin Soelberg: To my endlessly supportive parents, Doug and Cheri Soelberg; and my darling wife, Julie Soelberg Amr Abouleish: To my wife, Lamia Elerian, MD, for her support and patience

PREFACE “Good decisions come from experience, and experience comes from bad decisions.” —Mark Twain All medical providers are awash in information with more and more being published each week. The relevant publications are well summarized in a multitude of anesthesia textbooks to define the science of medicine. But what about the art of medicine? One could memorize Miller’s Anesthesia without having any idea how to plan or execute an anesthetic. While checklists guide the response to an emergency, experience guides the seasoned practitioner away from that emergency. This book guides the reader through means to identify potential problems, develop plans to avoid those problems, and to treat those problems to minimize their impact on the patient’s recovery. Many texts have been published that describe errors by extrapolating scientific studies and adding expert opinion. Those texts often neglect to spell out a plan. The Avoiding Common Errors series provides plans for avoiding and treating situations and communicates those plans in an informal and often humorous manner. As Mark Twain is quoted above, there is a lot to be learned from bad decisions. However, there is no reason to make all those bad decisions yourself! Reading about the risks and pitfalls of various strategies is a good way to avoid complications. The first edition of this book reviewed 215 situations in which common errors might occur as an effort to convey highlights from the published literature and expert opinions based upon the experiences of over 300 authors. It was very popular here in the United States and was also published in six foreign language editions. This second edition describes the cause, diagnosis, and treatment of a total of 305 situations. The text reflects on the conversations that occur between a seasoned attending anesthesiologist and a trainee before a case. Like those conversations, most chapters can be reviewed in 10 minutes or less. The situations can be used to spur conversations with trainees as well. Although some of these situations are infrequent, they are very relevant when they do present. Each patient is rightfully only concerned with their own situation and most patients fully expect to awaken perfectly well after their procedure, regardless of their preoperative status or the complexity of the procedure. Hospital administrators tend to agree with them. This text provides strategies to optimize the risks and benefits of anesthesia for your patients … and keep you off the podium at the Morbidity and

Mortality conference, and maybe even out of the courtroom. In reviewing, revising, and developing new content, we once again owe a tremendous debt to our contributing authors and section editors. Everybody who contributed to the book enthusiastically gave us their interest, time, and expertise. We literally could not have put Avoiding Common Anesthesia Errors, Second Edition together without them. Our section editors were just astounding in their dedication to the project and we are grateful for their patience and commitment. We would also like to give additional special mention to several individuals. These are the individuals who took topics and subjects on a moment’s notice and developed them with expertise, commitment, and good humor. First and foremost, we thank Raymond G. Graber, MD for joining us as Associate Editor-at-Large while the manuscript was “in preparation” and researching, reviewing, and writing up a number of important topics, with the quickest possible turnaround. We also thank Brandon Togioka, MD, Juraj Sprung, MD PhD, Toby Weingarten, MD, Erica Wittwer, MD PhD, Edwin G. Avery IV, MD, and the perioperative nursing staff at the University of Pittsburgh Medical Center for being terrific “go-to” people whenever we were stalled on a topic. We would also like to note the students and medical and legal professionals who took time away from their own educational programs, specialties, and busy clinical practices to contribute to ours with their ideas and expertise: Melissa R. George, DO, Matthew DeCaro, MD, F. Jacob Seagull, PhD, Albert Liao, LAc, Kristin King Liao, LAc, Scott Mist, PhD MAcOM LAc, Maria Lanzi, MS MPH ANP-BC COHN-s CTH, Sarah Foster-Chang, DNP APRN-BC COHN-s, Benjamin Conner, MSc MD/PhD3, Elizabeth Herzog, MD, Laura A. Donegan, MD, Carol F. Bodenheimer, MD, Daniel L. Glennon, JD MA, Renee A. Metal Esquire, Sara Lyons, MSN RN CNOR, Charles H. Sandson, BS IME’21, Lisa L. Sandson BArch’24, and Neil B. Sandson, MD. And thanks again as ever to the great Theresa Hanson at the Mayo Clinic! This book has its own dedicated section pertaining to perioperative drug--drug interactions (DDIs), naturally. In putting this material together, we once again reviewed just about every published paper of Evan Kharasch, MD PhD. And so we thank him, as before, for his pioneering research in the field of DDIs and the cytochrome P450 enzyme system—it continues to motivate and inform our educational efforts in this important and relevant area of clinical perioperative practice. We extend our gratitude to a number of senior physicians for their unique contributions: John L. Cameron, MD at Johns Hopkins for renewing his permission for us to quote him, Robert Gaiser, MD at the University of Kentucky for writing our foreword, David Zvara, MD FAHA for writing our concluding chapter, Peter Biro, MD for helping us with his unique expertise, Randal O. Dull, MD PhD for developing

content on the cytochrome P450 enzymes that we refer to constantly, Lorrie A. Lee, MD and Karen Domino, MD MPH for their expertise on the Anesthesia Closed Claims Project, Amr Abouleish, MD and Norman A. Cohen, MD for their contributions to the always important subject of professional practice, Poune Saberi, MD MPH for introducing us to our Occupational Health clinicians and authors, Jeffrey A. Grass, MD for reviewing chapters, and surgeons Mark K. Wax, MD FACS, Michael J. Moritz, MD FACS, Keith A. Chadwick, MD, Soon Park, MD, and Steven J. Busuttil, MD for their collective clinical expertise. We also extend our heartfelt thanks to John Kelly, MD, Chief of Staff of the Corporal Michael J. Crescenz Philadelphia VA Medical Center, for his commitment to the project and sponsorship of the time required to complete it. The editorial and development staff at Lippincott Williams & Wilkins Wolters Kluwer Health was once again great to work with and we must especially recognize David Murphy for his expertise, dedication, and patience. Dave was tops, by us, all the way through the project. We also send our gratitutde and compliments to Anamika Singh for her painstaking work in putting the book together and building the manuscript for us. This was a large and long project, with hundreds of contributors and thousands of chapter drafts, but we got it done with the steadfast support of the LWWWK Health folks who walked patiently beside us every step of the way. And to close, we must once again acknowledge our authors and editors—this time for their outstanding generosity. Incredibly, every person who contributed to this book once again concurred that all royalties from this project remain pledged in perpetuity to the Foundation for Anesthesia Education and Research. We are humbled and honored to be associated with this wonderful group of dedicated and caring providers! Catherine Marcucci, MD Brian T. Gierl, MD Jeffrey R. Kirsch, MD

FOREWORD It was Einstein who said, “Anyone who has never made a mistake has never tried anything new.” Any person, regardless of their level of experience, is at risk for error if approaching something new. No one wants to make a mistake and we do everything in our power to avoid it. As physicians, we are more in tune to mistake prevention because of the consequences of our mistakes. Any error may have a significant impact on the patient or their well-being. The best means to prevent an error is to practice the motto from the Boy Scouts, “Be prepared.” We become prepared by educating ourselves and by ensuring that all necessary equipment and personnel are available. What is the best means to educate ourselves? This book, Avoiding Common Anesthesia Errors, is a step in the right direction. With the information readily available and referenced, the book provides the knowledge to prevent common mistakes in anesthesiology. It is intended for the students in anesthesia, both medical students and residents. It allows them to enter a new situation informed and prepared. However, it would be a disservice to state that the book is only for the novice. As I advance in my years, some things which were previously old are now new as I am asked to perform an anesthetic or a technique that I haven’t done in several years. Furthermore, as the specialty advances, previously learned information and techniques no longer apply and new information must be learned. The book encompasses the entire range of patients from the pediatric to the geriatric, addressing the skills such as airway management, invasive monitoring, and regional anesthesia to name a few. This book is clearly one that should be readily available to both the trainee who is in the midst of medical school or residency and the expert who discovers their area of expertise is too narrow for the current practice in Anesthesiology. To err is human, to own and to read this book, sublime. Robert Gaiser, MD Professor and Chair Department of Anesthesiology College of Medicine University of Kentucky Lexington, Kentucky

ACKNOWLEDGMENTS The editors would like to acknowledge the following authors who contributed chapters for the previous edition for providing a strong foundation for us to build on as we developed the content for this new second edition: Shushma Aggarwal, MD Elizabeth E. Costello, MD Grant T. Cravens, MD Marisa H. Ferrera, MD Alan C. Finley, MD Bryan J. Fritz, MD J. Todd Hobelmann, MD Ying Wei Lum, MD

CONTRIBUTORS Kenneth R. Abbey, MD JD Clinical Associate Professor Portland VA Health Care System Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Amr E. Abouleish, MD MBA Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas Immaculeta Achilike, MD MPH Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Kareem Aggour, MD Instructor/Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Rashad Albeiruti, MD Anesthesia Practice Consultant Clinical Assistant Professor College of Human Medicine Michigan State University Grand Rapids, Michigan Navid Alem, MD Associate Clinical Professor Department of Anesthesiology and Perioperative Care UC Irvine School of Medicine Irvine, California Jafer Ali, MD Department of Anesthesiology & Pain Management Anesthesiology Institute Cleveland Clinic Cleveland, Ohio O. Layton Alldredge Jr, MD MS

Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Staci Allen, DO Chief Resident Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Michael D. Altose, MD PhD Section Head, Neurosurgical Anesthesiology Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Levana Amrock, MD Resident Physician Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Douglas W. Anderson, DMD (Retired) Clinical Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Paul C. Anderson, MD Department of Anesthesiology Jefferson Hospital Jefferson Hills, Pennsylvania Ryan Anderson, MD PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Chidi Ani, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Fiyinfoluwa Ani, MD MBA Resident Department of Anesthesiology and Perioperative Care University of California, Irvine Orange, California

Martin Anixter, MD Pittsburgh, Pennsylvania Benjamin L. Antonio, DO MBA American Anesthesiology of NC Department of Anesthesia and Critical Care UNC REX Healthcare Raleigh, North Carolina Gregory Applegate, DO Assistant Professor Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Faisal D. Arain, MBBS MD Assistant Professor Division of Cardiothoracic Anesthesiology Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Daniel I. Asher, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Edwin G. Avery IV, MD Professor of Anesthesiology Division of Cardiothoracic Anesthesiology Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Michael S. Axley, MS MD Anesthesiologist Oregon Anesthesiology Group Portland, Oregon Michael Aziz, MD Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Ann Bailey, MD FAAP Professor of Pediatrics and Anesthesiology The University of North Carolina

Chapel Hill, North Carolina Emily J. Baird, MD PhD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon David Barbara, MD Associate Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine Mayo Clinic Aurora BayCare Medical Clinic Green Bay, Wisconsin Natalie R. Barnett, MD Assistant Professor Department of Anesthesiology Cohen Children’s Medical Center New Hyde Park, New York Rodger E. Barnette, MD FCCM Consultant Anesthesiologist and Intensivist AIC Kijabe Hospital Kijabe, Kenya Professor Emeritus Department of Anesthesiology Lewis Katz School of Medicine Temple University Philadelphia, Pennsylvania Michael Barts, CRNA APRN BS Anesthesiology Staff Anesthetist Department of Anesthesiology Services Lovelace Hospital System Albuquerque, New Mexico Mark J. Baskerville, MD JD MBA MA Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Pavan K. Battu, MBBS DA FRCA Consultant in Anaesthesia Department of Anaesthesia and Intensive Care University Hospitals Birmingham (QEH) Birmingham, United Kingdom Katharina Beckmann, MD Associate Professor Department of Anesthesia University of Illinois at Chicago

Chicago, Illinois Bruce Ben-David, MD Clinical Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Charles Jeremy Bengson, MD Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Abiona Berkeley, MD JD Associate Professor Department of Anesthesiology Lewis Katz School of Medicine Temple University Philadelphia, Pennsylvania Peter Biro, MD DESA Professor and Senior Consultant Institute of Anesthesiology University Hospital Zurich Zurich, Switzerland Kimberly Blasius, MD Director of Education Scope Anesthesia of North Carolina Charlotte, North Carolina Carol Bodenheimer, MD Assistant Professor H. Ben Taub Department of Physical Medicine and Rehabilitation Baylor College of Medicine Staff Physician Spinal Cord Injury Care Line Michael E. DeBakey VA Medical Center Houston, Texas Michael L. Boisen, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Katarina Bojanić, MD PhD Staff Neonatologist Division of Neonatology Department of Obstetrics and Gynecology University Hospital Merkur Zagreb, Croatia

Ryan J. Bortolon, MD Anesthesiologist South Valley Anesthesia PA Plymouth, Minnesota Richard Botney, MD Assistant Professor Attending Anesthesiologist Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Kristin Bowden, CRNA DNAP MBA Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Ansgar M. Brambrink, MD PhD E.M. Papper Professor and Chair Department of Anesthesiology Columbia University/NewYork-Presbyterian Hospital New York, New York Daniel R. Brown, MD PhD FCCM Director, Multidisciplinary Critical Care Practice Professor of Anesthesiology Mayo Clinic Rochester, Minnesota John T. Bryant IV, MD Chief of Anesthesia Mission Hospital Asheville, North Carolina Abram H. Burgher, MD Chief Medical Officer The Pain Center of Arizona Associate Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic College of Medicine Scottsdale, Arizona David A. Burns, MD Anesthesiologist Department of Anesthesiology Providence Sacred Heart Medical Center Spokane, Washington Marion Bussay, MD Anesthesiology Resident Department of Anesthesiology University of Illinois at Chicago

Chicago, Illinois Steven J. Busuttil, MD Surgeon Vascular Surgery Geisinger CMC Vascular and Endovascular Surgery Geisinger Surgery Institute Scranton, Pennsylvania Matthew W. Caldwell, MD Assistant Professor Department of Anesthesia and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Maxime Cannesson, MD PhD Professor and Vice Chair Department of Anesthesiology and Perioperative Medicine University of California, Los Angeles Los Angeles, California Michael Carrigan, MD Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Philip Carullo, MD Pediatric Anesthesiology Fellow Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Keith A. Chadwick, MD Sean Parker Fellow in Laryngology and Instructor The Sean Parker Institute for the Voice Department of Otolaryngology—Head and Neck Surgery Weill Cornell Medical College/New York-Presbyterian Hospital New York, New York Walter Chang, MD Assistant Clinical Professor Department of Anesthesiology City of Hope Medical Center Duarte, California Benjarat Changyaleket, MD Assistant Professor Department of Anesthesiology University of Illinois at Chicago Chicago, Illinois Elliza M. Chen, MD

Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Grace Chen, MD Assistant Professor Director of Adult Pain Service Director of Pain Management Fellowship Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Zheyan (Jenny) Chen, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Alan Cheng, MD Associate Professor of Medicine (part time) Section of Cardiac Electrophysiology Johns Hopkins University School of Medicine Baltimore, Maryland Vice President Clinical Research, Medtronic, Inc. Mounds View, Minnesota Katya H. Chiong, MD FASA Assistant Professor Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Kathleen Cho, MD Chief Department of Anesthesiology and Perioperative Medicine University Hospitals Ahuja Medical Center Beachwood, Ohio Rose Christopherson, MD PhD (Retired) Anesthesiologist Department of Anesthesiology Portland VA Medical Center Portland, Oregon Linda Chung, MD Pediatric Anesthesiologist Good Samaritan Hospital San Jose, California Theodore J. Cios, MD MPH

Assistant Professor Division of Cardiothoracic and Vascular Anesthesiology Department of Anesthesiology and Perioperative Medicine Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania Norman A. Cohen, MD Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Thomas B. Comfere, MD Assistant Professor of Anesthesiology Mayo Clinic College of Medicine Rochester, Minnesota Benjamin C. Conner, MSc MD/PhD3 Student College of Medicine University of Arizona—Phoenix Phoenix, Arizona Nicole Conrad, MD Staff Anesthesiologist Legacy Emanuel Medical Center Portland, Oregon Etienne J. Couture, MD FRCPC Fellow in Adult Cardiothoracic Anesthesiology Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Vincent S. Cowell, MD FAACD Professor Vice Chair, Anesthesia Clinical Affairs Department of Anesthesiology Lewis Katz School of Medicine Temple University Philadelphia, Pennsylvania Daniela Damian, MD Clinical Assistant Professor Department of Anesthesiology Children’s Hospital of Pittsburgh Pittsburgh, Pennsylvania Chad T. Dean, MD Chief Resident Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center

Case Western Reserve University School of Medicine Cleveland, Ohio Diana S. DeAndrade, MD Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Matthew DeCaro, MD Director of Cardiovascular Intensive Care Associate Professor of Medicine Thomas Jefferson University Philadelphia, Pennsylvania Jennifer A. DeCou, MD Associate Professor Department of Anesthesiology University of Utah Salt Lake City, Utah J. Mauricio Del Rio, MD Assistant Professor Division of Cardiothoracic Anesthesia Department of Anesthesiology Duke University Durham, North Carolina James DeMeester, MD Director of Cardiac Anesthesia St. Joseph Mercy Hospital Ann Arbor, Michigan Daniel Diaczok, DO Resident/Fellow Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Brandon Dial, MD Chairman Department of Anesthesia Utah Valley Hospital Provo, Utah Heath Diel, MD Director, Cardiac Anesthesiology Benefis Health System Great Falls, Montana Jeffrey D. Dillon, MD Associate Chief of Anesthesia Salt Lake City VA Medical Center

Clinical Assistant Professor of Anesthesiology University of Utah School of Medicine Salt Lake City, Utah Sarah Elizabeth Dodd, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Karen B. Domino, MD MPH Professor and Vice Chair for Clinical Research Department of Anesthesiology and Pain Medicine University of Washington Seattle, Washington Laura A. Donegan, MD FACP Internist Department of Medicine University of Maryland St. Joseph Medical Center Towson, Maryland Randal O. Dull, MD PhD Professor and Chair Department of Anesthesiology University of Arizona COM, Banner-University Medical Center Tucson, Arizona Muhammad Durrani, MD Chief Department of Anesthesia Inspira Medical Center Vineland, New Jersey Jamey E. Eklund, MD Associate Professor of Clinical Anesthesiology and Pediatric Anesthesiology Department of Anesthesiology UI Health Chicago, Illinois Anila B. Elliott, MD Assistant Professor Department of Anesthesiology University of Michigan Ann Arbor, Michigan Margaret K. Menzel Ellis, MD Critical Care Anesthesiologist VA Portland Healthcare Center Assistant Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon

Hooman Rastegar Fassaei, MD Pain Medicine Specialist PIH Health Whittier, California Byron Fergerson, MD Clinical Professor Department of Anesthesiology University of California, San Diego San Diego, California Ryan J. Fink, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Michael G. Fitzsimons, MD Director Division of Cardiac Anesthesia Department of Anesthesiology, Critical Care and Pain Medicine Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Antolin S. Flores, MD Assistant Professor Department of Anesthesiology The Ohio State University Columbus, Ohio Patrick J. Forte, MD Associate Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Sarah Foster-Chang, DNP ANP-BC COHN-S Nurse Practitioner Environmental and Occupational Health Corporal Michael J. Crescenz Veterans Affairs Medical Center Philadelphia, Pennsylvania Alexander Y. Fu, MD Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Robert Gaiser, MD Professor and Chair Department of Anesthesiology College of Medicine

University of Kentucky Lexington, Kentucky Theresa A. Gelzinis, MD Associate Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Melissa R. George, DO Interim Chair and Associate Professor Department of Pathology Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania Stacey L. Gibbons, MD Assistant Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas Brian T. Gierl, MD Section Chief of Neuroanesthesiology Director, Neuroanesthesia and Supportive Care, UPMC Presbyterian Director, Neuroanesthesiology Fellowship Program University of Pittsburgh Medical Center Pittsburgh, Pennsylvania J. Saxon Gilbert, MD Anesthesiologist McKenzie Surgery Center Eugene, Oregon Stephen J. Gleich, MD Assistant Professor of Anesthesiology and Pediatrics Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Daniel L. Glennon, JD MA The Glennon Firm Philadelphia, Pennsylvania Jeffrey A. Gold, MD Professor of Medicine Division of Pulmonary and Critical Care Medicine Oregon Health & Science University Portland, Oregon Raymond G. Graber, MD Associate Professor Department of Anesthesiology and Perioperative Medicine

University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Heike Gries, MD PhD Associate Professor Pediatric Anesthesiology Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Matthew Griffee, MD Associate Professor Department of Anesthesiology University of Utah School of Medicine Salt Lake City, Utah Andrew M. Gross, MD Director of Interventional Pain Management Orthopedic Center of Florida Assistant Professor of Medicine Florida State University Fort Myers and Bonita Springs, Florida Dmitri Guvakov, MD Associate Professor Division of Cardiac Anesthesia Department of Anesthesiology and Perioperative Medicine Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania Patrick J. Hackett, MD Anesthesiologist Department of Anesthesiology Maine Medical Center Portland, Maine Rebecca Hall, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Karen Hand, MB BS FRCA Assistant Professor Department of Anesthesia and Perioperative Medicine Oregon Health & Science University Portland, Oregon Izumi Harukuni, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University

Portland, Oregon Sprague W. Hazard III, MD Assistant Professor of Anesthesia, Critical Care and Neurosurgery Division Director of Neuroanesthesia Department of Anesthesiology and Perioperative Medicine Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania R. Scott Herd, MD Pediatric Anesthesiologist Anesthesia Associates of Boise Boise, Idaho Raquel G. Hernandez, DO Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Elizabeth Herzog, MD University of Maryland School of Medicine Baltimore, Maryland James S. Hicks, MD MMM Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Ibtesam Hilmi, MBChB FRCA Professor of Anesthesiology Professor Clinical and Translational Science Institute Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Michael Hogan, MD Clinical Associate Professor Facility Site Chief Department of Anesthesiology and Pain Medicine University of Alberta Hospital Alberta, Canada Harriet W. Hopf, MD Professor Department of Anesthesiology University of Utah Salt Lake City, Utah Christopher Howson, MD

Anesthesiologist and Pain Medicine Specialist Pain and Rehabilitation Medicine BayCare Clinic Green Bay, Wisconsin Michael P. Hutchens, MD MA Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Critical Care Anesthesiologist and Research Scientist Operative Care Division Portland VA Medical Center Portland, Oregon James W. Ibinson, MD PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Clinical and Translational Science Institute University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania Ryan Ivie, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Serge Jabbour, MD FACP FACE Professor of Medicine Director Division of Endocrinology, Diabetes and Metabolic Diseases Sidney Kimmel Medical College Thomas Jefferson University Philadelphia, Pennsylvania Maggie A. Jeffries, MD Anesthesiologist Avanti Anesthesia Houston, Texas Andrea M. Johnson, DO Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Brian K. Johnson, MD MEd Program Director, Anesthesiology Residency Assistant Professor Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine

Cleveland, Ohio Jordan B. Johnson, MD Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Chauncey T. Jones, MD Anesthesiology and Acute Pain Specialist Anesthesiology and Acute Pain/Regional Northwest Anesthesiology and Pain Services Houston, Texas William Scott Jones, MD Clinical Assistant Professor Department of Anesthesiology and Perioperative Medicine UPMC Children’s Hospital of Pittsburgh Pittsburgh, Pennsylvania James Jonna, MD Anesthesiologist Carle Foundation Hospital Urbana, Illinois Zeev N. Kain, MD MBA Chancellor’s Professor, Anesthesiology and Medicine Executive Director UC Irvine Center on Stress & Health Director System Redesign and Value Based Healthcare HPRI University of California at Irvine School of Medicine Orange, California Anne Elizabeth Kamarchik, MD Clinical Assistant Professor Department of Anesthesiology UPMC Children’s Hospital of Pittsburgh Pittsburgh, Pennsylvania Ihab Kamel, MD MEHP Professor of Anesthesiology Vice Chair for Education Department of Anesthesiology Lewis Katz School of Medicine Temple University Philadelphia, Pennsylvania Joelle Karlik, MD Assistant Professor in Anesthesiology and Pediatrics Department of Anesthesiology Emory University Atlanta, Georgia

Elliott Karren, MD Anesthesiology and Critical Care Medicine Specialist McKay-Dee Hospital Ogden, Utah Paul Kempen, MD PhD Staff Physician Weirton Medical Center Weirton, West Virginia Angela Kendrick, MD (Retired) Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon David Y. Kim, MD Team Health/NVA Englewood Medical Center Englewood, New Jersey Jeffrey R. Kirsch, MD FASA Professor Associate Dean for Faculty Affairs Senior Medical Director, Perioperative Services Vice Chair, Faculty Development; Anesthesiology Medical College of Wisconsin/Froedtert Hospital Milwaukee, Wisconsin John C. Klick, MD FCCP FASE FCCM Associate Professor Department of Anesthesiology and Perioperative Medicine Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania Joshua Knight, MD Clinical Assistant Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Jeffrey L. Koh, MD MBA Professor of Anesthesiology, Pediatrics, and Dentistry Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Lavinia Kolarczyk, MD Associate Professor Division Chief Cardiothoracic Anesthesiology Executive Director

Enhanced Recovery After Surgery Department of Anesthesiology University of North Carolina Chapel Hill, North Carolina Gerhardt Konig, MD Assistant Professor of Anesthesiology and Bioengineering University of Pittsburgh Pittsburgh, Pennsylvania Oran Kremen, MD Attending Anesthesiologist MedStar Medical Group Anesthesiology MedStar Washington Hospital Center Washington, DC Admire Kuchena, MD Fellow Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Matthew B. Kunkel, DO Resident Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Alexander S. Kuo, MS MD Assistant Professor Harvard Medical School Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Robert W. Kyle, DO Clinical Professor of Anesthesiology Cardiothoracic Anesthesiology Section Department of Anesthesiology UNC School of Medicine Chapel Hill, North Carolina Kirk Lalwani, MD FRCA MCR Professor of Anesthesiology and Pediatrics Vice-Chair for Faculty Development Director Pediatric Anesthesiology Fellowship Program Oregon Health & Science University Portland, Oregon Robert Scott Lang, MD Assistant Professor of Anesthesiology

Assistant Professor of Pediatrics Thomas Jefferson University Philadelphia, Pennsylvania Director, Pediatric Liver and Kidney Transplant Anesthesia Nemours/Alfred I. duPont Hospital for Children Wilmington, Delaware Maria C. Lanzi, MS MPH ANP-BC COHN-S Nurse Practitioner/Program Coordinator Employee Occupational Health Corporal Michael J. Crescenz Veterans Affairs Medical Center Philadelphia, Pennsylvania Dean Laochamroonvorapongse, MD MPH Assistant Professor Department of Anesthesiology and Perioperative Medicine OHSU Doernbecher Children’s Hospital Portland, Oregon David Larsen, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Derek S. Lauter, MD Cardiothoracic Anesthesiologist Department of Anesthesiology Christiana Care Health System Newark, Delaware Melinda M. Lawrence, MD Associate Professor Program Director, Pain Medicine Fellowship Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Christina Lee, MD Anesthesiologist Medical Anesthesia Consultants, Inc. Walnut Creek, California Christopher R. Lee, MD Clinical Assistant Professor of Anesthesiology Indiana University School of Medicine West Lafayette, Indiana Eugene Lee, MD Assistant Professor Department of Anesthesiology Duke University School of Medicine

Durham, North Carolina Lorri A. Lee, MD Anesthesiologist Kadlec Regional Medical Center Richland, Washington Tim Lee, MD Staff Anesthesiologist Department of Anesthesiology and Perioperative Medicine Kaiser Permanente - South Sacramento Sacramento, California Anne Lemak, DMD Dentist and Dental Anesthesiologist Murrysville, Pennsylvania Jay K. Levin, MD Anesthesiologist Valley Anesthesiology & Pain Consultants An Envision Physician Services Provider Phoenix, Arizona Vincent Lew, MD Assistant Professor Department of Anesthesia University of California, San Francisco San Francisco, California Albert Liao, LAc Dipl. NCCAOM Acupuncturist Liao Acupuncture Group Towson, Maryland Kristin King Liao, LAc Dipl. NCCAOM Acupuncturist Liao Acupuncture Group Towson, Maryland Grace Lim, MD MS Assistant Professor Chief of Obstetric Anesthesia Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Erica P. Lin, MD Associate Professor Department of Anesthesiology Cincinnati Children’s Hospital Medical Center University of Cincinnati College of Medicine Cincinnati, Ohio

Asa C. Lockhart, MD MBA Principal Golden Caduceus Consultants Tyler, Texas Cherie Long, MD Anesthesiologist Bend Anesthesiology Group Bend, Oregon Nathalie Lunden, MD Assistant Professor Department of Anesthesia and Perioperative Medicine Oregon Health & Science University Portland, Oregon Sara Lyons, MSN RN CNOR Senior Professional Staff Nurse Operating Room University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Lisa MacBeth, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine University of Alabama in Birmingham Birmingham, Alabama Jeff E. Mandel, MD MS Assistant Professor Department of Anesthesiology and Critical Care Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Catherine Marcucci, MD Senior Research Anesthesiologist Corporal Michael J. Crescenz Veterans Affairs Medical Center Philadelphia, Pennsylvania Julie Marshall, MD Associate Professor Department of Anesthesiology University of Missouri Columbia, Missouri Christine S. Martin, MD Assistant Professor Department of Anesthesia and Perioperative Medicine Oregon Health & Science University Portland, Oregon David P. Martin, MD PhD Professor of Anesthesiology

Mayo Clinic Rochester, Minnesota Leena Mathew, MD Director, Pain Fellowship Associate Professor Department of Anesthesiology Columbia University New York, New York Gregory Maves, MD Clinical Assistant Professor Anesthesiology & Pain Medicine Nationwide Children’s Hospital Columbus, Ohio Dustin McGirr, DO Anesthesia Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Ryan McHugh, MD Interventional Pain Management Specialist Steward Medical Group Steward Health Care Network Port Arthur, Texas Peggy P. McNaull, MD Associate Professor Departments of Anesthesiology and Pediatrics University of North Carolina Chapel, North Carolina Naveen Mehra, MD Associate Professor Department of Anesthesiology University of Texas San Antonio, Texas Vipin Mehta, MD FFARCSI Assistant Professor Department of Anesthesia, Critical Care and Pain Medicine Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Vladyslav Melnyk, MD Adult Cardiothoracic Anesthesiology Fellow Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Li Meng, MD Associate Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Pilar R. Mercado, MD Associate Professor Department of Anesthesiology University of Illinois at Chicago Chicago, Illinois Matthias J. Merkel, MD PhD Professor and Vice Chair Department of Anesthesiology and Perioperative Medicine Knight Cardiovascular Institute Oregon Health & Science University Portland, Oregon Renee A. Metal, Esquire Attorney at Law Rosen Louik & Perry, P.C. Pittsburgh, Pennsylvania David G. Metro, MD Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania Carlyann Miller, DO Fellow, Pediatric Anesthesia Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Scott D. Mist, PhD MAcOM LAc Dipl. NCCAOM Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Brian Mitchell, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Staff Anesthesiologist VA Portland Health Care System Portland, Oregon Wilhelmina Moen Boston, Massachusetts

Hassan Mohamed, MD Faculty of Medicine Cairo University Cairo, Egypt Richard C. Month, MD FASA Assistant Professor of Clinical Anesthesiology Chief Obstetrical Anesthesia Department of Anesthesiology and Critical Care Medicine Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Laurel E. Moore, MD Clinical Associate Professor Departments of Anesthesiology and Neurosurgery University of Michigan Ann Arbor, Michigan Colleen Moran, MD Assistant Professor Department of Anesthesiology Duke University Durham, North Carolina Michael J. Moritz, MD FACS Professor of Surgery Morsani College of Medicine University of South Florida Tampa, Florida Chief Transplantation Services Lehigh Valley Health Network Vice Chairman for Operations Department of Surgery Lehigh Valley Health Network Allentown, Pennsylvania Medical Director Gift of Life Donor Program Principal Investigator Transplant Pregnancy Registry International Gift of Life Institute Philadelphia, Pennsylvania Jeff Mueller, MD FASA Associate Dean for Hospital Practice Assistant Professor of Anesthesiology Mayo Clinic Phoenix, Arizona Yasuko Nagasaka, MD PhD Chair and Director

Department of Anesthesia St. Luke’s International Hospital St. Luke’s International University Tokyo, Japan Andrew Neice, MD Anesthesiologist Oregon Anesthesiology Group Portland, Oregon Wayne T. Nicholson, MD PharmD Consultant Department of Anesthesiology and Perioperative Medicine Assistant Professor of Anesthesiology and Pharmacology Mayo Clinic College of Medicine Rochester, Minnesota Adam D. Niesen, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota L. Michele Noles, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Andrew Oken, MD Staff Cardiac Anesthesiologist Good Samaritan Regional Medical Center Corvallis, Oregon David A. Olsen, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Emily Olsen, MD Pediatric Anesthesiologist Denali Anesthesia, P.C. Anchorage, Alaska Siang Ombaba, MD Anesthesiologist Hill Country Anesthesia STAR Anesthesia, P.A. San Antonio, Texas Ayodele Omolola Oke, MD Resident

Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio James C. Opton, MD Staff Anesthesiologist Salem Hospital Salem, Oregon Todd M. Oravitz, MD Associate Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Chief, Hepatobiliary Transplant Anesthesia VA Pittsburgh Healthcare System Pittsburgh, Pennsylvania Steven L. Orebaugh, MD Professor Department of Anesthesiology University of Pittsburgh Pittsburgh, Pennsylvania Sarah Oswald, MD Associate Professor Division of Pediatric Anesthesia Department of Anesthesiology University of Illinois Hospital and Health Sciences System Shriners Hospitals for Children—Chicago Chicago, Illinois Vincent Pagano, MD Anesthesiologist Kalamazoo Anesthesiology, PC Kalamazoo, Michigan Seth Palesch, MD Partner Bend Anesthesiology Group Bend, Oregon Shawn R. Palmeri, MD Resident Department of Anesthesiology University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Soon Park, MD Cardiothoracic Surgeon Rochester General Hospital Rochester, New York

Anthony N. Passannante, MD Professor and Executive Vice-Chair UNC Anesthesiology Chapel Hill, North Carolina Ishan A. Patel, MD Resident Department of Medicine Oregon Health & Science University Portland, Oregon Sephalie Patel, MD Associate Member Department of Anesthesiology Moffitt Cancer Center and Research Institute Tampa, Florida Elizabeth Pedigo, MD Assistant Professor Pediatric Anesthesiology Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Angela Pennell, MD Vice President Anesthesia Consultants of Western Colorado St Mary’s Hospital Grand Junction, Colorado Jorge Alberto Pineda Jr, MD Associate Professor Department of Anesthesia and Perioperative Medicine Oregon Health & Science University Portland, Oregon Raymond M. Planinsic, MD FASA Professor of Anesthesiology and Perioperative Medicine University of Pittsburgh School of Medicine Chief of Transplantation Anesthesiology University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Emily Poynton, DO Fellow, Critical Care Medicine Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Rene Przkora, MD PhD Associate Professor Chief, Pain Medicine

Division Program Director Multidisciplinary Pain Medicine Fellowship Assistant Program Director, Anesthesiology Residency Department of Anesthesiology College of Medicine University of Florida Gainesville, Florida Anne E. Ptaszynski, MD Anesthesiologist and Pain Medicine Specialist Pain Medicine Kenosha Medical Center Kenosha, Wisconsin Juan N. Pulido, MD Medical Director CVICU Swedish Heart and Vascular Institute Swedish Medical Center US Anesthesia Partners Seattle, Washington Jason Zhensheng Qu, MD Cardiothoracic Anesthesiologist Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts Misty A. Radosevich, MD Assistant Professor Department of Anesthesiology, Perioperative Medicine and Critical Care Mayo Clinic Rochester, Minnesota Eugene Raggi, MD Resident Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Baskar Rajala, MBBS FRCA Clinical Assistant Professor Department of Anesthesiology University of Michigan Ann Arbor, Michigan Selina Read, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania Eliot Ro, MD Assistant Professor

Department of Anesthesia and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio S. Michael Roberts, DO Assistant Professor Department of Anesthesiology and Perioperative Medicine Penn State Health Milton S. Hershey Medical Center Pennsylvania State University College of Medicine Hershey, Pennsylvania Berklee Robins, MD MA Associate Professor of Anesthesiology and Pediatrics Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Stephen T. Robinson, MD Professor and Interim Chair Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Peter Rock, MD MBA FCCM Martin Helrich Professor and Chair Department of Anesthesiology Professor of Anesthesiology, Medicine, and Surgery University of Maryland School of Medicine Baltimore, Maryland Remigio A. Roque, MD Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Dan Rosenkrans, MD ACTA & CCM Fellow Department of Anesthesiology Duke University Hospital Durham, North Carolina Richard W. Rosenquist, MD Chairman Pain Management Department Anesthesiology Institute Cleveland Clinic Cleveland, Ohio Elizabeth Ross, MD Clinical Assistant Professor Department of Anesthesiology and Pediatrics

University of North Carolina Children’s Hospital Chapel Hill, North Carolina Leelach Rothschild, MD Associate Professor of Clinical Anesthesiology Division of Pediatric Anesthesia Department of Anesthesiology University of Illinois Hospital and Health Sciences System Shriners Hospitals for Children—Chicago Chicago, Illinois James R. Rowbottom, MD Professor of Anesthesiology Anesthesiology Institute Cleveland Clinic Foundation Cleveland, Ohio Kelly Ryan, MD Congenital Cardiac Anesthesiologist Nemours/Alfred I. duPont Hospital for Children Wilmington, Delaware Tetsuro Sakai, MD PhD MHA FASA Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Ajay Sampat, MD Assistant Clinical Professor Department of Neurology University of California, Davis Sacramento, California Charles H. Sandson Student Industrial and Management Engineering ’21 Rensselaer Polytechnic Institute Troy, New York Neil B. Sandson, MD Clinical Associate Professor Department of Psychiatry University of Maryland School of Medicine Staff Psychiatrist Director of Hospital-Based Services VA Maryland Health Care System Baltimore, Maryland Shashank Saxena, MD Clinical Assistant Professor Department of Surgery/Anesthesia and Pain Medicine Lake Erie College of Osteopathic Medicine

Erie, Pennsylvania Rachel E. Schlesinger, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Staff Anesthesiologist Louis Stokes Cleveland VA Medical Center Cleveland, Ohio Peter M. Schulman, MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon F. Jacob Seagull, PhD Assistant Professor Department of Learning Health Sciences University of Michigan Medical School Ann Arbor, Michigan Katherine M. Seligman, MD Assistant Professor Department of Anesthesiology and Critical Care Medicine University of New Mexico Albuquerque, New Mexico Surjya Sen, MD Anesthesiologist and Pain Medicine Specialist Hackensack Medical Center Hackensack, New Jersey Valerie Sera, DDS MD Associate Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Jarna R. Shah, MD Resident Physician Department of Anesthesiology University of Illinois Hospital and Health Services Chicago, Illinois Kushal Shah, DO Co-Chief Department of Anesthesiology Advocate Aurora Health Care Milwaukee, Wisconsin Amit Sharma, MD

Chairman Division of Pain Medicine SpineCare Long Island Good Samaritan Hospital Medical Center West Islip, New York Ravnita Sharma, MD FRCA Senior Staff Anesthesiologist Department of Anesthesia Henry Ford Health System Detroit, Michigan Yu Shi, MD MPH Assistant Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Philip Shin, MD Chief of Pain Management Department of Anesthesiology Southern California Permanente Medical Group Harbor City, California C. Tyler Smith, MD Resident Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Kathleen A. Smith, MD Associate Professor Department of Anesthesiology University of North Carolina Chapel Hill, North Carolina Mark M. Smith, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Cobin Soelberg, MD JD MBe Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Juraj Sprung, MD PhD Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota

Christina Stachur, MD MPH Assistant Professor Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Matthew C. Stansbury, MD Department of Anesthesia University of Michigan Ann Arbor, Michigan Evan Staszewski, DO Resident Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Erica Stein, MD Associate Professor Department of Anesthesiology Wexner Medical Center The Ohio State University Columbus, Ohio Michael Stella, MD Assistant Professor Department of Anesthesiology Duke University Durham, North Carolina Marcus C. Stepaniak, CRNA MSA BSN Nurse Anesthetist Anesthesia Services Baptist Health Lexington Lexington, Kentucky Lindsay M. Stollings, MD Assistant Professor Department of Anesthesiology and Perioperative Medicine UPMC Children’s Hospital of Pittsburgh Pittsburgh, Pennsylvania Scott Streckenbach, MD Assistant Professor Department of Anesthesia and Pain Medicine Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Esther Sung, MD Assistant Professor

Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Staff Anesthesiologist VA Portland Health Care System Portland, Oregon Christopher E. Swide, MD Professor Department of Anesthesiology and Perioperative Medicine Associate Dean for Graduate Medical Education Oregon Health & Science University Portland, Oregon Joseph F. Talarico, DO Clinical Associate Professor Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Brandon Michael Togioka, MD Assistant Professor Obstetric, Fertility, and Gender Identity Anesthesia Medical Director Anesthesia and Perioperative Medicine Oregon Health & Science University Portland, Oregon Terrence L. Trentman, MD Professor and Chair Department of Anesthesiology and Perioperative Medicine Mayo Clinic Arizona Phoenix, Arizona Michelle Tully, MD Resident Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Ashley R. Valentine, MD PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Oregon Health & Science University Portland, Oregon Eleanor Anne Vega, MD Assistant Professor Department of Anesthesiology Duke University Durham, North Carolina Sandhya Vinta, MD Associate Professor

Assistant Medical Director of Operating Rooms - League City Campus Department of Anesthesiology University of Texas Medical Branch Galveston, Texas Jennifer Vookles, MD MA Anesthesiologist TeamHealth Portland Anesthesia Specialists Portland, Oregon Rachel Elisabeth Waldinger, MD MPH Clinical Instructor Department of Anesthesiology University of Illinois at Chicago Chicago, Illinois Eva J. Waller, MD Assistant Professor Department of Anesthesiology University of North Carolina Chapel Hill, North Carolina Benjamin J. Wallisch, DO FASA Associate Professor Department of Anesthesiology UT Health San Antonio San Antonio, Texas William John Wallisch IV, MD Assistant Professor Division of Critical Care Medicine Department of Anesthesiology University of Kansas Kansas City, Kansas Mark K. Wax, MD FACS FRCS(C) Professor, Otolaryngology-HNS Professor, Oral-Maxillo-Facial Surgery Program Director Director Microvascular Reconstruction Coordinator Annual Program Meeting AAO-HNSF Past President AHNS Past President OPDO University Professional Services Portland, Oregon Toby N. Weingarten, MD Professor of Anethesiology Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota

Lindsay Wetzel, MD Department of Anesthesiology and Perioperative Medicine University Hospitals Cleveland Medical Center Case Western Reserve University School of Medicine Cleveland, Ohio Francis X. Whalen, MD Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Richard Wick, MD Anesthesiologist Providence St. Mary Medical Center Walla Walla, Washington Chelsea Willie, MD Assistant Professor of Anesthesiology Division of Pediatric Anesthesia and Critical Care Medical College of Wisconsin Milwaukee, Wisconsin Bradford D. Winters, PhD MD FCCM Division Director, Critical Care Medicine Departments of Anesthesiology and Critical Care Medicine and Surgery The Johns Hopkins University School of Medicine Baltimore, Maryland Erica D. Wittwer, MD PhD Assistant Professor Department of Anesthesiology and Perioperative Medicine Mayo Clinic Rochester, Minnesota Brian Woodcock, MBChB MRCP FRCA FCCM Assistant Professor Director of Medical Student Education Department of Anesthesiology and Critical Care Medicine University of Michigan Ann Arbor, Michigan Liora Yehushua, MD Department of Anesthesiology and Perioperative Medicine University of Pittsburgh Medical Center Pittsburgh, Pennsylvania Andrew Young, MD Medical Director Providence Medford Anesthesiology Department Anesthesia Associates of Medford Medford, Oregon Angela Zimmerman, MD

Assistant Professor Department of Anesthesia and Perioperative Medicine Oregon Health & Science University Portland, Oregon Josh Zimmerman, MD FASE Professor Department of Anesthesiology University of Utah Salt Lake City, Utah Laura Patricia Zung, MD Anesthesiologist Department of Anesthesiology Cedars-Sinai Medical Center Los Angeles, California David A. Zvara, MD Professor and Chair Department of Anesthesiology The University of North Carolina at Chapel Hill Chapel Hill, North Carolina

CONTENTS Preface Foreword Acknowledgments Contributors ■ VENTILATION AND AIRWAY 1 Introduction Steven L. Orebaugh, MD 2 Basics of Airway Management (Part I)—Always Keep in Mind Complications That Can Occur With Existing Endotracheal Tubes and Tracheal Extubation Toby N. Weingarten, MD, Adam D. Niesen, MD, and Juraj Sprung, MD PhD 3 Basics of Airway Management—Part II (More Tips and Tidbits to Read on the Train) Richard Wick, MD, Catherine Marcucci, MD, and Steven L. Orebaugh, MD 4 Optimize the Airway: Bag–Mask Ventilation Steven L. Orebaugh, MD 5 Optimize the Airway: Direct Laryngoscopy Steven L. Orebaugh, MD 6 Oxygen Is a Drug Eugene Raggi, MD and David G. Metro, MD 7 Advantages and Disadvantages of the Laryngeal Mask Airway (LMA) Paul C. Anderson, MD 8 Avoiding Challenges With Video Laryngoscopy Michael Aziz, MD 9 Do Not Overinflate the Cuff of the Endotracheal Tube

Shawn R. Palmeri, MD 10 Consider the Use of Lidocaine in the Cuff of the Endotracheal Tube, but Be Aware of the Risks and Alternatives Jamey E. Eklund, MD and Paul Kempen, MD PhD 11 An Easy Intubation Does Not Guarantee an Easy Reintubation—Especially After a Carotid Endarterectomy or Cervical Spine Surgery Steven L. Orebaugh, MD, Heath Diel, MD, and Randal O. Dull, MD PhD 12 Plan for an Airway Fire With Every Head and Neck Case Julie Marshall, MD 13 There Are Special Considerations Involved With Both Intubation and Chronic Airway Management of Burn Patients Joshua Knight, MD 14 To PEEP or Not to PEEP—That Is the Question Christopher Howson, MD and Ibtesam Hilmi, MBChB FRCA 15 This Is No Time for Wishful Thinking: Always Troubleshoot an Increase in Peak Airway Pressure Adam D. Niesen, MD and Juraj Sprung, MD PhD 16 The Key to the Smooth and Skilled Placement and Use of Double-Lumen Endotracheal Tubes Is to Take It One Step at a Time Patrick J. Hackett, MD and Jay K. Levin, MD 17 Avoid Common Airway and Ventilation Errors in Morbidly Obese Patients Francis X. Whalen, MD, Toby N. Weingarten, MD, and Juraj Sprung, MD PhD 18 Anesthesia for Awake Intubations Chauncey T. Jones, MD 19 Awake Intubations–Being Able to Do Them Comfortably and Safely for the Patient Is the Benchmark for the Airway Expert Chauncey T. Jones, MD 20 Airway Management in the ICU, Including the Dreaded Leaking Cuff—How to Bring Your Best Game Margaret K. Menzel Ellis, MD and Matthias J. Merkel, MD PhD

21 Ludwig’s Angina Anne Lemak, DMD, Todd M. Oravitz, MD, and William John Wallisch IV, MD 22 Jet Ventilation—How to Adequately Handle This Exotic Ventilation Technique and Earn the Admiration of Your Spectators Peter Biro, MD DESA 23 High-Frequency Jet Ventilation—The View From Philadelphia Jeff E. Mandel, MD MS 24 Know How to Perform a Cricothyroidotomy Keith A. Chadwick, MD and Mark K. Wax, MD FACS FRCS(C) 25 Don’t Make the Mistake of Thinking That a Tracheostomy Is a Guaranteed Airway Steven L. Orebaugh, MD 26 Helium for the Compromised Airway—You Have to Understand the Principles and Properties but We’ve Seen Some Amazing Saves Anne Elizabeth Kamarchik, MD, Theresa A. Gelzinis, MD, and J. Mauricio Del Rio, MD ■ LINES AND ACCESS 27 Introduction Brian T. Gierl, MD and Catherine Marcucci, MD 28 Remember That the IV Start Is Your First Chance to Make a Favorable Impression on the Patient Christina Stachur, MD MPH, Hassan Mohamed, MD, and Catherine Marcucci, MD 29 Never Use an Intravenous Line Without Palpating and Inspecting It Visually Mark M. Smith, MD, Ryan McHugh, MD, and Juraj Sprung, MD PhD 30 Intraosseous Access Toby N. Weingarten, MD 31 Central Line Placement: Never Neglect the Basics Hassan Mohamed, MD and Brian T. Gierl, MD

32 Avoid Technique-Related Central Venous Catheter Complications by Using Modern Tools J. Saxon Gilbert, MD and Karen Hand, MB BS FRCA 33 Pulmonary Artery Catheters—Still Relevant and Still Worthy of a Cautious Approach Valerie Sera, DDS MD, Jarna R. Shah, MD, Matthew W. Caldwell, MD, and Erica D. Wittwer, MD PhD 34 Don’t Overflush Lines Julie Marshall, MD and Peter Rock, MD MBA FCCM 35 Inadvertent Intra-Arterial Injection Can Result in Severe Patient Injury David Barbara, MD, Michael Hogan, MD, Surjya Sen, MD, Toby N. Weingarten, MD, and Juraj Sprung, MD PhD 36 Do Not Use the Subclavian Vein for Central Access of Any Type in a Patient Who Is On or Planned for Dialysis Catherine Marcucci, MD and Michael J. Moritz, MD FACS 37 Consult the Surgeons Immediately if Your Patient Loses a Patent Hemodialysis Fistula—This Is a Serious Complication for the Patient Steven J. Busuttil, MD ■ FLUIDS AND RESUSCITATION 38 Introduction Brian T. Gierl, MD and Catherine Marcucci, MD 39 Crystalloid Fluids: More Than Just a Dash of Salt Sephalie Patel, MD and Brian T. Gierl, MD 40 Hypertonic Saline: Still the “Solution” to the Solution Problem? Lavinia Kolarczyk, MD, Colleen Moran, MD, and Patrick J. Forte, MD 41 Synthetic Colloid Solutions Have Distinct Properties and Risk/Benefit Ratios That Require Your Attention! Lindsay M. Stollings, MD and Raymond M. Planinsic, MD FASA 42 Do Not Use CVP to Guide Fluid Resuscitation Ryan J. Fink, MD

■ TRANSFUSION MEDICINE 43 Introduction Melissa R. George, DO 44 Know What Screening Tests Are Performed on Volunteer Donor Blood Melissa R. George, DO and Andrew M. Gross, MD 45 Red Blood Cell Primer Melissa R. George, DO 46 Type and Screen or Type and Cross-Match? Diana S. DeAndrade, MD and Michael L. Boisen, MD 47 Special Circumstances: Patients With Antibodies Melissa R. George, DO and Sprague W. Hazard III, MD 48 Plasma—It’s Not Just to Fix an Abnormal INR Melissa R. George, DO, Brian T. Gierl, MD, and Raymond G. Graber, MD 49 Plasma Part II: Is This Plasma or Pea Soup? Catherine Marcucci, MD and Melissa R. George, DO 50 Remember That the “Universal” Donor Is Different for Red Cell and Plasma Products Derek S. Lauter, MD and Brian T. Gierl, MD 51 Platelets—Often a Mystery! Gerhardt Konig, MD 52 Cryoprecipitate—The Most Misunderstood Product in the Blood Bank Melissa R. George, DO and Sprague W. Hazard III, MD 53 Washed Blood Products Are a Source of Confusion—Here’s Some Help Melissa R. George, DO and Sprague W. Hazard III, MD 54 This TEG Tracing Looks Like a Rorschach Blot … Is It Time for a Transfusapalooza? Edwin G. Avery IV, MD, Daniel Diaczok, DO, and Melissa R. George, DO 55 Transfusion Reactions Melissa R. George, DO

56 Transfusion Outcomes Melissa R. George, DO and Sprague W. Hazard III, MD 57 Directed Donation Is Generally Not a Good Idea Melissa R. George, DO 58 Not All Acute Lung Injury After a Transfusion Is Transfusion-Related Acute Lung Injury Melissa R. George, DO and Sprague W. Hazard III, MD 59 Jehovah’s Witnesses and Bloodless Medicine Melissa R. George, DO and Sprague W. Hazard III, MD 60 The Ethics of Jehovah’s Witnesses and Transfusion Rose Christopherson, MD PhD (Retired) ■ MEDICATIONS 61 Introduction Wayne T. Nicholson, MD PharmD 62 What Just Happened! What You Need to Know About Medication Errors Raymond G. Graber, MD and Chad T. Dean, MD 63 Make Sure You Understand the Complex Medical and Legal Issues Surrounding Off-Label Drug Use Cobin Soelberg, MD JD MBe and Angela Pennell, MD 64 Perioperative Beta-Blocker Therapy for High-Risk Patients Having Noncardiac Surgery—New Data, New Recommendations Esther Sung, MD and Dustin McGirr, DO 65 Should I Withhold or Continue Angiotensin Receptor Blockers in the Perioperative Period? Thomas B. Comfere, MD and Juraj Sprung, MD PhD 66 Stop Metformin Before Elective Surgery or Intravascular Contrast Dye Study to Decrease the Risk of Lactic Acidosis Immaculeta Achilike, MD MPH and Serge Jabbour, MD FACP FACE 67 Should I Administer Steroids in the Perioperative Period?

Sarah Elizabeth Dodd, MD and Toby N. Weingarten, MD 68 Beware of the Bowel Prep Wayne T. Nicholson, MD PharmD and James C. Opton, MD 69 What Drugs Require Slow Administration? Maggie A. Jeffries, MD, Laurel E. Moore, MD, and Catherine Marcucci, MD 70 Ketamine—Use It Well Catherine Marcucci, MD 71 TIVA—What You Need to Understand to Do It Well Jeff E. Mandel, MD MS 72 Dexmedetomidine: Is There Such a Thing as a Free Lunch? Martin Anixter, MD and Tetsuro Sakai, MD PhD MHA FASA 73 Consider Chloroprocaine in Emergency Situations—It Is a Rapid-Onset Local Anesthetic With Low Systemic Toxicity Brandon Michael Togioka, MD, Josh Zimmerman, MD FASE, and Randal O. Dull, MD PhD 74 Use Bicarbonate as a Buffer to Local Anesthetics—Especially for Skin Infiltration Vladyslav Melnyk, MD, Hooman Rastegar Fassaei, MD, and Steven L. Orebaugh, MD 75 The Hows, Whys, Ins, and Outs of Succinylcholine or Succinylcholine—Still a Useful Anesthesia Adjunct Christopher R. Lee, MD and Edwin G. Avery IV, MD 76 Don’t Get Burned by Incomplete Reversal of Neuromuscular Blockade Christina Stachur, MD MPH, Matthew B. Kunkel, DO, Lindsay Wetzel, MD, and Raymond G. Graber, MD 77 Opioid Conversions—It’s Not Only About the Table Melinda M. Lawrence, MD 78 Not All Patients Are Naive—Management of Perioperative Pain in OpioidDependent Patients Melinda M. Lawrence, MD

79 The Basal Infusion Mode in Patient-Controlled Analgesia Is Both Friend and Foe Amit Sharma, MD 80 Keep Discussing the Use of Ketorolac (Toradol) With Your Surgical Team Before the Need Arises and Keep Your Eye on the Literature Catherine Marcucci, MD, Amit Sharma, MD, and Wayne T. Nicholson, MD PharmD 81 Special Topic I: Do Patient With Congenital Insensitivity to Pain Need Anesthetics and Postoperative Opioids? Katarina Bojanic´, MD PhD, Toby N. Weingarten, MD, and Juraj Sprung, MD PhD 82 Special Topic II: Can Your Patients Eat Their Way Out of Chronic Pain? Some Common Sense Advice Ashley R. Valentine, MD PhD 83 Attacking Acute Perioperative Hypertension— The Cleveland Group Shares Their Battle Plan Edwin G. Avery IV, MD, Matthew B. Kunkel, DO, and Brian K. Johnson, MD MEd 84 Cardiovascular Vasoactive Drugs That Pump You Up Brian K. Johnson, MD MEd, Matthew B. Kunkel, DO, and Edwin G. Avery IV, MD 85 Milrinone—The Not-So-Kidney-Friendly Intraaortic Balloon Pump in a Bottle James Jonna, MD and Edwin G. Avery IV, MD 86 Amiodarone and Alternative Antiarrhythmics— Double-Edge Swords for the Treatment of Atrial and Ventricular Fibrillation Muhammad Durrani, MD, Alan Cheng, MD, and Edwin G. Avery IV, MD 87 Ondansetron Is a Great Drug, We ALL Use It, But Watch for Headache and QT Prolongation Catherine Marcucci, MD and Michael J. Moritz, MD FACS 88 A Word About Haloperidol in the Perioperative Period Neil B. Sandson, MD

89 Remember That Not All Blue-Colored Compounds Are the Same Wayne T. Nicholson, MD PharmD and Chauncey T. Jones, MD 90 Clonidine Considerations Shashank Saxena, MD and Catherine Marcucci, MD 91 A Primer on the Psych Syndromes: Serotonin Syndrome Versus Neuroleptic Malignant Syndrome Elizabeth Herzog, MD, Neil B. Sandson, MD, Brian T. Gierl, MD, and Catherine Marcucci, MD 92 Drug-Drug Interactions Are Now Necessary Knowledge for the Anesthesia Provider and We Can Help Neil B. Sandson, MD and Catherine Marcucci, MD 93 The Six Patterns of Cytochrome P450 Drug-Drug Interactions Relevant to the Perioperative Clinician Catherine Marcucci, MD and Neil B. Sandson, MD 94 Don’t Spend Time Rereading Tom Clancy Novels Until You Have Mastered These Basic Drug-Drug Interactions Catherine Marcucci, MD, Randal O. Dull, MD PhD, Laura A. Donegan, MD FACP, and Neil B. Sandson, MD 95 Drug-Drug Interactions and the P-glycoprotein Pump—Be Vigilant With Patients on Digoxin Catherine Marcucci, MD, Erica D. Wittwer, MD PhD, and Neil B. Sandson, MD 96 Can You Name Six Perioperative Drug-Drug Interactions That Involve Oral Contraceptives? Okay, You Can Now! Catherine Marcucci, MD and Neil B. Sandson, MD 97 Wish We Knew Then What We Know Now— A Case of Serotonin Syndrome in the Operating Room Katarina Bojanic´, MD PhD, Juraj Sprung, MD PhD, and Toby N. Weingarten, MD ■ EQUIPMENT 98 Introduction Brian Mitchell, MD

99 Pulse Oximetry: Perhaps You Need a Refresher? Jorge Alberto Pineda Jr, MD and Stephen T. Robinson, MD 100 The End-Tidal CO2 Monitor Is More Than Just a Device to Tell You That “the Tube in the Airway” Brian Woodcock, MBChB MRCP FRCA FCCM 101 Noninvasive Blood Pressure Management— It’s Not Just a Piece of Nylon Around the Arm Jorge Alberto Pineda Jr, MD and Stephen T. Robinson, MD 102 Avoid Errors in Invasive Blood Pressure Measurement David Barbara, MD, Michael Hogan, MD, Toby N. Weingarten, MD, and Juraj Sprung, MD PhD 103 How, Why, and When to Use Brain Function Monitors Izumi Harukuni, MD 104 Do Not Improvise Techniques to Warm Patients—Use Warming Devices Only as Per Manufacturers’ Recommendations Jeff Mueller, MD FASA 105 Transesophageal Echocardiography: Contraindications, Complications, and Misinterpretations Andrew Young, MD and Andrew Oken, MD 106 Scavenging Waste Gases Is Perhaps the Only Action We Take That Benefits Us but Not the Patient Terrence L. Trentman, MD 107 Carbon Dioxide Absorbers Save Gas and Moisture but Create the Potential for Mechanical Hazards, Chemical Soup, or a Thermal Disaster Michael S. Axley, MS MD and Stephen T. Robinson, MD 108 Infusion Pumps: Get Them Going and Keep Them Going! Richard Botney, MD and Stephen T. Robinson, MD 109 Don’t Bring the Fiberoptic Scope Into the MRI Scanner! Andrew Young, MD and Brian Mitchell, MD 110 Understanding the Operating Room Circuit and the Line Isolation Monitor—

It’s Really Pretty Simple Richard Botney, MD and Jeffrey D. Dillon, MD 111 Cell Phones in the Operating Room—Here Are the Issues R. Scott Herd, MD and Juraj Sprung, MD PhD 112 Don’t Let the Tourniquet Cause Extra Pain or Complications Byron Fergerson, MD, Randal O. Dull, MD PhD, and Brian Mitchell, MD ■ PERIOPERATIVE 113 Introduction Ryan J. Fink, MD 114 Hurdles of the Electronic Health Record Ishan A. Patel, MD and Jeffrey A. Gold, MD 115 Hand Hygiene! History, Human Factors, and Helping Your Patients Harriet W. Hopf, MD, James W. Ibinson, MD PhD, and David G. Metro, MD 116 Remember That the Same Simple Mistakes at Induction (and Emergence) Happen Over and Over Again! Brandon Dial, MD and Randal O. Dull, MD PhD 117 Smoking Cessation Part I—ANYTIME Is a Good Time to Quit Yu Shi, MD MPH 118 Smoking Cessation Part 2—So Good for the Patient as Long as You Understand the Effects on CYP1A2 Drug Metabolism (Especially RWarfarin) Catherine Marcucci, MD, Brian T. Gierl, MD, and Neil B. Sandson, MD 119 Flying to the Mayo Clinic for Surgery? The Clot Thickens Misty A. Radosevich, MD, Abram H. Burgher, MD, and Juraj Sprung, MD PhD 120 Don’t Let Your Understanding of the Utility of Preoperative Stress Testing in Suspected Heart Disease Lapse Matthew DeCaro, MD 121 A Positive Troponin Does Not Always Mean a Myocardial Infarction—Will the New High-Sensitive Assays Help Sort It Out?

Michael P. Hutchens, MD MA, Bradford D. Winters, PhD MD FCCM, and Catherine Marcucci, MD 122 Preoperative Anxiolysis: It’s Not Just “Two of Midaz” Michael P. Hutchens, MD MA and Ryan J. Fink, MD 123 Schizophrenia Is a Devastating Mental and Medical Illness—and These Patients Have Significantly Greater Perioperative Risks Than Age-Matched Controls Catherine Marcucci, MD and Neil B. Sandson, MD 124 What to Do About the Tattoos and Body Jewelry Chidi Ani, MD and Andrew Neice, MD 125 We Now Know That Obstructive Sleep Apnea Is More Common Than We Thought—Manage These Patients Carefully and Conservatively Daniela Damian, MD and Ibtesam Hilmi, MBChB FRCA 126 Don’t be Shy About Borrowing ICU Equipment, Medications, and Personnel for the Critically Ill Patient Going to the Operating Room Elliott Karren, MD and Matthew Griffee, MD 127 The Dao of Positioning Raymond G. Graber, MD, Selina Read, MD, and Catherine Marcucci, MD 128 The Supine Position—Complications Can Still Arise! Kristin Bowden, CRNA DNAP MBA and Richard Botney, MD 129 Thinking Laterally—How to Safely Position a Patient in the “Sideways” Position for Surgery Gregory Applegate, DO, Carlyann Miller, DO, and Raymond G. Graber, MD 130 Positioning Patients for Spine Surgery Ihab Kamel, MD MEHP, David Y. Kim, MD, and Rodger E. Barnette, MD FCCM 131 Sit Back and Relax? Implications of the Sitting Position in Shoulder and Brain Surgery Evan Staszewski, DO and Michael D. Altose, MD PhD 132 Individuals With Cerebral Palsy and Other Spastic Disorders Need Your Best Positioning Prowess

Brandon Michael Togioka, MD, Benjamin C. Conner, MSc MD/PhD3, and Carol Bodenheimer, MD 133 Use Extra Care in Positioning Patients Who Have Had Amputations Carol Bodenheimer, MD and Catherine Marcucci, MD 134 Never, Ever Fire C. Tyler Smith, MD and Brian T. Gierl, MD 135 Malignant Hyperthermia: If You Get to the Point Where You See an Elevated Temperature, It’s Already Happening James C. Opton, MD 136 Good Old-Fashioned Basic Perioperative Blood Pressure Control Edwin G. Avery IV, MD and Brian K. Johnson, MD MEd 137 Some Additional Thoughts on Blood Pressure Management Techniques— What We Believe, How We Do It, and Where We Think the Science Is Going Edwin G. Avery IV, MD and Brian K. Johnson, MD MEd 138 Protect the Kidneys, Not the “UOP” Michael P. Hutchens, MD MA 139 Avoid a 70% Mortality Rate: Do Everything You Can to Prevent Perioperative Renal Failure Michael P. Hutchens, MD MA 140 Do Not Use Urine Output as an Indicator of Volume Status in Hypothermic Patients Juan N. Pulido, MD and Daniel R. Brown, MD PhD FCCM 141 Perioperative Hyperglycemia Is Associated With Poorer Clinical Outcomes so Consider Insulin Therapy for Both Diabetic and Nondiabetic Patients With Elevated Blood Glucose Tim Lee, MD 142 Seven Ways to Treat Hyperkalemia in the Perioperative Period Grace Chen, MD 143 Laparoscopic Procedures: Managing the Risks and Physiologic Effects

During Camera Placement, CO2 Insufflation, and Vertical Positioning Benjarat Changyaleket, MD, Jennifer A. DeCou, MD, and Randal O. Dull, MD PhD 144 Could This Be Methemoglobinemia, Maybe? Leena Mathew, MD, Philip Shin, MD, and Walter Chang, MD 145 The Eye Room—Is It the Easiest of Days? Or the Hardest of Days? Regardless, Vigilance Is Key! David Larsen, MD and Ryan J. Fink, MD 146 My Eye Hurts! Prevention, Diagnosis, and Treatment of Corneal Injuries After Anesthesia Raymond G. Graber, MD and David P. Martin, MD PhD 147 Never Forget That Patient Transport Within the Hospital Is One of the Most Dangerous Intervals in the Perioperative Period O. Layton Alldredge Jr, MD MS and Ansgar M. Brambrink, MD PhD 148 Seek Out Hypercapnia in the PACU and Remember That an Acceptable Pulse Oximeter Reading Is Not Assurance of Adequate Ventilation Michael P. Hutchens, MD MA 149 Let’s Go Over It Again: Avoid Residual Neuromuscular Blockade in the PACU! Eleanor Anne Vega, MD and Ryan J. Fink, MD 150 Give the Intensivist the Best Handover to Improve Patient Outcomes Andrew Young, MD and Matthias J. Merkel, MD PhD 151 Don’t Miss Out on Ultrasound—Which ICU Techniques Are Helpful for the Anesthesiologist? Margaret K. Menzel Ellis, MD and Peter M. Schulman, MD 152 Don’t Overlook the Potential of Perioperative Acupuncture Scott D. Mist, PhD MAcOM LAc Dipl. NCCAOM, Kristin King Liao, LAc Dipl. NCCAOM, Albert Liao, LAc Dipl. NCCAOM, and Catherine Marcucci, MD 153 Consider Acupuncture as an Adjunct for the Prophylaxis and Treatment of Postoperative Nausea and Vomiting

Scott D. Mist, PhD MAcOM LAc Dipl. NCCAOM, Kristin King Liao, LAc Dipl. NCCAOM, Albert Liao, LAc Dipl. NCCAOM, and Leena Mathew, MD 154 Don’t Warm Up a Cardiac Arrest Patient Unless They Are Dying of Hemorrhage! Admire Kuchena, MD and Michael P. Hutchens, MD MA 155 What to Do If You Get a Needlestick Injury Maria C. Lanzi, MS MPH ANP-BC COHN-S and Sarah Foster-Chang, DNP APN-BC COHN-S ■ REGIONAL ANESTHESIA 156 Introduction Raymond G. Graber, MD 157 Complications of Regional Anesthesia: Don’t Touch the Needle Before You Know Them David A. Burns, MD, Brian T. Gierl, MD, and Raymond G. Graber, MD 158 Make Time for a Timeout Before Placing a Block—the Preprocedure Check Mark J. Baskerville, MD JD MBA MA and Jeffrey R. Kirsch, MD FASA 159 Chlorhexidine: Killing Bacteria … and Allergic Patients? Levana Amrock, MD and Brandon Michael Togioka, MD 160 What Is the Correct Brachial Plexus Block to Perform? Nathalie Lunden, MD and Raymond G. Graber, MD 161 Getting the Right Ultrasound Image Ryan Ivie, MD 162 Interscalene Blocks—Preventing the Blues! Raymond G. Graber, MD and Lindsay Wetzel, MD 163 The Old-Fashioned “Bier” Block Is Still Relevant—The Trick Is to Not Let the Surgeons Get Ahead of You Raymond G. Graber, MD, Michael Barts, CRNA APRN BS Anesthesiology, and Surjya Sen, MD 164 Remember the Low-Risk/High-Yield Blocks

Raymond G. Graber, MD and Jennifer Vookles, MD MA 165 Preparing to Fail: The Dynamics of a Failed Block Joelle Karlik, MD and Andrew Neice, MD 166 Salvage Techniques for Incomplete Upper-Extremity Blocks Joelle Karlik, MD and Andrew Neice, MD 167 Salvage Blocks for Incomplete Lower Extremity Blocks Joelle Karlik, MD and Andrew Neice, MD 168 More Than a Stick and a Burn: Local Anesthetic Systemic Toxicity Charles Jeremy Bengson, MD and Brandon Michael Togioka, MD 169 Lipid Rescue—Where Are We Now? Ayodele Omolola Oke, MD, Katya H. Chiong, MD FASA, and Raymond G. Graber, MD 170 A Patient Who Is Planned for Spinal Anesthesia Asks “Can This Paralyze Me?” What Are the Facts and What Do You Say? Raymond G. Graber, MD 171 Spinals in the Lateral Position Liora Yehushua, MD and Catherine Marcucci, MD 172 Consider the Paramedian Approach for Spinal Anesthesia in the Hip Fracture Patient Raymond G. Graber, MD and Emily Poynton, DO 173 When Is a Whisper a Cry for Help? When the Patient Has a High Block Ryan J. Bortolon, MD and Juraj Sprung, MD PhD 174 Issues Related to Discharging the Postspinal Patient Christopher E. Howson, MD and Li Meng, MD 175 Epidural or Truncal Block? Sorting It Out Kareem Aggour, MD 176 Dang It! Wet Tap Brandon Michael Togioka, MD and Robert Gaiser, MD 177 Consider Continuous Paravertebral Block as Your Primary Analgesic

Technique Bruce Ben-David, MD and Brian T. Gierl, MD 178 Pneumothorax After Paravertebral, Supraclavicular, or Interscalene Block Nathalie Lunden, MD 179 Epidural Anesthesia for Mastectomy Jennifer Vookles, MD MA 180 What Is the Right Level for Postoperative Epidural Catheter Insertions Based on Type of Surgery? Joelle Karlik, MD and Andrew Neice, MD 181 Know the Complications of Epidural Corticosteroid Injections David A. Olsen, MD, Anne E. Ptaszynski, MD, and Toby N. Weingarten, MD 182 If You Are New to Neuraxial and Peripheral Nerve Block Infusions—a View From Both Academia and Private Practice Jordan B. Johnson, MD 183 What to Do With a Prolonged Block Zheyan (Jenny) Chen, MD and Ryan Ivie, MD 184 Regional Anesthesia in the ICU—What Should We Use and When Should We Use It? Benjamin L. Antonio, DO MBA ■ PEDIATRIC ANESTHESIA 185 Introduction Kirk Lalwani, MD FRCA MCR 186 Assent, Consent, and Refusal: Informed Consent and Decision-Making for Adult and Pediatric Patients Berklee Robins, MD MA 187 NPO Guidelines Made Easy—Always Maintain a Firm Hold on Current Principles, Best Practices, and Your Own Common Sense Gregory Maves, MD and Elizabeth Ross, MD 188 Aspiration and Food Injury—Or When Not to Extubate Deep

Marion Bussay, MD and Leelach Rothschild, MD 189 Don’t Underestimate the Power of Distraction During Separation and Induction of Anesthesia in Kids Emily Olsen, MD and Jorge Alberto Pineda Jr, MD 190 Parental Presence on Induction—It’s Your Call and How to Do It Nicole Conrad, MD and Kimberly Blasius, MD 191 The Child With a URI Ann Bailey, MD FAAP 192 Accept That You Will Have to Meet the Clinical Challenges of Obesity and Obstructive Sleep Apnea in Your Pediatric Patient Cohort Natalie R. Barnett, MD and Katharina Beckmann, MD 193 Neuromuscular Disease in Kids Can Be Very Challenging Because You Don’t Always Have a Definitive Diagnosis—Here’s How to Approach the Clinical Situations Anila B. Elliott, MD and Dean Laochamroonvorapongse, MD MPH 194 Pediatric Patients With Epilepsy: Considerations for Patients on a Ketogenic Diet and for Cortical Mapping Raquel G. Hernandez, DO and Heike Gries, MD PhD 195 Neonates Deserve Perioperative Analgesia, Too Raquel G. Hernandez, DO and Angela Kendrick, MD (Retired) 196 Anesthetic Considerations in Patients With Fontan Physiology Who Present for Noncardiac Surgery Kelly Ryan, MD and Angela Zimmerman, MD 197 Anesthesia for Kids and Neurotoxicity: You Are Going to Be Asked, So Don’t Be Surprised and Don’t Act Uninformed Emily Olsen, MD, and Ansgar M. Brambrink, MD PhD 198 Double Down on Pediatric Airway Equipment Eugene Lee, MD 199 Optimizing Bag Mask Ventilation and Direct Laryngoscopy in Children William Scott Jones, MD and Robert Scott Lang, MD

200 Why You Should Expect Hypoxemia During Induction and Emergence of the Pediatric Patient and What to Do About It Andrea M. Johnson, DO, Kirk Lalwani, MD FRCA MCR, and Michael Stella, MD 201 Why Air Bubbles and Air Emboli Can Be So Serious in Pediatric Patients and How to Safeguard Your Patients Erica P. Lin, MD 202 Pediatric Fluid Management Linda Chung, MD and Pilar R. Mercado, MD 203 Keeping Babies Warm in the Perioperative Period Is Important, Challenging, and at Times Dangerous! Kathleen A. Smith, MD and Daniel Rosenkrans, MD 204 Pediatric Arterial Access—And the Beat Goes On Rebecca Hall, MD, Kirk Lalwani, MD FRCA MCR, and Angela Kendrick, MD (Retired) 205 Pediatric Regional Anesthesia—The Karma of Caudals Eva J. Waller, MD and Elizabeth Ross, MD 206 Avoiding the One-Hour Wake Up or How to Save the Sanity of the Parents and Your Own Reputation at the Same Time Rachel Elisabeth Waldinger, MD MPH and Sarah Oswald, MD 207 When Not to Extubate Deep! And if the Patient Is Already Coughing or Swallowing, It’s Too Late Anyway Marion Bussay, MD and Leelach Rothschild, MD 208 Emergence Delirium—Don’t Overcall It, Don’t Undercall It, and Don’t Let It Happen Chelsea Willie, MD and Kimberly Blasius, MD 209 Too Much, Too Little, Just Right: Avoiding Opioid Withdrawal in Pediatric Patients on Chronic Opioids Jeffrey L. Koh, MD MBA and Elizabeth Pedigo, MD 210 Careful and Conservative Clinical Judgment Is Required Before Discharging a Pediatric Patient to Home

Peggy P. McNaull, MD and Eva J. Waller, MD 211 Chronic Pediatric Pain: There’s Always More Than Enough Pain for Everybody Involved and It’s Not About the Blocks! Elizabeth Pedigo, MD, Jorge Alberto Pineda Jr, MD, and Jeffrey L. Koh, MD MBA 212 “But, It’s Just an Herb!” Avoiding Problems Resulting From Nontraditional Pain Medications in the Pediatric Population Cherie Long, MD and Jeffrey L. Koh, MD MBA 213 Okay, There Are Herbals, but What About Those “Other Herbals?” Cherie Long, MD and Jeffrey L. Koh, MD MBA 214 Pitfalls in Pediatric Sedation Siang Ombaba, MD and Pilar R. Mercado, MD 215 Pitfalls of Pediatric Anesthesia for International Service Missions Christine S. Martin, MD and Berklee Robins, MD MA 216 Pediatric Cardiac Arrest Under Anesthesia—Predicting and Preventing the Most Devastating Event of All Kirk Lalwani, MD FRCA MCR ■ NEUROANESTHESIA 217 Introduction Laurel E. Moore, MD 218 The Neurophysiology You Learned in Medical School Is Always Relevant— Get a Grip on It and Don’t Let Go Laura Patricia Zung, MD and Laurel E. Moore, MD 219 Cerebral Aneurysm Versus “Routine” Craniotomy—The Anesthetic Goals Are Not the Same James DeMeester, MD and Brian T. Gierl, MD 220 Perioperative Visual Loss Is One of the Most Feared and Devastating Complications of Spine Surgery Ajay Sampat, MD and Laurel E. Moore, MD

221 Being Maximally Prepared for Minimally Invasive Pituitary Surgery Rashad Albeiruti, MD 222 Evoked Potentials: Don’t Approach the Surgeon or Neurophysiologist Until You Know These Principles Anthony N. Passannante, MD and Laurel E. Moore, MD 223 Awake Craniotomy Ravnita Sharma, MD FRCA and Laurel E. Moore, MD 224 Anesthesia for the Pregnant Patient With Neurosurgical Disorder: These Cases Actually Do Happen in Real Life ….. and on the Oral Boards Vincent Pagano, MD and Baskar Rajala, MBBS FRCA 225 Don’t Forget There’s No Such Thing as a Brain Transplant: Preventing Perioperative Stroke Matthew C. Stansbury, MD and Laurel E. Moore, MD 226 Anesthesia for Emergent Neurointerventional Procedures: “Neurology Just Called, They Have a Stroke Patient for Thrombectomy Down in Neuroradiology, Start Time is 2 AM” Laurel E. Moore, MD 227 Encephalopathy and Intracranial Hypertension in the Acute Liver Failure Patient Are Not the Same Thing! Pavan K. Battu, MBBS DA FRCA and Laurel E. Moore, MD ■ CARDIAC ANESTHESIA 228 Introduction Edwin G. Avery IV, MD 229 Cardiac Surgical Coagulopathy—You’ll Need the Blood Bank and a Genie in a Bottle Edwin G. Avery IV, MD and James R. Rowbottom, MD 230 A Is for Aortic, C Is for Cannulation, B Is for … Be Careful! Alexander S. Kuo, MS MD and Jason Zhensheng Qu, MD 231 Transesophageal Echocardiography in the Cardiac Surgery Suite— Strategies to Stay Out of Trouble

Robert W. Kyle, DO 232 Myocardial Protection Strategies During Cardiopulmonary Bypass—Do Everything You Can but Realize That Some Ischemic Damage Is Inevitable S. Michael Roberts, DO, Theodore J. Cios, MD MPH, and Dmitri Guvakov, MD 233 The Heartbreak of Left-Sided Valvular Dysfunction Jafer Ali, MD and Oran Kremen, MD 234 Anesthesia for the Descending Thoracic Aorta—Initiate Damage Control Measures Eliot Ro, MD and Edwin G. Avery IV, MD 235 Buckle Your Seat Belt: Taking Care of the Patient With Ascending Aortic Dissection Rachel E. Schlesinger, MD and Kathleen Cho, MD 236 Rolling in the Deep Hypothermic Circulatory Arrest Michael G. Fitzsimons, MD and Etienne J. Couture, MD FRCPC 237 Anesthesia for Left Ventricular Assist Device Surgery: Essentials to Bear in Mind Raymond G. Graber, MD and Daniel I. Asher, MD 238 Off-Pump Coronary Artery Grafting Is Like Working on an Engine (While It Is Still Running) Yasuko Nagasaka, MD PhD and Vipin Mehta, MD FFARCSI 239 What to Do and What Not to Do for Your Patients With Hypertrophic Obstructive Cardiomyopathy John C. Klick, MD FCCP FASE FCCM and Kushal Shah, DO 240 Cardiac Transplant—Gotta Get This One Right Edwin G. Avery IV, MD, Soon Park, MD, and Scott Streckenbach, MD 241 The Right Heart Should Never Play Second Fiddle to the Left Heart—What to Do When the Right Heart Just Really Ain’t Right at All Lindsay Wetzel, MD, Faisal D. Arain, MBBS MD, Daniel I. Asher, MD, and Edwin G. Avery, MD ■ OBSTETRIC ANESTHESIA

242 Introduction Christopher E. Swide, MD 243 Be Prepared for the Presence of a Doula in Both the Labor and Delivery Rooms Christopher E. Swide, MD 244 Guests on the Labor Deck and in the Delivery Room—How to Manage It and Keep Your Professional Demeanor Christopher E. Swide, MD 245 Alternatives to Epidural Analgesia for Labor Pain—What to Consider, What You Might Be Asked Karen Hand, MB BS FRCA 246 Epidural Labor Analgesia: Does It Prolong Labor? Remigio A. Roque, MD and Brandon Michael Togioka, MD 247 We Were Taught Once a C-section, Always a C-Section … What to Do When Your Hospital Now Wants to Provide Trial of Labor After Cesarean (TOLAC) Services Jordan B. Johnson, MD and James S. Hicks, MD MMM 248 Should We Place a Spinal for a Version? Anesthesia for External Cephalic Version Angela Pennell, MD and Brandon Michael Togioka, MD 249 Management of an Accidental Dural Puncture in the Laboring Patient “When the Hanging Drop Becomes a Flowing River …” Dustin McGirr, DO 250 “We Have an Urgent C-Section!” The Pitfalls of Intrapartum Monitoring of the Fetus Richard C. Month, MD FASA 251 Stat C-Section—The 30-Minute Rule and Beyond Karen Hand, MB BS FRCA and Christopher E. Swide, MD 252 Postpartum Hemorrhage: Don’t Forget That Having a Baby Is Major Surgery Alexander Y. Fu, MD and Brandon Michael Togioka, MD

253 From Glad to Sad (Part 1): Pain Control After Cesarean Section Michael Carrigan, MD and Brandon Michael Togioka, MD 254 From Glad to Sad (Part 2): Postpartum Neuropathy of the Lower Extremity Seth Palesch, MD and Brandon Togioka, MD 255 Obstetric Anesthesia/Analgesia Can Work in a Small Hospital: The Key Principles Are Commitment, Flexibility, and Planning James S. Hicks, MD MMM and Jordan Johnson, MD 256 Resuscitation of the Pregnant Cardiopulmonary Arrest Patient: Not Just Standard ACLS L. Michele Noles, MD 257 The Pregnant Anesthesia Provider (Part 1)—Managing the Occupational Exposures Michelle Tully, MD and Emily J. Baird, MD PhD 258 The Pregnant Anesthesia Provider (and New Adoptive Parent)—Part 2 Elliza M. Chen, MD and Colleen Moran, MD ■ HUMAN FACTORS 259 Introduction Brian T. Gierl, MD and Catherine Marcucci, MD 260 Understanding the Human Factor F. Jacob Seagull, PhD 261 Minimize Errors in Anesthesia: Lessons Learned From Aviation Stephen J. Gleich, MD and Juraj Sprung, MD PhD 262 Eliminate Communication Errors by Using a Spelling Alphabet and Spoken Digits Michael Carrigan, MD, Brian T. Gierl, MD, and Catherine Marcucci, MD 263 Don’t Ignore Your Intuition F. Jacob Seagull, PhD and Catherine Marcucci, MD 264 Ethics in Anesthesiology Practice Harriet W. Hopf, MD

265 Know When to Stop—Anesthesia Providers Have Got to Know Their Limitations Brian T. Gierl, MD, F. Jacob Seagull, PhD, and Catherine Marcucci, MD 266 Before You Press Play, Let’s Talk About Music in the OR Lisa MacBeth, MD, Toby N. Weingarten, MD, and Juraj Sprung, MD PhD 267 Never Rush Through a Signout John T. Bryant IV, MD and Ryan J. Fink, MD 268 Don’t Ignore the Folklore—It Can Be a Powerful Ally in Your Clinical Practice Raymond G. Graber, MD, F. Jacob Seagull, PhD, and Catherine Marcucci, MD 269 Don’t Underestimate the Role of Spirituality in Patients’ Perceptions of Disease and Healing, and Remember to Uphold the Right to SelfDetermination Christina Lee, MD and Grace Lim, MD MS 270 What’s in a Name? Charles H. Sandson and F. Jacob Seagull, PhD 271 We Are Not the Only People Who Care About the Patients Brian T. Gierl, MD, Sara Lyons, MSN RN CNOR, and F. Jacob Seagull, PhD 272 Working in the OR—Sometimes the Staff Gets Sick or Injured, Too Raymond G. Graber, MD 273 The Physician as Patient—What I Learned During the Last Five Times I Went to the OR on the Stretcher Instead of Pushing It Catherine Marcucci, MD 274 A Primer on Simulation in Anesthesiology— Definitions and Concepts Brian T. Gierl, MD, F. Jacob Seagull, PhD, and Jeffrey R. Kirsch, MD FASA 275 What Makes a Great Anesthesia Resident? Staci Allen, DO and Raymond G. Graber, MD ■ LEGAL 276 Introduction

Cobin Soelberg, MD JD MBe 277 A Brief on the Legal Process Abiona Berkeley, MD JD, Daniel L. Glennon, JD MA, Wilhelmina Moen, and Vincent S. Cowell, MD FAACD 278 How “Not” to End Up in a Closed Claims File—Lessons Learned From the ASA Closed Claims Project Lorri A. Lee, MD and Karen B. Domino, MD MPH 279 The Anesthesia Closed Claims Project— What’s Trending Now? Cobin Soelberg, MD JD MBe and Catherine Marcucci, MD 280 A Careful and Complete Anesthesia Record Is the Best Defense Against a Lawsuit Joseph F. Talarico, DO, David G. Metro, MD, and Renee A. Metal, Esquire 281 Documentation Disputes in the Medical Record—How to Avoid a Chart War and How to Survive One Cobin Soelberg, MD JD MBe, Catherine Marcucci, MD, and Jeffrey R. Kirsch, MD FASA 282 Reading in the Operating Room: Is It Worth the Risk? Michael S. Axley, MS MD 283 Going to the Operating Room With a Do-Not-Resuscitate Patient Kirk Lalwani, MD FRCA MCR and Vincent Lew, MD 284 Refusal to Do a Case on Moral or Ethical Grounds: More Practical Navigation Through Choppy Waters Kenneth R. Abbey, MD JD and Marcus C. Stepaniak, CRNA MSA BSN 285 Dental Injuries—Document Carefully and Do Not Overpromise Douglas W. Anderson, DMD (Retired) and Kenneth R. Abbey, MD JD 286 Apologizing to Patients After an Adverse Event Is the Ethical Thing to Do and Just Might Keep You Out of Court Cobin Soelberg, MD JD MBe* and Katherine M. Seligman, MD ■ PROFESSIONAL PRACTICE

287 Introduction Amr E. Abouleish, MD MBA 288 Marketing 101: Know Your Customers and What They Need! Stacey L. Gibbons, MD and Amr E. Abouleish, MD MBA 289 Improving OR Throughput: Don’t Say “No” Sandhya Vinta, MD and Amr E. Abouleish, MD MBA 290 Cost Analysis: You Always Want to Be at the Table Rene Przkora, MD PhD and Amr E. Abouleish, MD MBA 291 Strategic Planning: Failing to Prepare Is Preparing to Fail Naveen Mehra, MD and Asa C. Lockhart, MD MBA 292 Business Plan 101: Where You Want to Go and How You Are Going to Get There Benjamin J. Wallisch, DO FASA and Asa C. Lockhart, MD MBA 293 Avoid Being Labeled “Simply a Gas-Passer”: An Overview of the Perioperative Surgical Home Navid Alem, MD, Maxime Cannesson, MD PhD, Fiyinfoluwa Ani, MD MBA, and Zeev N. Kain, MD MBA 294 The Curriculum Vitae: Know Your Audience Antolin S. Flores, MD 295 Your Career: Interviewing Antolin S. Flores, MD 296 Your Career: Understanding the Basics of Ownership Jobs Erica Stein, MD 297 Your Career: Employee Jobs Erica Stein, MD 298 Your Career: Understanding the Basics of Locum Tenens Jobs Erica Stein, MD 299 Your Career—Understanding Solo Practice and the Basics of Medical Practice Finance and Legal Organization Norman A. Cohen, MD

300 Your Career: Make Sure You Understand the Compliance Plan Norman A. Cohen, MD 301 Your Career—Know the Risk-Management Strategies of the Practice Norman A. Cohen, MD 302 Avoiding Bad Employment Contracts: Due Diligence, Termination, and Restrictive Covenants Mark J. Baskerville, MD JD MBA MA 303 Avoiding Bad Employment Contracts: Duties, Compensation, and Benefits Mark J. Baskerville, MD JD MBA MA 304 MACRA—Robbing Peter to Pay Val (ue) Brian T. Gierl, MD and Philip Carullo, MD ■ CONCLUSION 305 Sage Advice to Close This Book: Anesthesiology and the Aphorisms of B. Franklin, Printer David A. Zvara, MD Index

SECTION I

VENTILATION AND AIRWAY

1 Introduction Steven L. Orebaugh, MD

Airway management is the centerpiece of anesthesia care. No other intervention is as emblematic of what we do to preserve patient safety as securing an airway and ensuring sufficient oxygenation and ventilation. Indeed, it can be considered a vital contract between anesthesiologists and their patients that this aspect of care will be competently provided. Whether for the induction of anesthesia, or during a resuscitation, most practitioners regard the establishment of an airway as the foundation of further management. Until this is accomplished, everything else seems to hang in the balance. When placement of an airway goes well, we on the anesthesia side may not attract much notice; however, when it does not proceed as planned, we develop a very high profile, very quickly. Beyond the obligation to patient safety, and the demonstration of professional competence, there looms the specter of medicolegal liability. Failure to secure the airway carries important physiologic consequences that may lead to severe morbidity and mortality in a very short time. The clear connection, in such a case, between failure to provide the expected intervention, and the consequences resulting from hypoxia and/or hypercarbia, makes for a very difficult defense if a claim is made against the provider. Indeed, failure to adequately secure the airway is a perennial source of medicolegal consequences in our profession, as evidence in both the American Society of Anesthesiologists (ASA) closed claims database and the UK airway registry. Highprofile cases of failed airway management featured in the lay press presuppose that the anesthesiologist failed to do his or her job, as we have seen quite recently. Some anesthesiologists’ careers have been challenged by such occurrences. Hence, recommendations to optimize airway management can be of benefit to all acute care providers. What follows is a selection of short articles to help ensure optimal decision making in this often difficult setting, when management must be instituted with immediacy, and risks to patient safety are considerable. These articles include discussion of the ASA airway management algorithm, tips for difficult situations, and descriptions of various airway management techniques, reflecting the knowledge and personal experience of highly qualified practitioners.

2

Basics of Airway Management (Part I)—Always Keep in Mind Complications That Can Occur With Existing Endotracheal Tubes and Tracheal Extubation Toby N. Weingarten, MD, Adam D. Niesen, MD, and Juraj Sprung, MD PhD

Anesthesia providers are specialists in establishing controlled airways for surgical procedures and mechanical ventilation. However, it is also essential that anesthesia providers be able to quickly diagnose and manage airway emergencies that can occur intraoperatively or in the intensive care unit, and during extubation.

Inability to Ventilate due to Endotracheal Tube Occlusion One of the most common airway emergencies is failure to ventilate a patient because of obstruction of an endotracheal tube (ETT). The lumen of the ETT typically becomes occluded from secretions or blood. ETT cuffs have been reported to cause obstruction secondary to overinflation and subsequent herniation into the distal aperture and/or Murphy eye of the ETT. Rarely, other objects, such as a dislodged nasal turbinate during traumatic nasotracheal intubation, can lead to occlusion. Tracheal pathology, such as tumors, can also occlude the ETT by covering the opening aperture(s) of the tube. The patency of an occluded ETT can be quickly confirmed, and in some circumstances cleared, by passage of a suction catheter. Irrigation with 5 to 10 mL of normal saline solution may be required to moisten dried secretions to make them amenable to suction. Occasionally, fiber-optic examination can be used to help establish the diagnosis, clear the obstruction, or guide repositioning of the ETT. In extreme circumstances, the ETT may need to be withdrawn and exchanged for a nonoccluded tube. The ETT can also become occluded from external compression, such as clenched teeth in the nonparalyzed patient who becomes “light” during anesthesia. This situation can be avoided by inserting orally a “bite block” or an oral airway. The use of a “soft” bite block, such as a roll of taped gauze, may be less likely to traumatize oral structures than rigid plastic oral airways. Another common cause of external compression of the ETT is kinking of the ETT. This typically occurs when surgical personnel inadvertently apply pressure (lean) on the patient’s face. Typically, relieving the external compression will allow the ETT to straighten and reestablish patency. However, an ETT enforced with metal (wire spiral or metal-jacketed laser ETTs) can permanently

kink or deform from extrinsic pressure and may need emergent exchange. Also some laser ETTs are prone to fracture and require emergent exchange.

Avoiding Unexpected Loss of the Airway in Already Intubated Patients Inadvertent extubation during surgery or mechanical ventilation represents a lifethreatening emergency. In order to avoid these situations, the ETT should be securely taped (adhesive tape), tied, or fixated with commercial ETT holders to avoid inadvertent dislodgement. In cases when the facial field is shared with the surgeon (e.g., oral procedures), additional ETT security may be achieved by pretreating the skin with liquid medical adhesives, such as benzoin, which increase surface stickiness. This may be important in a patient who presents for surgery unshaved. As a part of routine anesthetic management, ETT position (depth of insertion in regard to incisors) should be checked intermittently throughout the operation. One of the greatest risks of accidental tracheal extubation is during change of patient position or patient transfer. Before patient movement, the ETT should be inspected to ensure it is firmly secured. Further, manually guarding the ETT by holding it adds another layer of safety. Prior to any patient movement the anesthesia provider should give verbal confirmation that he/she is prepared. During movement, an anesthesia circuit can get caught on a piece of equipment and pull out an ETT. Therefore, when possible, the ETT should be disconnected from the anesthesia circuit prior to repositioning or moving the patient. The rare exceptions are high-risk patients who cannot tolerate uninterrupted oxygenation, and for those in whom oxygenation is dependent on high levels of positive end-expiratory pressures (PEEP). The same caution with ETT should be exercised when turning the operating room table. Caution is warranted in intubated patients during procedures of the head and neck, especially of the airway, and during endoscopic or esophageal procedures. Meticulous attention to securing the airway is mandatory. Manipulation of a gastroscope or transesophageal echocardiography probe can dislodge an ETT, and manually guarding the ETT may be recommended. Changes of body position also pose a risk of tube dislodgement. The Trendelenburg position can result in advancement of the ETT (up to 2 cm), and turning the head sidewise may result in similar ETT withdrawal (1.5 to 2 cm). In patients whose ETT was originally inserted close to the carina or just below the glottic opening, these maneuvers can result in mainstem intubation or tracheal extubation, respectively. Therefore, assuring proper ETT placement to approximately mid-trachea will assure these mishaps. Typically in adults, the ETT should be placed between 20 and 23 cm at the incisors, depending on the patient’s build and height. When placing

ETTs with a pre-existing bend, that is, down RAE ETTs, it is important that the bend be in the proper location to allow for optimal depth of the ETT. Downsizing a down RAE ETTs to a smaller internal diameter may not be feasible because of the location of the bend.

Anticipate Potential Difficulties and Be Prepared to Treat Airway Failure After Extubation Typical complications of premature tracheal extubation are hypoventilation, apnea, or obstructive breathing. Immediate postoperative apnea or hypoventilation is most often caused by residual anesthetic and opioid effects, incomplete reversal of neuromuscular blockade, or the excessive relaxation of oral tissues causing obstructive breathing. Some patients may have increased sensitivity to anesthetic agents (e.g., elderly, children, patients with obstructive sleep apnea), which can contribute to hypoventilation. Therefore, patients need to achieve extubation criteria before being extubated (Table 2.1). Specifically, before tracheal extubation, the risk of apnea or hypopnea can be minimized by achieving adequate spontaneous breathing. In addition, anesthetic levels should be low enough to ensure that the patient is able to follow simple commands as well as demonstrate adequate return of muscle strength (e.g., squeezing hands, head lift sustained >5 seconds). The neuromuscular reversal agents should be administered well before the end of the surgery to allow enough time for maximal inhibition of pseudocholinesterase (typically 5 to 15 minutes, depending on the reversal agent used). Patients who have received nondepolarizing muscle relaxants should receive reversal agents, even if the train-of-four ratio appears visually normal, since it has been shown that estimation of this ratio by eye is often inaccurate. Exception to that practice should be rare and well considered. Table 2.1 ■ General Criteria for Tracheal Extubation Vital Function

Parameter

Hemodynamics

Stable blood pressure Stable heart rate Body temperature at acceptable normothermic range Respiratory rate >8 per min Tidal volume >5 mL/kg IBW Vital capacity >15 mL/kg IBW

Metabolic Respiratory drive Respiratory muscle strength

Negative inspiratory pressure >−20 cm H2O Oxygenation/ventilation (on room air or O2 60 mm Hg PaCO2 20 cm H2O can tamponade mucosal perfusion and result in tissue necrosis. Fluid-filled intracuff pressures may be difficult to assess, with slow fluid flow between pilot and tracheal balloons. Anesthesia providers who are unfamiliar with or unaware of fluid-filled cuffs may not completely empty them at extubation during the 1- to 2-second deflation attempt that is typical for air. Thus, the noncompressible fluid-filled ETT balloon may lead to vocal cord trauma when it is inadvertently pulled through the glottic opening. Although extubation with air-filled balloons was not found to cause arytenoid subluxation in several cadavers, the effect of fluid-filled balloons is unknown. Albeit rare, cuff rupture has been reported, and lidocaine can be rapidly absorbed through the lung. Although diffusion from 10% lidocaine via intact ETT cuffs did not reach toxic plasma levels, systemic toxicity could occur if the cuff ruptures and releases >1 g of lidocaine into circulation. Cuffs with pinhole-sized defects filled at minimal pressure typically leak slowly, thus limiting peak and rapid uptake and potential lidocaine toxicity. Knight et al. studied high-dose administration of lidocaine in a

patient population to assess systemic toxicity. After induction with 6 mg/kg of lidocaine and maintenance anesthesia of 0.6 mg/kg diazepam and 50% N2O, a total of 21 mg/kg lidocaine via controlled intravenous infusion was administered up to the point of cardiac bypass without toxicity. Peak plasma concentrations of 9.5 mcg/mL were noted at sternotomy. Indeed, rapid parenteral injections carry a higher risk of toxicity; but based on this study, systemic toxicity should not be clinically evident in adults with doses smaller than 100 mg intravenous push or 160 mg via tracheal instillation. Time-dependent diffusion of lidocaine from the cuff effectively limits toxicity, as hepatic metabolism occurs with a T½of 90 minutes. With excessive pressure and resulting tracheal mucosa ischemia, systemic absorption may be further curtailed. In vitro studies demonstrated that higher concentrations of lidocaine (4% vs. 2%), prolonged duration for diffusion (360 minutes vs. 60 minutes), and “priming” cuff membranes (by prefilling them) resulted in a maximum diffusion of only 17.49-mcg lidocaine. A similar independent study noted as much as 1% of a 4% lidocaine solution diffusing after 6 hours, whereas alkalinized lidocaine resulted in 65% diffusion of the stock solution (2 mL of 2% lidocaine) after 6 hours. Sufficient time must elapse for an effective topical accumulation of mucosal lidocaine, making ICL questionably effective in surgeries lasting 1 hour in duration but may carry significant risks and requires significant preparation. Lower concentrations of lidocaine are more effective when alkalinized and are less likely to result in systemic toxicity should the cuff rupture. Use of manometry is useful to prevent mucosal ischemia but is underutilized. Endotracheal instillation appears to be a safe, easy, effective, and widely available technique.

Clinical skill and experience are required to safely match available techniques to appropriate patients, and the use of intratracheal local anesthetics to remove the ETT is typically contraindicated in patients “at risk” for aspiration. Suggested Readings Altinas F, Bozkurt P, Kaya G, et al. Lidocaine 10% in the endotracheal tube cuff: Blood concentrations, haemodynamic and clinical effects. Eur J Anaesthesiol. 2000;17(7):436–442. Asai T, Koga K, Vaughan RS. Respiratory complications associated with tracheal intubation and extubation. Br J Anaesth. 1998;80(6):767–775. Bidwai AV, Bidwai VA, Rogers CR, et al. Blood pressure and pulse-rate responses to endotracheal extubation with and without prior injection of lidocaine. Anesthesiology. 1979;51(2):171–173. Burton AW, Zornow MH. Laryngotracheal lidocaine administration. Anesthesiology. 1997;87(1):185–186. Daley MD, Norman PH, Coveler LA. Tracheal extubation of adult surgical patients while deeply anesthetized: A survey of United States anesthesiologists. J Clin Anesth. 1999;11(6):445–452. Diachun CA, Tunink BP, Brock-Utne JG. Suppression of cough during emergence from general anesthesia: Laryngotracheal lidocaine through a modified endotracheal tube. J Clin Anesth. 2001;13(6):447–451. Difazio C, Neiderlehner J, Burney RG. The anesthetic potency of lidocaine in the rat. Anesth Analg. 1976;55(6):818–821. Dollo G, Estebe JP, Le Corre P, et al. Endotracheal tube cuffs filled with lidocaine as a drug delivery system: In vitro and in vivo investigations. Eur J Pharm Sci. 2001;13(3):319–323. Estebe JP, Dollo G, Le Corre P, et al. Alkalinization of intracuff lidocaine improves endotracheal tube-induced emergence phenomena. Anesth Analg. 2002;94(1):227–230. Estebe JP, Gentili M, Le Corre P, et al. Alkalinization of intracuff lidocaine: Efficacy and safety. Anesth Analg. 2005;101(5):1536–1541. Fagan C, Frizelle HP, Laffey J, et al. The effects of intracuff lidocaine on endotracheal-tube-induced emergence phenomena after general anesthesia. Anesth Analg. 2000;91(1):201–205. Gefke K, Andersen LW, Freisel E. Lidocaine given intravenously as a suppressant of cough and laryngospasm in connection with extubation after tonsillectomy. Acta Anaesthesiol Scand. 1983;27(2):111–112. Gonzalez RM, Bjerke RJ, Drobycki T, et al. Prevention of endotracheal tube-induced coughing during emergence from general anesthesia. Anesth Analg. 1994;79(4):792–795. Himes RS, DiFazio CA, Burney RG. Effects of lidocaine on the anesthetic requirements for nitrous oxide and halothane. Anesthesiology. 1977;47(5):437–440. Huang CJ, Tsai MC, Chen CT, et al. In vitro diffusion of lidocaine across endotracheal tube cuffs. Can J Anaesth. 1999;46(1):82–86. Jee D, Park SY. Lidocaine sprayed down the endotracheal tube attenuates the airway-circulatory reflexes by local anesthesia during emergence and extubation. Anesth Analg. 2003;96(1):293–297. Kempen PM. Reply: laryngotracheal lidocaine administration. Anesthesiology. 1997;87(1):186. Kempen PM. Extubation in adult patients: who, what, when, where, how, and why? J Clin Anesth. 1999;11(6):441–444. Knight PR, Kroll DA, Nahrwold ML, et al. Comparison of cardiovascular responses to anesthesia and operation when intravenous lidocaine or morphine sulfate is used as adjunct to diazepam-nitrous oxide anesthesia for cardiac surgery. Anesth Analg. 1980;59(2):130–139. Leech P, Barker J, Fitch W. Proceedings: Changes in intracranial pressure and systemic arterial pressure during the termination of anaesthesia. Br J Anaesth. 1974;46(4):315–316. Miller RD, ed. Miller’s Anesthesia. 6th ed. New York: Elsevier; 2005. Navarro RM, Baughman VL. Lidocaine in the endotracheal tube cuff reduces postoperative sore throat. J Clin Anesth. 1997;9(5):394–397. Paulsen FP, Rudert HH, Tillmann BN. New insights into the pathomechanism of postintubation arytenoids

subluxation. Anesthesiology. 1999;91(3):659–666. Sant’Ambrogio G, Remmers JE, deGroot WJ, et al. Localization of rapidly adapting receptors in the trachea and main stem bronchus of the dog. Respir Physiol. 1978;33(3):359–366. Sconzo JM, Moscicki JC, DiFazio CA. In vitro diffusion of lidocaine across endotracheal tube cuffs. Reg Anesth. 1990;15(1):37–40. Soltani HA. Letter to the editor. J Clin Anesth. 2004;16(1):80. Steinhaus JE, Gaskin L. A study of intravenous lidocaine as a suppressant of cough reflex. Anesthesiology. 1963;24:285–290. Sumpelmann R, Krohn S, Strauss JM. Laryngotracheal administration of local anesthetics–is the effect mediated by systemic absorption? Anesth Analg. 1995;80(2):430–431. Yukioka H, Yoshimoto N, Nishimura K, et al. Intravenous lidocaine as a suppressant of coughing during tracheal intubation. Anesth Analg. 1985;64(12):1189–1192.

11 An Easy Intubation Does Not Guarantee an Easy Reintubation—Especially After a Carotid Endarterectomy or Cervical Spine Surgery Steven L. Orebaugh, MD, Heath Diel, MD, and Randal O. Dull, MD PhD

Anesthesia providers do not always appreciate the potential difficulties in reintubating patients who have undergone carotid endarterectomy and cervical spine surgery. Because these patients do not have tumors and usually do not initially present with stridor or signs of vocal cord paralysis (unless there has been a previous stroke), the initial intubation often is uncomplicated. During the operative phase there are many important physiologic issues, such as management of hemodynamics and maintenance of organ perfusion, that compete with the anesthesia provider’s attention to airway issues. Prompt emergence and extubation is desired to facilitate postoperative neurologic checks and to avoid hypertension and coughing at the time of emergence. However, at all times, anesthesia providers must be alert for postextubation airway issues. It can be extremely difficult to get the airway secured after failed extubation even if the initial intubation was uncomplicated. This is a situation to consider very carefully before planning a “trial of extubation” or a “let’s see how he does without the tube” maneuver. The causes of postoperative respiratory dysfunction after carotid endarterectomy or cervical spine fusion include laryngeal or pharyngeal edema, hematoma, cerebrospinal fluid (CSF) leak, recurrent laryngeal nerve dysfunction, carotid body dysfunction, cervical fusion, malalignment, and improperly applied bandages.

Edema/Hematoma Postoperative cervical edema is present in every anterior neck procedure to some degree and occurs in cervical laminectomy because of prone positioning. In carotid endarterectomy patients, computed tomographic studies have shown a 25% to 60% reduction in airway volume and a 200% to 250% increase in retropharyngeal mass as a result of edema alone. Edema of the larynx and pharynx is thought to be caused by venous and lymphatic disruption, as well as direct tissue trauma with increased capillary permeability secondary to release of local inflammatory mediators. Tissue

edema can be difficult to gauge clinically if the patient has remained in the supine position. There can be significant internal compression of airway structure with little or no change in neck circumference, and stridor may not be heard until the airway has narrowed to 4 mm. Also, unilateral tissue disruption can cause bilateral edema. Edema is rarely the sole cause of respiratory distress leading to reintubation, but it compounds the effects of other problems that might arise (such as hematoma) and can make visualization of the vocal cords for reintubation extremely difficult. If the edema has occurred because of prone positioning, elevating the head of the bed to 30 degrees during emergence can reduce soft tissue edema. Significant hematoma occurs in about 1.4% to 10.0% of carotid endarterectomy patients, with higher frequency in cases involving coagulopathies and heparin use without reversal. Frequently, hematomas do not develop until several hours into the postoperative phase, and the “carotid take-back” patient is often hypertensive, hypercarbic, and partially obtunded as well. Reintubation in this situation can be one of the most difficult airway situations to manage, and the airway can quickly become a truly emergency situation. Surgical evacuation of the hematoma without regard for aseptic technique may be sufficient to relieve the obstruction until oral direct laryngoscopy can be performed. The authors recommend that anesthesia providers have available maximum airway support in terms of personnel and equipment when reintubating any patient who has developed significant hematoma after carotid or cervical neck surgery.

Cerebrospinal Fluid Leak CSF leak is a possible complication of anterior cervical vertebral fusion and occurs when the integrity of the dura mater and arachnoid tissue is disrupted. Collection of CSF can cause impaired ventilation as a result of mass effect, very similar to hematoma formation.

Recurrent Laryngeal Nerve Injury Recurrent laryngeal nerve injury happens most often after thyroid surgery but is a recognized complication of carotid endarterectomy and anterior cervical spine surgery as well. Acute dysfunctions of the recurrent laryngeal nerve occur in about 0.2% to 10.0% of carotid surgery cases, but, fortunately, less than 1.0% involve permanent injuries. The recurrent laryngeal nerve runs in the groove between the trachea and esophagus and innervates all the muscles of the larynx except the cricothyroid muscle. Injury is usually the result of ischemia, surgical manipulation, dissection, stretching, or compression. Unilateral dysfunction results in unilateral vocal cord adduction and

hoarse voice. Bilateral dysfunction causes airway obstruction from bilateral cord adduction. The anesthesiologist should be aware of the preoperative function of the recurrent laryngeal nerves and patients with hoarse voice related to stroke or prior surgery. These patients may benefit from preoperative evaluation. Upon emergence and extubation, bilateral laryngeal nerve dysfunction presents as immediate airway obstruction requiring intervention.

Carotid Body Dysfunction The carotid body functions primarily as a chemoreceptor for blood oxygen and carbon dioxide content. Surgical denervation secondary to carotid endarterectomy impairs the patient’s physiologic response to hypoxia. Patients treated with respiratory depressants such as opiates are at greater risk for postoperative hypoxia.

Cervical Misalignment Cervical misalignment is an unusual but possible complication of cervical spinal fusion. Misalignment can cause structural impingement of the airway, which, coupled with edema, can lead to ventilation deficiencies. Also, cervical fusion limits neck extension, and this could contribute to difficult postoperative reintubation.

Surgical Dressings Supportive dressings after neck surgery can cause airway obstruction by impeding venous and lymphatic drainage and worsening edema. Large dressings also obscure visualization of the operative site and may cover signs of bleeding that would alert the anesthesia and postoperative acute-care staff to a developing hematoma. Cervical collars should be sized appropriately and allow for some postoperative expansion due to edema. It should be obvious but bears stating that excessively tight or circumferential neck bandages should never be used. The authors are aware of several cases of apparent airway obstruction after carotid endarterectomy that were relieved when the neck dressing was removed. TAKE HOME POINTS In addition to the specific pathologic situations described above, it has become increasingly apparent that extubation of the trachea is not uncommonly a precarious intervention for patients in the operating room or recovery areas, or those in the ICU. The most recent ASA guidelines suggest that “an extubation strategy is a logical extension of the intubation strategy.” Recommendations include consideration of clinical factors that could impact airway

patency or ventilation after extubation (as detailed above), development of an airway management plan that can be immediately applied if ventilation fails on removal of the tube, and potential use of an airway stylet or supraglottic airway as a guide for reintubation. In the most recent iteration of the National Audit Program (NAP4, 2011) from the United Kingdom, over 20% of morbid events related to airway management occurred at the end of anesthesia or in the recovery area after extubation. These data underscore the importance of a management plan for airway management should obstruction develop after removal of the endotracheal tube. Suggested Readings Allain R, Marone L, Meltzer L, et al. Carotid endarterectomy. Int Anesthesiol Clin. 2005;43(1):15–38. American Society of Anesthesiologists Task Force. A management of the difficult airway. Practice guidelines for management of the difficult airway. An updated report. Anesthesiology. 2003;95:1269– 1277. Apfelbaum JL, Hagberg CA, Caplan RA, et al. Practice guidelines for management of the difficult airway: an updated report by the American society of anesthesiologists task force on management of the difficult airway. Anesthesiology. 2013;118:251–270. Ballotta E, Da Giau G, Renon L, et al. Cranial and cervical nerve injuries after carotid endarterectomy: a prospective study. Surgery. 1999;125:85–91. Bukht D, Langford RM. Airway obstruction after surgery in the neck. Anesthesia. 1983;38:389–390. Carmichael FJ, McGuire GP, Wang DT, et al. Computed tomographic analysis of airway dimensions after carotid endarterectomy. Anesth Analg. 1996;83:12–17. Cook TM, Woodall N, Frerk C. Major complications of airway management in the uk: results of the fourth national audit project of the royal college of anaesthetists and the difficult airway society. Br J Anaesth. 2011;106:617–631. Curran AJ, Smyth D, Sheehan SJ, et al. Recurrent laryngeal nerve dysfunction following carotid endarterectomy. J R Coll Surg Edinb. 1997;42(3):168–170. Hughes R, McGuire G, Montanera W, et al. Upper airway edema after carotid endarterectomy: the effect of steroid administration. Anesth Analg. 1997;84:475–478. Ichinose K, Kozuma S, Fukuyama S, et al. A case of airway obstruction after posterior occipito-cervical fusion. Masui. 2002;51(5):513–515. Joseph MM, Kaufman WA, Shindo ML, et al. Complications of anesthesia for head-neck and reconstructive surgery. Semin Anesth. 1996;15:203–211. Jung A, Schram J, Lehnerdt K, et al. Recurrent laryngeal nerve palsy during anterior cervical spine surgery: a prospective study. J Neurosurg Spine. 2005;2(2):123–127. Kreisler NS, Durieux M, Spickermann BF. Airway obstruction due to a rigid cervical collar. J Neurosur Anesthesiol. 2000;2:118–119. McRae K. Anesthesia for airway surgery. Anesthesiol Clin North Am. 2001;19(3):497–541. Penberthy A, Roberts N. Recurrent acute upper airway obstruction after anterior cervical fusion. Anaesth Intensive Care. 1998;26(3):305–307.

12 Plan for an Airway Fire With Every Head and Neck Case Julie Marshall, MD

A 67-year-old woman with a history of chronic obstructive pulmonary disease (COPD), home oxygen requirement of 3 L/min by nasal cannula, and coronary artery disease was admitted to the burn unit. She had been involved in a house fire after falling asleep while smoking and dropping her cigarette. She sustained an inhalation injury and was intubated in the intensive care unit (ICU) for 2 weeks before coming to the operating room (OR) for a tracheostomy. The procedure was done using the in situ polyvinyl chloride endotracheal tube. During the procedure, you had trouble maintaining her blood pressure under anesthesia and were reluctant to use pressors due to recent skin grafts. Because she was tolerating only about 0.5% isoflurane and not much midazolam, you added 20% nitrous oxide to her inspired oxygen. Unfortunately, she suffered a desaturation of her SpO2 with attempts to further lower the FiO2. As the airway was entered with electrocautery at the tracheostomy site, a flame was noted that flashed from the tracheostomy. What might have been done to decrease this risk? Now that a fire has occurred, what should be done?

Introduction One of the responsibilities of the anesthesia provider is the management of the operating room environment, including prevention and management of operating room fires. Selecting an anesthetic plan that decreases the risk of fire is one of the first priorities in airway management. If a fire does occur, an anesthesia provider must know what to do to minimize harm to the patient.

Fire Triad The risk of fire occurs whenever the fire triad is present. The fire triad consists of an ignition source, fuel, and oxidizer. It must be recognized that these elements are nearly always present in the OR! During the head and neck surgery, these elements are not only

present but in close proximity. The oxidizer (oxygen or nitrous oxide) is provided by the anesthesiologist through the endotracheal tube into the surgical site. The ignition source is provided by the surgeon, usually in the form of an electrocautery device or laser for airway fires. The fuel source varies with the type of surgical procedure. Common Components to Fire Triad in an Operating Room Oxidizer

Ignition Source

Fuel

Oxygen Nitrous

Electrocautery Lasers Fiberoptic lights Defibrillator pads

Endotracheal tube Packing Patient tissue Drapes or gowns Surgical prep solutions—not dried Patient’s hair Nasal cannula or facemask

Procedures With Increased Risk for Fire Common procedures that carry a high risk of airway fire include tracheostomy, tonsillectomy, adenoidectomy, airway tumor debulking, and tracheal reconstructions. Head and neck procedures or ophthalmologic procedures requiring sedation with supplemental oxygen create a high risk of an operating room fire by trapping oxygen under the drapes, creating an oxygen-rich environment.

Surgical Fire If an endotracheal tube is ignited in a patient, the flow of gas through the tube can create a “blowtorch”-type flame that can injure more distal structures. Fires that occur at tracheostomy sites as the airway is entered have the potential for local injury, flames that enter the OR environment, or injury to the distal lungs. Oral and pharyngeal procedures performed in children with uncuffed tubes may result in airway fire because of the leak of oxygen-rich gas into the site of surgery. The endotracheal tube is the fuel source most consistently present in the airway. It has been shown that red rubber, polyvinyl chloride, and silicone endotracheal tubes are all flammable at lower than 27% oxygen. Commercially available “laser-resistant” tubes are more resistant to combustion and are the recommended endotracheal tube

when the use of a laser is planned. Filling the cuff of the endotracheal tube with saline tinted with methylene blue allows notification to the surgeon of cuff perforation if damage has occurred. For procedures involving the head and neck, when moderate to deep sedation are required, or in a patient with oxygen dependence, the anesthesiologist should consider a sealed gas delivery system such as a cuffed ETT or LMA. If the patient and case are deemed appropriate for an open gas delivery device (facemask or nasal cannula), care must be taken to avoid trapping of gases under drapes thereby creating a high-oxygen environment. In a closed claims analysis of operating room fires from 1985 to 2009, a large proportion of electrocautery-induced fires occurred using an open gas delivery system. The necessity for an endotracheal tube should be discussed with the surgeon as some procedures may be performed with intermittent apnea, although this may require a higher FiO2 during episodes of ventilation.

Communication and Prevention The surgeon and anesthesiologist should be in communication about the surgical plan throughout the case. The anesthesia provider should be notified as the airway portion approaches so that adjustment may be made to lower the FiO2 if needed. Minimizing the FiO2 is one of the trickiest aspects of managing the fire triad, even for experienced anesthesia providers. It is especially difficult in patients who have poor lung function or tenuous cardiovascular status. If there is difficulty in maintaining the patient at a low FiO2, the surgeon must be notified so that he or she can use non–heatgenerating surgical tools (scalpel instead of electrocautery) or modify the surgical plan. During intraoral or pharyngeal procedures, wet packing may be placed to decrease the leakage of oxygen-rich gas into the surgical site. Care must be taken that these stay moist, because dry packing will act as an additional source for ignition.

Management of OR Fires If an airway fire occurs, immediate action must be taken to prevent further harm. The most recent Practice Advisory for the Prevention and Management of OR Fires by the ASA provides the following steps in the Operating Room Fires Algorithm when airway fire is present: (1) Remove the tracheal tube, (2) Stop the flow of all airway gases, (3) Remove sponges and any other flammable material from the airway, and (4) Pour saline into the airway. A carbon dioxide fire extinguisher may be used if the fire is not extinguished following these steps. If a fire continues in the OR, activate the fire alarm and evacuate the patient. Assuming the fire was extinguished with the initial steps, the anesthesiologist should

reestablish ventilation by mask without supplemental oxygen or nitrous oxide if possible; extinguish the airway device and attempt to determine if airway fragments could be left in the airway. Consider bronchoscopy, if needed to retrieve parts of the tube or assess the degree of injury to the airway. Any additional relevant workup (arterial blood gas, chest x-ray) or treatment including airway support (reintubation, tracheotomy) should be implemented. For an OR fire not involving the patient airway, the airway device should be left in place. Remove all drapes and burning materials and extinguish flames with saline or a fire extinguisher appropriate for use in the OR. For all operating room fires, reporting to the local fire department should occur, based on local policy. All such cases should be evaluated within an institution’s quality reporting framework, to improve future patient outcome. So what could have been done differently for the patient above, who sustained an airway fire during tracheostomy? A discussion between all providers should occur prior to the procedure to determine the risk for airway fire. The steps for management if one does occur should be outlined, and agreed upon. Using a gas mixture of oxygen and air would have decreased the amount of oxidizer present. Notifying the surgeons of the increased FiO2 requirement may have resulted in an alternative method of entering the airway, such as a scalpel. And finally, all operating room personnel including the anesthesia providers should participate in periodic OR fire drills to plan for the potential of an OR fire. TAKE HOME POINTS The fire triad is both present and in close proximity to the airway in the cases noted above—develop a method to remind yourself of that for every case with airway fire potential. Minimize oxidizer FiO2 and nitrous oxide concentration for cases with risk of fire. Minimize ignition generators—electrocautery or laser time. Laser tubes are harder to ignite, but note that all tubes can combust. If an airway fire occurs, disconnect from the circuit, extubate, extinguish the flame, ventilate without supplemental oxygen if possible, evaluate, and support the airway as needed. Suggested Readings Apfelbaum JL, Caplan RA, Barker SJ, et al. Practice Advisory for the prevention and management of operating room fires: An updated report by the American Society of Anesthesiologists Teak Force on operating room fires. Anesthesiology. 2013;118(2):271–290. Ehrenwerth J, Seifert HA. Electrical and fire safety. In: Barash PG, Cullen BF, Stoelting RK, et al., eds.

Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:189–218. Mehta SP, Bhananker SM, Posner KL, et al. Operating room fires: A closed claims analysis. Anesthesiology. 2013;118(5):1133–1139. Modest VE, Alfille PH. Anesthesia for laser surgery. In: Miller RD, Eriksson LI, Fleisher LA, et al., eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Saunders; 2014:2598–2611. Wolf GL, Simpson JI. Flammability of endotracheal tubes in oxygen and nitrous oxide enriched atmosphere. Anesthesiology. 1987;67(2):236–239.

13 There Are Special Considerations Involved With Both Intubation and Chronic Airway Management of Burn Patients Joshua Knight, MD

Burns can result from thermal, chemical, electrical, or radiation injury. Carbon monoxide poisoning is the most frequent cause of death during and immediately after a fire. If the patient survives the first few hours, morbidity and mortality are related to the total body surface area (TBSA) involved, the depth of the burn, and the patient’s age. The likelihood of airway compromise increases with more serious burns. Characteristics of major burns include: Partial-thickness burns involving >25% of TBSA in adults Full-thickness burns involving >10% of TBSA Presence of inhalational injury Involvement of the face, eyes, ears, hands, feet, or perineum causing impairment Caustic chemical burn etiology High-voltage electrical burns Burns in patients with coexisting debilitating disease Table 13.1 ■ Rule of Nines Entire head and neck Each arm Anterior upper/lower trunk Posterior upper/lower trunk Each lower extremity Genitals and perineum

9% 9% 18% 18% 18% 1%

Each hand

1%

Characteristics of moderate burns include: Partial-thickness burns involving 15% to 25% of TBSA in adults Full-thickness burns involving 2% to 10% TBSA TBSA of burned skin is estimated using the “rule of nines” Body parts are divided into allotments or multiples of 9% (Table 13.1).

Acute Management Burn patients with inhalational injury may require endotracheal intubation and ventilator support in the field. If the patient has an endotracheal tube (ETT) on arrival to the hospital, do not change the tube; it may be difficult to get another one in place. Burn patients can present with asymptomatic airways, but can shortly become problematic because of subsequent respiratory sequelae that lead to a challenging airway. Burn patients develop excessive amounts of upper- and lower-airway edema as a result of mucosal destruction and capillary leakage that is further exacerbated by fluid resuscitation. Airway edema and narrowing continue for 12 to 24 hours after the initial burn insult. A thorough history and physical are helpful in determining which patients are candidates for early intubation. While assessing the patient, administer oxygen by facemask and monitor oxygen saturation with pulse oximetry. History. A burn injury that occurs in an enclosed space with highly combustible material is very suspicious for inhalation injury. Patients who report coughing, drooling, hoarseness, dysphonia, and dysphagia are at risk of airway swelling. Physical Exam. Facial burns and the presence of oral soot correlate highly with airway edema and impending airway compromise. Other signs include singed facial hair, soot in the nose, stridor, and respiratory distress. Diagnosis. The diagnosis of inhalation injury is made primarily by history and physical examination. Patients who demonstrate the above signs and symptoms should undergo prompt endotracheal intubation. Testing supportive of intubation include partial pressure of arterial oxygen (PaO 2) 50 mm Hg (acutely) on room air, or a PaO2 35 kg/m2, Age >50 years, Neck circumference >40 cm, and male Gender (BANG). Three positive responses indicated a high risk for OSA. It has been validated with polysomnography and has a sensitivity ranging from 83.6% to 100%. Another study found that the STOP-BANG model correlates with no, mild, moderate, and severe OSA on polysomnography. Yet another is the sleep apnea clinical score (SACS). Four variables (neck circumference, hypertension, habitual snoring, and nocturnal gasping or choking) generate a score ranging from 0 to 100. Validated by polysomnography, a score greater than 15 has a 25% to 50% likelihood of an AHI >10. A third commonly used screening tool is the

Berlin questionnaire with 10 variables (including nonrestorative sleep, sleepiness while driving, periods of apnea during sleep, BMI, and hypertension). When correlated with home polysomnography, the sensitivity and specificity for an AHI >5 is 86% and 77%; for AHI >15, 54% and 97%.

Associated Conditions Morbidly obese patients are more likely to have metabolic syndrome (diabetes, hypertension and abnormal cholesterol and/or, elevated triglycerides). These patients, when compared to non-OSA patients, are more likely to have myocardial infarction, stroke, and congestive heart failure. Diastolic dysfunction may contribute to congestive heart failure perioperatively. The combination of cardiac and pulmonary disease can result in cor pulmonale with pulmonary hypertension. Polycythemia may occur due to recurrent hypoxemia. These patients may also develop obesity-hypoventilation syndrome. Metabolic syndrome and decreased mobility can contribute to development of DVT and pulmonary embolism. Cor pulmonale with hepatic congestion may further contribute to liver dysfunction. Independently, morbidly obese patients can also have hepatosteatosis (the most serious stage of hepatosteatosis is cirrhosis) with possible liver dysfunction and abnormal drug metabolism.

Physiologic Alterations The respiratory system changes that occur in obese patients with OSA are of keen interest for anesthesiologists. Redundant oral and pharyngeal tissue can reduce the airway diameter and may contribute to difficulties in mask ventilation as well as tracheal intubation. They may also have restrictive lung disease due to increased body fat over the chest wall (decreased chest wall compliance) as well as compression by abdominal fat. All these factors lead to significant reduction in functional residual capacity (FRC), which results in lower oxygen reserve during periods of apnea during tracheal intubation and extubation. A lower FRC, larger alveolar-to-arterial oxygen gradient, and a higher tendency for hypoventilation during sedation may result in precipitous oxyhemoglobin desaturation during monitored anesthesia care and induction of general anesthesia. Oxygen consumption and carbon dioxide production is higher, further contributing to development of hypoxemia and respiratory acidosis.

Establishing the Airway Several studies have compared the difficulties in intubating the trachea in morbidly obese and normal-weight patients. Neither BMI nor OSA has been shown to be independent predictors of difficult tracheal intubation. Neck circumference and

Mallampati score have been shown to be indicators of a difficult airway: neck circumference of 40 cm was associated with a 5% incidence of a difficult airway, and a 60-cm circumference was associated with a 35% incidence of difficulty. Intubation difficulty is associated with increasing Mallampati class, decreased thyromental distance (50%) to gain maximal advantage from the helium, the administration system needs to be “helium tight.” Therefore, the most effective heliox systems are closed systems. The system should also be high flow to minimize the rebreathing of low-oxygen gas, with sufficient flow to meet or exceed the patient’s minute volume and peak inspiratory flow, and to minimize dilution with ambient air. Flushing a high flow of heliox into the patient’s airway is expensive and can be wasteful. Hence, the delivery method should include a reservoir and an on-demand delivery system that minimize total flow and helium requirements. Heliox can be used in patients who are breathing spontaneously, but also in the settings of both invasive mechanical ventilation (e.g., with tracheal intubation) and noninvasive mechanical ventilation. The beneficial respiratory effects of heliox include a reduction in transpulmonary pressure requirement (and thus work of breathing), increases in tidal volume, improvement in the homogeneity of gas distribution, improvement in the elimination of CO2, and improvement in the delivery of aerosolized medications. In many centers, heliox may be part of the pipeline supply of medical gases to the ICU or to the OR. In the OR, the administration may be titrated with oxygen via a specific heliox flowmeter in the anesthesia machine, assuming the flowmeter has been calibrated for such a mixture. Large academic centers will usually schedule airway cases in rooms with the capability to deliver heliox via the anesthesia circuit. In the ICU setting where pipeline supply of helium may be available, respiratory therapists typically connect a helium regulator and blender to the oxygen flowmeter and administer the selected mixture based on clinical needs (of note the pipeline supply is often a 80:20 mix already). Similarly, when administering helium from a tank, the appropriate helium regulator with an oxygen blender should be used. Of note, when used in this manner a conversion may be necessary to calculate the total flow delivered to the patient, as the oxygen flowmeter itself will underestimate the actual volume delivered secondary to the differential density between the two gases as the oxygen flowmeter itself is not calibrated for helium.

Possible Clinical Applications Upper-airway obstruction

Postextubation stridor Croup Bronchiolitis Asthma exacerbation Chronic obstructive pulmonary disease (COPD) exacerbation Pulmonary function testing When used for these purposes in different clinical trials, heliox therapy has been shown to relieve stridor, reduce the work of breathing, and reduce respiratory distress to act as a therapeutic bridge to allow time for definitive treatments to become effective; to prevent intubation in patients with impending respiratory failure and decrease the need for intubation or reintubation in perioperative settings; and to shorten the length of perinatal ICU stay in infants with bronchiolitis. Of note, heliox is of particular use in acutely ill patients, as it has no significant hemodynamic effects.

For Upper-Airway Obstruction and Stridor Stridor is a case of orifice flow and the low density of heliox mixtures improves the flow at the orifice. The literature from pediatric burn centers related to children with postextubation stridor reports improved outcomes. Specifically, such studies note less respiratory distress and fewer episodes of reintubation in patients who received early heliox therapy when they showed signs of postextubation stridor or retractions, than in those patients in whom heliox therapy was somewhat delayed. While data does not conclusively point to the routine use of heliox for this indication, it may certainly have a role in managing the acute upper-airway obstruction.

For Croup and Bronchiolitis Viral upper respiratory tract infections are a common cause of pediatric respiratory distress where they reduce the radius of lengthy segments of the tracheobronchial tree. However, this patient population is often hypoxic and therefore is unable to receive the low fractional inspired oxygen concentration required with heliox mixtures. At present, while heliox presents an alternative therapy for the management of moderate to severe croup, most sources do not recommend this as a routine therapy.

For Asthma Exacerbation Heliox can be effective for patients with severe air flow obstruction. The beneficial effects seem to be most efficacious when heliox is used within 24 hours of the onset of symptoms, as early use may decrease dyspnea and improve gas exchange especially while implementing conventional therapies which may require hours for full effect (e.g., steroids). Heliox can be used as a temporizing measure to prevent intubation and has a

relatively safe treatment profile. Usually, clinical benefits of this therapy are rapidly evident.

For Severe COPD Heliox may improve alveolar ventilation and gas transfer (decreasing PaCO2) as well as reduce the need for intubation. Heliox should be considered in individual cases when intubation is required, but would be undesirable. However, wide-scale use of heliox cannot be recommended based on clinical evidence.

New Avenues in Clinical Helium Use Unlike the noble gas xenon, helium does not possess any anesthetic properties. However, studies performed in animal models and in limited human paradigms have shown potential clinical applications related to the effects of heliox on several organ systems. Its utility may not simply be limited to the management of obstructive airflow disorders in the future.

Risks of Heliox Use Hypoxemia/Anoxia There is a possibility of delivering a gas mixture that contains 24 mEq/L is relatively alkylotic as compared to plasma, while a solution with an SID 24 mEq/L will push the pH toward 7.4. Several studies have evaluated whether diluting pRBCs with LR causes the blood to clot. Recall that pRBCs are in a citrate solution that binds the free calcium that is necessary to facilitate the coagulation cascade. The calcium in LR (2.6 mEq/L) is insufficient to overcome the citrate present in pRBCs based on three different studies. However, the FDA’s Circular of Information for Blood Products still lists diluting blood products with LR as an absolute no-no. And Canadian Blood Services agrees with the FDA. Diluting pRBCs with 0.45% NaCl (half-normal saline) will lead to RBC lysis. You will infuse a lot of free hemoglobin and potassium. What solution is appropriate for hyperkalemic patients? Contrary to popular belief, 0.9% NaCl will increase potassium concentration while LR and Plasma-Lyte A only increase plasma potassium when the patient is hypokalemic or both hyperkalemic and alkylotic. Recall that a great majority of total body potassium is intracellular. Potassium shifts into and out of cells to maintain electroneutrality when hydronium ions (H+) shift into and out of those same cells to maintain extracellular pH. The majority of hyperkalemic patients are acidotic and the shift of H+ into cells causes K+ to shift into the plasma. Balanced fluids with an SID greater than 25 mEq/L increase pH and shift K+ back into cells. O’Malley et al. found that renal transplant patients receiving LR versus NS are less likely to require bicarbonate therapy and develop hyperkalemia. So, if balanced fluid is good, how much should the patient receive? And are goaldirected therapy protocols to titrate cardiac preload and intravascular volume with sytemic vascular resistance and myocardial contractility to optimize end-organ perfusion valid? The choice of fluid for that optimization introduces the concept of the endothelial glycocalyx, an albumin- and carbohydrate-rich layer that is bound to the capillary surface by glycoproteins. It is an important portion of the vascular barrier and its breakdown increases vascular permeability and exposes platelets to endothelial

components that promote clot formation. Hypervolemia dilutes the glycocalyx, which leads to edema formation and aberrant clot formation. Thus, too much of any fluid can have consequences. While some studies found that the infusion of albumin or hydroxyethyl starch preserved or improved the thickness of the glycocalyx, neither have been shown to consistently improve patient outcomes. Realize that while the common 5% albumin solutions may help to preserve the glycocalyx, they are dissolved in NaCl with an SID of 0 which worsens acidosis.

The Evidence Studies have shown a lower rate of complications (infection, renal replacement therapy, blood transfusion, and acidosis) with use of Plasma-Lyte A over 0.9% NaCl for fluid replacement on the day of surgery. Additionally, use of a chloride-restrictive fluid strategy decreased the incidence of acute kidney injury (AKI) in Australian ICU patients without altering in-hospital mortality, hospital or ICU length of stay. From these studies, we conclude that administering large volumes of 0.9% NaCl is detrimental to patients who receive large volume resuscitation or are at high risk of a range of complications. The broad use of balanced crystalloids versus 0.9% NaCl in relatively healthy ASA I and II patients not requiring large volume resuscitation has not been demonstrated; the impact of fluid choice on the clinical outcomes of healthy people who present in a near euvolemic state is minimal or perhaps nonexistent. Balanced salt solutions are hypotonic as compared to plasma due to the lower concentration of sodium, which can be detrimental to patients who present with hypernatremia or patients who are receiving hyperosmolar therapy for intracranial hypertension. Infusion of LR can lead to elevated lactate levels in patients with impaired lactate clearance (sepsis, hepatic insufficiency) and when large volumes are used. Care should be used when drawing blood samples to avoid a location near the LR infusion. Whenever a large volume resuscitation occurs, serial laboratory values should be examined to identify electrolyte disturbances that can be treated. Underperfusion is the most common etiology of elevated lactate levels. Unlike in underperfusion, elevated lactate levels due to the administration of LR are not detrimental and treatments typically used for underperfusion (fluids, inotropes) are not appropriate for this type of hyperlactatemia. Balanced salt solutions cost more than 0.9% NaCl. Plasma-Lyte A costs ∼4× that of 0.9% NaCl, which is impressive. However the utilization of Plasma-Lyte A for an additional ∼$4.00 per liter during the acute resuscitation phase is easily recouped if the provider sends one fewer blood gas to analyze an acidosis. The number needed to treat (NNT) with Plasma-Lyte A versus 0.9% NaCl to prevent a meaningful complication that

has a known associated cost is not clear, making a cost–benefit calculation difficult.

The Practice In practice, for an adult with normal hepatic and renal function, infusing up to 40 cc/kg of 0.9%NaCl will not significantly alter acid–base status. The limit for patients with comorbidities and active illnesses that cause acidosis are not well defined, but there is very limited downside to the administration of balanced salt solutions in place of 0.9% “abnormal” NaCl; aside from cost. In the vignette that started the chapter, our patient received a large volume of 0.9% NaCl to treat his metabolic acidosis. One might argue that the resuscitation may have contributed to his acidosis. Regardless of judging the benefits of the 0.9% NaCl, it is reasonable to conclude that his acid–base status might be much closer to the physiologic norm of 7.4 if he would have received a similar volume of a “balanced” salt solution. The evidence shows that he would be less likely to experience AKI if he had received a “balanced solution” as well. TAKE HOME POINTS “Normal” saline is not a physiologic match to plasma! Infusing large volumes of 0.9% NaCl will lead to a hyperchloremic metabolic acidosis and can lead to worse outcomes, specifically AKI in susceptible patients. Balanced crystalloid solutions are increasingly recommended as first-line resuscitation fluids in surgical and trauma patients. The administration of large volumes of crystalloids will cause the glycocalyx to breakdown, leading to edema formation and aberrant activation of the coagulation cascade. But 5% albumin is diluted in 0.9% NaCl with an SID of 0 mEq/L. Lactated Ringer solution contains a small amount of calcium that is insufficient to cause clot formation when used to dilute pRBCs. Suggested Readings Hoste EA, Maitland K, Brudney CS, et al; ADQI XII Investigators Group. Four phases of intravenous fluid therapy: A conceptual model. Br J Anaesth. 2014;113(5):740–747. Lira A, Pinsky M. Choices in fluid type and volume during resuscitation: Impact on patient outcomes. Ann Intensive Care. 2014;4:38. Myburgh JA, Mythen MG. Resuscitation Fluids. New Eng J Med. 2013;369(13):1243–1251. O’Malley CM, Frumento RJ, Hardy MA, et al. A randomized, double-blind comparison of lactated Ringer’s solution and 0.9% NaCl during renal transplantation. Anesth Analg. 2005;100(5):1518–1524. Shaw AD, Bagshaw SM, Goldstein SL, et al. Major complications, mortality, and resource utilization after open abdominal surgery: 0.9% saline compared to Plasma-Lyte A. Ann Surg. 2012;255(5):821–829. Story DA. Stewart Acid-Base: A simplified bedside approach. Anesth Analg. 2016;123(2):511–515.

40 Hypertonic Saline: Still the “Solution” to the Solution Problem? Lavinia Kolarczyk, MD, Colleen Moran, MD, and Patrick J. Forte, MD

Analogous to the variety of beverages in your supermarket’s soda aisle, there exist numerous choices for fluids for patients. What is best for your patient’s needs? What fluid is appropriate for specific situations? How much fluid should be administered? Although these questions may seem trivial, the knee-jerk reflex for most residents is to use a fluid that they feel most comfortable administering. Let us wade out of the “normal saline” pool and explore the clinical uses of hypertonic saline. Fluids became the focus of prehospital resuscitation research more than 75 years ago. The same clinical problems encountered with fluid resuscitation efforts then remain the focus of today’s research. The search continues for an “ideal” fluid, that is, one that is inexpensive, generates sustained hemodynamic effects with minimal peripheral or pulmonary edema, and is effective even in small volumes. Traditionally, isotonic crystalloids such as lactated Ringer solution and normal saline have been considered first-line treatment for trauma patients. Although these fluids are inexpensive, readily available, nonallergenic, noninfectious, and efficacious in restoring total body fluid, they have limited intravascular half-life. A proposed solution to the “solution problem” is to augment the osmotic properties of traditional resuscitation fluids. In theory, this would extend the intravascular half-life and reduce the amount of third spacing. The “ideal” fluid search then focused on osmotic properties, and hypertonic saline (with and without colloid) became a prime subject of research. Hypertonic saline already had a role in the trauma setting, as it was used for patients with increased intracranial pressure secondary to traumatic head injury. Of note, mannitol (an osmotic diuretic and cerebral arteriolar vasoconstrictor) was traditionally used as first-line therapy in this patient population, but it was associated with rebound intracranial hypertension. It was believed that this effect was due to intravascular dehydration and an inability to maintain cerebral perfusion pressure when diuresis was not matched by appropriate fluid administration. Hypertonic saline became the agent of

choice, as it served a dual purpose as a diuretic and a resuscitative agent. In a battlefield setting, hypertonic saline has been suggested as a good alternative to normal saline for resuscitation since it is a smaller volume to carry. Further research in the use of hypertonic saline in the trauma setting revealed that it had vasoregulator, immunologic, and neurochemical effects (Table 40.1). Hypertonic saline increases blood pressure and cardiac output secondary to plasma volume expansion, and it is also thought to stimulate adrenocorticotropin and cortisol release. Hypertonic saline is also believed to counteract vasospasm occurring after traumatic brain injury through its vasodilatory effects. On a molecular level, hypertonic saline has been shown to improve microvascular perfusion by attenuating leukocyte–endothelial interactions. It has also been suggested that hypertonic saline can provide protection from bacterial illness by attenuating changes in extracellular sodium and excitatory neurotransmitters that occur after injury. These changes are thought to depress leukocyte adherence and neutrophil margination. Table 40.1 ■ Hypertonic Saline: Beyond Plasma Volume Expansion Vasoregulatory effects

Immunologic effects

Neurochemical effects

Counteracts vasospasm occurring after traumatic brain injury through its vasodilatory effects. Improves microvascular perfusion by attenuating leukocyte– endothelial interactions. Changes in extracellular sodium that occur after injury may be attenuated by hypertonic saline, which is thought to depress leukocyte adherence and neutrophil margination. Changes in excitatory neurotransmitters that occur after injury may be attenuated by hypertonic saline, which stimulates adrenocorticotropin and cortisol release.

Although the most common concentration of hypertonic saline used clinically is 3%, the concentrations studied in clinical trials range from 1.7% to 29.2%. In spite of concern for hypertonicity, acute increases in serum sodium levels to 155 to 160 mEq have not been shown to be harmful to most patients. However, too rapid correction of hyponatremia can result in osmotic demyelination syndrome and permanent brain damage. Another clinical problem with hypertonic saline is the transient nature of the

resulting hemodynamic improvement (30 to 60 minutes) when it is used as a resuscitative fluid, much like traditional resuscitative fluids. Proposed strategies to lengthen the hemodynamic effects of hypertonic saline include longer infusion times, subsequent or concomitant infusion of blood or conventional fluids, and adding 6% dextran to the hypertonic saline. Despite the claims surrounding the addition of colloid, there remains no clear answer as to the best strategy to lengthen hemodynamic effects of hypertonic saline. The reality is that the clinical efficacy of hypertonic saline resuscitation versus conventional fluids remains unclear because many prehospital studies compared only single boluses of experimental and control fluids. Furthermore, misleading conclusions exist about the clinical responses to different types of fluid resuscitation (including hypertonic saline with and without colloid additives). This is likely the result of studies comparing two or more regimens that alter more than one variable. In addition to the use of hypertonic saline in the prehospital and trauma setting, it has several well-established roles. These include the care of patients with severe, symptomatic hyponatremia (20 Fluid Estimates Calculation

2 1

Example 1. 100-kg person. (10 × 4) + (10 × 2) + (80 × 1) = 140 mL/hr Example 2. 23-kg child (10 × 4) + (10 × 2) + 3 = 63 mL/hr For surgical losses, the anesthesia provider must be vigilant, as underestimating surgical blood loss can have devastating consequences. The first obvious place to look is in the suction canister or at the sponges. Additionally, a 4 × 4 sponge may hold 10 mL of blood and a full-sized, soaked laparotomy pad may represent 100 mL of blood loss. Furthermore, one must account for the use of irrigation solution, and frequent communication between the surgical personnel when estimating this fluid is essential. With the increased use of cell salvage techniques, a second suction canister may be present. However, quick visual estimation of blood losses may account for only onethird of the “actual blood loss.” There may be a significant amount left unaccounted for in tubing, on drapes or the floor, or on the gloves and gowns of surgical personnel. Once estimated, surgical blood loss replacement, not including the use of blood products, can occur in the ratio of 1:3 for crystalloid solutions and 1:1 for colloid solutions. For example, a 300-mL blood loss could be corrected by giving 900 mL of crystalloid or 300 mL of colloid. But how does one decide whether to use crystalloid or colloid solutions and what are colloid solutions? Simply, colloid solutions are high–molecular-weight substances administered to maintain intravascular volume. They last intravascularly from 3 to 6 hours, up to six times longer than crystalloid solutions, such as normal saline or lactated Ringer’s. Some indications for the use of colloid solutions are for fluid resuscitation prior to blood product availability or in patients with severe hypoalbuminemia. One must also consider the context of care, such as a critically ill patient in the intensive care unit versus the intraoperative setting, which is the focus of this chapter, as the risk/benefit profiles differ. There are many different types of colloid solutions. One of the most familiar to anesthesia providers is albumin, which is available in 5% and 25% solutions. The albumin protein is relatively stable and is heated to 60°C for 10 hours to potentially remove pathogens such as HIV and hepatitis. Albumin is one of the most expensive

solutions, as it is derived from donated blood. Recently, the lower cost pentastarch and hetastarch (Hespan®) have been increasingly popular. Both are composed of glucose chains to which hydroxylated ethyl ether groups have been added in order to resist degradation. The average molecular weight of hetastarch is 450,000 kD, and comes in a 6% solution of either NaCl (Hespan®) or LR (Hextend®) (Table 41.2). Pentastarch, which has a slightly smaller molecular weight, was developed secondary to the fact that the large hetastarch molecules are sequestered in the reticuloendothelial system (RES), the kidney, and the liver. Although this has not been shown clinically, it may impair the RES. Outside the United States, but only since FDA approval in 2007, a tetrastarch (Voluven®) is available as well and recent analyses have suggested improved risk profiles as compared to hetastarches. For a comparison of hetastarch, pentastarch, and tetrastarch (all in NaCl solution) see Table 41.3. The polyhydroxylated starches have relative contraindications in patients with coagulopathies, fluid overload, renal impairments, or those undergoing cardiac surgery, and produce rare hypersensitivity reactions. However, recent data and regulatory agencies continue to make clinical decision making difficult regarding hydroxyethyl starch use. Hetastarch has been shown to have a decreased inflammatory response compared to albumin preparations. However, there is evidence showing possible impaired coagulation with Hespan as compared to albumin, particularly in cardiac surgery. This begs the question of whether hetastarch in a balanced salt (BS) solution (i.e., Hextend®) could avoid these coagulation issues. One must also be aware that HES/NS solution can cause a hyperchloremic metabolic acidosis, as it is not a balanced salt solution (similar to giving excess normal saline). In June 2002 the U.S. Food and Drug Administration (FDA) Blood Products Advisory Committee recommended that HES/BS (1) should not have a warning label for bleeding, (2) is pharmacologically different from HES/NS, (3) is equivalent to 5% albumin, and (4) is superior to HES/NS. However, in November 2013 the FDA revised the saftey warning recommending that the use of hydroxyethyl starches (1) be avoided in patients with renal dysfunction, at the first sign of renal injury, or severe liver disease, (2) requires monitoring of coagulation in patients undergoing open heart surgery associated with cardiopulmonary bypass due to increased risk of bleeding, and (3) HES/NS is to be avoided entirely in the perioperative setting in cardiopulmonary bypass patients due to the risk of bleeding. Table 41.2 ■ Hespan Versus Hextend HES/NS

HES (g/dL) Na (mEq/L) Cl (mEq/L) Lactate (mEq/L) Ca (mEq/L) K (mEq/L) Mg (mEq/L) Dextrose (mg/L)

HES/BS (Hextend)

(Hespan/Voluven)

60 143 124 28 5 4 0.9 99

60 154 154 — — — — —

Table 41.3 ■ Hetastarch Versus Pentastarch Versus Tetrastarch

pH Avg. MW Intravascular halflife Elimination Coagulation effects Liver effects

Maximum dose

Hetastarch

Pentastarch

Tetrastarch

5.5 450,000 25.5 hr

5 264,000 2.5 hr

4–5.5 70,000–80,000 12.5 hr

Renal Increases PT, PTT, bleeding time Temporarily increases amylase, increases indirect bilirubin 15–20 mL/kg, max. 1 L

Renal Increases PT, PTT, bleeding time Temporarily increases amylase

Renal Increases PT, PTT, bleeding time Temporarily increases amylase

15–20 mL/kg, max. 1 L

20–50 mL/kg

Avg. MW, average molecular weight; PT, prothrombin time; PTT, partial thromboplastin time.

Table 41.4 ■ Hespan Versus Hextend in Patients Needing Blood

Transfusions

Heart rate, beats/min EBL, mL PRBC, mL FFP, mL Platelets, mL Cryoprecipitate, mL

HES/NS

HES/BS

(N = 25)

(N = 31)

P Value

85 2,516 ± 1,856 1,516 ± 1,397 288 ± 697 83 ± 205 4 ± 20

78 1,560 ± 99 1,040 ± 639 73 ± 202 7 ± 38 0

0.049 0.02

EBL, estimated blood loss; FFP, fresh frozen plasma; HES/BS, Hespan/balanced salt solution; HES/NS, Hespan/normal saline; PRBC, packed red blood cells.

Gan and colleagues studied 120 patients undergoing major elective surgery who received HES/NS or HES/BS intraoperatively. Table 41.4 compares these solutions in patients who required blood transfusions. No statistical differences between groups were found for volume of HES, crystalloid, packed red blood cells (PRBC), fresh frozen plasma (FFP), platelets, or cryoprecipitate infused, or estimated blood loss. However, in the subgroup of patients who received intraoperative blood transfusions, there were significant differences in the mean heart rate and estimated blood loss. In addition, the thromboelastogram (TEG) r-time was measured, and patients who received ≥20 mL/kg of HES/NS had a statistically significant change in r-time from baseline to the end of surgery (p = 0.01). Patients who received HES/BS or 10 accompanied by symptoms or an AHI >30 regardless of symptoms. This technique has been proven to be efficient in preventing the collapse of the airway and improving breathing during sleep. CPAP therapy improves concentration, alertness, neurocognitive function, and mood. The CPAP has favorable effects on cardiovascular outcome but necessitates a strict commitment from the patient. The addition of humidification, bi-level positive airway pressure (BiPAP), and autotitration of positive airway pressure has been tried to improve compliance and patient comfort. Mandibular repositioning appliances represent a simple and noninvasive alternative method of treatment for mild OSA (AHI 5 to 15) and are used in patients who are unable to tolerate CPAP. The mechanism of action is similar to the jaw-thrust technique. Surgery is reserved for severe OSA or lack of response to CPAP. The main objective of any surgical technique is to enlarge the upper airway. Adenoidectomy, tonsillectomy, nasal polypectomy, septoplasty, uvulopalatopharyngoplasty, maxillomandibular advancement and hyoid expansion are all procedures used to alleviate the symptoms of OSA surgically. If these are unsuccessful and the obstruction is severe, the last option is tracheostomy. As adjuvant therapy, the following may be helpful: losing weight, position therapy, topical application of soft tissue lubricant, and the use of acetazolamide to increase respiratory drive to compensate for the metabolic acidosis caused by hypoxia. Most recently the application of high-flow nasal cannula (HFNC) in the perioperative care of OSA patients is proven to benefit this population during intraoperative moderate or deep intravenous sedation and during postoperative care after general anesthesia. HFNC has shown to be well-tolerated by the patient, easy to use and very useful in preventing hypoxia, and airway obstruction. Table 125.2 ■ Apnea–Hypopnea Index (AHI) and Severity of Obstructive Sleep Apnea (OSA) Severity of OSA None Mild OSA Moderate OSA

Adult AHI

Pediatric AHI

0–5 6–20 21–40

0 1–5 6–10

Severe OSA

>40

>10

Outcome The natural history of sleep apnea is not yet fully described, but the mortality is increased with the development of cardiovascular complications, especially in the middle-aged population. CPAP, surgery, and dieting can improve the outcome and lower the risk of death from cardiovascular complications. We also want to remind our readers that the Anesthesia Closed Claims Project maintains the Obstructive Sleep Apnea (OSA) Death and Near Miss Registry, which was jointly established by the Project and the Society of Anesthesia and Sleep Medicine. Case submission closed on December 31, 2016 and are undergoing analysis to (1) identify the level of monitoring, (2) provide increased understanding as to how and why OSA adverse events occurred, and (3) provide insight regarding how to best construct prospective studies to evaluate and develop best practices for the care of OSA patients.

Implications for Anesthesia In October 2005 that was updated in November 2014, the American Society of Anesthesiologists (ASA) developed practice guidelines for perioperative management of patients with OSA. This document should be considered required reading for every anesthesia provider.

Preoperative Evaluation Patients with an established diagnosis of OSA with the severity of the OSA graded from the results of the sleep study (AHI) (Table.125.1) should be managed according to certain practice guidelines that are recommended by the ASA. Otherwise, all surgical patients should be evaluated for OSA risk factors. Multiple screening methods are available, such as the Berlin Questionnaire, which has been proven to be specific and sensitive for OSA screening. The Berlin Questionnaire focuses primarily on symptoms of snoring, apnea, fatigue, hypertension, and body mass index (BMI). The ASA has come up with two models, one for identification and assessment of OSA and a second to be used as a scoring system (Tables 125.3 and 125.4) to predicate the possibility of OSA from the presence of various risk factors. The ASA modules need clinical validation and proof of their usefulness in the perioperative management of OSA. In patients who are evaluated as being at high risk for OSA and/or who are undergoing a major surgical procedure with a possible requirement for high doses of opioids for postoperative pain, it is advisable to postpone an elective surgery until

further evaluation and proper management of their OSA can be undertaken. During the preoperative evaluation of surgical patients with OSA, it is vital to perform a comprehensive history and physical examination to learn of any comorbidities or previous anesthesia-related complications and to document the settings of the patient’s CPAP/BiPAP. One should also make sure that the patient’s equipment will be available for postoperative use. The use of sedatives and analgesics should be avoided in the preoperative setting because of the increased sensitivity to any respiratory depression. The consequences of upper airway muscle tone relaxation could lead to devastating effects before the start of surgery and anesthesia. It is important not to underestimate the challenge of mask ventilation and/or intubation in these patients and to remember to have a clear plan for airway management before going ahead with a general anesthetic. Table 125.3 ■ ASA-Proposed Example for Identification and Assessment of OSA Clinical signs and symptoms suggesting the possibility of OSA 1. Predisposing BMI >35 kg/m2 (95th percentile for age and gender) physical Neck circumference >17 in or >43 cm (men); >16 in characteristics or >41 cm (women) Craniofacial abnormalities affecting the airway Anatomical nasal obstruction Tonsils touching or nearly touching in the midline 2. History of apparent Snoring (loud enough to be heard through closed airway obstruction door) during sleep Frequent snoring Observed pauses in breathing during sleep Awakens from sleep with choking sensation Frequent arousals from sleep Intermittent vocalization during sleep Parental report of restless sleep, difficult breathing, or struggling respiratory efforts during sleep 3. Somnolence Frequent somnolence or fatigue despite adequate “sleep” Falls asleep easily in a nonstimulating environment Parent or teacher comments that the child appears sleepy during the day, is easily distracted, overly

aggressive, or has difficulty concentrating Child often difficult to arouse at usual awaking time If patient has signs or symptoms in two or more of the above categories, there is a significant probability that OSA is present. Sleep study done Severity of OSAw Adult AHI Pediatric AHI None Mild OSA Moderate OSA Severe OSA

0–5 6–20 21–40 >40

0 1–5 6–10 >10

AHI, apnea–hypopnea index; ASA, American Society of Anesthesiologists; BMI, body mass index; OSA, obstructive sleep apnea.

Intraoperative Management OSA patients should be considered potential difficult airway management patients, and the anesthesia team should be prepared in advance for this possibility. As a general rule, whenever it is possible, a regional anesthesia technique should be used instead of general anesthesia. General anesthesia with a secured airway is a better choice than monitored anesthesia care (MAC) with spontaneous breathing and an unsecured airway. Short-acting anesthetic drugs represent an attractive choice for general anesthesia. For monitoring, standard noninvasive monitoring such as pulse oximeter, capnography, electrocardiography (EKG), and blood pressure are critical, especially for patients who are breathing spontaneously under MAC. Table 125.4 ■ ASA-Proposed Example for OSA Scoring System Severity of sleep apnea based on sleep study or clinical indicators if sleep study not available; point score (0–3) Invasiveness of Superficial surgery under

None Mild Moderate Severe

0 1 2 3

0

surgery and anesthesia; point score (0–3)

local or peripheral nerve block anesthesia without sedation Superficial surgery with 1 moderate sedation or general anesthesia Peripheral surgery with 1 spinal/ epidural anesthesia (no more than moderate sedation) Peripheral surgery with 2 general anesthesia Airway surgery with 2 moderate sedation Major surgery with general 3 anesthesia Airway surgery with general 3 anesthesia Requirement for None 0 postoperative Low-dose oral opioids 1 opioids; point score High-dose oral opioids, 3 (0–3) parenteral or neuraxial opioids Estimation of perioperative risk: overall score = score from A plus the greater of the score for either B or C; point score (0–6). Patients with score of 4 may be at increased perioperative risk from OSA; patients with a score of 5 or 6 may be at significantly increased perioperative risk from OSA. ASA, American Society of Anesthesiologists; OSA, obstructive sleep apnea. Modified with permission from American Society of Anesthesiologists. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: An updated report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2014;120(2):268–286. Copyright © 2013 American Society of Anesthesiologists, Inc.

Extubation should be done in the semiupright position when the patient is fully awake and completely recovered after muscular blockade.

Postoperative Care The main objectives in postoperative care are oxygenation and maintenance of a patent airway using supplemental oxygen and CPAP/BiPAP support. This is especially true for patients who are already on these treatments or high-risk patients. Adequate analgesia with minimal depression of respiratory drive provided by continuous analgesia through regional techniques such as continuous nerve blocks, paravertebral blocks, or epidurals are the best choice for postoperative pain control. When appropriate, regional techniques should be used, preferably without opioids. Nonsteroidal anti-inflammatory drugs or other adjuvants should be used whenever possible to decrease opioid requirements. The use of patient-controlled analgesia (PCA) without the continuous infusion mode represents a better alternative than opioids administered on a regular or as-required basis. The antidote for opioid overdose should be readily available to rescue the OSA patient with respiratory compromise. Supine position should be avoided, and lateral, prone, or sitting position should be used. Continuous monitoring of oxygenation, breathing, blood pressure, and heart rhythm are required because of the possibility of serious complications such as hypertension, dysrhythmias, hypoxia, and airway obstruction, the latter potentially requiring urgent reintubation. Studies have shown a 2 to 3× increase in all-cause mortality in patients with OSA, as well as a 2 to 3× increase in perioperative cardiopulmonary complications. The use of CPAP has only been studied in retrospective reviews, as there are ethical questions regarding holding someone’s home medical therapy, and they have achieved mixed results. In some studies it decreased the risk of mortality by ∼1/3rd but was not statistically significant in others. One study administered CPAP to patients after abdominal surgery without a high likelihood of OSA and it reduced postoperative cardiopulmonary complications. Studies have also shown that abrupt CPAP withdrawal increases blood pressure by an average of 10 mm Hg, but does not alter endothelial function to cause a significant change in myocardial or renal perfusion.

Discharge Criteria In addition to the standard discharge criteria used routinely in the postanesthesia care unit (PACU), patients with OSA should be able to maintain adequate oxygenation on room air with no hypoxemia or critical airway obstruction when they are asleep. OSA patients should stay at least 3 hours longer than non-OSA patients to ensure the required discharge criteria. OSA patients who develop an episode of hypoxemia or critical airway obstruction while in the PACU require an extended monitoring period of 7 hours (median time recommended by ASA guidelines in this circumstance) and the most careful evaluation thereafter (many anesthesia providers simply secure a postoperative bed in this instance). Patients with mild OSA who have undergone minor surgery

(superficial plastic surgery, eye procedures, and superficial orthopedics) under local or regional anesthesia can be discharged home on the same day. Patients with moderate OSA and intermediate comorbidities who have undergone intermediate-risk surgery (does not include abdominal, faciomaxillary, thoracic, or intracranial) should be hospitalized in a standard surgical unit. Patients with severe OSA, necessitating CPAP at home and/or who have had major surgical procedures, should be admitted to a stepdown unit or intensive care unit until the threat of respiratory complications is no longer present. Continuing CPAP in patients with severe OSA was associated with reduced perioperative complications in some series but not in others.

Outpatient Surgery Outpatient surgery for OSA patients remains controversial. According to Sabers et al., the presence of OSA does not increase the risk of readmission to the hospital after ambulatory surgery. However, this view is not shared by many same-day surgery anesthesia providers, and it is the practice in some ambulatory surgery centers to refuse care to sleep apnea patients (and sometimes even suspected sleep apnea patients). Risk must be assessed for each individual patient, because there are a large number of undiagnosed cases of OSA (Table 125.5).

OSA Characteristics for Children The peak period for OSA in the pediatric population is preschool age, with equal boy/girl distribution. The common causes are adenotonsillar hypertrophy, obesity, and craniofacial anomalies. Usually, children with OSA suffer growth retardation, hyperactivity disorders, developmental delay, or attention deficit disorders. Excessive daytime somnolence is uncommon in children with OSA. Sleep studies show normal sleep architecture and a 5 are positive for OSA diagnosis. In the absence of sleep study, have a high index of suspicion to the diagnosis of OSA in the presence of risk factors. Avoid preoperative benzodiazepines or opioids. Use regional anesthesia whenever appropriate or general anesthesia with secured

airway (an endotracheal tube or, controversially, a laryngeal mask airway). Extubate in semiupright position, when the patient is awake and fully recovered from neuromuscular blockade. Use supplemental oxygen with or without CPAP and monitor oxygen saturation. Avoid the supine position. Use adjuncts to decrease opioid requirement. Discharge adult patients when they reach their baseline room air oxygen saturation and have no hypoxemia or critical airway obstruction when not stimulated. Pediatric patients with moderate to severe OSA should be hospitalized overnight after surgery. Suggested Readings American Academy of Sleep Medicine Task Force. Sleep related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of SleepMedicine Task Force. Sleep. 1999;22(5):667–689. American Society of Anesthesiologists. Practice guidelines for the perioperative management of patients with obstructive sleep apnea. Anesthesiology. 2014;120(2):1–19. Bandla P, Brooks LJ, Trimarchi T, et al. Obstructive sleep apnea syndrome in children. Anesthesiol Clin North America. 2005;23(3):535–549. Cielo CM, Silvestre J, Paliga JT, et al. Utility of screening for obstructive sleep apnea syndrome in children with craniofacial disorders. Plast Reconstr Surg. 2014;134(3):434e–441e. Cortuk M, Kiraz K, Sonmezler A, et al. Perioperative evaluation for the patients with obstructive sleep apnea. Tuberk Toraks. 2015;63(1):53–59. Fava C, Montagnana M, Favaloro EJ, et al. Obstructive sleep apnea syndrome and cardiovascular diseases. Semin Thromb Hemost. 2011;37(3): 280–297. Hiestand MD, Britz P, Goldman M, et al. Prevalence of symptoms and risk of sleep apnea in the US population. Results from the National Sleep Foundation Sleep in America 2005 Poll. Chest. 2006;130(3):780–786. Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131(7):485–491. Sabers C, Plevak DJ, Schroeder DR, et al. The diagnosis of obstructive sleep apnea as a risk factor for unanticipated admissions in outpatient surgery. Anesth Analg. 2003;96(5):1328–1335. Suzuki YJ, Jain V, Park AM, et al. Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases. Free Radic Biol Med. 2006;40(10):1683–1692.

126 Don’t be Shy About Borrowing ICU Equipment, Medications, and Personnel for the Critically Ill Patient Going to the Operating Room Elliott Karren, MD and Matthew Griffee, MD

A 46-year-old male refinery worker suffers an explosive burn injury to his trunk. Over the initial week of hospitalization in the burn ICU, he develops acute lung injury and requires venovenous extracorporeal membrane oxygenation to treat refractory hypoxemia. The ventilator mode is airway pressure release ventilation. His respiratory failure, volume overloaded state, and lung contusions lead to pulmonary hypertension, treated with inhaled nitric oxide. Cardiac output and pulmonary artery pressure are monitored with a pulmonary artery thermodilution catheter. Your burn trauma surgical colleague schedules OR time for debridement of eschar. The anesthesia technician assisting you with transport asks, “What equipment do you need in the OR for this case?” Anesthesiologists spend substantial time managing stable patients undergoing elective surgical procedures. However, we are also asked to manage critically ill patients in the OR. Certain aspects of critical care are routine for anesthesiologists, for example, ventilator management and titration of vasoactive medications. Other aspects of care for the ICU patient may be less familiar. The aim of this chapter is to highlight some medications, devices, and personnel used in the ICU that may be useful for the intraoperative care of critically ill and injured patients.

Pulmonary Arterial Vasodilators Inhaled nitric oxide, epoprostenol, and iloprost are some medications used to manage pulmonary hypertension and right heart failure after cardiothoracic surgery or in patients with severe acute lung injury. Inhaled nitric oxide (iNO) is given as a continuous inhalational agent, while epoprostenol can be given either parentally, via a central line, or as a continuous nebulized solution. Iloprost is unique in that it is given intermittently

via nebulizer. Inhaled nitric oxide is started at a dose of 40 ppm, titrated down rapidly to 20 ppm, and then more gradually as oxygenation and ventilation improve, until a dose of 5 ppm is reached. It is then slowly weaned in increments of 1 ppm until discontinuation. Epoprostenol is initiated at 25 to 50 ng/kg/min by continuous inhalation. As with iNO, epoprostenol is weaned in half-dose increments, but without the need for as slow a taper at the end. It is important that these medications are continued intraoperatively, since abrupt discontinuation of any of these medications can be associated with a number of side effects, including hypoxia (due to decreased ventilation–perfusion matching) and rebound pulmonary hypertension. For the same reasons, rapid intraoperative titration should be performed with caution. Because the epoprostenol and nitric oxide delivery systems must travel with the patient between the OR and ICU, the simplest solution may be to travel with the ICU ventilator as well. The iloprost atomizer, by contrast, can be connected to the anesthesia circuit, but it requires a different adapter than the interface used for albuterol. Alternatively, inhaled iloprost therapy can be scheduled for a time just prior to any patient transport, negating the need for delivering it during imaging or procedures outside the ICU. Beware of serious potential adverse effects! Nitric oxide can cause methemoglobinemia. Both administration of nitric oxide and prostaglandins have been associated with pulmonary edema in the setting of LV systolic dysfunction, due to improved right-sided cardiac output. Epoprostenol has been associated with thrombocytopenia. All three inhaled agents are known to inhibit platelet aggregation. Due to mucosal vasodilatation, any inhaled vasodilator can cause bronchoconstriction and systemic vasodilation can occur at higher doses of inhaled vasodilator therapy.

Antibiotics and Immunosuppressive Agents Critically ill patients with sepsis require a regimen of antibiotics. Antibiotics require constant plasma concentrations above the bactericidal or bacteriostatic threshold in order to be efficacious. Drops in plasma concentration due to missed doses can lead to bacterial resistance or ineffective resolution of infection. Remember to check with the ICU staff to see if the patient is due for important medications before starting the case. The same consideration applies to immunosuppression medications for organ transplant recipients.

Temporary Pacemakers During cardiac surgery, temporary pacemaker leads are attached to the epicardium. Temporary pacemaking may be indicated if severe bradycardia is discovered during

weaning from bypass or if damage to the conducting system occurs during surgical intervention. Epicardial pacing wires are for temporary use (hours to a few days). Patients with epicardial leads who have effective endogenous pacing still remain at risk for bradycardia or high-degree heart block if they require multiple trips to the operating room. Prior to taking a patient with epicardial pacing leads to the OR, be sure to determine why the leads are in place, and whether the patient is pacemaker dependent. You want to make sure that you know the settings of the temporary pacemaker, as well as the rate and rhythm of the endogenous conduction system.

ICU Ventilator ICU ventilators almost exclusively employ piston-based designs for mechanical ventilation. Piston-based designs have the advantage of delivering more accurate tidal volumes, which may be challenging in bellows-driven ventilators (commonly used in the OR) in patients with reduced lung compliance, such as in acute lung injury or pulmonary edema. Additionally, older generation OR ventilators may not be able to generate sufficient minute ventilation to prevent severe hypercarbia and respiratory acidosis. When you are planning an anesthetic for a patient with stiff lungs, don’t forget the option of taking the ICU ventilator to the OR, because stiff lung areas can easily become atelectatic, leading to an increase in shunt and hypoxemia. It is important to take note of the ICU ventilator settings when transitioning to the anesthesia machine ventilator. The standard-of-care for critically ill patients with respiratory failure is to use physiologic tidal volume settings (6 to 8 mL/kg predicted body weight) and higher PEEP settings. Clinical trials demonstrate that patients with lung injury benefit from lower tidal volumes. Clinical trials have also shown that patients undergoing thoracic surgery and major intra-abdominal surgery benefit from lung protective ventilation. Thus, careful consideration of the risks and benefits of limiting plateau pressure and tidal volume are warranted when caring for ICU patients who require perioperative mechanical ventilation. Patients with the most severe lung injury may require rescue ventilator modes such as airway pressure release ventilation, high-frequency oscillatory ventilation, or venovenous extracorporeal membrane oxygenation—collectively termed rescue strategies—that are not available on the anesthesia ventilator. In such cases, ask yourself whether surgery should be delayed until the lung injury improves and the ventilator setting is changed to a conventional mode, or whether surgery should be done in the ICU. In rare cases, a ventilator capable of these advanced ventilator modes or the ECMO circuit will need to be transported to the OR. Airway pressure release ventilation maintains a high time-averaged mean airway pressure to avoid de-recruitment, while still allowing a patient to have spontaneous

ventilation. Take note that patients with a lot of dead space ventilation may be getting a substantial amount of alveolar ventilation with spontaneous breaths during the P high phase of breathing. Be vigilant to see if the patient is taking breaths at P high and what the total minute ventilation is on the ICU ventilator. If the patient requires a paralytic, the loss of spontaneous ventilation may cause a substantial decrease in minute ventilation. It may be necessary to increase tidal volume or respiratory rate to maintain acceptable CO2 levels during anesthesia.

ICU Personnel Respiratory Therapist It is challenging to transport and care for patients who require rescue ventilator modes or inhaled pulmonary vasodilators. While some providers may be familiar with these therapies, the additional equipment makes transport and intraoperative care more complex. In these cases, having a respiratory therapist during transport and potentially for some of the time during the case may be helpful. Respiratory therapists are well trained in the practical aspects of administering airway medications, and changing ventilator settings on ICU ventilators. Having them available allows you to focus more attention on resuscitation of a critically ill patient and less attention on the ICU ventilator alarms and buttons.

Ventricular Assist Device Coordinator We have all noticed increasing numbers of patients obtaining ventricular assist devices (VADs) for heart failure. Given this growth, all anesthesia providers should be familiar with practical anesthesia implications of VADs. Because there are several VAD manufacturers, adjustment and troubleshooting of VAD parameters is complex. Mechanical heart support hospitals have VAD coordinators who are on call to ensure patients with temporary or permanent VAD support can be transported safely. A VAD coordinator may be indispensable in the OR if the VAD needs to be adjusted at a time when the other people in the room have to focus attention on resuscitation and surgery. Keep in mind that a patient dependent on a VAD for most of the cardiac output may have little or no pulse pressure, resulting in inaccurate readings of automated blood pressure cuffs and poor waveforms of a pulse oximeter. The recommended technique for taking noninvasive blood pressure in this circumstance is to use a vascular Doppler probe and a manual BP cuff. The first flow detected in the brachial artery with releasing the cuff is the mean arterial pressure.

Lung De-recruitment

If the ETT gets disconnected in transitioning from the ICU vent to the transport breathing circuit and the patient has been needing PEEP to maintain adequate oxygenation (due to stiff lungs), you may need to do a recruitment maneuver when getting into the OR or upon return to the ICU. One way to do a recruitment maneuver is to use manual ventilation and keep airway pressure 40 cm water for 40 seconds. On a ventilator, the tidal volume and PEEP can be increased for a few minutes, then slowly decreased to maintenance settings. TAKE HOME POINTS Anesthesiologists can profoundly impact the care of the critically ill patient. Patients get the best care when there is a seamless articulation of ICU and OR care. So pay very careful attention to key details of the ICU care plan in order positively affect the clinical outcome in ways that may not be manifest immediately in the OR. Spending a little extra time getting a complete sign out from the ICU nurse and intensivist, and making sure that the ICU equipment, medications, and personnel the patient needs are available for intraoperative care may prevent serious problems during a challenging case. Suggested Readings Celebi S, Koener O, Menda F, et al. The pulmonary and hemodynamic effects of two different recruitment maneuvers after cardiac surgery. Anesth Analg. 2007;104(2):384–390. Griffiths MJ, Evans TW. Inhaled nitric oxide therapy in adults. N Engl J Med. 2005;353(25):2683–2695. Liu LL, Aldrich JM, Shimabukuro DW, et al. Special article: Rescue therapies for acute hypoxemic respiratory failure. Anesth Analg. 2010;111(3):693–702.

127 The Dao of Positioning Raymond G. Graber, MD, Selina Read, MD, and Catherine Marcucci, MD

The Problem First, let’s start off this topic with a bit of wishful thinking—wouldn’t it be nice if surgery could always be performed on a patient in a neutral or “natural” position? Alas, sometimes the surgeon desires variations or even extremes of positioning that diverge from what is safest for the patient. Although the entire operative team is responsible for positioning of the patient, the practical and even legal truth is that the anesthesia team is “most responsible.” After all, we are the ones who have caused the lack of consciousness and insensate condition that prevents the patient from recognizing trouble and correcting it by literally moving out of harm’s way. Included in this overall “positioning” responsibility is the necessity to take into account the patient’s anatomy and physical vulnerabilities, baseline physiology and comorbidities, and the perturbations that occur with positioning and surgical manipulations. You also need to understand the proper use of a wide variety of positioning devices and equipment. On an existential level, why is your job as a “positioner” so crucial? Basically, because we are in the business of preventing pain! Remember always that both acute and chronic positioning injuries can be extremely painful. We tend to think about the acute issues such as soft tissue damage, corneal abrasions, vascular compression, and nerve compression or stretch, but don’t forget that there can be long-term problems such as chronic pain, neuropathy, nerve regeneration pain, and the ever-dreaded and devastating complication—visual loss. We have found that positioning injuries to the face, arms and hands, and genitals are especially difficult and painful complications for patients, and hence us. Positioning injuries are also painful for legal and financial reasons. The American Society of Anesthesiologists sponsors the Closed Claims Project—a database of adverse anesthetic outcomes obtained from the closed malpractice claims files of liability insurance companies. A 1999 review of this data revealed a significant number

of claims that asserted perioperative peripheral nerve injury. The most common nerve involved was the ulnar nerve (4.5% of all claims in the project). Some of these injuries may have been secondary to brachial plexus block, but 85% occurred on patients who received general anesthesia. The next most common nerve injury was to the brachial plexus (3.3% of all claims) of which about 75% occurred in patients who were under general anesthesia. Claims also involved sciatic/peroneal, median, radial, and femoral nerves. There are also other position-related injuries in the database—including vision loss, and neurologic injury after shoulder surgery performed in the sitting position.

The Lessons We were fortunate to have received some superb instruction on patient positioning early in our training, and these lessons in the “philosophy of positioning” have stayed with us down through the years. Here are some recommendations on how you should think about and approach patient positioning. (a) First principles: Remember that there are both primary and secondary positioning complications. Primary positioning injuries involve actual tissue damage from torquing, twisting, gravity, pressure injuries, pinch points, and improper use of positioning equipment. Secondary positioning complications result from the physiologic consequences of an unnatural and prolonged position or turning, such as prolonged beach chair position with its deleterious effects on cerebral perfusion. We must be ever vigilant in every case to prevent positioning injuries. (b) Let’s talk terminology: There are different components to positioning. “Moving” is easiest—generally it’s the process of sliding the patient from one bed to another by either lifting sheets or using a rolling device. A supine-to-supine move, in a pure lateral direction. Then there is “turning”—the process by which a patient gets moved from the supine to a lateral or prone position (or back to supine at the end of the case). A turn-to-prone generally involves turning off a cart and on to a special frame or chest rolls placed on the OR table. There is a variety of bed maneuvers that can happen next —such as flexing, extending, tilting, etc. Lastly, there is “rotation”—which is turning the whole bed on its axis so that now it’s not the head that is nearest to the anesthesia machine, but the side of the patient or even the feet. With each of these maneuvers, there is potential for patient injury or dislodgment of airways and vascular access. (c) Checking: Each time one of these maneuvers is completed, the patient’s position should be checked. What does that actually mean? Well, the head and neck and spine should be in alignment and neutral. Arms should not be abducted so high as to risk brachial plexus stretch injury. Breasts and genitals should not be trapped or pinched. Potential pressure points should be padded. Axillae should be free from compression.

(d) Preparing to turn: Turning is the most complicated component of positioning, and proper preparation makes a big difference. Tape your lines (both venous and arterial) such that you do not make loose “purse handles” or loops that can easily be caught when you flip a patient. Place your leads and pads such that a minimum of replacement is required after you turn. Have adequate staff available to do the turn— at minimum one on each side, one at the foot of the bed, and a member of the anesthesia team at the head of the bed. We take responsibility for managing the head and neck and airway during the turn. It’s helpful to have one additional person to watch the arms and lines during the turn. Disconnect most monitors prior to the turn. We generally like to disconnect the anesthesia circuit from the airway immediately prior to turning, to decrease the risk of pulling the airway out. (e) Turning: There are many individual styles of turning or flipping a patient and they all work if they are done carefully and consistently. We were taught to envision the patient as occupying an envelope in space (a burrito-shaped package, if you will) and try to turn everything as a unit. When turning from supine to prone, lines and monitors on the arm closest to the bed serve as an axis which the body can be rotated around. The person handling the head and neck calls the turn. The head and neck should be kept in alignment with the spine. Arms and legs are controlled so that nothing gets torqued or twisted or dropped. Gravity is not our friend here. Once the turn is completed, the airway is hooked up, tube position is rechecked, and the rest of the monitors are reattached. If a monitoring pad gets dislodged, do not try to reuse it or restick it—just get a new one. (f) Airway issues: Of course, the most important “line” is the oxygen line, i.e., the airway device or endotracheal tube. After an airway is placed, you have to secure it in a way that it won’t be lost with changes in position. You can imagine the scenario where the patient is prone, drooling up a storm, tape adhesive is dissolving, the circuit is under tension, and the tube starts working its way out. There are many tricks to deal with this. You can give 0.2-mg glycopyrrolate IV to any patient who is going to be prone, to reduce the drools. You can use benzoin or Mastisol ® to better secure tape. Some practitioners will put sterile transparent IV dressings over the tape to keep it dry. You can also double cover and secure with both tape and a tube tie. The good thing about a tie is that it won’t loosen up and fall off, but you can’t leave a tie in place when the neck is going to be prepped out. Next, after you have turned the patient, hooked the circuit back up, and verified breath sounds, make sure the circuit is supported or secured so that there is no weight pulling on the tube. Make sure that the airway circuit is long enough to tolerate any changes of the position of OR table within the room. Make sure the endotracheal tube and airway circuit are as accessible as possible for suctioning and checking.

Alright, now let’s talk about some airway rescue scenarios. You should know, before it happens, what you are going to do if the patient is accidentally extubated during a turn. The best approach is to quickly turn back supine and resecure the airway. What about the situation where the case is underway and the patient gets extubated in the prone position? You won’t be able to immediately turn the patient— the surgeon will have to do something to cover the incision, and a bed has to be brought in to the OR to flip on to. Yes, there are stories about legendary anesthesiologists who have rushed into rooms when prone patients in pins were extubated and reintubated patients from the floor underneath the patient—and in the famous case at Hopkins, it’s actually true—but you don’t want to have to rely on being a legend. An easier alternative is to place an LMA if you need to attempt to oxygenate and ventilate prior to the turn. (g) Equipment issues: You must really understand how to use positioning equipment, including frames, sleds, arm boards, arm rests, and the OR table itself. Positioning complications can occur easily as a result of the patient–equipment interface—for example, pressure points and stretch injuries. A classic example is peroneal nerve palsy secondary to compression from stirrups. On another note, remember to adjust the height of transducers when you turn or position a patient, in order to maintain accurate readings. Also, check all equipment when you have raised or lowered a patient vertically. We once saw a case where a patient was raised vertically and his hand became trapped under a Mayo stand, which resulted in skin necrosis to his thumb and forefinger—not a happy day for anybody in the room. (h) Bean bags: These ubiquitous “patient positioning devices” are frequently used for positioning in the operating room, and are most commonly used for securing patients in the lateral position for orthopedic, thoracic, and urologic procedures. How are they used? The patient starts out supine on the bean bag, and is then turned to the lateral position. The flexible bean bag is molded around the patient, suction is attached to the device, and the bean bag now becomes a rigid structure. Sometimes, surgeons will want to flex the bed as part of their positioning plan—this is common for thoracic surgery. This bed maneuver should be done prior to placing the bag on suction. At the end of surgery, the bean bag suction is removed, and it will become flexible again. There are a few things to watch out for. The bean bag should not be positioned so high that it is compressing the axilla. An axillary roll is commonly used, but may not always be necessary if the bean bag has adequately raised the chest wall off the bed. Also, remember that there is potential for pressure points that can result in injury. Injury to the dependent lateral femoral cutaneous nerve (meralgia paresthetica) has been reported in hip replacement surgery (secondary to compression at the anterior superior iliac spine). We have also seen a dependent radial nerve injury due to the

beanbag compressing the nerve against the posterior lateral aspect of the humerus. (i) The Survey: The absolute best thing we were ever taught was to stand back after a patient is positioned but before surgical prep commences and make a quick visual head-to-toe survey from all sides of the patient. Does the patient look comfortable and as “neutral” as possible? Could you imagine yourself in such a position for the duration of surgery? Remember to consider both the degree of deviation from neutral anatomical position and the length of time the patient will be mobilized. If any changes need to be made, this is the time to do it. Use your best social skills with your surgeon to accomplish your goals. Also make sure that all limbs are well-secured, and not at risk of falling from their designated spots. Once the drapes go up, it is much harder to deal with these issues. (j) Rotations: Surgeons will frequently request rotation of the OR table. A 90-degree rotation is frequently used—this allows the anesthesia team to have good access to one side of the body and to not be too far away from the head. Some surgeons request a 180-degree rotation of the OR table so that they have unrestricted access to the head and neck. This can be problematic for us, because now you only have access to the bottom of the feet. Work with your surgeons to see if they can tolerate a 165- to 170degree rotation instead. Try to preserve access to one arm and one leg—this allows you to put in extra peripheral IVs, an arterial line, or even femoral lines if you need to without totally displacing and disrupting the surgeon. You do not want to have your only working IV located in the arm or hand that is away from you or is tucked. (k) Lines: When planning where you are going to place intravenous and arterial access, try to keep in mind what limb you will have easiest access to once the patient is in their final position. If at all possible, it pays to have your arterial line and best IV access in the limb you have access to. It is also not a bad idea to place a spare IV before positioning. It can be capped for the turn, but be available later in the case if needed. (l) Extremes: The very thin patient may be more prone to pressure point injuries, and need more padding—because they have less built in cushioning. The obese patient may require special OR tables which are rated for heavier patients. You will need more help to position these patients safely. (And by safely—I mean for the patient and for the staff!) It may be worth discussing with the surgeon whether that planned prone case could be done in the lateral position instead. The obese patient also requires extra padding because of the extra weight. Brachial plexus injuries have been reported in obese patients who have been placed in prolonged Trendelenburg position where shoulder braces were being used to prevent the patient from sliding down the OR table. These injuries have also been seen in the obese patient in the supine

position when there was inadequate padding behind the arms, and this may be further potentiated by being in the reverse Trendelenburg position. The elderly patients may also be more prone to pressure point injury, and need good padding. We have seen elderly with tissue paper skin get tears in their skin with turning and moving. (In some cases, we have wrapped the arms with protective cotton roll or gauze prior to a move.) Also watch out for arthritic necks and shoulders, which do not have the same range of motion that they once had. You can check range of motion during your preop exam, and simulate the position that they will be in during surgery to see if it is tolerable. (m) Documentation: The patient’s position must be checked and documented throughout the case. This certainly includes documenting the steps that were taken to avoid any and all of the recognized positioning complications at the time of the initial turn or positioning. This cannot be stressed strongly enough. There are positioning complications that arise from the anatomic and physiologic sequelae that occur in certain positions, even if every precaution is taken. You can do “everything right” and still have a complication. Thorough documentation may prevent these situations from becoming malpractice situations. We were also taught that the patient should be surveyed every 15 minutes as much as possible and a note made in the anesthesia record. TAKE HOME POINTS Assume that you have the primary responsibility for safe positioning and minimizing the risks of positioning complications and injuries. Positioning injuries and complications can be very painful and difficult for the patient to deal with. You have to give these clinical issues your utmost attention. Plan for the turn and/or position from the time you bring the patient into the OR. This includes planning the placement of monitors, lines, and leads. Consider redundant intravenous access when it can be accomplished quickly and with little risk to the patient. You might need it only once in a while, but if you do need it, you won’t be sorry you have it. When turning a patient, imagine that he is a neatly packaged bundle and turn the whole bundle as a unit. Pay special attention to whatever crosses the boundaries of the bundle. You must prevent equipment elements and body parts from being dragged, torqued, or hyperextended in a turn or repositioning maneuver. Somebody, as in a specifically designated anesthesia person, has to assume primary responsibility for the head, neck, and airway. It starts with proper securing, then disconnecting, safely turning, and reconnecting the airway. This includes establishing that the ETT remains where you want it after the turn.

Take a moment to carefully survey the patient in the final “turned” or positioned patient before the surgical prep begins. If the OR table is to be rotated to facilitate the surgeon’s access to the operative site, negotiate for a few degrees in order to preserve your access to a hand, arm, arm board, and leg. The closer to 90 degrees, the better. Use special care when dealing with patients with extremes of weight and age. Document the initial positioning safety checks and ongoing intraoperative positioning checks as possible! Suggested Readings Barash PG, Cullen BF, Stoelting RK. Clinical Anaesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2017; 809–817. Brunette KE, Hutchinson DO, Ismail H. Bilateral brachial plexopathy following laparoscopic bariatric surgery. Anaesth Intensive Care. 2005;33(6):812–815. Cheney FW, Domino KB, Caplan RA, et al. Nerve injury associated with anesthesia: A closed claims analysis. Anesthesiology. 1999;90(4):1062–1069. Miller R, Eriksson L, Fleisher L, et al. Miller’s Anesthesia. 4th ed. Philadelphia, PA: Elsevier Saunders; 2014; 1241–1249. Miller RD, Pardo M. Basics of Anesthesia. 6th ed. Philadelphia, PA: Elsevier Saunders; 2011; 300–314. O’Connor D, Radcliffe J. Patient positioning in anesthesia. Anaesth Intensive Care. 2015;16(11):543–547. Thomas J. Post-operative brachial plexus neuropraxia: A less recognised complication of combined plastic and laparoscopic surgeries. Indian J Plast Surg. 2014;47(3):460–464. Weier CA, Jones LC, Hungerford MW. Meralgia paresthetica of the contralateral leg after total hip arthroplasty. Orthopedics. 2010;33(4); DOI: 10.3928/01477447-20100225-24.

128 The Supine Position—Complications Can Still Arise! Kristin Bowden, CRNA DNAP MBA and Richard Botney, MD

The operating room schedule reads “supine position.” At first, most anesthesia providers would be pleased to see this neutral–recumbent position listed. Almost all anesthetics are initiated with the patient in the supine position. If the patient remains in this position after induction, efforts and risks associated with repositioning are minimal. No manipulation of limbs means no overstretching or pulling of extremities, and no strategic placement of excessive bulky padding in places where ischemia can manifest due to excessive pressure. Accessing intravenous lines and placing invasive monitors can be accomplished with ease. Most importantly, the airway is readily accessible. The supine position produces minimal strain and stress on the body and its systems, and although the type of operation ultimately determines the patient position, presumably, the supine position is optimal for many surgical procedures. Nonetheless, there are complications related to the supine position! And it is very important that the anesthesia provider be aware of these. In some cases, the risk arises because of specific patient conditions, as we highlight in our chapters on patients with spastic conditions or who have undergone amputations. For most cases, however, the risk results from interactions between patient physiology and the specific effects of positioning, creating difficulties in achieving optimal anesthetic management, for example ventilatory challenges in the morbidly obese individual. Alternatively, there are specific complications that can result in patient morbidity and adverse outcomes, such as nerve or ocular injuries. The anesthesia provider should employ various strategies to minimize these risks.

General Considerations for Patient Positioning It is important when situating patients that they should never be placed into a position they would not or could not assume when awake. For example, a patient with limitations in range of motion (ROM) of the upper extremity due to arthritis should not have their limb placed in a position outside their normal ROM. Discussion about ROM limitations

due to pain, fractured bones, arthritis, or other conditions that can result in mechanical limitations to ROM should be clarified with patients during the preoperative evaluation. The anesthetic plan should involve all members of the operating room (OR) team, w i th shared responsibility for the movement and positioning of the patient. This includes the patient, as after a patient is transferred to the OR table, they can participate in positioning themselves prior to the induction of anesthesia. In so doing, they can verbalize their own comfort. This will help reduce the risk of positioning-related complications and increase the likelihood of an injury-free outcome. Once the patient has been anesthetized, pressure points should be properly padded and the neck, spine, and other joints should remain in a neutral position. Limb positions should not be stretched beyond acceptable limits, and limbs should be well secured to ensure they do not fall off the table during surgery. A pillow placed under the knees can reduce lumbar strain and the possibility of the patient experiencing back pain, especially in patients with pre-existing back discomfort. If this is done before induction, the patient can provide feedback about how well the pillow reduces back pain. If steep Trendelenburg, reverse Trendelenburg, or tilting the table side to side is to be used during the surgical procedure, a preassessment should be done to ensure the patient is completely secured and will not slide during the procedure. The following checklist is a useful tool for evaluating the correct position (including the supine position!) and safety of a patient when an anesthetic is being administered.

Positioning Checklist 1) Airway. No alteration of ETT patency or placement (including depth). Recheck capnograph for waveform tracing formation. 2) IV lines and invasive monitors. Check patency of IVs and flow of IV fluid, and arterial tracing should not be dampened (e.g., if arms are tucked). 3) Eyes. Closed and protected. Do NOT rush this step. 4) Neurovascular. Vulnerable areas padded and excessive extension/abduction avoided. 5) Cables, catheters, and electrodes. Should not be pressed into skin (e.g., from being underneath patient or passing over the face). 6) Access. At-risk areas should remain accessible for review, if possible.

Complications Related to Physiologic Changes The supine position is associated with a number of physiologic changes that can influence anesthetic management, making it more complicated and resulting in the possibility of undesirable outcomes. Changes of particular interest may occur to the respiratory and cardiovascular systems.

Respiratory In the supine position, the intra-abdominal contents and diaphragm shift cephalad and compress the adjacent lung tissue. Functional residual capacity (FRC) decreases with a change from the upright to the supine position. This is exacerbated in anesthetized patients, even more so when the patient is obese. Small airways begin to collapse, resulting in a decline in closing capacity. Healthy, spontaneously breathing patients have a normal tidal volume that is typically above closing capacity, and their small airways remain open for gas exchange. This function changes as the body grows older: By age 45, normal tidal breathing causes some airway collapse in the supine position, and by age 65, collapse happens in the upright position. As the FRC decreases there is potential for the closing capacity to exceed the FRC, which can lead to ventilation– perfusion (V/Q) mismatch and subsequent hypoxemia. Demographics at risk for this include the elderly, who have higher closing capacities, and obese or pregnant patients who already have a reduced FRC. The effect can be moderated with positive endexpiratory pressure (PEEP). Positive pressure ventilation in the supine position in obese patients and during laparoscopic procedures is associated with reduced pulmonary compliance. This necessitates greater inspiratory pressures to deliver adequate tidal volumes. The Trendelenburg position exacerbates these effects significantly. Also, these patients are at increased risk of an increase in pCO2 due to hypoventilation. The supine position and general anesthesia decrease FRC. Pneumoperitoneum from laparoscopic surgery and the Trendelenburg position shift the diaphragm cephalad, further decreasing FRC, possibly to values less than closing volume. This causes airway collapse, atelectasis (more so in obese patients, because of the negative effects of thoracic wall weight and abdominal fat mass on pulmonary compliance), V/Q mismatch, potential hypoxemia, and hypercarbia. The use of PEEP raises intraoperative FRC, reduces hypoxemia, and may also help to reduce postoperative atelectasis. However, PEEP can reduce cardiac output, especially in the presence of a pneumoperitoneum; therefore, it should be used with caution.

Cardiovascular Changing from an upright position to the supine position results in an increase in venous return, which is associated with a redistribution of blood from the lower extremities into the central circulation. This increase in preload increases the cardiac output, with a concomitant reflexive decrease in heart rate, stroke volume (SV), and contractility. These changes are mediated through aortic and carotid baroreceptors via the vagus and glossopharyngeal nerves. The body tries to maintain a stable blood pressure but the mechanisms that

accomplish this are altered with the addition of general anesthesia, neuraxial anesthesia, or PEEP. The effects of anesthesia on the cardiovascular system cause a decrease in the systemic vascular resistance (SVR) and reduce return of venous blood to the heart. The mechanisms that compensate hemodynamic changes are disrupted, causing the blood pressure to be more labile. Placing patients in the Trendelenburg or reverse Trendelenburg position has a pronounced effect on systemic blood pressure while supine and under general anesthesia, more so than in awake and spontaneously breathing patients. The Trendelenburg position in awake and anesthetized patients results in an increase in pulmonary arterial pressure (PAP), central venous pressure, (CVP) and pulmonary capillary wedge pressure (PCWP), changes that may be poorly tolerated by patients with decreased cardiac reserve. In contrast, patients in the reverse Trendelenburg position under anesthesia are at risk for a decrease in cerebral perfusion, due to the hydrostatic pressure difference between the head and heart, where blood pressure is normally measured. For every 13 cm of vertical height difference of the head above the heart, the mean arterial blood pressure at the head will drop by 10 mm Hg. Special attention is needed with a parturient, as the gravid uterus in the supine position can cause aortocaval compression leading to a supine hypotension syndrome and uteroplacental insufficiency. Every effort should be made not to place her in a true supine position; in order to maintain placental perfusion, a left lateral tilt of 15 to 30 degrees is usually sufficient to prevent inferior vena cava (IVC) obstruction and maintain placental perfusion. It’s important to keep in mind that when the tilt position is used, the pregnant patient must be secured to the table to prevent fall and injury.

Specific Complications The supine position is related to numerous potential adverse outcomes and patient morbidity. The most significant of these are peripheral nerve injuries, injuries involving the eyes, and skin-related problems.

Peripheral Nerves Although nerve injuries are infrequent, they represent 16% of all closed claims, the second largest class of adverse outcomes in the ASA Closed Claims Study database. Internal and external compression, stretch, ischemia, direct trauma, and direct nerve laceration can all result in nerve injury. Although the mechanisms of the nerve injuries are not always understood, they are usually preventable with proper positioning and padding. The ulnar nerve and brachial plexus can commonly sustain damage if positioned incorrectly; however, any peripheral nerve may be subject to compression or traction injuries.

Ulnar Nerve The ulnar nerve is the most commonly injured nerve, accounting for 28% of peripheral nerve injuries. In the past, ulnar neuropathy was thought to be due to malposition of the elbow and compression of the nerve. Pronation of the arm, which may result in direct external pressure on the nerve, and extreme elbow flexion, puts the ulnar nerve at risk. Other factors, including male gender (males have a lower elbow fat content compared to women), prolonged hospitalization, anatomic variations at the elbow, and either thin or obese body habitus, may also increase the overall risk. In addition, a pre-existing subclinical compression can make the ulnar nerve more susceptible to injury. Ulnar nerve injury is also more common following cardiac surgery compared to noncardiac surgery. To minimize the risk of injury to the ulnar nerve, the arms should either be tucked at the patient’s side with the thumbs pointing upward or abducted to less than 90 degrees with the forearm supinated. Supination of the forearm in the abducted position puts the least amount of pressure on the ulnar nerve, decreasing the risk of compression-related injury. Padding can help to prevent direct compression of the ulnar nerve as it traverses the cubital tunnel. Flexion of the elbow greater than 90 degrees should be avoided, for example, when the arm is folded tightly across the chest.

Brachial Plexus To reduce the risk of brachial plexus injury in the supine position, the arm should not be placed in extremes of abduction, extension, or external rotation. Brachial plexus neuropathies can be avoided by ensuring abduction of the arms is kept to less than 90 degrees, limiting stretch or compression of the plexus. External rotation of the arm and posterior displacement should be avoided, and the head should be maintained in the neutral position. Lateral flexion of the head away from a fixed contralateral shoulder should be avoided, to reduce the risk of stretch on the contralateral plexus.

Head The head should rest on a soft, low-profile, circular foam piece or gel headrest to minimize pressure on the occipital area. The weight of the head should lie on the headrest and not hang unsupported above the operating room table, avoiding hyperextension of the neck. If possible, the head should be maintained in the neutral position. Alopecia may occur due to pressure on the back of the head during prolonged procedures. Repositioning the head every 30 minutes may prevent this.

Skin

A reduction in perfusion leads to tissue ischemia and subsequent skin tissue breakdown. Pressure areas of concern during the supine position include the occiput, elbows, sacrum, calves, and heels. Careful padding of all pressure points is key for preventing pressure sores. Gel pads or ankle supports, which raise the heels off the table, can eliminate pressure points. Arms should not be wrapped too tightly, to prevent pressure on the skin from IV tubing or monitoring devices. Wrinkling of the sheets can occur when moving to the OR table, especially with obese patients. Every effort should be made to smooth out wrinkles under the patient, otherwise compromised circulation and pressure ulcers can occur. The common OR mattress is foam covered with nylon or vinyl; a gel mattress is an ideal alternative. Research results, however, have not provided a definitive answer regarding which type is best for preventing intraoperative skin injuries and pressure ulcers. When purchasing OR tables, the most important safety factors to take into consideration are the mattresses and the ability to evenly distribute body pressure to prevent circulatory disturbances and pressure ulcers at the bony prominences. Periodic pressure-relieving maneuvers may help to prevent skin problems.

Eyes Eye injuries are infrequent but can potentially result in serious complications. The most common type of injury in the supine position is corneal abrasion, which may occur in part because of reduced lacrimation during general anesthesia. There are no strict guidelines for how to protect the cornea and globe from abrasions or injuries; however, it is commonly accepted that taping the eyes shut helps, when possible. The risk of abrasion can be further reduced by use of lubrication; however, this is not a routine practice at many sites. Often, the use of lubricant is a matter of practitioner preference. Plastic corneal protectors coated with lubricant and inserted under the eyelids, usually by the surgeon, can be an effective and safe method of protection and can be easily removed at the end of the procedure. In some procedures, surgeons will suture the eyes closed if they are within the surgical field. At a minimum, using eye lubricant may be desirable if the eyelids cannot be taped or protected otherwise; this simple intervention might help to avoid a corneal abrasion. To help reduce the risk of direct pressure on the eyes, goggles can also be placed over a patient’s eyes, with careful attention paid to the bony eye sockets and the bridge of the nose. Frequently, tubes and monitoring cables will cross over the face; this is not only a problem at the beginning of the case but throughout the procedure. Inspect the patient’s eyes, ears, and nose frequently to ensure the face is free of pressure or possible trauma, even in a short procedure. TAKE HOME POINTS

Safe positioning requires planning and good communication between all team members involved in the patient’s surgical procedure. Adequate numbers of attentive and well-informed personnel are required at the beginning and at the end of a surgical procedure to facilitate safe positioning. Knowledge of physiologic changes associated with the position can help predict and prevent potential problems. All equipment should be secured and rechecked after every change in position. Sometimes complications do not become evident until several days after surgery. Suggested Readings Barash P, Cullen BF, Stoelting RK, et al., eds. Patient positioning and potential injuries. Handbook of Clinical Anesthesia. Philadelphia, PA: LWW; 2013; 434–440. Hansen JE, Botney R. Safe patient positioning. In: Young VL, Botney R eds. Patient Safety in Plastic Surgery. St. Louis, MO: Quality Medical Publishing, Inc; 2009; 511–549. Martin JT, Warner MA. Positioning in Anesthesia and Surgery. 3rd ed. Philadelphia, PA: WB Saunders; 1997. Prielipp RC, Morell RC, Butterworth J. Ulnar nerve injury and perioperative arm positioning. Anesthesiol Clin North America. 2002;20(3):589–603.

129 Thinking Laterally—How to Safely Position a Patient in the “Sideways” Position for Surgery Gregory Applegate, DO, Carlyann Miller, DO, and Raymond G. Graber, MD

An 88-year-old man with a history of hypertension, morbid obesity, and obstructive sleep apnea presents with a right hip fracture and is scheduled for a hemiarthroplasty. The surgeon plans a lateral position to help with exposure. What anesthetic approach should you chose for a lateral surgery? What are the anesthetic ramifications and potential risks of the lateral position? What supplies should you have readily available for the lateral position? The lateral decubitus position is used to optimize surgical exposure for numerous types of surgery. A few examples include surgeries on the hip, lung, and kidney. Below we will discuss some important things to consider when planning and performing surgical procedures in the lateral position. When the lateral position is planned, either general or neuraxial anesthetic techniques can be appropriate. The choice is frequently dictated by the type of surgery. For a patient with a hip fracture, either a general or spinal anesthetic could be appropriate, whereas a patient undergoing a thoracotomy will be managed with general anesthesia. The ideal case for a spinal is one in which you have an experienced surgeon doing a case that they routinely perform in a time that is predictably within about 2 to 3 hours. For example, a primary total hip at the author’s institution can reliably be completed within 2 hours of performance of the spinal. On the other hand, there are cases where the time course is not predictable, such as acute care of orthopedic trauma, especially if there are residents working. For a long and unpredictable surgery, it is frequently easiest and safest to just use a general anesthetic. You have control of the airway, and it is easier to place extra intravenous, central or arterial lines if needed. If a neuraxial technique is desired in this situation, then a catheter-based technique such as an epidural or a combined spinal/epidural (CSE) should be used. When considering a spinal anesthetic, you also need to consider issues such as whether the patient can tolerate the position, and what the airway will be like while

under sedation. If the patient has a high risk of airway obstruction, then you have to discuss with the patient whether they would be willing to be more awake. If the patient prefers to be oblivious, then maybe it would be safer to put an endotracheal to and control the airway. If you plan to do a general anesthetic for a patient who will be the lateral position, it may be OK to place an LMA if it is a short case in a healthy patient with a good airway. However, for the vast majority of cases, we favor an endotracheal tube. The airway is secured—and you have no worries about the LMA getting displaced and obstructing the airway. Another thing to think about is how to deal with the scenario where the surgery is taking longer than planned, and the spinal is wearing off. You need to have a plan B! The author’s preference is to first try converting to total intravenous anesthesia (e.g., propofol/ketamine) and allowing the patient to breath spontaneously (a nasal airway is helpful). If this is not successful, then you have the choice of trying to secure the airway in the lateral position by direct laryngoscope or LMA insertion. The author’s experience is that it is much easier to place an LMA in the lateral position then it is to intubate! Do not wait too long to implement your adjunctive anesthesia plans and do not ever tell the patient to “hang on” while their surgeon completes their hip replacement. That is simply unacceptable. If the surgery is in the finishing stages, the surgeon should be encouraged to use local anesthetic where possible. There are multiple possible positioning-related injuries that can occur in the lateral position. In our experience, patients are especially sensitive to perioperative injuries of any type—they present to the OR to get a problem fixed, and do not expect to come out of the OR with a new problem. For example, the dependent radial nerve can be compressed posterior-laterally in the upper arm where it wraps around the humerus. The ulnar nerve can be compressed at the medial epicondyle of the elbow. The dependent brachial plexus can be injured by compression. The dependent peroneal nerve is vulnerable to compression against the head of the fibula. The dependent eye and ear, and breasts/male genitalia may be vulnerable to compression injury. Significant edema of the dependent periorbital tissues and lips and face can occur in prolonged lateral cases, especially if large volumes of IV fluid have been administered or if the bed is also positioned in Trendelenburg (head down). We teach that the process of turning to the lateral position requires your utmost attention. First, make sure that all lines are free and in position so that they will not get pulled out with the turn. All facial piercings that will be dependent should already have been removed, no exceptions. The anesthesia provider is responsible for managing the head, neck and airway during the turn. Our practice is to disconnect the circuit from the endotracheal tube during the turn, so that no inadvertent snag on the circuit extubates the

patient. Typically, the patient is first turned laterally, then lifted a second time to insert an “axillary roll.” This roll is placed under the chest caudad to the axilla to prevent compression of the brachial plexus and axillary artery. Either a wrapped liter bag of intravenous fluid or a rolled blanket is commonly used for this purpose. Ensure that the roll is not directly against axilla by checking that at least 1 to 2 fingerbreadths can be placed between the roll and the skin of the axilla. A palpable pulse or good pulse oximetry waveform will confirm that the dependent arm axillary artery is not compressed. After the patient is turned laterally, the dependant arm is typically placed on an arm board. The arm should be padded to prevent compression of the ulnar nerve at the elbow. The nondependent arm should mimic the dependent arm and is supported with either an arm-holding device or a secured stack of blankets. We usually favor an armholding device in our personal practices. This allows easy access to each arm so that IV sites can be observed, more lines can be started if needed, and also minimizes the weight on the dependent arm. If a stack of blankets is used, err on the side of a stack that is too tall as opposed to too short. Otherwise, the nondependant axilla may become compressed by the weight of the upper arm being drawn too perpendicularly and laterally (at too sharp an angle) across the chest. We were taught to visualize the arms of a lateral patient as in position to hold a large beach ball—there should be a natural and gentle rounded posture of the arms at the axilla and shoulders and the elbows should be just slightly flexed. After arm positioning, make sure that there are no pressure points between arm-holding devices and the patient’s skin, and that all intravenous lines are functioning properly. The head should be kept in a neutral position and it will usually require two or more blankets to keep the head and neck in line with the spine. A foam “donut” pillow is useful to prevent compression of the ear and dependent eye. (Central retinal artery occlusion is a known complication of prone cases, but has also been reported in a few cases in the lateral position.) It is known that patients in the lateral position have a higher incidence of corneal abrasions, so an eye lubricant is typically used, and the eyes are secured shut with either tape or a transparent IV dressing. A pillow is commonly placed between the lower legs, which should not be overextended at the hips, knees, or ankles. Finally, a quick head-to-toe survey will prove useful to make sure that the eyes, ear, breasts, and genitalia are not compressed or pinched, the neck is in a neutral position and not laterally flexed, and that bony prominences are padded. Safety belts or stability devices such as a bean bag should be used to keep the patient stable. If the patient has a spinal anesthetic, we typically keep the patient awake during the positioning process. After the patient has been positioned, we will check with them to make sure arms, shoulders and neck all feel comfortable. After the patient confirms this,

it is time to start propofol. During lateral positioned surgery, noninvasive blood pressure (NIBP) cuff values will vary between the dependent and nondependent arm. In comparison to an arterial pressure measured with transducer placed at the level of the heart, the pressures measured in the dependent arm will be about 10 to 15 mm Hg higher, while those in the nondependent arm will be 10 to 15 mm Hg lower. Pulmonary physiologic changes do occur in the lateral position. The nondependent lung receives excess ventilation and the dependent lung experiences excess pulmonary perfusion. Fortunately, the ventilation–perfusion mismatch is clinically insignificant unless the patient has severe pulmonary compromise and/or is undergoing one-lung ventilation. When moving a patient from supine to lateral position, the endotracheal tube is at risk of migration—which may result in either endobronchial intubation or extubation. It is good practice to confirm bilateral breath sounds by chest auscultation after changing from supine to lateral positions. For thoracic surgery with double lumen tubes or bronchial blockers, we strongly recommend fiberoptic bronchoscopy to reconfirm proper endotracheal tube placement after moving from supine to lateral. Peripheral intravenous lines and arterial lines are easier to place prior to moving to the lateral decubitus position. These lines can be placed in the lateral position, but sites and access will be limited. The clinician must use his or her clinical judgment to decide what lines should be performed prior to positioning. Central line access should always be performed prior to turning the patient. Sometimes the dependent arm may be concealed under a stack of blankets. Be aware that if intravenous line flow is slow, it may not just be a compressed or positional IV, but an infiltrated IV. Excessive fluid delivered through a hidden infiltrated IV can lead to compartment syndrome. TAKE HOME POINTS When deciding on regional versus general anesthesia for the patient in the lateral position, make sure the planned regional can cover the duration of the planned surgery, and that the patient can tolerate the position. Prior to placing a patient in the lateral position, make sure you have the appropriate supplies: axillary roll, nondependent arm support, foam “donut” pillow, extra blankets/pillows for neck support. Remember that an operative case in the lateral position is really two moves—the first is the 90-degree rotation and the second is the lift for placement of the axillary roll. During the positioning process, check that the neck is neutral, and that known nerves at risk are not under undue compression or stretch. An arterial line or pulse-ox on the

dependent arm can help alert you to axillary artery compression. Ensure monitors and lines on the dependent arm are properly functioning after positioning. Understand the differences in blood pressure that may be obtained in the dependent and nondependent arm with NIBP. Be aware of the potential for endotracheal tube (ETT/DLT/bronchial balloon) migration when moving from supine to lateral. Check and recheck this! Suggested Readings Cassorla L, Lee J. Patient positioning and anesthesia. In: Miller RD, ed. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone; 2010: 1151–1170. Lawson NW, Meyer DJ Jr. Lateral positions. In: Martin JT, Warner MA, eds. Positioning in Anesthesiology and Surgery. 3rd ed. Philadelphia, PA: WB Saunders; 1997:127–152. McCaul CL, Harney D, Ryan M, et al. Airway management in the lateral position: A randomized controlled trial. Anesth Analg. 2005;101(4):1221–1225.

130 Positioning Patients for Spine Surgery Ihab Kamel, MD MEHP, David Y. Kim, MD, and Rodger E. Barnette, MD FCCM

The obligatory positions required for spine surgery subject patients to significant risk above and beyond the inherent risk of the procedure itself. These risks include, but are not limited to, injury to the eyes, ears, nose, breasts, penis, extremities, and peripheral nerves. Peripheral nerve injury is a well-recognized anesthetic complication and is the second largest cause of malpractice actions in anesthesiology, accounting for 16% of claims. Minimizing potential injury to peripheral nerves through proper positioning and monitoring is extremely important. Monitoring of somatosensory evoked potentials (SSEPs) is frequently utilized during spine surgery (75%) and is available in most institutions in the United States (94%). In addition to monitoring spinal cord function, SSEP can detect potential peripheral nerve injury during spine surgery. Conduction changes, such as a decrease in amplitude or an increase in latency of the signal, are believed to indicate impending upper-extremity nerve injury. Modification of the arm position by the anesthesiologist often improves the SSEP signal and may return it to baseline. Reversal of position-related SSEP changes can influence impending nerve injury and prevent postoperative peripheral nerve injury. The prone position is a dangerous position for patients. Attention to securing the airway is very important, as it is difficult to re-establish an airway in the prone position. Though we must always be cautious regarding protection of the eyes, this position raises additional concerns. Both ophthalmic ointment and occlusive eye tape may be appropriate if the procedure involves the cervical spine; prep solution that comes into direct contact with the eyes can lead to corneal injury. Additionally, we must assure that there is no direct pressure on the eye, ears, or nose. Pressure on eye may lead to loss of vision due to central retinal artery occlusion. Pressure can lead to loss of function and/or a disfiguring ischemic injury. For the same reason, it is important when positioning chest rolls to assure yourself that the breasts in women and the genitalia in men are free from undue compression of any sort. With regard to the patients’ extremities, the mechanisms of nerve injury associated with surgical positioning and anesthesia are not completely understood. Peripheral nerve injury may be due to direct trauma or more commonly due to ischemia.

Compression of peripheral nerves or stretch beyond 15% of original length may cause peripheral nerve injury due to compression of intraneural capillaries. Diabetes, hypertension, tobacco use, and uremia are known to affect peripheral nerves and predispose them to injury; intraoperative conditions such as prolonged hypotension and anemia are believed to facilitate ischemic injury. Peripheral nerve injury has been associated with neurosurgical and orthopedic surgeries. Finally, certain operative positions are known to place patients at increased risk for nerve damage. During spine surgery the overall incidence of impending upper-extremity peripheral nerve injury, as defined by changes in the SSEP, is >6%. The ulnar nerve and the brachial plexus are the most commonly injured neural structures during this type of surgery. Risk factors for ulnar nerve injury include male gender, very thin or very obese patients, and prolonged hospitalization for >14 days. Risk factors for brachial plexus injury include the use of shoulder braces, the prone head-down position, and some regional anesthetic techniques such as interscalene and axillary blocks. There are five positions commonly employed during spine surgery: supine, arms out; supine, arms tucked; lateral decubitus; prone “Superman” position; and prone, arms tucked. The prone “Superman” position and the lateral decubitus position have been identified as high-risk positions for upper-extremity nerve injury, especially if the surgical procedure is prolonged. Techniques for minimizing injury in these positions are reviewed below. The incidence of impending upper-extremity nerve injury during spine surgery in the supine arms-out position is 3.2%. Overstretch of the brachial plexus can occur as a result of abduction of the shoulder >90 degrees and should be avoided. Direct compression of the ulnar nerve against the medial epicondyle may occur, especially if the forearm is in the prone position. Placing the forearm in the supine or neutral position decreases pressure over the ulnar nerve at the elbow. Elbows should be padded to further protect the nerve from compression. Direct compression of the radial nerve in the spiral groove of the humerus can be avoided with proper padding. Overextension of the elbow should be avoided because it may stretch the median nerve. The patient’s head and neck should ideally be maintained in a midline position. Tilting the head and neck laterally may stretch the contralateral brachial plexus. The incidence of impending upper-extremity nerve injury during spine surgery in the supine arms-tucked position during spine surgery is 1.8%. The tucked arms should be placed in neutral positions to decrease the pressure over the ulnar nerve. The ulnar nerve should be padded at the elbow for additional protection. Shoulder tape, which is often applied by the surgeon to pull the shoulders down and maximize the lateral radiographic view of the spine, may compress the brachial plexus. The duration of

application of this shoulder tape should be minimized. The head and neck should be maintained in midline position. Placement of the patient’s forearms on the lower abdomen should be avoided, as excessive flexion at the elbow joint can simultaneously stretch and compress the ulnar nerve. The lateral decubitus position is a challenging position for the anesthesiologist. The incidence of impending upper-extremity peripheral nerve injury during spine surgery in the lateral decubitus position is 7.5%. Compression of the brachial plexus is the most common mechanism of injury. The dependent brachial plexus can be compressed between the clavicle and first rib as well as against the humeral head. Obese patients and patients placed in a head-down position are at higher risk, as compressive forces are augmented. A chest roll should be placed to elevate the dependent chest and decrease the likelihood of compression. The chest roll should not be placed in the axilla, but under the lateral, superior chest; the goal is to prevent compression of the contents of the axillae between the chest and humeral head. The dependent arm should be padded at the elbow and maintained in the supinated position to avoid compression of the ulnar nerve. To minimize the likelihood of brachial plexus stretch, abduction of the dependent and nondependent arm should be less than 90 degrees. Excessive flexion or extension at the elbow should be avoided. The elbow in the nondependent forearm should be padded, and lateral rotation of the shoulder should be avoided. The patient’s head and neck should be maintained in a midline neutral position without excessive flexion or extension. The prone “Superman” position is another challenging position with a relatively higher incidence of impending upper-extremity nerve injury (7%). Stretching forces on the brachial plexus is the commonest mechanism of injury. Again shoulder abduction beyond 90 degrees should be avoided, and the patient’s head and neck should be in a neutral midline position. Elbows should be padded and the forearm and hand placed in a neutral position. Placing patients in steep head-down position should be avoided or limited if possible. Pressure from chest rolls should not be directly on the shoulders and the clavicle, as they may compress the brachial plexus, especially in obese patients. In women, the position of the chest rolls should be checked to ensure that there is no possibility of ischemic injury to the breasts. In men, the position of the lower roll should be checked to confirm that the genitalia are free from direct compression. The prone arms-tucked position is relatively lower risk compared to the prone “Superman” and the lateral decubitus positions. The incidence of impending nerve injury in the prone arms-tucked position during spine surgery is 2.1%. Special attention should be given to positioning the head and neck as described in the previous paragraph. The forearms should be in neutral positions. Shoulder tape, applied to maximize the lateral radiographic view of the neck, should be minimized. The elbows

should be padded to avoid compression by arm sleds. Direct compression by the chest rolls is of concern as in the prone “Superman” position. Attention to detail is one of the reasons for our specialty’s superior safety record. When caring for patients undergoing spinal surgery, we must assume an integral role in positioning, monitoring, and interceding as appropriate. TAKE HOME POINTS The prone position can be dangerous for patients. Attention must be given to preventing injury to eyes, ears, nose, breasts, penis, extremities, and peripheral nerves. SSEP monitoring can be used to detect and prevent peripheral nerve injury during spine surgery. The lateral decubitus position and the prone “Superman” position are high-risk positions for nerve injury during spine surgery. Abduction of the shoulder beyond 90 degrees should be avoided because it stretches and may injure the brachial plexus. Excessive flexion of the elbow should be avoided; it stretches and compresses the ulnar nerve. Excessive extension of the elbow should be avoided because it stretches the median nerve. The forearm in the supinated position may be safest because of the decreased pressure on the ulnar nerve; the neutral position is a good second choice. Appropriate padding can minimize excessive pressure on the radial nerve in the spiral groove. Suggested Readings Caplan RA. Will we ever understand perioperative neuropathy? A fresh approach offers hope and insight. Anesthesiology. 1999;91(2):335–336. Edgcombe H, Carter K, Yarrow S. Anaesthesia in the prone position. Br J Anaesth. 2008;100(2):165–183. Kamel IR, Drum ET, Koch SA, et al. The use of somatosensory evoked potentials to determine the relationship between patient positioning and impending upper extremity nerve injury during spine surgery: A retrospective analysis. Anesth Analg. 2006;102(5):1538–1542. Kroll DA, Caplan RA, Posner K, et al. Nerve injury associated with anesthesia. Anesthesiology. 1990;73(2):202–207. Lawson NW, Meyer DJ Jr. Lateral positions. In: Martin JT, Warner MA, eds. Positioning in Anesthesiology and Surgery. 3rd ed. Philadelphia, PA: WB Saunders; 1997:127–152. Martin JT. The ventral decubitus (prone) positions. In: Martin JT, Warner MA, eds. Positioning in Anesthesiology and Surgery. Philadelphia, PA: WB Saunders; 1997:155–195. Prielipp RC, Morell RC, Walker FO, et al. Ulnar nerve pressure: Influence of arm position and relationship to somatosensory evoked potentials. Anesthesiology. 1999;91(2):345–354. Schwartz DM, Drummond DS, Hahn M, et al. Prevention of positional brachial plexopathy during surgical

correction of scoliosis. J Spinal Disord. 2000;13(2):178–182. Welch MB, Brummett CM, Welch TD, et al. Perioperative peripheral nerve injuries: A retrospective study of 380,680 cases during a 10-year period at a single institution. Anesthesiology. 2009;111(3):490–497.

131 Sit Back and Relax? Implications of the Sitting Position in Shoulder and Brain Surgery Evan Staszewski, DO and Michael D. Altose, MD PhD

The sitting position (beach chair position) is most commonly used during shoulder surgery, particularly arthroscopic procedures. This position has several surgical advantages compared with the lateral position: decreased incidence of brachial plexus traction neuropathy and neurovascular complications; decreased surgical duration; a more bloodless surgical field and reduced blood loss; better access to the shoulder from both the anterior and posterior aspect; more physiologic arm movement by the surgeon; and easier conversion to an open procedure. There are anesthetic advantages as well, including: better access to the airway, face and thorax; lower airway pressures and better diaphragmatic excursion which can improve ability to ventilate; increased vital capacity and functional residual capacity (FRC); better access to extremities; and less risk of swelling of the tissues in the eyes, face, and airway. In the sitting position, the arms are pulled caudad by gravity, and traction on the shoulder muscles can lead to stretching of the brachial plexus and other neurovascular structures. The arms therefore must be supported, while avoiding pressure on the ulnar area of the elbow, a common site of nerve injury. This can be done with padded arm supports, or the arms can be secured across the patient’s abdomen. Hips should be flexed 45 to 60 degrees and knees should be flexed about 30 degrees to reduce stretching on the sciatic nerve; but excessive knee flexion should be avoided to prevent abdominal compression. Ensure there is no compression of the common peroneal nerve, which is also commonly injured. Feet should be supported and padded, avoiding excessive plantar flexion. Shoulder surgery in the sitting position can be done under general or regional anesthesia, or a combination. The patient is seated at an angle of 30 to 90 degrees from the horizontal plane, with the head stabilized on a head rest using a specialized face mask or a wrap of gauze or tape. Some anesthesiologists prefer to secure the airway with an endotracheal tube, but, many shoulder surgeries can be done with a supraglottic airway if the surgeon does not require neuromuscular blockade and the patient is an

appropriate candidate. Several hemodynamic changes occur in the sitting position, primarily due to venous pooling in dependent tissues. Pulmonary and systemic vascular resistance increase, while venous return, cardiac output and cerebral perfusion pressure (CPP) decrease, and hypotension may occur. Hypovolemia can also lead to V/Q mismatch, due to decreased perfusion of the upper lung. Hypotensive bradycardic events have been described in patients who have regional blocks using epinephrine, and are thought to be caused by the Bezold–Jarisch reflex. The decrease in CPP can lead to devastating complications including cerebral ischemia, retinal ischemia, and spinal cord injury. Surgeons may request deliberate hypotension in order to provide a bloodless surgical field and improve visualization through the arthroscopy camera, which can increase the risk of hypoperfusion. Many sources recommend keeping systolic blood pressure (SBP) >90 mm Hg and mean arterial pressure (MAP) >70 mm Hg to minimize risk of cerebral hypoperfusion. Ideally, SBP and MAP should be maintained within 20% of baseline values. There are several strategies to minimize the risk of cerebral hypoperfusion. First, most sources recommend paying attention to the difference between CPP and MAP, recognizing that for each 1.25 cm elevation of the head above the level of the heart, local arterial pressure is reduced by approximately 1 mm Hg. This difference becomes quite significant in the sitting position, especially if the blood pressure cuff is placed on the leg. Incremental positioning, intravenous fluids and vasopressors can attenuate the severity of hypotensive episodes and preserve cerebral oxygenation, while elastic stockings and active leg compression devices can help maintain venous return. One study has suggested that adding PEEP (5 cm H2O) reduces the amount of hemorrhage in the surgical field and increases surgeon satisfaction during arthroscopic shoulder surgery, without requiring controlled hypotension. Maintaining end-tidal CO2 in the 40 to 42 mm Hg range (as compared with 30 to 32 mm Hg) can provide better cerebral blood flow and oxygenation. Cerebral oximetry may be appropriate in higherrisk patients to identify cerebral hypoperfusion. Very high–risk patients may benefit from using regional anesthesia only without general anesthesia, which will better preserve cerebral autoregulation. The sitting position is also used, albeit infrequently, during neurosurgical procedures involving the posterior cervical spine and the posterior fossa. Surgeons may prefer this position rather than the prone position due to improved surgical exposure and decreased blood in the surgical field. The head is usually fixed in place with a 3-pin head holder that is attached to the operating table. It is highly preferable to secure the frame to the back portion of the bed (and not the portion that supports the patient’s thighs). This will allow the head of the bed to be flattened in the event of venous air embolism (VAE),

severe hypotension, or cardiac arrest. Flexion of the cervical spine may be needed to improve surgical exposure. Excessive cervical flexion or rotation should be avoided, as it can impede arterial blood flow (causing cerebral hypoperfusion) as well as venous blood flow (leading to venous congestion of the brain). Extremes in neck flexion/extension can impair spinal cord autoregulation, especially when coupled with a reduction in hemodynamic parameters, and spinal cord infarction and quadriplegia have been reported. Excessive cervical flexion can also lead to obstruction or kinking of the endotracheal tube in the pharynx and place significant pressure on the tongue causing swelling. In adults, one should try to maintain at least 2 fingerbreadths (2 to 3 cm) of distance between the mandible and the sternum. If transesophageal echocardiography (TEE) is used for air embolism monitoring, extra caution should be taken since the esophageal probe increases the potential for compression of laryngeal structures and the tongue. Similarly, large oral airways or bite blocks should be avoided. As discussed above, the sitting position may lead to decreased cardiac output and cerebral perfusion. During neurosurgical procedures, most anesthesiologists prefer to position the arterial pressure transducer at the external auditory canal (Circle of Willis) to more accurately reflect true CPP. The dysrhythmias that can occur with surgical manipulation of the cranial nerves or brainstem (bradycardia, tachycardia, PVCs, asystole) may have an exaggerated effect on cardiac output in the sitting position. Elevation of the surgical field above the heart can reduce dural sinus pressure by up to 10 mm Hg. These dural venous sinuses cannot collapse because of their bony attachments, so the risk of VAE is a constant concern. If enough air is entrained, arrhythmia, desaturation, pulmonary hypertension, circulatory compromise, or even cardiac arrest may occur. If an intracardiac shunt is present (e.g., patent foramen ovale), even small amounts of venous air may result in a stroke or myocardial infarction as a result of paradoxical embolism. Nitrous oxide is often avoided, as it increases the size of intravascular bubbles (but it has not been shown to worsen perioperative morbidity in patients undergoing posterior fossa surgery). Some centers perform screening echocardiography before considering the sitting position for neurologic surgery. In the OR, early detection of entrained air with the use of TEE or precordial Doppler ultrasound may decrease the incidence and severity of VAE, and placement of a central line to aspirate large collections of air from the right heart is advised. TAKE HOME POINTS Surgery in the sitting position has advantages for the anesthesiologist and surgeon, but patient injury can occur if precautions are not taken.

To avoid spinal cord or nerve injury, avoid excessive neck flexion/extension/rotation, ensure that arms are properly supported, and take steps to prevent compression of the ulnar and peroneal nerves. Decreased cardiac output and CPP in the sitting position can have profound hemodynamic and neurologic sequelae. Be aware of the difference between noninvasive blood pressure cuff measurements and CPP. Cerebral oximetry and/or a regional-only anesthetic may be helpful when caring for patients at very high risk for cerebral hypoperfusion. VAE can occur during craniotomy in the sitting position, and should be avoided in patients at high risk for paradoxical embolism. Be prepared to detect and manage intraoperative VAE. Suggested Readings Cassorla L, Lee J. Patient positioning and associated risks. In: Miller RD, ed. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier; 2015: 1240–1265. Ersoy A, Çakırgöz M, Ervatan Z, et al. Effects of positive end-expiratory pressure on arthroscopic shoulder surgery under general anesthesia. Acta Orthop Traumatol Turc. 2016;50(1):82–88. Laflam A, Joshi B, Brady K, et al. Shoulder surgery in the beach chair position is associated with diminished cerebral autoregulation but no differences in postoperative cognition or brain injury biomarker levels compared with supine positioning: The anesthesia patient safety foundation beach chair study. Anesth Analg. 2015;120(1):176–185. Larsen SL, Lyngeraa TS, Maschmann CP, et al. Cardiovascular consequence of reclining vs. sitting beachchair body position for induction of anesthesia. Front Physiol. 2014;5:187. Mannava S, Jinnah AH, Plate JF, et al. Basic shoulder arthroscopy: Beach chair patient positioning. Arthrosc Tech. 2016;5(4):e731–e735. Rains DD, Rooke GA, Wahl CJ. Pathomechanisms and complications related to patient positioning and anesthesia during shoulder arthroscopy. Arthroscopy. 2011;27(4):532–541. Schlichter RA, Smith DS. Anesthetic management for posterior fossa surgery. In: Cottrell JE, Patel P, Warner DS, eds. Cottrell and Patel’s Neuroanesthesia. 6th ed. Edinburgh: Elsevier; 2017: 210.

132 Individuals With Cerebral Palsy and Other Spastic Disorders Need Your Best Positioning Prowess Brandon Michael Togioka, MD, Benjamin C. Conner, MSc MD/PhD3, and Carol Bodenheimer, MD

An 18-year-old female patient with cerebral palsy and contractures of her knees and hips presents to you for an MRI under anesthesia. The patient first presented to the MRI technician yesterday, but they were unsure how to position the patient on the MRI table. There is a note in the anesthesia posting requesting neuromuscular paralysis so that “the patient’s contractures can be straightened for imaging.” Is this a reasonable request? How do you proceed? Positioning is quite important for preventing postoperative pain and neurologic complications. Over the last a few chapters you have learned how to position patients to facilitate surgery while minimizing physiologic perturbations and the opportunity for neurologic injury. Now we are going to take it up a level. Patients with cerebral palsy (CP) have musculoskeletal deficits that make them among the most prone to positioningrelated pain and injury. While there has yet to be a formally agreed upon definition for CP, most providers would agree that it is a nonprogressive disease of motor dysfunction related to central neurologic pathophysiology that is sustained very early in life. CP is the most common cause of severe childhood motor disability. While early studies seemed to point to a peripartum asphyxia etiology, intrapartum hypoxia has recently been estimated as the cause in only 6% of all patients with CP. The incidence of CP is estimated at between 2 and 2.5:1,000 live births. There are different types of CP, based upon the area of brain injury. The most common type of CP is spastic, which is due to lesions in the cerebrum. Patients with spastic CP often have normal intelligence. Individuals with spastic CP have an imbalance between their excitatory and inhibitory neural impulses. It is believed that this imbalance (due to a lack of inhibitory signals from the brain) leads to a relative

excess of excitatory impulses, overexcitation of the muscle, and a state of constant contraction. Over time, the muscle’s state of constant contraction leads to permanent shortening due the fibrosis, which limits range of motion. Other types of CP include dyskinetic CP, involving injury to the basal ganglia, and ataxic CP, involving injury to the cerebellum. It is also possible to have a mixed form of CP that includes characteristics of multiple forms. For purposes of this chapter, we focus on spastic CP as it is the contractures that cause most positioning issues. If there is one lesson to remember from this chapter, it is that patients with CP should be put in a comfortable position, which minimizes muscle tone. If possible, allow the patient to place themselves on the operating room table while awake, so that you can see what is natural and a neutral position for them. Consider having the care provider in the room for initial positioning to decrease patient fear. The patient will naturally place themselves in a position that minimizes the chance for skin, muscle, and bone damage; however, because of the difference in surfaces, this may not avoid skin damage. Please note that the neutral position for a patient with CP may not result in symmetric joint placement. This is okay. After the patient is asleep, the provider can make minor adjustments in positioning. General anesthesia and neuromuscular paralysis can facilitate final positioning; however, keep in mind that it is not wise to extend a joint that does not want to stretch. This can lead to permanent muscle, nerve, and bone damage. Patients with CP need postural support in ways that patients without CP do not. This may mean using extra pillows, cushioning pads, and adjunct support structures. As is the case for all patients, extremities should never hang under their own weight, but rather have a support structure built up to them. Individuals with CP have an underdeveloped musculoskeletal system and osteopenia, especially of the lower extremities. This predisposes them to low-energy fractures, or fractures from an insult that would not usually cause injury. Over one quarter of all CP patients experience a fracture before adulthood. Many of these fractures occur during positioning or transfers. Because these injuries occur during an insult that one would typically not expect to cause injury, many of these diagnoses are delayed. In other words, you may cause a fracture during patient positioning without even knowing it. Remember, neuromuscular blockade will abolish spasticity-related joint limitations, but not contractures (due to permanent shortening of the muscle and tendon). Again, forceful positioning is a no-go in patients with CP. Positioning the hip deserves special attention when it comes to patients with CP. As we previously discussed, patients with CP often have abnormal gait, sitting posture, muscle tightness, and spasticity which leads to abnormal loading on joints. Bones remodel in response to stress leading to osteophyte formation, bone deformation, and osteoarthritis. The hip is particularly prone to dislocation in CP as spastic muscle

forces lead to nonuniform stress across the femoral head. This concentrates stress on the superolateral part of the femoral head leaving the rest of the femoral head relatively unloaded and predisposed to separating from the acetabulum. Hip subluxation, or dislocation, during transfers has been documented in both adult and child patients with CP. Preoperative questioning of individuals with CP should include questions about prior hip dislocations. In order to prevent hip dislocation, special attention must be paid in supporting the hip and pelvis during transfers and final positioning on the operating room table. Patients with CP are prone to complications from skin injury. Patients often have metabolic derangements and also often have thin, poorly vascularized skin, a thin subcutaneous fat layer, and less contractile muscle fibers for padding. This can lead to skin tears, pressure ulcers, and muscle necrosis. Careful attention to common pressure points is warranted to help decrease the chance for skin injury. Common areas that require padding in all patients include the following: the ears, the elbows, the hips, the knees, the heels, the back of the head, and any areas where lines or drains are entering the patient, such as the site of a G-tube button. In addition, every patient with CP will have additional areas where they are prone to skin injury secondary to their particular pattern of contractures. These areas will typically be obvious at the time of positioning. An intermittent massage (or repositioning if possible) to improve circulation in any area of concern during long surgery can also be helpful. Hypothermia is the most commonly encountered adverse event in the perioperative period for patients with CP. Patients with CP are prone to hypothermia because they typically lack muscle and fat while having a compromised central nervous system, which may lead to abnormal thermoregulation. Hypothermia has many deleterious side effects such as an increased rate of wound infection, prolonged neuromuscular blockade, delayed emergence, postoperative shivering, and potentially increased perioperative blood loss. Preventing hypothermia should always be on the provider’s mind when positioning patients with CP. This can be accomplished by using convective warming blankets, warmed intravenous fluids, humidification of gasses, and controlling the operating room temperature. Lastly, it is worth noting that positioning difficulties in patients with CP do not go away once the operation is over. Positioning in the PACU, ICU, and floor patient locations is equally, if not more, important as patients will typically spend more time in these locations. Providing adequate analgesia in the postoperative period is of utmost importance for patients with CP. Ineffective analgesia can lead to muscle spasms, worsening pain, further immobility, and a higher risk for skin breakdown. As communication can be difficult in patients with CP, continuous pain regimens may be better than on-demand regimens. Behavioral indicators of inadequate pain control are

very important to pay attention to. Regional anesthesia has been used safely, but keep in mind that regional anesthesia also typically implies less mobility, which can predispose to skin necrosis. TAKE HOME POINTS CP is a nonprogressive disease of motor dysfunction that is sustained in utero, during birth, or immediately thereafter. When positioning patients with CP, place them in a comfortable position that minimizes muscle tone. Do not force joints that do not want to stretch as this can lead to permanent muscle and nerve damage or bone fracture. Patients with CP are especially prone to hip dislocation during transfers and positioning. When positioning patients with CP, pay special attention to avoid skin breakdown and hypothermia. Suggested Readings Albright AL. Spastic cerebral palsy. CNS Drugs. 1995;4(l):17–27. Carter DR, Tse B. The pathogenesis of osteoarthritis in cerebral palsy. Dev Med Child Neurol. 2009;51 Suppl 4:79–83. http://doi.org/10.1111/j.1469-8749.2009.03435.x Gormley ME Jr. Treatment of neuromuscular and musculoskeletal problems in cerebral palsy. Pediatr Rehabil. 2001;4(1):5–16. http://doi.org/10.1080/13638490151068393 Presedo A, Dabney KW, Miller F. Fractures in patients with cerebral palsy. J Pediatr Orthop. 2007;27(2):147–153. Prosser DP, Sharma N. Cerebral palsy and anaesthesia. Continuing Education in Anaesthesia Critical Care & Pain. BJA Educ. 2010;10(3):72–76. Wass CT, Warner ME, Worrell GA, et al. Effect of general anesthesia in patients with cerebral palsy at the turn of the new millennium: A population-based study evaluating perioperative outcome and brief overview of anesthetic implications of this coexisting disease. J Child Neurol. 2012;27(7):859–866.

133 Use Extra Care in Positioning Patients Who Have Had Amputations Carol Bodenheimer, MD and Catherine Marcucci, MD

With over 2 million people living with limb loss in the United States, caring for patients with prior amputations is more common during other surgical procedures. All anesthesia providers must take extra care with patients with amputations to avoid positioning injuries. Be aware that limbs that have sustained partial amputation have undergone subtle but very real changes in musculoskeletal structure, skin integrity, and somatic and autonomic innervation. The contralateral limb is at risk as well and care must be taken with its positioning. The joints proximal to an amputation are often affected on both the contralateral and ipsilateral sides. For example, because of increased weight bearing in the contralateral leg, it is very common after lower-limb amputation for the contralateral hip to develop significant osteoarthritis. This is true even for patients who use a prosthesis. On the ipsilateral side in above-knee amputations, a hip flexure contracture results from immobility (more time sitting) and a hip abduction contracture from loss of the insertions of the adductors to the distal femur. On the ipsilateral side in below-knee amputations, a knee flexion contracture develops as a result of impaired mobility and loss of quadriceps extension strength. This is very common even in relatively young and active patients and will predispose a patient to injury in any position involving extension at the knee, such as the simple supine position. A pad below the distal thigh allows mild knee flexion and protects the integrity of the skin at the end of the stump. In all types of amputation, there can be subcutaneous fibrosis at the amputation site that puts the overlying skin at risk because of increased tension and decreased blood flow. In many patients with amputations, the underlying medical reason for the amputation (diabetes or vascular disease) may mean that the skin of the residual limb is at high risk for skin breakdown independent of amputation. Up to 55% of those with an amputation due to medical disease will require amputation of the second leg within 2 to 3 years. Even in patients whose limb loss was due to trauma, there is a higher risk of skin breakdown because of concomitant skin disorders such as contact dermatitis and

verrucous hyperplasia. Patients who show skin breakdown or ulceration on a residual limb should be positioned so that there is minimal chance of further pressure injuries. Perturbations in both the somatic and autonomic nervous systems can cause patients who have had amputations to experience a variety of hypersensitivity and chronic pain syndromes, including causalgia and phantom limb pain. Positioning injuries therefore can also cause an acute-on-chronic pain syndrome that can be especially distressing to the patient. Upper limb loss is a less common occurrence—the ratio of upper limb to lower limb amputation is 1:4. However, positioning a patient with an upper limb amputation may be even more complex than a patient with lower limb amputation. Padding for support must be balanced with the need to access the upper extremities for monitoring access intraoperatively. Upper residual limbs may have nerves with less muscle and skin protection, and special attention to nerve protection is appropriate. Surgical positioning in lateral or prone will be especially challenging in patients with high above-elbow or forequarter (in which the arm, scapula and clavicle are all removed) amputations. It is now understood that the perception of pain involves cortical processing of afferent input to the nervous system. There is also a tremendously complex interplay among all types of pain and psychological and emotional resilience. Amputation patients have an array of psychological “defenses” pertaining to their amputations, ranging from Vietnam War veterans who say simply, “Stepped on a toe-popper my third week in-country,” as if there is nothing more to the story, to patients who carefully guard their residual limbs. Patients who have had recent amputations may also be prone to depression. Ask if there is pain in the limb and discuss the plan for careful positioning with the patient. This can lessen anxiety, which is a good start to preventing pain. It is also appropriate to check for changes in the usual pain pattern during the postoperative check. TAKE HOME POINTS A new generation of war-wounded patients will be entering care in both civilian and veterans hospital—a significant percentage of whom will have had one or more amputations. Be attentive to changes in musculoskeletal structure, skin, and innervation. Above-knee amputees can have hip flexion and abduction contractures requiring positioning that must account for this. Below-knee amputations can result in knee flexion contractures. Upper-extremity amputations are less common than lower-extremity amputations but more complicated to position.

Subcutaneous fibrosis can put the overlying skin at increased tension with decreased underlying blood flow. Positioning injuries can result in acute-on-chronic pain in amputated limbs. If possible, involve the patient in the positioning before induction of anesthesia. Suggested Readings Bryant PR, Pandian G. Acquired limb deficiencies in children and young adults. Arch Phys Med Rehab. 2001;82(3 suppl 1):S3–S8. McAnelly RD, Faulkner VW. Lower limb prostheses. In: Braddom, RL, ed. Physical Medicine and Rehabilitation, Philadelphia, PA: WB Saunders; 1996:289–320. Pandian G, Huang ME, Duffy DA. Perioperative mangement in acquired limb deficiencies. Arch Phys Med Rehab. 2001;82(3 suppl 1):S9–S16. Wikoff, EK. Preprosthetic management. Phys Med Rehab: State Art Rev. 1994;8(1):61–72.

134 Never, Ever Fire C. Tyler Smith, MD and Brian T. Gierl, MD

Operating room fires can occur away from the patient, on the patient, or worse—inside the patient. Each fire location has its own consequences and subsequent management. The Emergency Care Research Institute (ECRI) estimates that in the United States the annual incidence of surgical fires in 2012 was 200 to 245 fires, which is down from 550 to 650 reported in 2009. Of fires reported, 76% occurred in the outpatient setting and 81% are cases in which the patient received Monitored Anesthesia Care. Surgical fires were distributed as 34% in the airway, 28% on the head or face, and 38% elsewhere on or inside the patient. A fire causing harm to a staff member or a patient is a never event because with appropriate preventive strategies they can be entirely avoided, yet one occurs every weekday in the United States. This chapter will take you through the risks and how to avoid them. We have all heard of the fire triad: oxidizers, fuels, and ignition sources. But what are the usual suspects in the OR? Oxygen is the most common oxidizer in the operating room, and is reported in 95% of all fires in the ASA Closed Claims Database. Open sources of oxygen (e.g., nasal cannula, simple facemask) are the major source of oxidizing agents for surgical fires. Remember that laughing gas is not funny, nitrous oxide will support combustion almost as well as oxygen. Fuels are the combustible materials that maintain a fire. Common fuels in the operating room include prep solutions—that is, 2% chlorhexidine in 70% isopropanol—surgical drapes and covers, dressings, hair, anesthesia equipment, and other equipment. Realize that an alcoholbased prep solution dries quickly on open skin, but requires more time to dry in hair or under a drape. A variety of other things have rarely been reported to burn, including bone cement. Bowel gas is both very putrid and highly flammable. An ignition source is any source of energy (open flames, sparks, static electricity, and hot surfaces) that initiates the process of igniting a fire or explosion. Caffeine is a source of energy for anesthesia providers but does not ignite. Ignition sources in the operating room include Electrosurgical Units (ESUs), surgical lasers, fiberoptic lights, drills, defibrillators, CO2 absorbers (sevoflurane and dehydrated soda lime), or short circuits in OR

equipment. In a report from the ECRI, 58% of fires involved ESUs, 38% involved fiberoptic cords, and 3% involved lasers. When oxidizers, fuels, and ignition sources are all present in the OR, patient surgical fire risk assessments should be taken.

Risk Assessment The risk of fire in the operating room should be assessed for each patient in every type of case. This assessment should be done jointly by the whole perioperative team— including the surgeon, anesthesiologist, and nursing staff, and can be incorporated into the preoperative timeout or “huddle” process. A simple tool has been developed to facilitate this process—the “Silverstein Fire Risk Assessment Tool” ( Table 134.1). This tool basically checks whether you are providing free oxygen near the surgical field and if you are using an energy source that could ignite it. Answer these three questions and add 1 point for each yes answer: A score of 3 out of 3 is a warning that the operation carries a high risk for surgical fire. Score of 2 indicates intermediate risk. And if only one or no conditions are met the operation is considered low risk. This risk assessment will guide what preventative measures should be used for the operation.

Preventative Measures The appropriate use of preventative measures is the key to avoiding surgical fires and communication between the various OR teams is the first line of defense. The fire triad and its components can be broken down into which team member has the most influence. Anesthesiology controls the oxidizer, while surgeons have the ignition source and nursing primarily influences the fuel. However, all members of the teams play crucial roles in minimizing all components of the fire triad. In low to intermediate surgical fire risk procedures based on the “Silverstein Fire Risk Assessment,” standard fire precautions should be followed. These precautions include limiting the oxygen to the lowest FiO2 that maintains patient oxygenation (ideally 30% prior to introducing an ignition source into the surgical field, the surgeon should wait 3 to 5 minutes to allow appropriate dissipation of the accumulated oxygen. You can briefly sample such an area with your capnogram tubing to determine the local oxygen level. Also, prep solutions should be allowed to adequately dry (for at least 3 minutes or per manufacturers recommendations), drapes should be configured in such a way that oxidizing agents do not accumulate, ignition sources should be protected by storing them in their appropriate holsters and away from surgical fuels, and appropriately reinforced endotracheal tubes should be used with lasers—although no ETT is LASER-Proof. In high-risk surgical fire procedures, standard fire precautions should be employed in addition to avoiding open oxygen delivery systems: avoid nitrous oxide, ensure that a syringe and basin containing saline is accessible, fill the endotracheal tube cuff with normal saline, use wet sponges, avoid ESU if possible or if not feasible then use alternative ESU devices such as bipolar ESU or a harmonic scalpel. Bipolar ESU requires less energy and has less current leakage than monopolar electrodes, making fires much less likely but not impossible—nothing is impossible. Class 4 LASERS by definition transfer enough energy to ignite a fire and include CO2 and YAG LASERS; class 3 LASERS cannot ignite a fire. Any facility that uses LASERS should have a LASER Safety Officer that can address your concerns. Table 134.1 ■ Silverstein Fire Risk Assessment Tool Item

+1 Point for each “Yes” response

Is the surgical site or incision above the xiphoid process? Is there an open source of oxygen including nasal cannula or simple facemask? Is there an available ignition source such as ESU, laser, fiberoptic light source, etc.? Total:

Management of the Surgical Fire

When the fire occurs each team member plays a vital role in minimizing harm or possibly eliminating it entirely. A fire inside the operating room but away from the patient warrants activation of the emergency response system. A carbon dioxide fire extinguisher should be utilized. A water extinguisher will damage operating room equipment and cause more sparks that could ignite more fires—your bad day just got worse. The acronym RACE serves as a guide in the initial steps of fire management.

Race to Fire Safety Remove the patient from the burning source Activate the alarm system Confine the doors to the OR once the patient has been evacuated Extinguish the fire. Staff should be familiar with the location of medical gas supply shut-off valves to limit the entry of oxidizing agents into a large fire. In the event of a fire located on the patient, the drapes should be doused with water and quickly removed. It is important to remove the drapes in a horizontal direction, away from the patient’s airway to prevent mixing of oxidizing agents. The anesthesiologist should discontinue the oxygen supply and ventilate with air until the fire has been extinguished. If the fire is located in the patient’s airway, the anesthesiologist should immediately remove the endotracheal tube and shut off all gas flow to the circuit. The sequence of events has been a controversial topic, but the time to remove the endotracheal tube (ETT) and turn off gas flow should be dictated by what can be completed first by the anesthesiologist depending on the proximity of items at the time of the fire—if the ETT is within arm’s reach but the gas flow meter is not you should pull the ETT before turning off the gas and vice versa. Saline—or any fluid— should then be poured into the patient’s airway. It is probably best to pour saline down a burning tube before removing it from the patient, but that should be weighed against the time required to obtain the fluid. Reassessment of the patient’s airway will allow the anesthesiologist to verify the airway fire has resolved and subsequently proceed to management of the postsurgical fire with preparations to send the fire victim to an American Burn Association (ABA) burn center.

Postsurgical Fire Management After it has been verified that the fire has been exhausted, it is essential to establish ventilation and oxygenation. Bag mask ventilation should resume with the minimal FiO2 that the patient can tolerate, minimizing the oxidizing agent until a secured airway can be established or the procedure comes to completion. Bronchoscopy may be warranted in

large fires to assess the structural damage to the lungs and the airway. However, antibiotics and steroids that have been described in the literature, are not universally adopted. Admission to an ABA burn center should be considered if the patient meets requirements: evidence of inhalational injury, full thickness burns of >10% total body surface area, burns involving the eyes, ears, hands, feet, or perineum likely to result in cosmetic functional impairment, or chemical or electrical burns. TAKE HOME POINTS Although rare and preventable, surgical fires occur every day in the United States, and it is important to prevent them and to be prepared in the instance that one happens. And OR fires are something that you should expect to see in your professional lifetime. Most of the editors have seen at least one. They happen in a flash—literally and figuratively. Cathy Marcucci once saw a surgeon set his own surgical gown on fire. The fire triad components are: the oxidizer, the fuel, and the ignition source. Communication is paramount in the risk reduction of surgical fires. The “Silverstein Fire Risk Assessment Tool” assesses whether an ignition source will be near the oxygen supply. Preventative measures should be employed based on the risk of surgical fire determined at the beginning of the procedure. Consider the use of an oxygen blender to deliver gas with a set oxygen concentration of no more than 30%; even oxygen administered as a low flow rate can pool under the drapes and create a fire hazard. In the event of an airway fire, the endotracheal tube should be removed and fresh gas flow should be turned off in whichever succession is fastest. Drapes, airways, and airway devices (ETT or LMA) should be doused with saline and the surgical fuel should be removed as quickly as possible. Ventilation and oxygenation should be reestablished once the fire has been exhausted. Postsurgical fire management may include bronchoscopy and admission to an ABA burn center. Any patient who suffers an airway fire should be treated at a burn center. Suggested Readings Apfelbaum JL, Caplan RA, Barker SJ, et al. Practice advisory for the prevention and management of operating room fires: An updated report by the American Society of Anesthesiologists Task Force on Operating Room Fires. Anesthesiology. 2013;118(2):271–290.

Clarke JR, Bruley ME. Surgical fires: Trends associated with prevention efforts. Pa Patient Saf Advis. 2012;9:130. Hart SR, Yajnik A, Ashford J, et al. Operating room fire safety. Ochsner J. 2011;11(1):37–42. Mathias JM. Scoring fire risk for surgical patients. OR Manager. 2006;22(1):19–20. Mehta SP, Bhananker SM, Posner KL, et al. Operating room fires: A closed claims analysis. Anesthesiology. 2013;118(5):1133–1139. Roy S, Smith LP. What does it take to start an oropharyngeal fire? Oxygen requirements to start fires in the operating room. Int J Pediatr Otorhinolaryngol. 2011;75(2):227–230. Surgical fire prevention. ECRI Institute. https://www.ecri.org/Accident_Investigation/Pages/Surgical-FirePrevention.aspx. Accessed October 28, 2017.

135 Malignant Hyperthermia: If You Get to the Point Where You See an Elevated Temperature, It’s Already Happening James C. Opton, MD

Malignant hyperthermia (MH) is a clinical syndrome characterized by uncontrolled skeletal muscle metabolism. First defined in 1960 by Denborough and Lovell, it is classically “triggered” by volatile anesthetics and the depolarizing muscle relaxant succinylcholine in genetically susceptible individuals. MH is caused by uncontrolled calcium release in skeletal muscle cells as a result of abnormal function of the ryanodine receptor (RYR1). Diagnosis can be made clinically, by caffeine–halothane contracture testing of a muscle biopsy specimen, or by genetic testing. The caffeine– halothane test is very sensitive. However, it is invasive and expensive (about $800). Genetic testing for one of several known mutations of the RYR-1 genes is done via a simple blood test. Although it is not very sensitive, it is very specific and much less costly (about $200). The overall incidence of MH-susceptible patients in the general population is hard to estimate, because it is a “cluster” disease. However, in 2005, there were 12 confirmed cases and an additional 10 probable cases in the United States, according to an official at the Malignant Hyperthermia Association of the United States (MHAUS). MH can occur at any time during anesthesia or in the immediate postoperative period. It is the standard of care to ask every patient exposed to a triggering agent if he or she has a family history suspicious for MH (“Has a family member ever had a dangerous or unusual reaction to anesthesia?,” etc.). Although it is a rare disease, it is an important one in terms of anesthetic practice—anesthesiologists are expected from a medical/legal standpoint to be able to recognize and treat MH even if they are seeing it for the first time. The most consistent indicator of potential MH is a large increase in end-tidal carbon dioxide. End-tidal CO2 can double or triple in minutes (although it may increase over hours). Masseter rigidity is another early sign, and tachycardia, arrhythmias, unstable or rising blood pressure, cyanosis and mottling, myoglobinuria, and tachypnea follow.

Whole-body rigidity is a specific sign of MH and is seen in the limbs, abdomen, and chest if muscle relaxants have not been used. Respiratory and metabolic acidosis indicate fulminant MH and are typically followed by temperature elevation, a late sign. The temperature rise can be rapid and may exceed 43°C. Rhabdomyolysis and disseminated intravascular coagulation (DIC) may also occur. Death is usually from cardiac arrest secondary to acidosis or hyperkalemia. In the dantrolene era, mortality from MH is less than 10%.

Treatment of Acute MH Call for help! Get dantrolene! Discontinue volatile anesthetics and succinylcholine. Hyperventilate with 100% oxygen at high fresh gas flows. Give dantrolene 2.5 mg/kg by intravenous (IV) bolus. Repeat dose as needed until signs of MH are controlled. Place two large-bore peripheral IV lines and an arterial line. Treat acidosis with bicarbonate as guided by blood gas analysis. Actively cool patient with IV cold saline, nasogastric lavage, rectal lavage, and surface cooling. Discontinue cooling when temperature has fallen to 38°C. Treat hyperkalemia with hyperventilation, bicarbonate, insulin with glucose. Lifethreatening hyperkalemia should be treated with calcium. Dysrhythmias usually respond to treatment of acidosis and hyperkalemia. If not, use appropriate antiarrhythmics with the exception of calcium-channel blockers. Serially monitor end-tidal CO2, arterial blood gases (ABG), serum potassium and other electrolytes, urine output, and international normalized ratio (INR)/prothrombin time (PTT). Ensure urine output of at least 2 mL/kg/h by hydration and/or diuretics. In severe cases, consider more intensive monitoring for volume status and cardiac output, such as with a noninvasive cardiac output monitor (pulse pressure or stroke volume variation monitor) or pulmonary artery catheter. Call the MH Hotline.

Treatment of Postacute MH Observe in intensive care unit (ICU) for at least 24 hours, as recrudescence may occur. Give dantrolene 1 mg/kg IV every 4 to 6 hours for 24 to 48 hours after the episode. Follow arterial blood gases, creatine kinase (CK), potassium, coagulation factors, urine myoglobin, and temperature until they return to normal. CK may stay elevated for up to 2 weeks.

Report patients to the North American MH Registry of MHAUS and refer patients to MHAUS for information.

What to Stock in the Malignant Hyperthermia Cart The MHAUS is very specific about what needs to be stocked in the MH cart. In addition to the standard American Society of Anesthesiologists (ASA) monitors, all locations where general anesthesia is administered should have a posted plan to treat MH; a means to continuously monitor end-tidal CO2, blood oxygen saturation, and core body temperature; and a means to actively cool a patient. A malignant hyperthermia cart stocked with the following should be immediately available wherever general anesthesia is administered:

Drugs 1) Dantrolene sodium for injection: 36 vials (each able to be diluted at the time of use with 60 mL sterile water). With the conventiionally available dantrolene, mixing of the drug can take 15 to 20 minutes. A new injectable solution of dantrolene sodium (Ryanodex) was approved by the FDA in 2014, which will be available in 250-mg single-use vials. This formulation has the potential to reduce the time needed to prepare and administer the correct dose of dantrolene during an MH crisis. 2) Sterile water for injection USP (without a bacteriostatic agent) to reconstitute dantrolene: 1,000 mL × 2. 3) Sodium bicarbonate (8.4%): 50 mL × 5. 4) Furosemide 40 mg/ampule × 4 ampules. 5) Dextrose 50%: 50-mL vial × 2. 6) Calcium chloride (10%): 10-mL vial × 2. 7) Regular insulin 100 U/mL × 1 (refrigerated). 8) Lidocaine for injection, 100 mg/5 mL or 100 mg/10 mL in preloaded syringes (× 3). Amiodarone is also acceptable. Advanced cardiac life support (ACLS) protocols, as proscribed by the American Heart Association (AHA), should be followed when treating all cardiac derangements caused by MH.

General Equipment 1) Syringes (60 mL × 5) to dilute dantrolene 2) Mini-spike IV additive pins × 2 and Multi-Ad fluid transfer sets × 2 (to reconstitute dantrolene). Call MHAUS for ordering info 3) Angiocaths: 16G, 18G, 20G, 2-in; 22G, 1-in; 24G, ¾-in (four each) for IV access and arterial line 4) Nasogastric (NG) tubes: sizes appropriate for your patient population

5) Blood pump. 6) Irrigation tray with piston syringe (×1) for NG irrigation. 7) Toomey irrigation syringes (60 mL ×2) for NG irrigation. 8) Microdrip IV set (×1).

Monitoring Equipment 1) Esophageal or other core temperature probes 2) Central venous pressure (CVP) kits (sizes appropriate for your patient population) 3) Transducer kits for arterial and central venous cannulation

Nursing Supplies 1) A minimum of 3,000 mL of refrigerated cold saline solution 2) Large sterile Steri-Drape (for rapid drape of wound) 3) Three-way irrigating Foley catheters (sizes appropriate for your patient population). 4) Urine meter × 1. 5) Irrigation tray with piston syringe. 6) Large clear plastic bags for ice × 4. 7) Small plastic bags for ice × 4. 8) Bucket for ice.

Laboratory Testing Supplies 1) Syringes (3 mL) for blood gas analysis for ABG kits × 6. 2) Blood specimen tubes (each test should have 2 pediatric and 2 large tubes): (A) for CK, myoglobin, SMA 19 (LDH, electrolytes, thyroid studies); (B) for PT/PTT, fibrinogen, fibrin split products; (C) complete blood count (CBC), platelets; (D) blood gas syringe (lactic acid level). 3) Urine-collection container for myoglobin level. Pigmenturia indicates that renal protection is mandated; unless the centrifuged or settled sample shows supernatant, i.e., the coloration is due to ret cells in the sample. 4) Urine dipstick: hemoglobin.

Forms 1) Laboratory request forms: ABG form × 6; hematology form × 2; chemistry form × 2; coagulation form × 2; urinalysis form × 2; physician order form × 2. 2) Adverse Metabolic Reaction to Anesthesia (AMRA) Report form (obtained from MH Registry). 3) Consult form, if needed, for requesting a consultation from another physician.

Preparing the Anesthesia Machine for MH-Susceptible Patients Ensure that vaporizers are disabled by removing, draining, or taping in the “OFF” position. Some consultants recommend changing the CO2 absorbent. Flow 15 L/min O2 through circuits via ventilator for at least 20 to 40 minutes. Given differences in design and manufacturing, consider checking the manufacturer recommendations for minimal washout times. Place new, disposable breathing circuit and breathing bag. Use expired-gas analyzer to confirm absence of volatile gases. Consider removing succinylcholine from the operating room, especially if there will be a change of personnel (i.e., for breaks or end-of-day relief).

Contact Information MH Hotline: 1-800-644-9737 or 1-315-464-7079 (outside US). North American MH Registry of MHAUS registers information about specific families and patients. Registry is located at Children’s Hospital at the University of Pittsburgh. See www.mhreg.org or call 1-888-274-7899. MHAUS provides educational and technical information to patients and health care providers at www.mhaus.org. They generally do not register cases in other countries, but do field calls from all over the world. TAKE HOME POINTS As above! Suggested Readings American Society of Anesthesiologists. A. Practice of Anesthesia for Infants and Children. 3rd ed. Philadelphia, PA: WB Saunders; 2001. website. www.asahq.org.Coté. Denborough MA, Lovell RRH. Anaesthetic deaths in a family. Lancet. 1960;2:45–46. Malignant Hyperthermia Association of the United States website. www.mhaus.org.

136 Good Old-Fashioned Basic Perioperative Blood Pressure Control Edwin G. Avery IV, MD and Brian K. Johnson, MD MEd

A 66-year-old male with severe claudication, peripheral arterial vascular disease, hypertension, chronic renal insufficiency (glomerular filtration rate 27), dyslipidemia, diabetes mellitus type II, and chronic low back pain presents for elective bilateral lower-extremity arterial angiography with likely balloon angioplasty and stenting planned. His chronic back pain obviates his ability to lie still with a conscious sedation-based anesthetic. Once safely induced into general anesthesia with the airway secured, his blood pressure is noted to be 141/65 mm Hg, heart rate 67 beats per minute (sinus rhythm) and SpO2 99% (FiO2 0.4). His preoperative blood pressure was 172/89 mm Hg and he had taken all of his antihypertensive medications as directed on the morning of surgery. Where should you keep the blood pressure for him and what are you concerned with if his BP runs either too high, too low, or both during the procedure?

Blood Pressure Control in the 21st Century We spent a considerable amount of time developing this chapter of the book. Emails and discussion points went back and forth as we debated the practices at our respective institutions as well as our individual predictions for the future standards of perioperative blood pressure management. We did not come to a complete consensus on every point! But we did come to joke among ourselves that managing perioperative blood pressure is like making the basic lasagna—a couple of simple ingredients make a dish that is deceptively more than the sum of its parts. Similarly, the basic “ingredients” of blood pressure are taught and learned pretty easily in medical school—the inotropic state of the heart, the state of the vasculature, and volume status, of course. But these physiologic factors can combine into perioperative management challenges that are deceptively more than you bargained for. So anesthesiologists must guard against the mindset that blood pressure (BP) control is simple and straightforward. And we must ask ourselves—do we have a true

understanding of what BP goals are appropriate perioperatively? And are we as routinely successful as we would like to be in managing a patient’s BP? We all have those roller-coaster days of blood pressure lability and we all intensely dislike and are frustrated by them; so the authors think perhaps not. In most cases, we continue to use slightly more advanced but still basic principles from our basic science physiology classes to determine an individual patient’s ideal BP range in the perioperative setting. For example, we aim for a mean arterial pressure (MAP) of 70 mm Hg, or MAP of 50 mm Hg to 150 mm Hg to remain within the cerebral autoregulatory range, or the baseline BP on day of surgery or 20% lower than baseline BP if the patient is hypertensive. But we now know that these basic concepts of perioperative blood pressure control are just the basics. We also now have a significant body of peerreviewed literature that supports the concept that poor perioperative BP control, even for just a handful of hours in the operating room, can have a significant impact on postoperative morbidity and mortality, including neurocognitive dysfunction, renal injury, myocardial infarction, and stroke. In addition, goal-directed therapy (aka enhanced surgical recovery) in almost all varieties of surgical patients is in fact a multidimensional concept with effective blood pressure management being just one important aspect of optimizing perioperative care. So we must not become complacent in our belief that BP management is a ho-hum and easy-peasy topic, because it most definitely is not.

It’s a Big World but Here is BP Management That Should Work for Everyone Even if you are fortunate enough to get a vigilant patient with a diagnosis of hypertension who presents you with spreadsheets of daily blood pressure readings with accompanying multicolored graphs and a detailed medications list (and don’t hold your breath waiting for a patient like this to wander into your OR), you have to consider that the challenge of determining an optimal perioperative BP range is still not so simple. General anesthesia is accompanied by various degrees of sympathectomy as well as frequent temperature, acid–base, and intravascular volume dynamics which are encountered in more complex surgeries that will challenge the effectiveness of the body’s autoregulatory mechanisms and reflex physiologic responses. In a patient with limited organ reserve, such as our vasculopath presented in the vignette with shoddy kidneys, we certainly don’t want to make his renal function, or any other organ function for that matter any worse. As discussed above, poor perioperative BP control has been strongly linked to increased perioperative morbidity and mortality and it is for these reasons that we personally advocate for the use of advanced parameter monitoring in patients with limited organ reserve, as we discuss in more depth in Chapter 137.

However … what should you actually do? Not every institution and/or anesthesia department has the same access and availability with respect to equipment, not to mention the same clinical practices, expertise, analysis, opinions, and ICU management philosophies. And to make matters even more confusing, review of the published literature on perioperative blood pressure control is full of conflicting information. But you have to do something—you have a patient in front of you, he’s going to have an internal cardiovascular state and organ perfusion status, one way or the other. And you sure do want to control the blood pressure, because you don’t want the blood pressure to control you. So, we finally decided to put our collective experiences together and craft an approach for you to strongly consider while pondering BP management for a patient like our vignette patient. These recommendations should work for a variety of clinicians in a variety of settings: 1) In patients that have a systolic blood pressure greater than 180 mm Hg and/or diastolic pressure greater than 120 mm Hg with clear evidence of end-organ damage (e.g., myocardial ischemia, acute congestive heart failure, new evidence of acute kidney injury, changes in vision, new cerebral pathology), this is the definition of a hypertensive emergency and the nonemergent case should be cancelled with immediate referral of the patient to inpatient treatment. 2) In patients with the same blood pressure detailed in point #1 without clear evidence of end-organ damage, this is the definition of a hypertensive urgency (if anxiolysis does not improve the blood pressure). These patients should have their systolic or mean arterial pressure slowly lowered by 20% to 25% (over 30 to 60 minutes) and maintain this goal perioperatively while closely monitoring for signs and symptoms of neuroischemia. 3) In hypertensive patients that do not meet the hypertensive emergency/urgency criteria (i.e., those with systolic blood pressure greater than 140 mm Hg and/or diastolic blood pressure greater than 80 mm Hg), lower the systolic pressure by 20% and maintain that goal perioperatively. Finally, there are certainly many patients that we provide care for that are younger, possess sufficient organ reserve function and undergo elective noncomplex surgery with minimal fluid shifts (e.g., knee arthroscopy), and present with only relatively mild increases in blood pressure. In such cases more involved monitoring modalities can be foregone and patients can be managed with more contemporary enhanced surgical recovery techniques that include permitting the patient to drink clear carbohydratecontaining beverages up to 2 hours prior to surgery, use of multimodal analgesics to reduce narcotic dosing, and early use of the gastrointestinal tract (i.e., feed patients a

light meal in the postanesthesia care unit). Consider that intravascular volume contraction related to NPO guidelines can result in significant systemic arterial vasoconstriction with accompanying observed hypertension and these patients may respond favorably to cautious IV fluid replacement therapy. Those that fail to respond to volume expansion can be managed with the approach detailed in point #3 above. TAKE HOME POINTS Perioperative hypertension is a common problem for anesthesia clinicians and recent literature suggests that mismanagement for even a few hours around the time of surgery can have significant physiologic/outcome consequences (e.g., watershed stroke or myocardial ischemia). Merely targeting a mean arterial pressure of greater than or equal to 70 mm Hg may not be an acceptable strategy to manage perioperative hypertension. Individuals presenting for elective surgery with a hypertensive emergency as defined in the first point above should have their surgery cancelled and be referred for inpatient treatment. Adequately anxiolysed individuals presenting for surgery with a hypertensive urgency or less severe hypertension as detailed in the second and third points should have their systolic blood pressure lowered by approximately 20% through either volume expansion in those suspected of significant volume contraction or administration of antihypertensives. Suggested Readings Ameloot K, Palmers PJ, Malbrain ML. The accuracy of noninvasive cardiac output and pressure measurements with finger cuff: A concise review. Curr Opin Crit Care. 2015;21(3):232–239. Aronson S, Dyke CM, Levy JH, et al. Does perioperative systolic blood pressure variability predict mortality after cardiac surgery? An exploratory analysis of the ECLIPSE trials. Anes Analg. 2011;113(1):19–30. Ono M, Brady K, Easley B, et al. Duration and magnitude of blood pressure below cerebral autoregulation threshold during cardiopulmonary bypass is associated with major organ morbidity and operative mortality. J Thorac Cardiovasc Surg. 2014;147(1):483–489. Salmasi V, Maheshwari K, Yang D, et al. Relationship between intraoperative hypotension, defined by either reduction from baseline or absolute thresholds, and acute kidney and myocardial injury after noncardiac surgery: A retrospective cohort analysis. Anesthesiology. 2017;126(1):47–65.

137 Some Additional Thoughts on Blood Pressure Management Techniques—What We Believe, How We Do It, and Where We Think the Science Is Going Edwin G. Avery IV, MD and Brian K. Johnson, MD MEd

In Chapter 136, we reviewed the fundamental principles and targets of perioperative blood pressure (BP) control. But here’s the thing: the world of patient care is a big place with a wide range of clinical practices, expertise, analysis, and opinions. In our lively editorial debate, it became apparent that not every institution has the same access and availability with respect to equipment. Institutions that have the same equipment use it differently at their respective locations. Anesthesiologists within the same institutions and in different subspecialties vary in their opinions and practices. Practitioners evolve their practices and then evolve them back. And postoperative ICU management philosophies vary, of course, which has a ripple effect on patient management backward through the perioperative timeline. At the authors’ institution, the cerebral oximeter used together with the noninvasive oscillatory/near infra-red BP technology provides the best way to maintain vital organ perfusion in the perioperative setting—and all without poking any extra holes in the patient. We are certainly aware that there are numerous clinicians who do not have or use these technologies for blood pressure management and these folks rely on the traditional metrics discussed in Chapter 136, such as targeting baseline mean/systolic/diastolic arterial pressure, absence of tachycardia, moistness of mucous membranes, and observed urine output to determine if the vital organs are adequately perfused and if volume status is optimal. However, in our clinical practice and academic work, we are focused on moving past the traditional metrics toward developing and promoting the precision metrics. Our tagline among ourselves in our corner of the world is: when these two distinct approaches of perioperative BP management are compared it’s like the Flintstones meet the Jetsons … The patient in the vignette in Chapter 136 was a 66-year-old man with hypertension,

diabetes, vascular disease, and diabetes. How would we personally manage this patient? Our anesthetic plan for this challenging but common clinical situation would involve the use of a cerebral oximeter and a noninvasive blood pressure monitor that can provide beat-to-beat BP data as well as cardiac performance data. We feel the cerebral oximeter has supreme utility in protecting the brain’s oxygen balance as has been demonstrated by multiple randomized controlled trials and observational studies (discussed below), in that there is significantly lower incidence of postoperative neurocognitive dysfunction in a variety of surgical settings. Think of the brain like “the canary in the coal mine” because if you protect the brain’s oxygen balance the rest of the organs should be OK since the brain uses proportionally more oxygen and has limited reserve to tolerate ischemia. During a general anesthetic, the brain should have a lower cerebral metabolic rate and if it is extracting more oxygen while the patient is asleep, as opposed to when the patient is awake and doing mental long division in their head, it should not be increasing its oxygen extraction. The cerebral oximeter tells you when there is increased oxygen extraction in the brain by revealing a decrease below the patient’s baseline regional saturation (rSO2) values (N.B. less than 15% to 20% below the established baseline is considered a significant desaturation and less than 25% is a critical desaturation). A decrease in cerebral oxygen saturation most commonly heralds a decrease in oxygen delivery for any number of reasons—hypotension or relative hypotension below the lower limit of cerebral autoregulation is just one possibility, while others may include hypoxia, hypocarbia, hypovolemia, low cardiac output, and anemia. The cerebral oximeter is effectively a poor man’s way to determine the lower limit of cerebral autoregulation which has been well demonstrated to be a moving target during general anesthesia. For example, if a patient’s mean arterial pressure (MAP) is 80 mm Hg at baseline and during anesthesia you keep the MAP at 80 mm Hg but see a bilateral cerebral desaturation of 15% to 20% or more below the patient’s baseline then you know there is decrease in oxygen delivery to the head. If raising the MAP to 90 mm Hg resolves the desaturation then we know the patient’s cerebral blood flow was pressure passive and the patient was below the lower limit of cerebral autoregulation. We can do all this noninvasively with two adhesive near-infrared sensor pads applied to the patient’s forehead in lieu of complex and cumbersome transcranial Doppler monitoring; the use of cerebral oximetry in this capacity is well-validated in the peerreviewed literature. While the cerebral oximeter is a great tool for determining vital organ perfusion and maintaining oxygen balance, we should also consider another noninvasive option such as the ClearSight® device (Edwards Lifesciences, Irvine, CA). This noninvasive finger BP cuff uses a combination of near-infrared technology and oscillatory manipulation of

the finger arteries to produce a beat-to-beat arterial waveform as obtained with an arterial catheter. Shortly after, in about 10 seconds or so, analysis of the constructed arterial waveform, the device will also produce accurate cardiac index/output, stroke volume, stroke volume variation, and systemic vascular resistance parameters under most clinical conditions. Furthermore, these cardiac performance parameters are updated several times each minute giving clinicians the most up-to-date hemodynamic information on a continuous basis. Appropriate use of these parameters not only permits maintenance of adequate tissue oxygen delivery but also a means by which to provide optimal fluid management in the perioperative setting—another clinical area that we frequently score low marks in during the perioperative period. It is well documented that both underresuscitation and fluid-overload may result in an increased rate of perioperative complications that are proven to have significant economic consequences. The management of perioperative hypertension remains a challenge to clinicians and approaches will vary until additional large-scale randomized controlled trials are conducted to help guide therapies. That said, a number of studies that we feel are important are discussed in the Take Home Points below. Finally, the unconvinced reader should review the studies cited below that demonstrate how the cerebral oximeter can accurately find the lower limit of cerebral autoregulation in the majority of patients undergoing cardiac surgery as well as work on the clinical impact (i.e., acute kidney injury and increased mortality) of having cardiac surgical patients below the lower limit of cerebral autoregulation. Disclosure: Dr. Avery is an educational consultant to Medtronic on the topic of the clinical use of NIRS cerebral oximetry; he delivers both peer-to-peer education as well as speaker’s bureau lectures for which he has accepted honoraria. Dr. Avery has received research funding support from Medtronic for an Investigator-initiated protocol evaluating the use of cerebral oximetry in thoracic surgery.

TAKE HOME POINTS We feel the cerebral oximeter and an advanced hemodynamic parameter monitoring device finger cuff provides a novel approach to perioperative blood pressure management for clinicians with access to the equipment and technology. In our practice, this technique provides highly accurate blood pressure information as well as cardiac index and stroke volume index, and is likely the best way to find a safe blood pressure range in the perioperative period. Using the brain’s frontal lobes as the “canary in the coal mine” can provide optimal end-organ protection for the body. Patients with cerebral desaturations of 15% to

20% or more below their established awake baselines that demonstrate pressure passive flow should have their mean arterial pressure raised (e.g., with intravascular volume expansion, vasoconstrictors, or inotropes) to reverse any observed cerebral desaturation. And now a personal note from Dr. Avery : First, I am completely aware that there are not enormous numbers of people using cerebral oximeters in the manner that our cardiac anesthesiologists do. Second, I feel strongly about making the appropriate upfront disclosures when discussing or debating pretty much any aspect of cerebral oximetry for which I have received direct or indirect compensation. That said, I feel that researching this technology, teaching about it, and using it in my practice (including frequently outside of cardiac surgery) has given me a unique perspective. I have a sincere belief in the use of cerebral oximetry and hope that the rest of the anesthesia world will soon catch up. I do recognize that this is not a universal opinion, at present. I have great respect for my colleagues who do not use this technology but also great respect for and confidence in my colleagues who were the early proponents of this technology and who believe that it has the ability to help find the lower limits of cerebral autoregulation without transcranial Doppler. As I began to use these techniques, it was then my own realization that even with the near infrared spectroscopy (NIRS) data you still need to know about flow to the organs and blood pressure if you want to get it right every time. I like to think of combining NIRS cerebral oximetry with an advanced parameter noninvasive hemodynamic monitor as the perfect cocktail to ensure both optimal end-organ perfusion and appropriate maintenance of intravascular volume status. In “Suggested Readings”, we have included information on the prospective randomized controlled trials that demonstrate NIRS effectively reduced neurocognitive dysfunction in cardiac surgical patients. Neurocognitive dysfunction, of course, is a frequent complication of cardiac surgery and an expensive one. We also direct your attention to John Murkin’s work that demonstrated reduced complications and reduced ICU length of stay in cardiac surgery patients. The Andrea Casati prospective, randomized, controlled trial paper covers major abdominal surgery and, in this study, mini-mental status examination scores were favorable in those randomized to open NIRS monitoring with an interventional algorithm. The Casati study also showed dramatic reduction in both PACU and hospital length-of-stay. Suggested Readings Ameloot K, Palmers PJ, Malbrain ML. The accuracy of noninvasive cardiac output and pressure measurements with finger cuff: A concise review. Curr Opin Crit Care. 2015;21(3):232–239. Casati A, Fanelli G, Pietropaioli P, et al. Continuous monitoring of cerebral oxygen saturation in elderly patients undergoing major abdominal surgery minimizes brain exposure to potential hypoxia. Anesth

Analg. 2005;101(3):740–747. Colak Z, Borojevic M, Bogovic A, et al. Influence of intraoperative cerebral oximetry monitoring on neurocognitive function after coronary artery bypass surgery: A randomized, prospective study. Eur J of Cardiothor Surg. 2015;47(3):447–454. Joshi B, Ono M, Brown C, et al. Predicting the limits of cerebral autoregulation during cardiopulmonary bypass. Anesth Analg. 2012;114(3):503–510. Mohandas BS, Jagadessh AM, Vikram SB. Impact of monitoring cerebral oxygen saturation on the outcome of patients undergoing open heart surgery. Ann Card Anesth. 2013;16(2):102–106. Murkin JM, Adams SJ, Novick RJ, et al. Monitoring brain oxygen saturation during cardiac surgery: A randomized, prospective study. Anesth Analg. 2007;104(1):51–58. Ono M, Arnaoutakis G, Fine DM, et al. Blood pressure excursions below the cerebral autoregulation threshold during cardiac surgery are associated with acute kidney injury. Crit Care Med. 2013;41(2):464–471. Ono M, Brady K, Easley B, et al. Duration and magnitude of blood pressure below cerebral autoregulation threshold during cardiopulmonary bypass is associated with major organ morbidity and operative mortality. J Thorac Cardiovasc Surg. 2014;147(1):483–489.

138 Protect the Kidneys, Not the “UOP” Michael P. Hutchens, MD MA

It is axiomatic in anesthesiology that abundant, or at least physiologically normal, intraoperative urine output (UOP) is essential to a good postoperative renal outcome; and consensus guidelines state that intraoperative volume administration should be based on objective measures of hypovolemia and that fluid excess should be avoided because it is deleterious even without overt complications. Although it is still true that the best monitor of intraoperative renal function is UOP, this is unfortunately true only in the sense that there is no other monitor of even passable use. One should not confuse poor data from a bad monitor with excellent data (such as from end-tidal capnography) from a monitor that demands action. Urine output is often used as a measure of hypovolemia, but it is not necessarily objective. This chapter focuses on situations in which the anesthesia provider must be cautious in the use of oliguria as a sign of hypovolemia. Unfortunately, the differential diagnosis of intraoperative oliguria is not hypovolemia alone. Aggressive volume resuscitation of a patient with intraoperative oliguria due to unsuspected acute kidney injury (from sepsis, cardiorenal syndrome, or perioperative nephrotoxins) without monitoring of central venous pressure may result in intravascular volume overload without correction of the oliguria. In these patients, volume resuscitation in excess of normal volume status can lead to heart failure and pulmonary edema also. Occasionally, large volumes of fluid are administered to a physiologically normal but oliguric patient in an attempt to correct presumed hypovolemia when in fact the problem is a kinked urinary catheter or an unsuspected urinary tract injury in the surgical field. In the first case, delayed diagnosis of the kinked catheter and volume resuscitation will result in an overdistended bladder and ultimately obstructive renal failure. In the second case, renal function may be unaffected. It has been frequently observed that patients undergoing laparoscopic surgery have lower-than-expected intraoperative UOP. Aggressive volume resuscitation in these patients may or may not increase their UOP. Euvolemia or slight relative hypervolemia may be necessary to ensure adequate blood pressure in this setting (because of increased intrathoracic pressure reducing return to the right heart). But does the

reduced UOP reflect a danger to the kidney? Early laparoscopists thought this was the case—that pneumoperitoneum caused renal vein and parenchymal compression, which resulted in oliguria and eventually renal injury. There is now good evidence to show otherwise. In multiple studies in animal models, pneumoperitoneum of 15 mm Hg or less (the upper limit for most laparoscopic procedures is 15 mm Hg) predictably reduces UOP but does not result in significant changes in ultrasound, pathologic, or chemical indicators of renal function. This question has also been evaluated in humans. As laparoscopic gastric bypass was being developed, Nguyen et al. reported on renal physiology in more than 100 patients assigned randomly to either laparoscopic or open gastric bypass. Despite a longer operative time and 64% lower intraoperative UOP in the laparoscopic group, there was no significant difference in postoperative blood urea nitrogen (BUN), creatinine, antidiuretic hormone (ADH), aldosterone, or renin levels, strongly suggesting that the reduced UOP reflects a reversible noninjurious physiologic consequence of pneumoperitoneum. Similarly, the development of the laparoscopic donor nephrectomy offered an opportunity to study the effect of pneumoperitoneum directly, in both the retained and the transplanted (hence stressed) kidney. Hawasli et al. studied the effect on donated and retained kidneys of two different levels of pneumoperitoneum (10 and 15 mm Hg). They found no difference in UOP or other indices of renal function between the groups. Importantly, the transplanted kidneys functioned equally well whether harvested at high or low pressure. Intraoperative UOP is generally controlled aggressively with fluids, hypervolemia, and diuretics during donor nephrectomy, so it is impossible to assess relative oliguria in this population, but studies have shown that the laparoscopic donor operation produces allograft function that is equivalent to that of the open operation. Laparoscopic surgery is not the only setting in which relative oliguria may not be harmful. Patients undergoing radical head and neck surgery have also been observed to have relative oliguria intraoperatively. Priano et al. studied “dry” versus “wet” resuscitation strategies in head/neck surgery patients with normal preoperative renal function, finding that resuscitation of more than 1 L/hr produced a UOP of 1.3 mL/kg/hr; half-dose resuscitation was associated with significantly less UOP (0.4 mL/kg/hr). Both groups had normal intraoperative and postoperative hemodynamics, and normal postoperative renal function. The anesthetic doctrine of “plentiful pee,” then, has important exceptions. This is the case because a “normal” UOP is a second-line surrogate marker for instantaneous renal function, analogous to depending on the surgeons’ assessment of blood color to measure adequacy of oxygenation. New technologies such as continuous renal ultrasound and near-infrared regional oximetry offer some hope of improving the monitoring of intraoperative renal function. In the meantime, we must use the monitor we have with

intelligence, sophistication, and a high level of skepticism. TAKE HOME POINTS Urine output is a poor monitor of renal function, but it’s the only one we have in the operating room. Laparoscopic surgery patients can have low intraoperative UOP without detriment to postoperative renal function. Radical head and neck surgery patients can have low intraoperative UOP without detriment to postoperative renal function. Suggested Readings Feldheiser A, Aziz O, Baldini C, et al. Enhanced recovery after surgery (ERAS) for gastrointestinal surgery, part 2: Consensus statement for anaesthesia practice. Acta Anesth Scand. 2015;60(3):289–334. Hawasli A, Oh H, Schervish E, et al. The effect of pneumoperitoneum on kidney function in laparoscopic donor nephrectomy. Am Surg. 2003;69(4):300–303; discussion 303. Nguyen NT, Perez RV, Fleming N, et al. Effect of prolonged pneumoperitoneum on intraoperative urine output during laparoscopic gastric bypass. J Am Coll Surg. 2002;195(4):476–483. Priano LL, Smith JD, Cohen JI, et al. Intravenous fluid administration and urine output during radical neck surgery. Head Neck. 1993;15(3):208–215.

139 Avoid a 70% Mortality Rate: Do Everything You Can to Prevent Perioperative Renal Failure Michael P. Hutchens, MD MA

Acute renal failure in the postoperative period is appallingly common and has abysmal outcomes. In high-risk populations the incidence may be as high as 25%, and patients who require critical care services and renal replacement therapy have repeatedly been shown to have a mortality rate >70%. Despite this, perioperative resuscitation strategies are frequently formed solely with cardiac and pulmonary outcomes in mind. An early extubation is a pyrrhic victory if it condemns the patient to a slow death or lifetime dialysis. Despite decades of research, the risk factors, etiology, prevention, and treatment of perioperative acute renal failure all remain murky. Numerous interventions have been assessed, with few promising results. There are a few tools at hand, though, and the devastating effect of acute renal failure obligates anesthesiologists to use the tools available with the best possible dexterity. The most consistent risk factor for perioperative renal failure is preoperative renal dysfunction. Elevated creatinine or decreased creatinine clearance, or a preoperative diagnosis of renal insufficiency, all significantly increase the risk of postoperative renal failure. Preoperative heart failure and diabetes mellitus are also significant predictors, as are the acute comorbidities rhabdomyolysis, fulminant liver failure, abdominal compartment syndrome, and sepsis. Surgical procedures involving cardiopulmonary bypass or aortic cross-clamp (any aortic cross-clamp, not just suprarenal clamping) increase the risk as well. Perioperative diagnostic studies involving nephrotoxic radiocontrast and medical management of concurrent nonsurgical disease (chemotherapy, aminoglycosides, nonsteroidal anti-inflammatory drugs [NSAIDs]) can further elevate the risk. Anesthetic management directed at preventing acute renal failure ranges from banal to complex. If possible, stop nephrotoxic medications preoperatively. Certainly do not give preoperative NSAIDs to improve analgesia in at-risk patients. For procedures that will take 2 hours or more, a Foley catheter should be placed. Ensure that urine enters

the Foley catheter when it is placed, as a misplaced Foley and subsequent obstruction can cause renal failure. In current practice there is no longer a fixed “goal” for hourly urine output; the objective is to monitor urine output diligently, and if it drops, intervene—increase perfusion pressure, give a fluid challenge, and inform the surgeon. If need be, place a central venous pressure (CVP)— while this may not allow for the estimation of volume status or volume responsiveness, a high CVP (i.e., >8 mm Hg) may impede microcirculatory flow, especially in the kidney, and may need an intervention. Eschew nephrotoxic agents in your anesthetic plan—ketorolac, dextran or synthetic starches, and aminoglycosides—should be avoided. It is clear that hypoperfusion contributes to perioperative renal failure; in at-risk patients, maintaining perfusion pressure is a high priority. What does this mean? There is some evidence to support that MAPs should be maintained greater than 60 mm Hg in the normotensive patient. Patients with chronic hypertension, due to changes in renal autoregulation, may need even higher pressures. Have a low threshold for placing an intra-arterial monitoring line, and use vasoactive agents, if necessary, to treat hypotension. No therapeutic agent has shown broad renal-protective effect in the perioperative setting. Although there is lasting enthusiasm for low-dose dopamine, extensive study has shown it to have no effect on need for dialysis or mortality. Use of dopamine predictably causes tachycardia, which may be deleterious in a patient with concurrent coronary artery disease and increases the incidence of perioperative atrial fibrillation. Mannitol is commonly used in aortic cross-clamp cases; however, evidence to support this use is slim at best. Mannitol has been shown to be effective in preventing acute renal failure when used properly during renal transplant procedures. Although furosemide is popularly used to increase urine output, there is 30 years of evidence that furosemide can cause acute renal failure, and its use in the hypoperfused patient in the operating room (OR) is anathema. Other agents that have been used as putative intraoperative renal protectants include atrial natriuretic peptides, N-acetylcysteine, and fenoldopam. All have shown benefits in small studies that have not been replicable in large studies, suggesting that each may have use in a confined population, but what population remains unclear. A tantalizing study by Gandhi et al. in 2005 showed a significant association between intraoperative hyperglycemia and postoperative renal failure (defined as a doubling of creatinine, a creatinine >2, or new requirement for dialysis) in cardiac surgical patients. As intensive insulin therapy in the intensive care unit (ICU) reduces the need for dialysis, and as diabetes mellitus is a known risk factor, this raises the possibility that intraoperative insulin treatment may be renoprotective. TAKE HOME POINTS

Although the anesthesiologist may not see it happening in the OR, acute renal failure is an anesthetic outcome with gargantuan impact on patient morbidity and mortality. Remember that we can see only oliguric acute renal failure, because typically we don’t check the BUN and creatinine. The alert anesthesiologist must consider renal outcome in the anesthetic plan. Recognize the patient who is at risk because of preoperative disease or medical interventions. Maintain adequate circulating volume and perfusion pressure, and at all costs avoid doing harm with nephrotoxic agents. Consider tight intraoperative glucose control with insulin in diabetic patients. Finally, if you are concerned that the patient may be at risk for postoperative renal failure, communicate this to the surgeons, because early recognition and intervention in the postoperative period may improve the outcome. Suggested Readings Gandhi GY, Nuttall GA, Abel MD, et al. Intraoperative hyperglycemia and perioperative outcomes in cardiac surgery patients. Mayo Clin Proc. 2005;80(7):862–866. Jarnberg PO. Renal protection strategies in the perioperative period. Best Pract Res Clin Anaesthesiol. 2004;18(4):645–660. Levy EM, Viscoli CM, Horwitz RI. The effect of acute renal failure on mortality. A cohort analysis. JAMA. 1996;275(19):1489–1494. Mahon P, Shorten G. Perioperative acute renal failure. Curr Opin Anaesthesiol. 2006;19(3):332–338. Metnitz PG, Krenn CG, Steltzer H, et al. Effect of acute renal failure requiring renal replacement therapy on outcome in critically ill patients. Crit Care Med. 2002;30(9):2051–2058.

140 Do Not Use Urine Output as an Indicator of Volume Status in Hypothermic Patients Juan N. Pulido, MD and Daniel R. Brown, MD PhD FCCM

Hypothermia is a clinical entity defined as a core body temperature less than 35°C (95°F) and is classified in four stages depending on the temperature, symptomatology, and effect on specific organ physiology (Table 140.1). All organs are ultimately affected by hypothermia, including the kidneys. The renal response to cold is rapid and varies with the different stages of hypothermia. Initially, peripheral vasoconstriction results in relative central hypervolemia producing an increase in urine output. This response, termed “cold diuresis,” has been described even in patients with mild to moderate hypothermia. The etiology of this phenomenon is multifactorial and includes an initial increase in cardiac output and renal blood flow resulting from hypothermia-induced changes in vascular capacitance. Other important contributors are nonosmotic suppression of antidiuretic hormone (ADH) release by the hypothalamus and subsequent decreased renal tubular reabsorption. These responses usually begin as soon as the core body temperature reaches 35°C and become more pronounced until moderate hypothermia, when decreased renal blood flow and glomerular filtration rate (reduced 50% at 27°C to 30°C) may lead to acute kidney injury. Even in the setting of a large diuresis (the urine is usually dilute, with osmolarity 100th/mm3. Even if the preoperative platelet count was normal the long CPB run and diffuse bleeding suggest that platelets should be administered. Administer 1 to 2 pheresis platelet units through a nonwarmed, filtered line and do not inject concentrated calcium or epinephrine in the same intravenous line as the platelets, as it may activate them in the tubing! With all due respect to our surgical colleagues, “rescue rFVIIa” is not indicated until hemorrhaging patients have received at least two rounds of allogeneic hemostatic products without evidence of improvement in the bleeding. Further, rFVIIa may be effective at much lower doses (e.g., 35 µg/kg) than the package insert recommendation of 90 µg/kg which is the dose for bleeding hemophiliacs. If crossmatched hemostatic products are not immediately available consider activating your institutional massive transfusion protocol (MTP) and administer RBCs, FFP, and platelets in a 1:1:1 ratio; however, algorithmic POCT-guided therapy, for example, TEG or rotational thromboelastometry (ROTEM®) is currently preferred over MTP use as the issued components may not be type specific and will not be cross matched thus increasing the risk of allergic reaction. TEG/ROTEM can be useful as it will help diagnose the specific nature of many coagulopathies within about 15 to 20 minutes. Cardiac surgical patients are among those most likely to experience perioperative coagulopathy. These patients have temporally variable CPB exposure and regardless of the CPB circuit employed their coagulopathy has been shown to correlate with the length of time spent on CPB (i.e., there is an increasing incidence of coagulopathy as CPB time increases). CPB times exceeding 3 hours should alert clinicians to the potential for development of a significant coagulopathy. Blood to CPB element interfaces within circuitry initiate activation of systemic inflammatory pathways that are tied to the coagulation system and can provoke imbalance toward hypocoagulability. CPB-associated mechanical trauma to the blood elements causes anemia, thrombocytopenia, and a functional platelet defect (i.e., shear stress injury activates platelets). Dysfunctional platelets are quantified with a complete blood count (CBC) but do not actively contribute to hemostasis. The platelet count will frequently underestimate the need for a platelet transfusion because CPB creates a dysfunction-based thrombocytopenia. Additionally, cardiac surgery reproducibly creates a fibrinolytic state that may only be partially overcome through the pre-CPB initiation of antifibrinolytic agents. Further, since many cardiac surgery patients have undergone previous percutaneous coronary interventions or present with a low cardiac output syndrome, they are routinely treated with antiplatelet and/or antithrombotic agents. Antecedent antithrombotic/antiplatelet therapies are associated with increased postoperative hemorrhage and the increased need for transfusion of allogeneic blood

products. Several antithrombotic agents (e.g., low–molecular-weight heparin) and antiplatelet agents (e.g., ADP antagonists) cannot be effectively neutralized pharmacologically and will require the administration of allogeneic blood components to overcome their effects. Other antithrombotic agents such as oral factor X inhibitors may be neutralized by administration of a balanced prothrombin complex concentrate (i.e., contains balanced amounts of factors II, VII, IX, X, proteins C and S, and antithrombin III). Like rFVIIa, prothrombin complex concentrate is another “genie in a bottle.” Use of a balanced prothrombin complex concentrate to reverse a factor X inhibitor or to treat cardiac surgery–associated coagulopathy is an off-label use of the product and has been associated with thromboembolic complications, so be careful! As with rFVIIa, much lower doses of the balanced prothrombin complex concentrate (KCentra®) are used to treat cardiac surgical coagulopathy (i.e., 20 to 25 IU/kg of factor IX activity) than are recommended in the package insert for its labeled indication (i.e., Coumadin reversal). Off-label use of factor concentrates (prothrombin complex concentrates or rFVIIa) to treat cardiac surgical coagulopathy should not be pursued until at least two rounds of banked hemostatic allogeneic blood products have been administered without improvement. The potentially costly and morbid consequences of mistreating the coagulopathy observed in the clinical situation described above calls for the use of POCT as well as standard central laboratory hematology/coagulation tests, such as Hb, platelets, INR, and activated partial thromboplastin time (aPTT). Please remember that the isolated use of the INR is not a strong predictor of postoperative hemorrhage in this setting. The aPTT may be a better test to assess coagulopathy severity but does not distinguish between residual heparin effects. The ACT is the POCT that is used in cardiac surgery to monitor the effect of blood heparin levels and may correlate with the severity of coagulopathy. It does not correlate well with plasma heparin levels in hypothermic, hemodiluted patients on CPB. It is also a poor test of trace amounts of heparin and thus is not a good test to distinguish coagulopathy from residual heparin effects. It may be prolonged in patients with marked thrombocytopenia. Given its multiple shortcomings, the ACT is not a good test to diagnose the specific etiology of cardiac surgical coagulopathy. TEG/ROTEM are among the more useful POCTs to rapidly evaluate the integrity of the coagulation cascade. Both assays allow semispecific evaluation of the functional level of soluble coagulation proteins, functional fibrinogen levels, functional platelet levels, the presence of fibrinolysis and through the use of specialized assays the degree of platelet inhibition related to arachidonic acid inhibitors and ADP antagonists. Several cardiac surgical trials have confirmed that use of TEG with a transfusion algorithm is a more effective means to reduce the amount of transfused blood

components compared to physician discretion. Cardiac surgery–associated hypofibrinogenemia can be a major contributor to hemorrhage as it functions to form the proteinaceous scaffolding of a blood clot. Each unit of FFP contains the equivalent amount of fibrinogen found in one unit of Cryo. If TEG/ROTEM or laboratory testing reveals dys- or hypofibrinogenemia, then a target fibrinogen level of >200 mg/dL in a bleeding cardiac surgical patient is the goal and Cryo administration is indicated. In the absence of readily available Cryo the use of fibrinogen concentrate (RiaSTAP ®) should be considered—yet another genie in a bottle. A single vial of concentrate contains approximately 1 g of fibrinogen (i.e., equivalent to the amount of fibrinogen present in 5 units of either Cryo or FFP). Fibrinogen concentrate use to treat cardiac surgery bleeding is off-label (N.B. thromboembolic complications have been associated with its use) and it may take up to 20 minutes to solubilize this biologic depending on its temperature. Thawed Cryo is only good for 4 hours and must be stored at room temperature; it cannot be refrozen. Finally, remember that any variety of coagulopathy can be exacerbated by hypothermia, electrolyte disturbances and/or acid–base imbalance, thus the use of fluid/patient warming systems and attention to blood gas/electrolyte analysis results is vital. TAKE HOME POINTS Effective treatment of cardiac surgical coagulopathy requires that both central laboratory coagulation/hematology tests (e.g., the aPTT, INR, fibrinogen concentration, Hb and platelet count) and POCT; for example, TEG/ROTEM are used to guide blood component/factor concentrate and protamine administration. Given its multiple shortcomings the ACT is not a good POCT to diagnose the specific etiology of cardiac surgical coagulopathy. Platelet count frequently underestimates need for platelet transfusion because CPB creates a functional thrombocytopenia. Post-CPB initiation, or “rescue” antifibrinolytic therapy, such as aminocaproic or tranexamic acid, is not recommended as a primary usage pattern since the efficacy and safety of this practice has not been established. “Rescue” therapy may be an option for patients with significant hemorrhage who did not receive pre-CPB treatment. Coagulopathy should be anticipated in patients that have undergone CPB times greater than 3 hours—so have hemostatic blood bank components in the operating room! Several antithrombotic and antiplatelet agents cannot be neutralized pharmacologically and require the administration of allogeneic blood products to

overcome their effects. Patients treated with these agents may benefit from the delay of elective cardiac surgery. Use of factor concentrates (e.g., balanced 4-factor prothrombin complex concentrates and rFVIIa) to treat cardiac surgery bleeding is off-label and should be reserved until after the administration of at least two rounds of banked hemostatic products have not slowed bleeding. Doses for this indication are not established and thus should be conservative (i.e., 20% to 30% of the package insert dose) as their use is associated with thromboembolic complications. Use of fibrinogen concentrate to treat cardiac surgical-related bleeding in hypofibrinogenemic patients is off-label but has been demonstrated to be effective in increasing the fibrinogen concentration and quelling hemorrhage. Consider its use when Cryo or FFP is not readily available. Goal fibrinogen level in bleeding cardiac surgical patients is >200 mg/dL. Note that any variety of coagulopathy can be exacerbated by hypothermia, electrolyte disturbances and/or acid–base imbalance, thus the use of fluid/patient warming systems and attention to blood gas/electrolyte analysis results is imperative in the management of any coagulopathy. Suggested Readings Achneck HE, Sileshi B, Parikh A, et al. Pathophysiology of bleeding and clotting in the cardiac surgery patient: From vascular endothelium to circulatory assist device surface. Circulation. 2010;122(20):2068– 2077. Avery EG. Massive post-cardiopulmonary bypass related hemorrhage: A rational approach to management. ASA Refresher Courses in Anesthesiology. 2013; 41(1):8–14. Klick JC, Avery EG. Anesthetic considerations for the patient with anemia or coagulation disorder. In: Longnecker DE, Brown DL, Newman MF, et al., eds. Anesthesiology. 2nd ed. New York: The McGrawHill Companies, Inc.; 2012, Chapter 15.

230 A Is for Aortic, C Is for Cannulation, B Is for … Be Careful! Alexander S. Kuo, MS MD and Jason Zhensheng Qu, MD

A 64-year-old female with insulin-dependent diabetes, severe aortic atheromatous disease and peripheral vascular disease presents for coronary revascularization. Surgery is planned to include the use of cardiopulmonary bypass (CPB) with aortic cross clamp. Intraoperative pre-CPB transesophageal echocardiography (TEE) exam reveals a “mine field” of an ascending aorta with multiple mobile elements and protruding atheromatous plaques. The surgeon requests your help to find an appropriate site for insertion of the arterial perfusion cannula. What is your move in this situation? Answer: An epiaortic scan will help better define the extent of atheromatous disease in the ascending aorta. The epiaortic scan did not suggest that it would be safe to place the cannula in the ascending aorta because the stroke risk from atheroma dislodgement would likely be too great. The surgeon begins to prepare for cannulation of the right axillary artery. Will your left radial arterial line be appropriate for systemic pressure monitoring? Yes, as long as the blood pressure in the left upper extremity is not substantially lower than the right. Minimizing stroke risk in this patient is a big challenge given his severe atheromatous disease and the planned use of an aortic cross clamp; iatrogenic aortic dissection should also be of major concern. Cannulation for cardiac surgery does not often follow a straightforward formula. While the ascending aorta is the most common site of arterial cannulation for CPB, the presence of ascending aortic aneurysms, dissections, intramural hematoma, severe atherosclerosis or previous ascending aortic surgery may preclude safe cannulation in this region. In severely atherosclerotic ascending aortas, the site of arterial cannula insertion and aortic cross clamping should be carefully chosen to avoid dislodging atheromas and minimize risk of embolization. Optimal selection of the aortic cannulation site is facilitated with epiaortic and transesophageal ultrasound assessment to avoid disrupting aortic atheromas. In cases of

aortic dissection, TEE can be used to identify and guide cannulation of the true lumen. TEE findings identifying the true lumen include: antegrade flow during systole, maximal expansion during systole, and being able to visualize the intact vascular intima. Regardless of arterial cannulation site, CPB line pressures should be checked with a test infusion prior to initiation of full flow to reduce the risk of arterial dissection or expansion of existing dissection. Alternative sites for arterial cannulation include: the femoral artery, axillary artery, innominate artery, common carotid artery, and cardiac apex. Each cannulation site has unique implications for perfusion techniques and hemodynamic monitoring.

Femoral Artery Cannulation Although having a higher dissection rate than the aorta, the femoral artery is the most common alternative site for CPB cannulation. This vessel is readily accessible and therefore often used for cannulation in emergent CPB or when the ascending aorta is not suitable. Upon initiation of CPB, the arterial blood flows retrograde through the aorta from the groin toward the aortic arch. In select emergent cases (e.g., massive pulmonary embolism), femoral cannulation can be accomplished under local anesthesia to avoid the potential hemodynamic collapse that may accompany induction of general anesthesia (related to the blunting of sympathetic outflow) and the initiation of positive pressure ventilation. In cases of aortic dissection, the descending aorta and femoral artery are often involved. Retrograde perfusion via femoral cannulation may disrupt atheromatous plaques or elevate intima dissection flaps causing obstruction of branch vessels with consequent neurologic or visceral organ ischemia. In severely atherosclerotic vessels, perfusion from the femoral artery may also cause retrograde embolization from the atherosclerotic aortic wall. Commonly the right femoral artery is cannulated for CPB in patients with descending thoracic aortic dissections because it is more common for dissections to extend into the left femoral artery.

Axillary Artery Cannulation In comparison to the femoral artery, the axillary artery is usually less affected by atherosclerosis or dissection. Axillary artery cannulation minimizes the need to manipulate an atherosclerotic ascending aorta which may reduce the potential for atheroembolic sequelae. Further, since the arterial inflow is further away from the cerebral vessels and not directly aimed at them, cerebral embolic load may be decreased. For an operation that requires prolonged deep hypothermic circulatory arrest (DHCA), it is necessary to have a cannulation strategy that promotes cerebral

protection. Right axillary artery cannulation can provide anterograde right common carotid artery perfusion in conjunction with innominate artery occlusion during DHCA (Fig. 230.1). Axillary artery cannulation for CPB can be either direct or via an end-toside interposition graft. The use of right axillary artery cannulation may confound ipsilateral radial blood pressure monitoring. If the axillary artery is too small to accommodate full CPB flow, additional femoral or aortic artery cannulation is also needed to achieve target CPB flow.

Figure 230.1. Right axillary artery cannulation with interpositional graft and antegrade selective cerebral perfusion. With the innominate artery clamp off, the CPB pump provides systemic blood flow via the interpositional graft through the axillary artery (dashed arrows). The arterial pressure recorded from right radial artery will be significantly higher than that of the left radial or femoral arteries. When the innominate artery is clamped, the CPB pump provides antegrade cerebral perfusion via right carotid artery (solid arrows).

The efficacy of antegrade or retrograde brain perfusion for neurologic protection during DHCA is controversial. Most authors agree that there is not enough evidence to support retrograde cerebral perfusion (perfusing the brain via superior vena cava with oxygenated blood) compared to anterograde cerebral perfusion or simply deep hypothermia only. In any cerebral protection strategy employed during DHCA, be sure

to use a cerebral oximeter as it can be very useful to determine regional cerebral oxygenation and may prompt changes in the protection strategy that can minimize the incidence of stroke.

Innominate Artery Cannulation This technique provides all the above-mentioned advantages of right axillary artery cannulation, but with greater simplicity since there is no need of an adjunctive incision. It is especially useful in emergency cases (e.g., acute type A dissection).

Line Placement and Pressure Monitoring The radial artery is the most common peripheral artery used to monitor systemic blood pressure during CPB. In the absence of significant arterial stenosis, the laterality of radial artery cannulation is not clinically significant. Patients should be screened for differential upper extremity blood pressures prior to CPB if radial, brachial, or axillary artery monitoring is used. However, when axillary or innominate arterial cannulation for CPB is planned, bilateral radial or single femoral arterial pressure measurement is recommended to more accurately assess true systemic perfusion pressure. There are several techniques used to access the right axillary artery during CPB, such as end-to-side anastomosis or direct cannulation. Depending on the technique, the right radial artery pressure may be significantly higher or lower than aortic pressures due to the small caliber of the axillary artery, the close proximity to the perfuser, and the angle of the cannula/interposition graft. Therefore, it is crucial to have femoral or left radial artery pressures to reliably monitor systemic perfusion pressure on CPB. Hypoperfusion of the brain and other organs could occur if right radial artery pressure is depended upon for monitoring systemic blood pressure with an axillary cannulation strategy and use of a cerebral oximeter may be the only clue to the occurrence of this potentially devastating problem. TAKE HOME POINTS In severely atherosclerotic ascending aortas, the site of arterial cannula insertion and aortic cross clamping should be carefully chosen to avoid dislodging atheromas and minimize the risk of embolization. Regardless of arterial cannulation site, CPB line pressures should be checked with a test infusion prior to initiation of full flow to reduce the risk of arterial dissection or expansion of existing dissection. In select emergent cases (e.g., massive pulmonary embolism), femoral cannulation can be accomplished under local anesthesia to avoid the potential hemodynamic

collapse that may accompany induction of general anesthesia (related to the blunting of sympathetic outflow) and the initiation of positive pressure ventilation. Commonly the right femoral artery is cannulated for CPB in patients with descending thoracic aortic dissections because it is more common for dissections to extend into the left femoral artery. For an operation that requires prolonged DHCA, it is necessary to have a cannulation strategy that promotes cerebral protection. Right axillary artery cannulation can provide anterograde right common carotid artery perfusion in conjunction with innominate artery occlusion during DHCA. In any cerebral protection strategy employed during DHCA, be sure to use a cerebral oximeter as it can be very useful to determine regional cerebral oxygenation and may prompt changes in the protection strategy that can minimize the incidence of stroke. When axillary or innominate arterial cannulation for CPB is planned, bilateral radial or single femoral arterial pressure measurement is recommended to more accurately assess true systemic perfusion pressure. Suggested Readings Di Eusanio M, Quarti A, Pierri MD, et al. Cannulation of the brachiocephalic trunk during surgery of the thoracic aorta: A simplified technique for antegrade cerebral perfusion. Eur J Cardiothorac Surg. 2004;26(4):831–833. Evangelista A, Flachskampf FA, Erbel R, et al. Echocardiography in aortic diseases: EAE recommendations for clinical practice. Eur J Echocardiogr. 2010;11(8):645–658. Milewski RK, Pacini D, Moser GM, et al. Retrograde and antegrade cerebral perfusion: Results in short elective arch reconstructive times. Ann Thorac Surg. 2010;89(5):1448–1457. Orihashi K, Sueda T, Okada K, et al. Detection and monitoring of complications associated with femoral or axillary arterial cannulation for surgical repair of aortic dissection. J Cardiothorac Vasc Anesth. 2006;20:20–25. Spielvogel D, Kai M, Tang GH, et al. Selective cerebral perfusion: A review of the evidence. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S59–S62. Watanabe K, Fukuda I, Osaka M, et al. Axillary artery and transapical aortic cannulation as an alternative to femoral artery cannulation. Eur J Cardiothorac Surg. 2003;23:842–843.

231 Transesophageal Echocardiography in the Cardiac Surgery Suite—Strategies to Stay Out of Trouble Robert W. Kyle, DO

Perioperative transesophageal echocardiography (TEE) use has become a standard of care for cardiac surgical patients in most centers. While strong outcome data on TEE use are still lacking (does TEE result in lower overall morbidity and mortality compared to patients treated without TEE?), perioperative decision making can be significantly impacted by TEE. One study showed that in a cardiac surgical population of roughly 12,500, intraoperative decision making was impacted overall by 9%. TEE use and its subsequent impact will likely continue to increase with the expansion of hybrid surgical techniques (transcutaneous aortic valve replacement or TAVR, for example) and the increasing age and frailty of the surgical patient population. Like all forms of invasive monitoring, the use of TEE needs to be scrutinized to ensure that the monitor itself does not harm the patient. Fortunately, there are relatively few seriously adverse complications of TEE. Untoward events can include, but are not limited to, severe odynophagia, esophageal rupture, bleeding varices, bleeding ulcers, endotracheal tube dislodgement, and dental/oral trauma. Table 231.1 ■ Absolute and Relative Contraindications to Transesophageal Echocardiography Relative Contraindications

Absolute Contraindications

History of radiation to neck and mediastinum History of gastrointestinal surgery Recent upper GI bleed Barrett’s esophagus

Perforated viscus Esophageal stricture Esophageal tumor Esophageal perforation, laceration

History of dysphagia Active upper gastrointestinal bleed Resrictrion of neck mobility (severe cervical arthritis, atlantoaxial joint disease) Esophageal varices Coagulopathy, thrombocytopenia Active esophagitis Active peptic ulcer disease The reported incidence of mortality related to TEE use is less than 0.02% and carries an overall incidence of complications of about 0.2% (with severe odynophagia and upper gastrointestinal bleeds being among the most common)—most would agree that these are numbers we can all live with! However, the literature on TEE complications sends a clear signal that our older, female, and more frail patients appear to be at significantly higher risk for injury related to TEE use. The key with TEE use is to focus on staying out of trouble-–not getting out of it! TEE probes should not be placed in patients who have an absolute contraindication and clinicians have different ideas about which patients fall into this category. The 2010 American Society of Anesthesiology and Society of Cardiovascular Anesthesiology Task Force on TEE’s Practice Guidelines for Perioperative TEE consider the following absolute contraindications for TEE: esophageal stricture, tracheoesophageal fistula, postesophageal surgery, and esophageal trauma. Other disease states all fall into the realm of relative risk assessment, meaning that the benefit of TEE to patient care should be carefully weighed against any potential harm. More recently published guidelines on absolute and relative contraindications are presented in Table 231.1. The bottom line on determining what a relative versus absolute contraindication is for TEE use is involves a thorough assessment of the patient being considered and a full, patient-specific risk/benefit analysis. With these guidelines for reference and an in-depth perioperative history and physical, one can appropriately employ TEE, minimize risk, and successfully avoid the malpractice attorneys. Table 231.2 lists general indications for TEE use. In order to know if a patient has a contraindication to TEE, you must ask the patient about their medical history, as well as signs and symptoms pertinent to their comorbidities. Pertinent signs and symptoms include dysphagia, odynophagia, coffeeground emesis or hematochezia, liver disease, history of varices or variceal banding, significant long-standing (especially untreated) GERD, and hiatal hernia.

When placing a TEE probe, get your focus on and follow these three basic guiding principles: (1) NEVER force the probe. If there is resistance, reevaluate your current approach and optimize the patient’s position; (2) Use an adequate amount of sterile, water-based lubrication (note that many of the ultrasonic gels used for topical applications come with clearly labeled warnings—FOR EXTERNAL USE ONLY and thus should not be used for TEE); (3) Gently displace the mandible anteriorly while placing the probe to create an appropriate passage to the esophageal orifice. Laryngoscopy can be used effectively to assist in creating the necessary room to accommodate and place the TEE in more challenging placements. Be cognizant of the hemodynamic effects of placing the TEE probe and adjust anesthetic depth or analgesia accordingly. Lastly, applying mild anteflexion may assist the probe into the esophagus in certain patients by better approximating the anatomical angle of the pharynx. Care should be made, though, to have the probe in the neutral position when moving the probe in the upper and midesophagus. Table 231.2 ■ General Indications for Transesophageal Echocardiography 1) Evaluation of cardiac and aortic structure and function in situations where the findings will alter management and TTE (transthoracic echocardiography) is non-diagnostic or TTE is deferred because there is a high probability that it will be non-diagnostic. a. Detailed evaluation of the abnormalities in structures that are typically in the far field such as the aorta and the left atrial appendage. b. Evaluation of prosthetic heart valves. c. Evaluation of paravalvular abscesses (both native and prosthetic valves). d. Patients on ventilators. e. Patients with chest wall injuries. f. Patients with body habitus preventing adequate TTE imaging. g. Patients unable to move into the left lateral decubitus position. 2) Intraoperative TEE a. All open heart (i.e., valvular) and thoracic aortic surgical procedures. b. Use in some or all coronary artery bypass graft surgeries. c. Noncardiac surgery when patients have known or suspected cardiovascular pathology which may impact outcomes (also known as “Rescue TEE” in acute clinical situations).

3) Guidance of transcatheter procedure a. Guiding management of catheter-based intracardiac procedures (including septal defect closure or atrial appendage obliteration, and transcatheter valve procedures). 4) Critically ill patients a. Patients in whom diagnostic information is not obtainable by TTE and this information is expected to alter management. If your moves are spent and you are still unable to pass the probe, but feel that the surgery necessitates TEE, consider obtaining a surgical consult (i.e., evaluate the esophagus with an endoscope) and use of a pediatric TEE probe. Pediatric omniplane probes are of sufficient length (especially in women) and less likely to cause injury due to their small diameter. Another alternative to inserting a TEE probe may be to switch strategies and perform either epiaortic/epicardial (for cardiac cases) or transthoracic echocardiography (for cases not involving the thorax). TAKE HOME POINTS The key with TEE use is to focus on staying out of trouble—not getting out of it. Fortunately, the reported incidence of mortality related to TEE use is less than 0.02% and carries an overall incidence of complications of about 0.2% (with severe odynophagia and upper gastrointestinal bleeds being among the most common). Older, female, and more frail patients appear to be at significantly higher risk for injury related to TEE use. The bottom line on determining what a relative versus absolute contraindication is for TEE use is involves a thorough assessment of the patient being considered and a full, patient-specific risk/benefit analysis. When placing a TEE probe get your focus on and follow these three basic guiding principles: NEVER force the probe. Use an adequate amount of sterile, water-based lubrication (note that many of the ultrasonic gels used for topical applications come with clearly labeled warnings— FOR EXTERNAL USE ONLY and thus should not be used for TEE). In general TEE probe placement is facilitated by mild anteflexion of the probe, gentle anterior mandible displacement, judicious use of a laryngoscope and in the most difficult placement possible the use of a smaller diameter pediatric TEE probe.

Suggested Readings Eltzschig HK, Rosenberger P, Löffler M, et al. Impact of intraoperative transesophageal echocardiography on surgical decisions in 12,566 patients undergoing cardiac surgery. Ann Thorac Surg. 2008;85(3):845– 852. Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination: Recommendations from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiagr. 2013;26(9):921–964. Hensley FA, Martin DE, Gravlee GP. A Practical Approach to Cardiac Anesthesia. 3rd ed. Philadelphia, PA: Lippincott Williams &Wilkins; 2003. The American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography: An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology. 2010;112(5):1084–1096.

232 Myocardial Protection Strategies During Cardiopulmonary Bypass—Do Everything You Can but Realize That Some Ischemic Damage Is Inevitable S. Michael Roberts, DO, Theodore J. Cios, MD MPH, and Dmitri Guvakov, MD

A 62-year-old male with advanced heart failure related to ischemic cardiomyopathy presented for an orthotopic heart transplant. Following successful separation from cardiopulmonary bypass (CPB) the aorta was injured to an extent that required return to CPB and rearrest of the new heart to repair the aorta. A medical student observing the case has some questions about “the whole cardioplegia thing.”

Why Do We Need to Protect the Heart? The most important thing to remember is that some myocardial damage is inevitable during CPB; our goal is to minimize its extent and hope that the majority of the insult is reversible over time. Only a portion of the damage is due to ischemia; the majority of myocardial damage during CPB is due to reperfusion injury. Reperfusion releases free radicals causing direct myocardial dysfunction, intracellular acidosis, edema, calcium overload, inflammatory cascade initiation, and complement activation. Normally functioning myocardium consumes 9 mL O2/100 g/min. Emptying the heart decreases the myocardial work and the consumption to 5.5 mL O2/100 g/min. Inducing asystole via cardioplegia further reduces this to 1.8 mL O2/100 g/min, and cooling the still heart to 22°C reduces the basal consumption to 0.3 mL O2/100 g/min. Unfortunately, fibrillation increases these values to 6.5 mL O 2/100 g/min at 37°C and 2.0 mL O2/100 g/min at 22°C. Clearly a cold, empty, motionless heart would result in the lowest oxygen consumption and favor the best balance between supply and demand. Key factors in minimizing myocardial damage are avoiding ventricular fibrillation and ventricular distention during CPB (especially during antegrade cardioplegia

delivery in patients with aortic insufficiency). Other factors, such as direct trauma from surgical manipulation, excessive inotropes, and coronary emboli (either plaque or air), can contribute. Even microscopic air emboli are associated with endothelial dysfunction. These ischemic events generally result in myocardial stunning— dysfunction that resolves within 48 to 72 hours. Excessive ischemia can result in more significant and lasting damage. As a secondary insult, reperfusion injury occurs when the aortic cross-clamp is removed. Understandably, our goals should be to maximize the oxygen supply–delivery balance during CPB and minimize the effects of reperfusion. Effective myocardial protection is essential for successful cardiac surgery.

How Do We Protect the Heart? Cardioplegia! The ideal cardioplegia solution would quickly arrest all areas of the heart, allow early return of function, and minimize the need for inotropes. The most common method of protecting the myocardium is through giving cold, potassium-rich (10 to 40 mEq/L) cardioplegia. Anterograde cardioplegia is delivered proximal to the aortic cross-clamp into the coronary ostia, whereas retrograde involves the placement of a coronary sinus catheter through a right atriotomy or via transesophageal echocardiography (TEE)guided transjugular approach. While administering retrograde cardioplegia, keep the coronary sinus pressures under 40 mm Hg, in contrast to 100 mm Hg with anterograde delivery, to avoid rupturing coronary venules and capillaries. High-risk patients appear to do better when given both anterograde and retrograde cardioplegia but, with that said, some clinicians favor the isolated use of just anterograde or retrograde cardioplegia. The myocardial protection literature is complex and previously conducted studies may no longer be applicable as CPB techniques evolve. The potassium-rich cardioplegia arrests the myocardium in diastole through the inactivation of sodium channels. The makeup of cardioplegia solution varies with manufacturer and institutional preferences. Regardless of its delivery route (anterograde vs. retrograde) the goals of administering any cardioplegia solution are the same: reduce oxygen demand, calcium overload, myocardial edema, and provide an energy supply for the myocardium.

How Often Is the Cardioplegia Given? Any exogenously administered inotropes should be discontinued upon initiation of CPB to decrease myocardial oxygen consumption. The timing of cardioplegia delivery depends on the type of solution. Traditional solutions require administration approximately every 20 minutes to maintain asystole and consistent temperature. New solutions have recently come to market which are more dilute, have less calcium, and contain lidocaine. The main advantage is that they can be administered as a single dose

for most pump runs. Other techniques involve delivery of cardioplegia that is almost all blood with addition of key electrolytes (e.g., potassium and magnesium); this technique is referred to as “microplegia” and is thought to minimize myocardial edema as less than 100 mL of crystalloid may be delivered during a long aortic cross-clamp time in contrast to several liters of crystalloid with other techniques.

How Warm or How Cold Is the Cardioplegia Solution? Cardioplegia can be delivered as warm (37°C), cold (9°C), or tepid (29°C). Cold solution may decrease oxygen consumption, but may cause cellular damage via fluidity, transmembrane gradients, and edema. Evidence supports tepid cardioplegia for balancing the reduction of myocardial metabolic demands and enhancing oxygen delivery while allowing prompt recovery of myocardial function. Other studies have demonstrated a clinical benefit with the use of warm cardioplegia (i.e., lower troponin levels and shorter duration of intubation and hospitalization). No matter what cardioplegia solution is used, warm blood should be given through the cardioplegia pump prior to weaning from CPB to reverse the effect of cardioplegia and wash out the evil humors.

Should the Cardioplegia Be Mostly Crystalloid or Blood? Cardioplegia can be given as crystalloid or mixed in variable ratios of blood to crystalloid to improve oxygen-carrying capacity and provide endogenous buffers. Some literature suggests that there is no significant difference in the reduction of perioperative myocardial infarction in the use of cold blood cardioplegia compared to cold crystalloid cardioplegia. The rate of return of spontaneous sinus rhythm, 30-day mortality, incidence of atrial fibrillation and stroke were not significantly different between the two groups. Other studies have shown that myocardial metabolism is better with blood cardioplegia but there is no improvement in myocardial damage or clinical outcome. While the use of microplegia (i.e., whole blood with concentrated electrolytes) may seem appealing, large randomized studies are needed to verify whether its use is superior to traditional cardioplegia.

What Is the Deal With Hyperpolarizing Versus Depolarizing Cardioplegia Solutions? Depolarizing cardioplegia is most often used for myocardial protection during CPB. The high concentration of potassium serves as a depolarizing agent. Intracellular sodium influx causes calcium to be released from the sarcoplasmic reticulum, causing myocardial injury. Newer agents induce asystole via opening potassium channels,

triggering hyperpolarization of the myocardium and inhibiting contraction and preserving energy. There is evidence to suggest hyperpolarizing solutions preserve coronary endothelial function better than depolarizing solutions but consensus has not been reached.

Does Transesophageal Echocardiography Play a Role in Cardioplegia Delivery? In today’s cardiothoracic operating room, TEE can be considered a “standard” monitor. Using a modified midesophageal four-chamber view, the anesthesiologist can assist in confirming and documenting the placement of the retrograde coronary sinus catheter. Other views may also be helpful. Presence of a large coronary sinus could indicate a persistent left superior vena cava, rendering retrograde cardioplegia administration ineffective and redirecting the solution to the brain with the possibility of creating a watershed cerebral stroke. Difficulty placing a catheter may be due to the presence of a thebesian valve occluding the ostia of the coronary sinus. Color flow Doppler can be used to look for the flow of cardioplegia into the sinus and for antegrade flow down the left and right coronary arteries in the midesophageal aortic valve short axis view. For minimally invasive procedures, TEE is used to place the coronary sinus catheter via the internal jugular vein.

Is There Anything Else We Can Do to Protect the Heart? Ischemic preconditioning has long been recognized in reducing myocardial injury by protecting the heart from repeated ischemic events by endogenous mechanisms. Volatile anesthetics have been shown to produce a preconditioning effect and their use, when compared to intravenous anesthetics, have been shown to improve perioperative cardiac surgical clinical outcomes. A similar theory of ischemic postconditioning suggests protection via a post-survival kinase mechanism. Administering opioids, bradykinin, magnesium, adenosine, and cyclosporine-A at reperfusion have all shown promising results in various investigations. Results of select studies are promising in decreasing postoperative troponin levels and inotrope requirements. Another modality with beneficial results is the use of acute normovolemic hemodilution which is associated with decreases in serum biomarkers, inotrope requirements, and arrhythmias postoperatively by improving rheology for low-flow coronary collaterals and causing endogenous erythropoietin release. Erythropoietin causes endogenous nitric oxide release in the coronaries causing vasodilation and endothelial protection. Other myocardial protective techniques include the use of perioperative carvedilol, glucocorticoids, and nesiritide, all of which show promising

results for the future. TAKE HOME POINTS Some myocardial damage is inevitable during CPB; our goal is to minimize its extent and hope that the majority of the insult is reversible over time. Effective myocardial protection is critical for successful cardiac surgery. CPB-associated myocardial damage is due to ischemic insults and reperfusion injury. Regardless of its delivery route (anterograde vs. retrograde) the goals of administering any cardioplegia solution are the same: reduce oxygen demand, calcium overload, myocardial edema, and provide an energy supply for the myocardium. While administering retrograde cardioplegia, keep the coronary sinus pressures under 40 mm Hg, in contrast to 100 mm Hg with anterograde delivery, to avoid rupturing coronary venules and capillaries. Following the initiation of CPB, all exogenous inotropes should be discontinued. There is a lack of absolute consensus on which cardioplegia solution is clinically superior. Retrograde cardioplegia is useful in valve surgery and for patients with significant coronary artery disease and aortic insufficiency. TEE has an important role in verifying placement of coronary sinus catheters. Volatile anesthetics confer a protective preconditioning effect against ischemic damage. A warm, whole blood infusion is the best form of a “myocardial wake-up call” following cardioplegic arrest of the heart. Suggested Readings Grocott HP, Stafford-Smith M, Mora Mangano CT. Cardiopulmonary bypass management and organ protection. In: Kaplan JA, Reich DL, Savino JS, eds. Kaplan’s Cardiac Anesthesia: The Echo Era. 6th ed. Philadelphia, PA: Saunders/Elsevier; 2011: Chapter 28. Kinoshita T, Asai T. Preservation of myocardium during coronary artery bypass surgery. Curr Cardiol Rep. 2012;14(4):418–423. Zeng J, He W, Qu Z, et al. Cold blood versus crystalloid cardioplegia for myocardial protection in adult cardiac surgery: A meta-analysis of randomized controlled studies. J Cardiothorac Vasc Anesth. 2014;28(3): 674–681.

233 The Heartbreak of Left-Sided Valvular Dysfunction Jafer Ali, MD and Oran Kremen, MD

A 73-year-old female presents with a fractured right hip secondary to a mechanical fall. She is scheduled for urgent right total hip replacement under general anesthesia. She has been followed for many years with echocardiographs for a history of aortic stenosis (AS) but has not undergone corrective surgery. Her past medical history is also significant for diabetes mellitus type II, chronic obstructive pulmonary disease, and obesity. She notes being able to walk one to two city blocks before becoming winded. Upon physical examination she has a harsh, blowing IV/VI systolic ejection murmur that is loudest at the right sternal border and radiates up into both common carotid arteries. Her lungs are clear bilaterally. Chest film does suggest cardiomegaly but there is no appreciable pulmonary edema. There is time for an urgent transthoracic echocardiograph, but what would you do with that information? She needs the hip fixed urgently or she risks developing osteomyelitis and sepsis. What are your anesthetic goals for this patient? What are the biggest pitfalls that are associated with this valvular lesion? The anesthetic management of patients with cardiac valvular disease may span all types of surgery and is not really that complicated in that it involves four basic questions: 1) Which valve(s) is/are affected? 2) Is the lesion stenotic, regurgitant, or mixed? 3) What is the severity of the stenosis and/or regurgitation? 4) What are the secondary signs and symptoms related to the valvular pathology? Anesthesia providers do a good job of knowing how normal physiology may change under the influence of general anesthesia and surgical interventions. When it comes to patients with valvular lesions, it is of paramount importance that the anesthesia provider has goals in mind with regard to the physiologic variables of preload, afterload, contractility, heart rate, and rhythm. The good news is that these goals are

basically formulaic so you can either commit them to memory or save a table or reference paper in your phone or tablet for quick reference. This chapter will focus on left-sided cardiac valves.

Need-to-Know Information for Aortic Valve Disease Aortic Stenosis Normal aortic valve anatomy is three cusps and an aortic valve area (AVA) of 2.6 to 3.5 cm2 but the important number to remember is 1.0 cm2 because when the AVA drops to or below 1.0 cm2 that is considered severe AS and can be either congenital or acquired disease. Congenital AS may include a unicuspid, bicuspid (most common), tricuspid, or quadricuspid valve. Calcification of a bicuspid aortic valve can lead to early-onset AS (i.e., late fifties or early sixties so it is unlikely our clinical vignette patient has a bicuspid aortic valve). AS may also be acquired by degenerative calcification, which is the most common cause in the developed world whereas rheumatic AS is more common worldwide and it frequently affects the mitral valve concurrently. The severity of AS is classified by aortic jet velocity (m/s), mean gradient (mm Hg), and AVA (cm 2) . Be aware that a low cardiac index can underestimate the severity of AS and in some cases severe AS may present with a low gradient (e.g., an individual with normal left ventricular systolic function may have severe AS but, due to ventricular noncompliance secondary to hypertrophy, can have a low gradient.) Associated findings in patients with AS include abnormalities of the aorta (i.e., aortic root dilation and increased risk of aortic dissection). These patients typically present with angina (most common presenting symptom), syncope, or congestive heart failure (i.e., resulting from ventricular noncompliance in the setting normal systolic function). As the AS worsens, the transvalvular gradient increases in most patients. This increased pressure gradient causes a compensatory concentric left ventricular hypertrophy which ultimately renders the ventricle preload dependent.

Hemodynamic Goals for Aortic Stenosis—“Slow, Sinus, and Tight” Preload—Normovolemia; decreased ventricular compliance that accompanies AS necessitates a higher end diastolic volume/pressure to allow for adequate preload augmentation. Consider preoperative volume loading with a goal of normovolemia and be aware that rapidly delivered volume loads can result in acute, diastolic congestive heart failure. Afterload—Normal to high systemic vascular resistance (i.e., “tight”) is desirable. Systemic and coronary perfusion pressure depends on maintenance of systemic blood

pressure and systemic vascular resistance—so use of alpha-1 agonists to vasoconstrict is strongly recommended, especially accompanying anesthesia induction when sympathectomy is pronounced. Contractility—Avoid major cardiac depressants and remember these patients have normal to supranormal systolic function. Heart Rate—Lower rate normal sinus rhythm heart rate is ideal (50 beats/min to 70 beats/min). Tachycardia limits diastolic filing time both in the left ventricle and the coronary arteries. Tachyarrhythmias will be poorly tolerated and should be electrically cardioverted if hemodynamically significant. Additional Clinical Pearls for AS management: Attach external defibrillator pads to a patient prior to induction to be ready for a possible need for cardioversion. Strongly consider a preinduction arterial line and phenylephrine drip. Be cautious with vasodilators, especially nitroglycerin and nitroprusside as it can wreak havoc on preload and arterial pressure concurrently. Administer your anesthetic drugs slowly in smaller increments to allow time for some compensation from native physiology or if necessary to give you time to support the patient as needed with vasoconstrictors or volume administration to maintain organ perfusion.

Aortic Insufficiency Insufficiency (or regurgitation) is the failure of a valve to prevent backflow of blood. Causes of aortic insufficiency (AI) can be congenital or acquired. Congenital lesions include aortic valvular abnormalities and aortic root dilation (which can be associated with Marfan disease or other connective tissue disorders). Acquired etiologies include chronic hypertension, atherosclerosis, aortitis, aortic dissection, trauma, and aortic valve endocarditis. Severe acute AI can be life threatening and can lead to shortness of breath, pulmonary edema, and cardiovascular collapse. Acute AI may require urgent surgical treatment secondary to hemodynamic instability. Chronic AI may develop over the course of many years and patients may develop symptoms such as angina and fatigue after the onset of left ventricular dysfunction.

Hemodynamic Goals for Aortic Insufficiency—“Fast, Full, and Forward” Preload—Euvolemia with a preference toward being “full” and be cautious of drugs with significant venous dilatory effects as this may lead to further decreases in cardiac

output. Afterload—Low normal as there is improved cardiac performance and forward flow with decreased systemic vascular resistance. Contractility—Maintain contractility and avoid negative inotropes. Patients with chronic AI may develop eccentric left ventricular hypertrophy and/or dysfunction. Any inotropic decreases can be treated with beta-1/2 agonists (e.g., dobutamine) and inodilators (e.g., milrinone). These drugs have the perfect combination of peripheral vasodilation and inotropic support. Heart Rate—Fast (goal in the range of 90 beats/min to 100 beats/min). Patients with a faster heart rate have decreased diastolic time during which the regurgitation is manifested. This will lead to a smaller regurgitant fraction and improved cardiac performance. Additional Clinical Pearls for AI management: Many anesthetic drugs cause a drop in systemic vascular resistance and this can be very beneficial in patients with aortic regurgitation. Always remember that severe AI is an absolute contraindication for intra-aortic balloon pump placement (like shooting yourself in both feet!) The process of weaning from cardiopulmonary bypass can be more difficult than expected due to pre-existing left ventricular dysfunction and inadequate cardiac protection on CPB (difficult to deliver antegrade cardioplegia with AI). Keep inotropic agents ready to go! As with AS give your anesthetic drugs slowly as to allow native physiology to compensate or to permit administration of drugs to support physiology that maintains organ perfusion.

Need-to-Know Information for Mitral Valve Disease Good news is that as far as predictability the mitral valve is the valve most commonly affected with disease and is usually related to insufficiency (i.e., mitral stenosis [MS] accounts for less than 1% of cardiac diseases). Bad news is that when you come up against MS it can be the most challenging valvular pathology to manage during an anesthetic.

Mitral Stenosis MS is classically caused by rheumatic fever, which is rare in the United States, but may be seen more commonly in developing countries. Another common cause of MS is

mitral annular calcification. A normal mitral valve area is 4 to 6 cm2 but the important number to remember is that severe MS is defined as a valve area less than 1cm2 (just like severe AS). MS inhibits left ventricle filling and this process causes left atrial pressure to increase, which can lead to left atrial dilation, atrial fibrillation, pulmonary hypertension, congestive heart failure, and ultimately right-sided heart failure if the valvular dysfunction is not corrected.

Hemodynamic Goals for Mitral Stenosis Preload—Maintain preload and avoid hypovolemia. Afterload—Maintain systemic vascular resistance and decrease pulmonary vascular resistance to maximize left heart filling (i.e., avoid light anesthesia, hypercapnia, hypoxia, acidosis, and hypothermia). Heart Rate—Definitely avoid tachycardia! Slower heart rates allow for atrial emptying, but extreme bradycardia is dangerous given that cardiac output is fixed due to the stenotic mitral valve. Rhythm—Maintain sinus rhythm to get the filling benefit of the atrial kick—this is a key point! Contractility—Maintain contractility and be aware that chronic underfilling of the left ventricle may lead to a deconditioned state; inotropes may be needed. Also there may be right ventricular dysfunction in the setting of long-standing pulmonary hypertension, so don’t blow off right heart assessment!

Mitral Regurgitation The most common cause of mitral regurgitation (MR) is mitral valve prolapse followed by functional MR. Mitral valve prolapse can be caused by damage to heart muscle after a myocardial infarction. Myocardial infarction may cause chordae tendineae and/or papillary muscle rupture resulting in acute MR that necessitates intra-aortic balloon pump placement or emergency surgery; more commonly myocardial infarction with associated (and unwelcome) ventricular dysfunction related to papillary muscle dysfunction/displacement is the cause of MR. Rheumatic disease and infection/endocarditis of the mitral valve can also cause valvular dysfunction. Conditions that cause dilation of the left heart, such as ischemic or nonischemic left heart failure, can cause the mitral valve annulus to stretch with resultant leaflet malcoaptation and regurgitation (also termed functional MR). MR creates a state of left ventricular volume overload. Untreated, MR causes initial increases in left ventricular compliance, but progresses to left ventricular hypertrophy

as the heart must work harder to eject blood into systemic circulation as well as the regurgitant fraction back into the left atrium. As the left ventricle thickens, its compliance begins to decrease which results in diastolic dysfunction. Be aware that following mitral valve replacement/repair, preload to the left ventricle suddenly decreases and the left ventricle can no longer pump into the low pressure “pop-off” left atrium. These physiologic changes can cause acute left heart failure and the need for inotropes.

Hemodynamic Goals for Mitral Regurgitation Preload—Slightly increased preload is the goal but fluid responsiveness needs to be titrated individually as the increased preload can worsen MR. Afterload—Reduce systemic vascular resistance to decrease regurgitant fraction and improve cardiac output. Decrease pulmonary vascular resistance (i.e., avoid light anesthesia, hypercapnia, hypoxia, acidosis, and hypothermia and take note that the intraaortic balloon pump can be very helpful in these situations). Heart Rate—Aggressively avoid bradycardia as slow heart rates will cause increased left ventricular volume, reduced forward cardiac output, and increased regurgitant fraction. Normal to slightly elevated heart rate is preferred. Rhythm—Sinus rhythm is ideal, but atrial fibrillation is common and usually physiologically compensated when chronic, acute atrial dysrhythmias may respond well to synchronized cardioversion. Contractility—Maintain contractility and consider that inotropic support is frequently needed post mitral valve replacement. TAKE HOME POINTS When it comes to patients with valvular lesions, it is of paramount importance that the anesthesia provider has goals in mind with regard to the physiologic variables of preload, afterload, contractility, heart rate, and rhythm. For both aortic and mitral stenosis, the important number to remember is 1.0 cm2 because when the valve area drops to or below 1.0 cm2 that is considered severe stenosis. Be aware that a low cardiac index can underestimate the severity of AS and in some cases severe AS may present with a low gradient (e.g., an individual with normal left ventricular systolic function may have severe AS but, due to ventricular noncompliance secondary to hypertrophy, can present with a low gradient).

Basic anesthetic-related hemodynamic goals for AS are normovolemia, slow to normal sinus rhythm (50 to 70 beats/min), and slightly elevated systemic vascular resistance (well achieved with low doses of alpha-agonists). Basic anesthetic-related goals for aortic regurgitation are euvolemia, faster heart rate (90 beats/min), and low normal systemic vascular resistance. Anesthetic-related goals for MS are euvolemia, normal systemic vascular resistance, decrease pulmonary vascular resistance to maximize left heart filling (i.e., avoid light anesthesia, hypercapnia, hypoxia, acidosis, and hypothermia), and avoid tachycardia as well as extreme bradycardia. Anesthetic-related hemodynamic goals for MR are slightly increased preload, normal to slightly elevated heart rate (70 to 90 beats/min), maintain sinus rhythm (but atrial fibrillation is common in these patients), and decreased systemic as well as pulmonary vascular resistance. Suggested Readings Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22(1):1–23. Lee ES, Ha EL, Yang EH, et al. Diagnosis and management of valvular heart disease. Hospital Medicine Clinics. 2014;3(3):e305–e333. Nishimura RA. Aortic valve disease. Circulation. 2002;106(7):770–772. Skubas NJ, Lichtman AD, Sharma A, et al. Chapter 41: Anesthesia for cardiac surgery. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:1073–1107. Townsley MM, Martin DE. Chapter 12: Anesthetic management for the surgical treatment of valvular heart disease. In: Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia. (Practical Approach Series). 5th ed. Philadelphia, PA: Lippincott William & Wilkins; 2013:319–358. Turi ZG. Mitral valve disease. Circulation. 2004;109(6):e38–e41. Zoghbi WA, Enriquez-Sarano M, Foster E, et al; American Society of Echocardiography. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16(7):777–802.

234 Anesthesia for the Descending Thoracic Aorta —Initiate Damage Control Measures Eliot Ro, MD and Edwin G. Avery IV, MD

A 68-year-old male presents to the emergency ward complaining of acute onset of severe back pain. He has a past medical history of hypertension, hyperlipidemia, coronary artery disease, chronic obstructive pulmonary disease, and morbid obesity. His chest film reveals a widened mediastinum and just after completing computed tomography imaging he becomes unresponsive and develops pulseless electrical activity arrest. While the emergency ward team is resuscitating him the radiologist notes from his scan that contrast dye is extravasating from an aneurysm in the descending thoracic aorta(DTA). The surgical team is given a heads-up that he is being transported up to the operating room STAT while administering advanced cardiac life support measures. How are you going to use the little time you have to prepare for this patient? What are the most important aspects of this anesthetic? DTA procedures present a huge anesthetic challenge. The general categories of aortic pathology affecting the DTA include: aneurysm, pseudoaneurysm, coarctation, aortic rupture, dissection, intramural hematoma, infection, and atherosclerotic disease (with or without penetrating ulcers). Successfully designing an effective anesthetic plan for these patients mandates a detailed knowledge of an individual’s aortic pathology, the planned procedure and strategies to minimize the hit to various organs related to surgical manipulation of the aorta. In some cases of DTA aneurysms and other pathologies, the repairs occur electively and are commonly addressed using endovascular stenting technologies that considerably reduce the complexity of the surgery. In other scenarios, such as the clinical vignette above, they present in an urgent or emergent fashion with little time to evaluate the serious comorbidities that frequently accompany aortic disease (e.g., coronary and cerebrovascular disease). Ideally, the anesthesiologist will review the details of all available imaging studies and create an anesthetic plan that focuses on providing protection and support for all bodily systems affected by the planned procedure. In

emergent surgical procedures involving the DTA, it becomes a “damage control situation” with the goals of simultaneously ordering blood components, establishing robust intravenous access, invasive monitors, some degree of acceptable hemodynamics and amnesia; thus, recruiting additional anesthesia and/or surgical personnel is necessary so that preoperative preparation is carried out with optimal efficiency.

Monitoring for DTA Procedures Successful anesthetic monitoring for DTA surgery considers that the nature of these procedures creates hemodynamic instability and multi-organ hypoperfusion. To partially circumvent the effects of interrupting blood flow with aortic cross-clamping the distal aorta is often perfused using a Gott shunt or partial left-heart bypass (left atrium to distal aorta, iliac, or femoral artery bypass with centrifugal pump assist). Upper body arterial as well as femoral arterial blood pressure monitoring is therefore necessary to assess both proximal and distal arterial perfusion pressure relative to the aortic cross-clamp(s). Distal aortic mean arterial pressure (MAP) is commonly maintained between 60 mm Hg and 70 mm Hg during the partial bypass period while proximal MAP is maintained at approximately 90 mm Hg. Near-infrared tissue oximetry monitoring of the frontal lobes as well as somatic monitoring of the quadriceps bilaterally may assist in fine-tuning individually appropriate MAP values above and below the cross-clamp, respectively. Be aware that partial left-heart bypass circuits do not routinely incorporate a heater/cooler exchange unit and therefore the risk of developing a profound hypothermia is greatly increased as heat is lost through the extracorporeal circuit. Hypothermia increases the risk of coagulopathic hemorrhage and hyperglycemia (which may exacerbate ischemic injury to the brain, cord and/or heart) in these patients and thus patient warming systems (e.g., forced convective warm air blankets or hydrogel energy conduction pads) should routinely be used in these anesthetics. Alternatively, a customized extracorporeal membrane oxygenator (ECMO) venous to arterial circuit could be employed that would accomplish the same result and allows for incorporation of a heater/cooler exchange device which obviates hypothermia issues. Invasive monitoring and central venous access are essential for DTA surgery. Exercise caution in choosing a site for radial arterial cannulation because atherosclerosis is highly prevalent in these patients and severe subclavian or axillary artery plaquing can result in inaccurate hemodynamic data. Checking bilateral noninvasive cuff pressures can identify significant gradients between the upper extremities. Central venous access is useful to permit rapid volume and vasoactive medication administration as well as to monitor cardiac function and filling pressures

(e.g., by insertion of a pulmonary artery catheter). Alternatively, use of specialized arterial monitoring transducers can provide acceptable continuous indexes of cardiac output without pulmonary artery catheterization. Intraoperative transesophageal echocardiography (TEE) can also be useful for hemodynamic monitoring when the needed equipment and skillset are available. Aortic cross-clamping acutely increases afterload on the left heart that may result in myocardial ischemia and/or acute left ventricular failure in susceptible patients. Careful monitoring for ischemic ECG changes and/or signs of acute left ventricular failure (e.g., an acute increase in the pulmonary capillary wedge pressure, drop in cardiac output or new wall motion abnormalities observed with TEE) during aortic cross-clamping is necessary. Pharmacologic-based afterload reduction (e.g., administration of a shortacting dihydropyridine calcium channel blocker or nitric oxide donor) is often indicated during aortic cross-clamping. Aortic cross-clamp removal can also be accompanied by hemodynamic instability (e.g., hypotension) related to an acute reduction in left ventricular afterload and to the release of lactic acid from ischemic tissue beds distal to the clamp if partial left-heart bypass is not employed. The transient increase in circulating lactic acid and potassium associated with cross-clamp removal can also instigate ventricular irritability or arrhythmias. Fluid loading and pharmacotherapy (e.g., administration of alpha-1 agonists and sodium bicarbonate) just prior to and after unclamping can be useful to quell the hemodynamic deterioration.

DTA Surgery and Organ Ischemia/Protection The temporary interruption of aortic blood flow associated with DTA surgery to allow for aortic interposition grafting places all distal organs (e.g., kidneys, bowels, spinal cord) at risk for ischemic injury and infarction. Potential ischemic injury to the spinal cord is of paramount concern, thus the anesthetic plan is tailored to both monitor for and prevent such damage. Protection of the spinal cord during DTA surgery is accomplished with maneuvers that promote blood flow to the cord. Suggested interventions include the preoperative insertion of a lumbar spinal drain, arterial pressure augmentation, neurophysiologic monitoring techniques, and pharmacologic support measures. Lumbar cerebral spinal fluid (CSF) drainage is employed to both prevent cord ischemia as well as a treatment for postoperative paraplegia resulting from DTA surgery (i.e., removing CSF to offset the swelling of the cord promotes lower intradural pressures and better perfusion). These lumbar catheters are managed without the use of a heparinized or pressurized transducer flush apparatus. CSF is permitted to drain if the lumbar CSF pressure exceeds 10 mm Hg. Care is taken to ensure a normal coagulation profile prior to catheter insertion and removal. Arterial pressure augmentation is achieved by maintaining a spinal cord perfusion pressure (MAP-–

intrathecal pressure) of at least 70 mm Hg which is accomplished by achieving an MAP of 80 mm Hg to 100 mm Hg. Intraoperative neurophysiologic monitoring can reveal the acute development of spinal cord ischemia and is accomplished through the use of somatosensory-evoked potentials or motor-evoked potentials. Pharmacologic support measures include the intrathecal administration of preservative-free papaverine (in conjunction with lumbar CSF drainage) and the systemic administration of glucocorticoids, thiopental, mannitol, magnesium, calcium channel blockers, and naloxone. Supportive studies of these drugs in this clinical setting are difficult to interpret and no widely used standard pharmacologic regimen has been established to date. Intravenous naloxone given at 1 μg/kg/hr has been demonstrated to be associated with improved neurologic outcomes (including reversal of paraplegic symptoms) in this clinical setting.

DTA Anatomical Considerations Left thoracotomy or a thoracoabdominal incision is the most common surgical incision used for exposure of the DTA. These surgical approaches often necessitate single-lung ventilation, most often of the right lung. Options for single-lung ventilation include lung retraction, insertion of a left bronchial blocker, or the use of a double lumen endobronchial tube (DLT) (i.e., commonly a left DLT is employed). The DLT permits pulmonary maneuvers such as the ability to suction the airways and apply continuous positive airway pressure which may be obviated with the use of a blocker. However, its use may require transition to a single-lumen endotracheal tube at the end of the procedure with the inherent risks after a major surgery.

DTA Analgesia Consideration of postoperative analgesia is of major concern in this clinical setting because of the painful nature of a thoracotomy. The intra- and postoperative use of thoracic epidural analgesia can provide excellent pain control and permit early extubation to allow for the prompt assessment of neurologic function (e.g., rule out paraplegia related to spinal cord ischemia); care must be taken to ensure normal function of the coagulation cascade for both insertion and removal of the catheter to prevent bleeding-related neurologic complications. Emergent procedures obviate the preoperative insertion of an epidural catheter but postoperative insertion remains an option in most cases. TAKE HOME POINTS In emergent surgical procedures involving the DTA, it becomes a “damage control

situation” with the goals of simultaneously ordering blood components, establishing robust intravenous access, invasive monitors, some degree of acceptable hemodynamics and amnesia; thus, recruiting additional anesthesia and/or surgical personnel is necessary so that preoperative preparation is carried out with optimal efficiency. Invasive monitoring and central venous access are essential for DTA surgery. Exercise caution in choosing a site for radial arterial cannulation because atherosclerosis is highly prevalent in these patients and severe subclavian, or axillary artery plaquing can result in inaccurate hemodynamic data. Both upper- and lower-extremity arterial monitoring are often required. Potential ischemic injury to the spinal cord is of paramount concern and thus the anesthetic plan is tailored to both prevent such damage and to monitor for it. When DTA surgery involves the use of partial left-heart bypass, femoral arterial blood pressure monitoring is necessary to assess distal arterial perfusion pressure. Hypothermia increases the risk of coagulopathic hemorrhage and hyperglycemia (which may exacerbate ischemic injury to the brain, cord and/or heart) in these patients and thus patient/fluid warming systems are routinely used. Pharmacologic-based afterload reduction (e.g., administration of short-acting vasodilators including clevidipine, sodium nitroprusside, and nitroglycerin) is often indicated during aortic cross-clamping to prevent acute left-heart failure. The transient increase in circulating lactic acid and potassium associated with aortic cross-clamp removal can instigate ventricular arrhythmias. Fluid loading and pharmacotherapy (e.g., administration of alpha-1 agonists and sodium bicarbonate) just prior to aortic unclamping can be useful to quell the associated hemodynamic deterioration. Lumbar CSF drainage is employed to prevent/treat spinal cord ischemia. These catheters are managed without the use of a heparinized or pressurized transducer flush apparatus. Consideration of the use of postoperative thoracic epidural analgesia is important in this clinical setting because of the painful nature of a thoracotomy. Suggested Readings Bittner E, Dunn PF. Anesthesia for vascular surgery. In: Hurford WE, Bailin MT, Davison JK, et al., eds. Clinical Anesthesia Procedures of the Massachusetts General Hospital. 6th ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2002:350–365. Moskowitz DM, Kahn RA, Reich DL. Anesthesia for the surgical treatment of thoracic aortic disease. In: Thys DM, Hillel Z, Schwartz AJ. Textbook of Cardiothoracic Anesthesiology. McGraw-Hill; 2001:680–710. Pantin EJ, Cheung AT. Thoracic Aorta. In: Kaplan JA, Reich DL, Lake CL, et al., eds. Kaplan’s Cardiac Anesthesia. 5th ed. Philadelphia, PA: Saunders-Elsevier; 2006:723–764.

235 Buckle Your Seat Belt: Taking Care of the Patient With Ascending Aortic Dissection Rachel E. Schlesinger, MD and Kathleen Cho, MD

A 72-year-old female arrives to the emergency ward gripping her chest complaining of intense tearing pain; she is also wailing about unbearable burning pain in her left leg (like it’s on fire). Medical history is significant for poorly controlled hypertension, emphysema, and hyperlipidemia. Vital signs are notable for blood pressure (BP)—left arm: 188/124 mm Hg, right arm: 125/110 mm Hg; pulse 124/minute; respirations 25/minute. Physical examination is remarkable for confusion, diminished breath sounds bilaterally, and a loud holodiastolic murmur. Pulses are unequal with the right radial grossly weaker than the left and left pedal pulse weaker than the right. She has a 14gauge venous catheter in the left forearm. Electrocardiogram reveals sinus tachycardia with inferior lead ST-segment elevations, likely related to the dissection in the aortic root partially obstructing coronary blood flow in the proximal right coronary artery. Chest film demonstrates widening of the mediastinum and a computed tomography (CT) scan confirms an ascending aortic dissection extending from the aortic root to the iliac bifurcation (we call that a stem-to-stern dissection in cardiac OR lingo). Next, you get paged to the operating room to assist with management of this challenging patient, so strap in and hold on because you’re in for a ride! What is the next most appropriate management step? ANSWER: First, establish arterial monitoring in the left radial artery (i.e., higher BP on the left so the right side is probably lower because the aortic dissection (AD) involves the innominate and right subclavian arteries thus yielding a falsely lower central BP), then reduce the aortic shear stress and systolic BP (i.e., to approximately 110 mm Hg) by first initiating a short-acting intravenous β-blocker (i.e., esmolol) and next start an intravenous systemic arterial selective vasodilator (i.e., clevidipine) infusion. Order four units of blood and get a quick transthoracic (or transesophageal) echocardiogram to assess for cardiac tamponade and to determine the mechanism of her aortic insufficiency (AI) which the holodiastolic murmur tipped you off to. Get extra help in the room

because time is of the essence in these cases, and even when you do your job just right, the patient can still have a bad outcome. Dissections of the ascending aorta, representing 60% to 70% of all ADs, are lifethreatening emergencies that involve a tear of the intimal wall of the aorta creating a false channel that may contain blood flow or intramural hematoma. AD are commonly spontaneous but can be related to trauma (e.g., motor vehicle accident when the chest wall strikes the steering wheel). AD of the ascending aorta is a true medical emergency and carries a mortality rate of 1% to 2% per hour in the first 48 hours, following initial onset of symptoms. (We suggest quoting this mortality statistic if you are stopped by local law enforcement on the way to the hospital to treat a patient with an AD as it often results in a sirens blaring/blue lights flashing escort to the hospital.) Reported surgical mortality varies from 3% to 24% and is highest with dissections at the level of the aortic arch. It is common for the aorta to be aneurysmal in the area where it dissects. Aneurysm formation is clinically occult over a period of years and is most commonly associated with uncontrolled hypertension and a genetic defect resulting in the production a dysfunctional fibrillin protein located in the aortic wall. Another possible mechanism for AD is rupture of the vasa vasorum, creating an intramural hematoma and propagation of the dissection; this variant lacks an intimal tear but has the same mortality as an AD with a tear. The areas of highest mechanical stress are the ascending aorta and the area just distal to the left subclavian artery. Due to the shear stress created by hypertension and pulsatile perfusion, the dissection flap can continue to dissect in its proximal or distal extent (often in a spiral manner) and potentially compromise blood flow to multiple vital organs. It is very common to hear from our surgical colleagues that the tear in the aortic intima is located just above the ostia of the right coronary artery, another area of high mechanical stress in the aorta. In any case, identifying the location of the tear is not an anesthesia-related priority. Risk factors for AD include male gender, chronic and/or uncontrolled hypertension, age >60 years, connective tissue disorders (e.g., Marfan syndrome), uni-, bi-, or quadricuspid aortic valve, aortic aneurysm, pregnancy, toxins (e.g., cocaine use), trauma, and postaortotomy. Two classification systems are in use to detail the extent of an AD that include the Stanford and DeBakey systems (see Table 235.1). The most common presentation of ascending AD is chest pain described as either ripping, tearing, sharp, stabbing, or pressure-like and there may be pulse deficits in the extremities, suggesting limb ischemia or systemic hypoperfusion. Note that in our vignette patient she was also complaining of severe left leg pain that was likely due to AD-related lower limb ischemia. AD resulting in cardiac tamponade (i.e., commonly from aortic root rupture or more commonly blood

weeping through the dissected aorta into the transverse pericardial sinus) may produce jugular venous elevation, systemic hypotension, syncope, stroke, and cardiovascular collapse. Note that extension of the AD into the head vessels can result in a range of neurologic symptoms from mild confusion to frank stroke and obtundation. In most cases if there is a true rupture of the aorta into the pericardial space via the transverse sinus it will result in acute and often irreversible cardiac arrest. If the dissection causes severe AI, signs of congestive heart failure (e.g., pulmonary edema) may be present. Table 235.1 ■ Classification Systems for Aortic Dissection Classification System Stanford Stanford DeBakey DeBakey DeBakey

Type A B I II III

Description Involves Involves Involves Involves Involves

the ascending aorta the descending aorta the entire aorta only the ascending aorta only the descending aorta

Figure 235.1. Line art drawing of aortic short axis as imaged with transesophageal echocardiography in aortic dissection.

The degree of AI related to AD can vary from none all the way up to severe and

really depends on how badly the AD has undermined the function of the aortic valve. Additional respiratory symptoms may include hoarseness due to compression of the recurrent laryngeal nerve, dysphagia, and stridor. Diagnosis of ascending AD is commonly made by CT, aortic angiography, magnetic resonance imaging with angiography (most sensitive and specific), or transesophageal echocardiography (TEE). TEE is particularly useful as it allows one to rule out cardiac tamponade, determine mechanism/severity of AI, better characterize the extent of the dissection, and assess for proximal coronary artery involvement plus related wall motion abnormalities. Intraoperatively, TEE can help identify both the true and false aortic lumens, which will facilitate the arterial cannulation required for the initiation of cardiopulmonary bypass (CPB) (Fig. 235.1). Any attempt to perform a preoperative diagnostic TEE must be made in conjunction with an experienced anesthesiologist because inadequate sedation and blunting of sympathetic autonomic outflow could result in immediate aortic rupture with unrecoverable hemodynamic collapse. Complications associated with ascending AD are listed in Table 235.2. The high degree of morbidity and mortality is usually related to involvement of the coronary ostia, dissection into the aortic root causing severe AI, and proximal dissection causing cardiac tamponade. Acute medical management is directed at control of systemic BP to reduce the shear stress or change in pressure over time (ΔP/Δt) transmitted to the aortic wall. Control of hemodynamics for AD is initially accomplished with a bolus of esmolol (i.e., 20 to 50 mg IV) and an infusion (25 to 300 mcg/kg/min) (this reduces the shear stress on the aortic wall) followed by initiation of a clevidipine or nicardipine (dihydropyridine calcium channel blockers are preferred here due to their arterial selectivity note that clevidipine and nicardipine have the same mechanism of action but clevidipine has an approximately 1 minute half-life and nicardipine has a 12- to 14-hour half-life) which will help limit extension of the dissection. Although there has not been any pressure range proven to be best, 100 to 110 mm Hg systolic is the generally accepted goal. This pressure will likely maintain adequate organ perfusion while minimizing risk of aortic rupture. Table 235.2 ■ Complications of Acute Ascending Aortic Dissection (N = 513) Complication All neurologic deficits Coma/altered consciousness

Percentage of Occurrence (%) 18 14

Myocardial Acute renalischemia/infarction failure Hypotension Cardiac tamponade Mortality

4 6.2 26 17 30

Adapted from Bossone E, Rampoldi V, Nienaber CA, et al. Usefulness of pulse deficit to predict inhospital complications and mortality in patients with acute type A aortic dissection. Am J Cariol. 2002;89(7):851–855. Copyright © 2002 Excerpta Medica Inc. With permission.

Anesthetic management is directed at establishing both arterial and venous access and includes multiple large-bore intravenous catheters on blood warmers, a rapid infusion device, central venous access (i.e., permits monitoring of central filling pressures, cardiac index, mixed venous oxygenation as well as a delivery route for potent vasoactives). At least one arterial line must be placed depending on the surgical plan for arterial CPB cannulation. Always be thoughtful about where you place your arterial monitoring catheter because the surgeon may cannulate an upstream arterial site that will make your observed BP inaccurate (i.e., lower than the actual central systemic BP). Pre-induction arterial monitoring is a standard of care. Ultrasonic examination of the carotid arteries prior to central line placement can reveal vessel location and whether the dissection has extended into the neck. Such involvement is common with ascending AD, but flow obstruction–related carotid dissection is not common and portends increased mortality. Have at least four units of cross-matched red blood cells available in the operating room before the procedure begins. Necessary monitoring and adjuncts include standard American Society of Anesthesia monitors and use of cerebral oximetry is strongly suggested as corrective surgery for AD very commonly involves deep hypothermic circulatory arrest which is best managed with this technology. During the period of circulatory arrest the cerebral oximeter functions much like a sand-filled hourglass as one can literally observe a slow deterioration of the cerebral saturation percentage over a period of just minutes as the cold, unperfused brain extracts the remaining oxygen from the hemoglobin in the brain’s microcirculation. For surgeons that configure a unilateral selective anterograde perfusion setup, the cerebral oximeter can verify adequate perfusion and oxygenation of both sides of the brain. Unilaterally observed desaturation on the contralateral side of the brain during selective anterograde perfusion can alert clinicians to the absence of a complete circle of Willis and the potential need for insertion of a second anterograde cannula into the head vessels (i.e., most commonly the left common carotid artery). Further, insertion of a Foley catheter (with temperature-monitoring capability), orogastric tube, and temperature of the shell and core are considered

standard of care. High-dose narcotic is a preferred induction method due to hemodynamic instability frequently observed in these patients but be careful as bradycardia in the setting of severe AI can result in cardiovascular collapse. Induction of general anesthesia for patients with AD must always prioritize prevention of hypertension. If securing the airway necessitates rapid sequence intubation, then esmolol and/or clevidipine boluses can be used to treat/prevent the hypertensive response to laryngoscopy. Clevidipine is preferred over nitroprusside as it is an ultra-short acting, arterial selective, lacks toxic metabolites (in contrast to cyanide-laced nitroprusside) and does not depend upon renal or hepatic function for its metabolism. Place the TEE probe after induction and perform a complete TEE examination with special attention to the extent of the dissection and degree/mechanism of AI. If the dissection has caused a significant degree of cardiac tamponade, the transition to positive-pressure ventilation during the induction of general anesthesia can be deleterious for right heart filling and result in cardiovascular collapse. Maintain cardiac filling pressures with intravenous volume administration and a short inspiratory-toexpiratory ratio to maximize right heart filling. If pericardial tamponade is diagnosed or suspected, femoral cannulation for CPB under local anesthesia should be considered, followed by induction and immediate sternotomy. Decompression of cardiac tamponade prior to bypass may cause rebound hypertension, resulting in aortic rupture and a tremendous increase in mortality risk. (For every AD-related problem we know how to anticipate and fix, an acute ascending AD knows how to throw two more right back at us so turn your internal vigilance dial to “combat mode.”) If femoral cannulation for CPB cannot be instituted under local anesthesia prior to inducing general anesthesia, then a careful induction with the gradual transition to assisted and, finally, positive pressure ventilation should be performed to minimize the risk of cardiovascular collapse. Such cases have the entire shooting match ready to go (e.g., low room temperature, the surgeon scrubbed, patient prepped and draped, ice bags made up to place on the head, perfusionists ready to go on bypass). If one is unsure about the magnitude of a pericardial effusion or the presence of pericardial tamponade, then a quick pre-induction transthoracic echocardiogram is strongly indicated to rule out a surprise hemodynamic collapse on induction. Support of hemodynamics during anesthesia induction of an AD patient with vasoconstrictors and/or inotropes is risky and can result in aortic rupture if there is an unintended overshoot. The bottom line with induction of an AD patient is that the cardiac surgical, perfusion, and OR nursing teams should all be in the room and ready to go prior to anesthesia induction. Finally, TEE is useful to assess the adequacy of repair post-CPB including

restoration or augmentation of flow within the true aortic lumen, assessment of aortic valve repair/replacement, and evaluation of cardiac function. Cerebral oximetry can alert one to the presence of compromised cerebral blood flow post-CPB. Alternatively, the common carotid arteries can be directly assessed with a surface ultrasound probe via color Doppler interrogation to confirm that bilateral blood flow is present. Following confirmation of a successful surgical repair, the anesthesia team should be prepared to both evaluate (e.g., via thromboelastography and core laboratory hematology/special coagulation studies) and aggressively treat coagulopathic hemorrhage. The cold temperatures used to preserve organ function during deep hypothermic circulatory arrest commonly result in both platelet dysfunction and sequestration in the sinusoidal organs (i.e., the liver and spleen); thus it is standard to have platelets in the operating room before bypass separation. TAKE HOME POINTS AD of the ascending aorta is a true medical emergency and carries a mortality rate of 1% to 2% per hour in the first 48 hours, following initial onset of symptoms. Ascending AD and intramural hematoma both carry the same risk of mortality. Due to the shear stress created by hypertension and pulsatile perfusion, the dissection flap can continue to dissect in its proximal or distal extent (often in a spiral manner) and potentially compromise blood flow to multiple vital organs. The most common presentation of ascending AD is chest pain described as either ripping, tearing, sharp, stabbing, or pressure-like, and there may be pulse deficits in the extremities, suggesting limb ischemia or systemic hypoperfusion. AD resulting in cardiac tamponade (i.e., commonly from aortic root rupture or more commonly blood weeping through the dissected aorta into the transverse pericardial sinus) may produce jugular venous elevation, systemic hypotension, syncope, stroke, and cardiovascular collapse. Extension of the AD into the head vessels can result in a range of neurologic symptoms from mild confusion to frank stroke and obtundation. In most cases if there is a true rupture of the aorta into the pericardial space via the transverse sinus it will result in acute and often irreversible cardiac arrest. Any attempt to perform a preoperative diagnostic TEE must be made in conjunction with an experienced anesthesiologist because inadequate sedation and blunting of sympathetic autonomic outflow could result in immediate aortic rupture with unrecoverable hemodynamic collapse. Acute medical management of AD includes control of hemodynamics initially accomplished with a bolus of esmolol (i.e., 20 to 50 mg IV) and an infusion (25 to 300 mcg/kg/min) followed by initiation of a clevidipine or nicardipine

(dihydropyridine calcium channel blockers are preferred here due to their arterial selectivity note that clevidipine and nicardipine have the same mechanism of action but clevidipine has an approximately 1 minute half-life and nicardipine has a 12- to 14-hour half-life) which will help limit extension of the dissection. A systolic pressure of 100 to 110 mm Hg is the generally accepted goal. Have at least four units of cross-matched red blood cells available in the operating room before the procedure begins. Always be thoughtful about where you place your arterial monitoring catheter because the surgeon may cannulate an upstream arterial site that will make your observed BP inaccurate (i.e., lower than the actual central systemic BP). Preinduction arterial monitoring is a standard of care. Induction of anesthesia for patients with AD must always prioritize prevention of hypertension. The short half-lives of esmolol and clevidipine make them ideal for BP control in these patients. Necessary monitoring and adjuncts include standard American Society of Anesthesia monitors and use of cerebral oximetry is strongly suggested. Insertion of a Foley catheter (with temperature monitoring capability), orogastric tube, and temperature of the shell and core are considered standard of care. Depending on the distal extent of the dissection, circulatory arrest may be required to perform an adequate surgical repair; neuroprotection is of paramount concern in cases requiring deep hypothermic circulatory arrest. If the dissection has caused cardiac tamponade, the transition to positive-pressure ventilation during the induction of anesthesia can be deleterious for right heart filling and result in cardiovascular collapse. Decompression of cardiac tamponade prior to the bypass may cause rebound hypertension, resulting in aortic rupture and an increased mortality risk. The bottom line with induction of an AD patient is that the cardiac surgical, perfusion and OR nursing teams should all be in the room and ready to go prior to anesthesia induction. Following confirmation of a successful surgical repair, the anesthesia team should be prepared to both evaluate (e.g., via thromboelastography, core hematology/special coagulation labs) and aggressively treat coagulopathic hemorrhage. Suggested Readings Augoustides JG, Pantin EJ, Cheung AT. Thoracic aortic surgery. In: Kaplan JA, Reich DL, Savino JS, eds. Kaplan’s Cardiac Anesthesia. 6th ed. Philadelphia, PA: Saunders/Elsevier; 2011: Chap 21. Isselbacher EM. Diseases of the aorta. In: Goldman L, Schafer AI, eds. Goldman’s Cecil Medicine. 24th ed. Philadelphia, PA: Saunders Elsevier; 2011:Chap 78.

236 Rolling in the Deep Hypothermic Circulatory Arrest Michael G. Fitzsimons, MD and Etienne J. Couture, MD FRCPC

A 38-year-old male with a history of Marfan disease presents with a dilated aortic root (65 mm), ascending aorta (60 mm), aortic arch (57 mm), descending aorta (43 mm) and mild aortic insufficiency. He is scheduled for a valve-sparing aortic root replacement, complete arch replacement, reimplantation of the arch vessels, and “elephant trunk procedure” to the distal aorta. His surgeon is planning on addressing the descending aorta at a future date. The surgeon notes that the procedure will be performed under deep hypothermic circulatory arrest (DHCA) that he believes will take less than 60 minutes. Bilateral radial arterial lines are placed along with two large-bore peripheral intravenous catheters. Near infrared spectroscopy (NIRS) is placed on the forehead for cerebral oximetry monitoring along with processed electroencephalogram (pEEG) monitoring. Baseline regional cerebral oxygen saturation (rSO2) reads 77% on the right and 76% on the left. General anesthesia is induced with propofol, fentanyl, and rocuronium. A pulmonary artery catheter is placed via the right internal jugular vein. Transesophageal echocardiography (TEE) is utilized and a nasopharyngeal temperature probe is placed before systemic anticoagulation. The patient is cooled to a nasopharyngeal temperature of 18°C, cooling occurs for another 45 minutes while the surgeon performs portions of the aortic root reconstruction. Cerebral oximetry shows an rSO2 of 90% on the right and 91% on the left. The surgeon completes the distal arch elephant trunk anastomosis, arch replacement, and arch vessels reimplantation under DHCA. Individual selective cerebral perfusion is performed on the arch vessels. DHCA ends after 46 minutes and systemic perfusion is resumed while the surgeon completes the root replacement and final anastomosis. The patient is successfully weaned from cardiopulmonary bypass (CPB). TEE demonstrates absence of significant aortic insufficiency or stenosis. The patient is brought to the intensive care unit, is extubated and makes a complete recovery.

DHCA is a surgical technique where the body is cooled to 18°C. This profound hypothermia reduces the cerebral metabolic rate of oxygen consumption (CMRO2) as well as systemic tissue oxygen consumption for the entire body. Once the temperature measures in the nasopharynx reaches 18°C, the body is generally cooled for an additional period of time to achieve a uniform temperature. Circulation from the CPB is then stopped and blood is drained into the CPB venous reservoir. The absence of flow allows the surgeon to remove the aortic cross clamp to facilitate surgery in locations where a cross clamp interferes. Distal aorta and aortic arch work is completed then CPB is resumed. DHCA may also be utilized for pulmonary thromboendarterectomy, surgery involving descending aorta, excision of renal cell carcinoma that has extended in to the right atrium and certain cerebral aneurysm clipping procedures.

Mechanisms of Benefits of DHCA The brain has a high CMRO2 and is very sensitive to lack of oxygen. This is largely related to a limited supply of high-energy phosphates and glucose unlike other organs such as the liver or muscles. Cerebral injury occurs due to anaerobic glycolysis and entry of calcium into brain cells activating enzymes. DHCA reduces oxygen consumption significantly which increases the safe time that the brain can go without blood flow. CMRO2 decreases approximately 5% to 7% for every 1°C below 37°C. When the body reaches a temperature of 18°C, metabolism is less than 25% that at normal body temperature. Other potential benefits include inhibition of caspases, reduction of toxic free radicals, reduction of inflammation, and maintenance of microvascular integrity. Several physical, pharmacologic, and surgical adjunctive techniques have been suggested to enhance the degree of protection as well as the duration of DHCA to facilitate longer procedures.

Direct Application of Ice to the Head Many will utilize direct application of ice from initiation of cooling until resumption of circulation and rewarming. The thought is that ice will facilitate additional cooling and prevent passive rewarming from the room. The thickness and density of the skull prevents any additional benefit to that provided by full-body cooling from CPB. The operating room temperature is usually decreased below 18°C which would eliminate any temperature gradient between the patient and the room. No human randomized studies have conclusively demonstrated advantages to external application of ice during DHCA. Care must be taken to avoid thermal injury to the eyes, ears, and other tissue if direct application of ice is utilized.

Pharmacologic Adjuncts Several single pharmacologic agents and combinations of medications have been suggested to augment the safety of DHCA. The steroid methylprednisolone has been utilized to reduce the inflammatory effects of DHCA including edema, free radical formation, and lipid peroxidation. Barbiturates act by reducing CMRO2, free fatty acids, free radicals, cerebral edema, and seizure activity and are associated with burst suppression. Magnesium is a cerebral vasodilator. Lidocaine may improve short-term cognitive outcome. Mannitol is proposed to scavenge free radicals and reduce cerebral edema. No pharmacologic agents have been demonstrated to reduce cerebral injury alone or in combination with others.

Blood Gas Management There are two means to manage blood gas during DHCA, (1) pH-STAT and (2) alpha (α)-STAT. The pH-STAT technique focuses on maintaining a pH of 7.40 and PaCO 2 of 40 mm Hg. Changing body temperature results in the perfusionist needing to add CO2 to the circuit resulting in a respiratory acidosis. The respiratory acidosis results in an increase in cerebral vasodilation and an increased cerebral blood flow (CBF). The increase in CBF theoretically results in more rapid and uniform cooling of the brain, but at the risk of increases in cerebral embolic events due to higher flows. The α-STAT technique focuses on preserving cerebral autoregulation by achieving a normal pH and PaCO2 at 37°C and respiratory alkalosis results with reductions in CBF. No CO2 is added. CBF is lower and the risk of emboli may be lower. The risk though is that cooling may not be uniform. No study has clearly demonstrated one blood gas management technique to be superior to another. The pH-STAT approach (respiratory acidosis and increased CBF) during the cooling period may improve cerebral cooling while use of α-STAT (respiratory alkalosis and cerebral vasoconstriction) during warming may reduce embolic events yet preserve cerebral autoregulation and coupling of blood flow to CMRO2.

Selective Cerebral Perfusion The brain is a highly metabolically active organ and highly vulnerable to any period of ischemia. Selective cerebral perfusion involves the delivery of blood and oxygen to the brain during the period that the rest of the body is subject to arrest and deprived of blood flow. Selective cerebral perfusion has been shown to prolong the period of systemic DHCA so that critical work on the aortic arch can be completed. A general

downside of these techniques is the addition of additional equipment or blood flow into the field. Retrograde cerebral perfusion (RCP) involves perfusion of the brain through the venous system via the superior vena cava. Blood is pumped from the circuit at a rate of approximately 200 to 300 mL/min to a measured central venous pressure of 15 to 20 mm Hg. The mechanism of potential benefit of his technique is unclear. RCP may “flush” the cerebral vasculature of air and debris that accumulated during surgery. RCP may also provide additional cooling. This technique is becoming less popular. Antegrade cerebral perfusion (ACP) can be hemispheric through the right axillary, subclavian or innominate artery. It can also be bihemispheric by adding an antegrade perfusion cannula to the left common carotid artery. There is no consensus for the perfusion pressure or flow however, blood flow is generally maintained between 5 to 20 mL/kg/min according to uni- or bilateral cerebral perfusion. Pressure is generally measured via the right radial arterial catheter and should be between 40 to 70 mm Hg. Higher pressure ACP may appear appealing but has been associated with increased CBF, intracranial pressure, higher post-CPB CMRO 2 and poorer neurologic recovery. Blood gases are often managed with a pH-STAT technique. ACP is more popular than RCP and permits longer periods of DHCA.

Temperature Management During Rewarming Rewarming involves resumption of systemic flow and increasing the patient’s body temperature from 18°C to a temperature at which the problems associated with hypothermia are minimized without causing injury associated with hyperthermia in the vulnerable brain. Reperfusion will generally be initiated at 18°C for 5 minutes before beginning the rewarming process. The gradient between the warming inlet water temperature and the venous blood should be 10°C or less to avoid excessive rapid rewarming of the brain. The pH-STAT (respiratory acidosis and increased CBF) technique may be used until the brain temperature reaches 28°C then an α-STAT technique (respiratory alkalosis, preservation of auto-regulation) may be used to potentially reduce emboli-associated injury. A nasopharyngeal temperature of >36°C and a bladder temperature of >35°C but less than 37°C is adequate to initiate weaning from CPB. Inflow temperatures in excess of 37°C may result in cerebral hyperthermia and injury.

Monitoring Cerebral Protection During DHCA Since CMRO2 is reduced significantly with hypothermia, the temperature of the brain must be followed accurately. The jugular bulb temperature is the most accurate reflector of brain temperature during DHCA but is difficult to access. The nasopharynx

temperature is most commonly utilized and is more accurate than measurement in the bladder or oropharynx. The probe should be placed gently in the naris before systemic anticoagulation for CPB to avoid trauma which may result in bleeding. NIRS is a noninvasive means to assess cerebral oximetry through rSO2. Within the brain 70% to 80% of the blood is venous (deoxygenated) and 20% to 30% is arterial (oxygenated). Differences in oxygen saturations between arterial (≈100%) and venous (≈ 60–70%) blood result in an average calculated rSO2 of 60% to 70%. This reflects the balance between oxygen supply and demand. NIRS is a means to continuously monitor rSO2. Decreases in rSO2 may be correlated with postoperative neurologic dysfunction such as stroke, cognitive dysfunction, and delirium but it is unclear whether interventions such as increased perfusion pressure or maintenance of a high hematocrit improve outcomes. It is unclear what rSO2 below which cerebral injury will occur. Drops in rSO2 below 75% of the patient’s baseline may result in cerebral injury. Electrical brain activity can be monitored using traditional electroencephalographic (EEG) or pEEG monitoring. During cooling, change in electrical activity can be appreciated and during DHCA, electrical silence can be documented. It can also serve as a brain ischemia monitor while reduced cerebral electrical activity can be associated with hypoperfusion related to reduced CPB flows or hypotension. It can also serve to detect epileptiform activity which can also be caused by ischemia. Limitation of cerebral oximetry using NIRS and EEG resides in the inability to monitor activity of deeper structures such as hippocampus and basal nuclei that are highly vulnerable to ischemia.

Additional Monitoring Hypothermia induces resistance to insulin and hyperglycemia is generally seen during the cooling part. Conversely, insulin perfusion must be adjusted during rewarming to avoid hypoglycemia. Hyperglycemia has been shown to increase morbidity and mortality in cardiac surgical patients with and without diabetes. The Society of Thoracic Surgeons recommends that glucose levels be maintained below 180 mg/dL in the perioperative period. TAKE HOME POINTS Gradual systemic cooling to a body temperature of 18°C should occur when DHCA is chosen as a technique for cerebral protection. The use of topical application of ice during cooling and DHCA has not been demonstrated to provide any additional benefit to DHCA. If utilized, protection of

tissue against thermal injury is critical. No single pharmacologic agent or group of agents has been demonstrated to be beneficial during DHCA. Use of a pH-STAT technique during cooling results in a respiratory acidosis and increased uniform cerebral cooling associated with cerebral vasodilation. Use of an α-STAT technique during DHCA (if antegrade perfusion utilized) and during warming may reduce the risk of cerebral embolic events. Retrograde or antegrade cerebral perfusion may increase the safe period if DHCA is likely to last more than 20 minutes. During rewarming, inflow temperature should never exceed 37°C. A pH-STAT technique may be utilized until 28°C is reached then α-STAT. The temperature gradient between the inlet water temperature and venous blood temperature should be ≤10°C. Decreases in rSO2 may be associated with postoperative neurologic decline such as stroke, cognitive dysfunction, and delirium but it is unclear whether interventions to increase rSO2 improve these outcomes. Suggested Readings Foley LS, Yamanaka K, Reece TB. Arterial cannulation and cerebral perfusion strategies for aortic arch operations. Semin Cardiothorac Vase Anesth. 2016;20(4):298–302. Keenan JE, Benrashid E, Kale E, et al. Neurophysiological intraoperative monitoring during aortic arch surgery. Semin Cardiothorac Vasc Anesth. 2016;20(4):273–282. Zheng F, Sheinberg R, Yee MS, et al. Cerebral near-infrared spectroscopy monitoring and neurologic outcomes in adult cardiac surgery patients: A systematic review. Anesth Analg. 2013;116(3):663–676. Ziganshin BA, Elefteriades JA. Deep hypothermic circulatory arrest. Ann Cardiothorac Surg. 2013;2(3):303– 315.

237 Anesthesia for Left Ventricular Assist Device Surgery: Essentials to Bear in Mind Raymond G. Graber, MD and Daniel I. Asher, MD

A 57-year-old man with idiopathic cardiomyopathy and end-stage heart failure presents for elective left ventricular assist device (LVAD) destination therapy. Left ventricular (LV) ejection fraction is estimated to be less than 15%; right ventricular (RV) systolic function is moderately depressed. He has a biventricular implantable cardioverter/defibrillator (ICD). His congestive heart failure symptoms are medically well-managed, but he still has some pulmonary edema, significant pulmonary hypertension, mildly impaired renal function, and hepatic congestion despite being on milrinone and clevidipine infusions. What is the anesthetic plan for this patient? Do you stop his infusions? What is the invasive monitoring plan? What induction/anesthesia maintenance drugs will you use? Is the pre-cardiopulmonary bypass (CPB) and/or postCPB transesophageal echocardiography examination (TEE) important? Are you concerned about post-CPB bleeding in this elective, “virgin chest” patient? What is the risk of right heart failure? Will you plan to extubate in the operating room? Anesthesia for ventricular assist device (VAD) implantation surgeries can be very challenging. Let us consider our patient in this clinical vignette—where do we start when putting together the anesthetic plan for a patient like this? We will be tackling all these issues head on because ignoring even one of them can mean a disaster in the operating room and/or the intensive care unit.

Introduction to Ventricular Assist Devices Short-term VADs are implanted to provide support for a period of days to weeks in conditions that are presumably reversible (e.g., viral cardiomyopathies, acute cardiogenic shock, acute right heart failure after LVAD placement). Thus, these are placed as a “bridge to recovery” (the patient gets better, device is removed) or as a “bridge to decision” (patient doesn’t get better, so patient is either converted to a long-

term device or decision made to withdraw support). Since these are placed for shortterm indications, the pump is external to the body. For LV support, an inflow cannula is placed in the left atrium (LA) or apex of the LV, and blood is then returned via an outflow cannula into the ascending aorta. For RV support, an inflow cannula is placed in the right atrium or apex of the RV, and blood is then returned via an outflow cannula into the pulmonary artery. Longer-term VADs are implanted as a “bridge to transplantation” in patients that are listed for cardiac transplantation but are failing conventional supportive therapy, or as permanent devices in patients who are not transplant candidates, which is known as “destination therapy.” These pumps are implanted internally. In general, an inflow cannula is placed in the apex of the LV, and blood is then routed via a pump into an outflow graft which is sewn onto the ascending aorta. The pump is connected via a cable (that exits through the upper abdominal wall) to an external controller unit.

Preoperative Concerns Some important areas of focus during the preop evaluation: Review preoperative right heart cardiac catheterization and echocardiography data prior to taking these patients to the OR. You know the LV is going to be bad, but how about the RV? How is the function of the liver and kidneys? Have they been impaired by the combination of low flow and venous congestion? What is the status of the coagulation system? Liver production of clotting factors may be impaired. Many patients are on chronic coumadin or other anticoagulant therapy. This information may help guide what clotting factors should be ready and on hold at the time of surgery. Does the patient have an ICD and/or pacemaker? The ICD will need to be shut off prior to surgery, and the pacemaker may need to be re-programmed. Is the patient on inotropic support? Many patients are on dobutamine, milrinone, or vasodilator therapy when they present for surgery. Make sure appropriate blood products are on order for surgery. There should be 6 units of packed red cells in the room at the start of the case. The type of clotting factors ordered will to a certain extent depend on the preop clotting status. However, usually at least 6 units fresh frozen plasma and 10 units of platelets, are placed on hold, and need to be in room when you come off pump. Finally, cryoprecipitate may also be necessary if preoperative fibrinogen level is low. We generally prefer to keep fibrinogen level over 200 mg/dL when we are off pump and trying to dry up.

Invasive Monitoring

Standard American Society of Anesthesia monitors are supplemented with an arterial line, pulmonary artery (PA) catheter, and TEE. An arterial line is placed pre-induction. At our center, brachial arterial lines are frequently utilized to minimize post-CPB waveform damping issues. However, radial or femoral sites are also acceptable. You need to know where your surgeon is going to arterially cannulate for CPB. Don’t place a right arm arterial line if the surgeon is going to cannulate the right axillary artery! A pulmonary artery catheter may be placed prior to or after induction. Use ultrasound to scan the planned internal jugular (IJ) site prior to skin prep. These patients may have had multiple IJ sticks in the past, and may have thrombosed veins or other abnormal anatomy. A 9F introducer or a double lumen (9F/12 Ga) introducer is placed first, then the PA catheter is floated. Some centers utilize continuous cardiac output/mixed venous oxygen capable PA catheters to continuously assess adequacy of oxygen delivery. The PA catheter will help guide your inotropic and vasodilator choices. TEE is invaluable in managing these patients, and will be discussed further later.

Careful Induction and Maintenance If the patient has been on inotropic support, it is maintained. If not on support, it is frequently helpful to start a low dose of inotrope (dopamine or epinephrine) to support heart function and blood pressure through the induction period. If a patient presents on a vasodilator (like sodium nitroprusside or clevidipine), these are turned off prior to induction, to avoid bottoming out the blood pressure. Most of these patients will not tolerate lying flat, so anesthetic induction may have to be initiated with the patient in a head-up position. Most anesthesiologists will want to avoid significant vasodilation or cardiac depression, so will induce with etomidate in conjunction with moderate doses of fentanyl and midazolam. The idea is to minimize the sympathectomy as there is really very little, if any, cardiac reserve in VAD patients. Remember that these patients may have a prolonged induction time due to slow circulation. Low doses of inhalation agent can be added as tolerated. Maintenance anesthesia is usually accomplished with a balanced technique of inhalational anesthetic, narcotic, benzodiazepines, and muscle relaxants.

Other Management Issues Baseline coagulation labs should be drawn: CBC, PT/TT, INR, fibrinogen. At our center we also use thromboelastogram (TEG) to help guide administration of clotting factors. Good IV access is required. For example, two large-bore peripheral lines and double lumen (9F/12 Ga) introducer. At least two lines should be warmed for administration

of fluids and clotting factors. Tranexamic acid or ε-aminocaproic acid (Amicar ®) is administered to reduce bleeding and blood product requirements. Hypotension can be multifactorial, but is frequently related to the use of angiotensinconverting enzyme (ACE) inhibitors, angiotensin receptor blockers, and milrinone. The vasodilatation induced by these agents can exacerbate anesthetic-induced vasodilatation. A vasoconstrictor such as vasopressin or norepinephrine may be needed if the SVR remains excessively low. Vasopressin has less effect on pulmonary vascular resistance, so is frequently used first. Methylene blue (1.5 to 2 mg/kg) is also sometimes used to treat refractory vasoplegia.

Pre-CPB TEE Evaluation Pre-pump, a complete TEE examination is performed. There are some specific areas of focus in LVAD patients: Is a patent foramen ovale (PFO) or ventricular septal defect (VSD) present? After LVAD initiation and LV decompression, the pressure gradient across the septa will increase, tending to cause or exacerbate right-to-left shunts if a PFO or VSD is not surgically closed. Is there significant aortic insufficiency (AI)? When AI is present, LVAD flow into the ascending aorta will circle back into the LV. A small amount of preop AI may become much more significant post LVAD activation as the pressure gradient across the aortic valve increases. Significant AI will need to be dealt with surgically—valve replacement or valve closure may be required. RV function is assessed. A failing right heart may require increased support, either with inotropes, nitric oxide, or RVAD. Worsening tricuspid regurgitation is an indicator of RV dilatation. The aorta is assessed for calcification, plaque, or dilation in order to assess the aortic graft site. The LV and LA are examined for thrombus, particularly at the apex of the LV where the LVAD inflow cannula is inserted.

During CPB CPB is managed as with any type of cardiac pump case. Vasopressors may be needed for blood pressure support in patients chronically on vasodilators. One should use this time wisely, to prepare for coming off CPB. All clotting factors and platelets should be prepared and in the room prior to termination of CPB. If nitric oxide is planned, it is hooked up to the anesthesia circuit during this time in preparation for coming off bypass. Inotropic support drugs should all be ready to go.

When getting close to coming off CPB, start the planned inotropic meds to support right heart function. Frequently, epinephrine and milrinone are used in combination. Also, TEE should be used to confirm adequate deairing of the heart. Air has a tendency to make its way down the right coronary artery—leading to RV dysfunction. If this does occur, the systemic pressure should be raised to at least 80 to 90 mm Hg to drive the air bubbles through the coronary circulation. This should be followed by a recovery period while still on bypass.

Separation From Bypass When a patient is weaned off pump with an LVAD in place, the focus is on adequately volume loading the patient and monitoring the right heart to make sure it is tolerating the load. (More on that later!) After successful separation from CPB, you must be able to multitask, and deal with reversing protamine, managing underlying coagulopathy, maintaining euvolemia, keeping the patient warm, and correcting any metabolic derangements. Obtain frequent arterial blood gases to monitor for issues with potassium, glucose, metabolic acidosis, and adequacy of ventilation.

Post-CPB TEE Evaluation The post-CPB TEE examination focuses on the following: Assess the position and orientation (toward the mitral valve) of the LV apex inflow cannula. If obstruction is present, turbulent inflow will be seen, along with high velocity flows (>1.5 m/sec). However, some devices which lie directly adjacent to the LV apex will generate noise when Doppler is pointed at that location, and this precludes the ability to measure velocity. The outflow graft flow into the ascending aorta can frequently be assessed. If obstruction is present, turbulent flow may be seen, or high velocity flows (>2.0 m/sec) may be seen. RV size and function and the severity of tricuspid regurgitation are monitored. Assess the size of the LA and LV. If the LA and LV are noted to be too small, there may be inadequate RV preload or right heart failure. Treatment may include adding volume, temporarily cutting back on LVAD flow rate, or increasing right heart support. If the LV collapses, catastrophic air entrainment around the inflow cannula can occur. Keep an eye on the ventricular septum. If it deviates significantly in either direction, something needs to be addressed! The aortic valve should be reexamined to look for worsening of preexisting AI. Also reexamine the septa for shunts.

Right Heart Support When an LVAD is placed, preservation of RV function becomes a major priority. The right heart may fail in up to 20% of patients. Therefore, we always administer some kind of RV support when coming off CPB. The degree of support necessary will depend on the degree of underlying right heart dysfunction and the severity of pulmonary hypertension. We generally will start a beta agonist such as epinephrine prior to coming off CPB, and then also consider whether to add in milrinone +/− inhaled nitric oxide. Some centers use inhaled epoprostenol (Flolan®) as an alternative to nitric oxide. We monitor the right heart in several ways. The CVP and PA pressures give us an indication of preload and afterload. The RV can be seen on the surgical field. TEE is used to monitor size and function of the RV, and to assess severity of tricuspid regurgitation. A failing right heart must be promptly addressed (e.g., increasing epinephrine dose, adding milrinone, ensuring that oxygenation and ventilation are adequate). In maybe 5% of cases, short-term RV assist device support may be required.

Extubation Timing Intraoperative extubation is pretty much never a good idea for a VAD operation. The idea is to support cardiac physiology and let the body get used to the weird new spinning do-dad that the surgeon just buried in the chest! In order to get extubated, the patient must be warm, not bleeding, not metabolically deranged, off nitric oxide, on reasonable levels of inotropic support, and hemodynamically stable. That takes time, and that means the patient is going to the ICU intubated. TAKE HOME POINTS LVAD patients are extremely ill, and are at risk for crashing on induction. These patients must be aggressively supported and monitored—with the goal being getting safely on bypass. Pre-CPB and post-CPB TEE is extremely important in the care of these patients. After CPB, the major areas of attention are preserving RV function, monitoring the LV/LVAD combination, and getting the patient dried up so you can get the patient out of the OR. Suggested Readings Feldman D, Pamboukian SV, Teuteberg JJ. The 2013 International society for heart and lung transplantation guidelines for mechanical circulatory support: Executive summary. J Heart Lung Transplant. 2013;32:157–187. Hensley FA, Martin DE, Gravlee GP. A Practical Approach to Cardiac Anesthesia. 4th ed. Philadelphia, PA:

Lippincott Williams & Wilkens; 2008:587–603. Mets B. Anesthesia for left ventricular assist device lacement. J Cardiothoracic & Vascular Anesthesia 2000;14:316–321. Miller LW, Guglin M. Patient selection for ventricular assist devices: A moving target. J Am Coll Cardiol. 2013;61:1209–1221. Savage RM, Aronson A, Shernan SK. Comprehensive Textbook of Perioperative Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkens; 2011:622–660. Stainback RF, Estep JD, Agler DA, Birks EJ, Bremer M, Hung J, Kirkpatrick JN, Rogers JG, Shah NR; American Society of Echocardiography. Echocardiography in the management of patients with left ventricular assist devices: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr 2015;28:853–909.

238 Off-Pump Coronary Artery Grafting Is Like Working on an Engine (While It Is Still Running) Yasuko Nagasaka, MD PhD and Vipin Mehta, MD FFARCSI

A 58-year-old female attorney presents with triple vessel coronary disease and elective coronary revascularization was planned. The left ventricular ejection fraction (LVEF) is 40% by echocardiogram. Preoperative imaging studies reveal a heavily calcified thoracic aorta (a.k.a. porcelain aorta). The patient’s past medical history is notable for hypertension (HTN), Type II diabetes mellitus (DM), obesity, a 45 pack-year smoking history and intermittent claudication. In addition, she underwent left carotid endarterectomy (CEA) 5 years ago when she suffered a transient ischemic attack (TIA); recent blood tests have revealed mild renal insufficiency and elevated HbA1c. The surgeon plans an off-pump coronary artery bypass (OPCAB) surgery. The patient is very fearful of stroke risk as an uncle of hers recently had one when undergoing coronary surgery. She asks you during her preoperative assessment what the risks and benefits of OPCAB versus conventional coronary surgery are. OPCAB is a good option for this patient, given possible contraindications for aortic cannulation of the porcelain aorta. Her preoperative comorbidities suggest she certainly has increased stroke risk, especially if the procedure will involve aortic manipulation.

Background OPCAB has been practiced for many decades and following development of improved stabilization systems reached the height of its use in 2004. OPCAB is technically demanding both for anesthesiologists as well as surgeons and there is NO PUMP BREAK for the anesthesiologist! In contrast to the United States, OPCAB is practiced more frequently in other countries (e.g., Japan, China, India, Brazil). When conducted by experienced teams OPCAB is clinically as safe and effective as on-pump surgery with no difference in costs.

Who Best Qualifies for OPCAB? OPCAB patient selection depends upon multiple factors: patient’s comorbidities as well as the number and location of vessels to be revascularized. For example, intramyocardial vessels are technically more difficult to graft during OPCAB surgery. Relative contraindications of OPCAB include: Poor quality target vessels (intramyocardial vessels, diffusely diseased vessels, calcified coronary vessels) Cardiomegaly/congestive heart failure Critical left main disease Small distal targets Recent or current acute MI Poor left ventricular function (LVEF 6 Woods unit, BMI >35 kg/m2), reprogramming the ICD, and insuring that the patient has the clear understanding that although a potential donor has been identified, the process can be aborted for a number of reasons even after the transplant wheels have started turning. Immunosuppression protocols are of great importance for OHT patients to minimize organ rejection. This process is initiated prior to surgical incision so one must insure that these protocols are appropriately followed. Related to this issue is the need to use strict aseptic technique with the indwelling catheters. Timing of anesthesia induction is dependent upon multiple variables, such as predicted time of recipient preparation and predicted transport time of donor organ. Communication with the organ harvesting surgical team is of the highest priority to avoid unnecessarily prolonged donor organ ischemic time.

Establishing both arterial blood pressure monitoring and central venous access can be very challenging in OHT candidates, so allow plenty of time to get these lines in. Right heart failure is the most feared acute complication of OHT, so you must vigilantly monitor the patient for any sign of this issue and be ready to treat it immediately. Coagulopathy is common in OHT patients given the nature of their disease process, so you must have hemostatic allogeneic blood components readily available to aggressively treat this problem if it is observed. Suggested Readings Quinlan JQ, Murray AW, Casta A. Anesthesia for heart, lung and heart-lung transplantation. Chapter 26. In: Kaplan JA, Reich DL, Lake CL, et al., eds. In Kalpan’s Cardiac Anesthesia. 5th ed. Philadelphia, PA: Saunders Elsevier; 2006. Thomas Z, Rother AL, Collard CD. Anesthetic management of cardiac transplantation. Chapter 14. In: Hensley FA, Martin DE, Gravlee GP, eds. In Cardiac Anesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.

241 The Right Heart Should Never Play Second Fiddle to the Left Heart—What to Do When the Right Heart Just Really Ain’t Right at All Lindsay Wetzel, MD, Faisal D. Arain, MBBS MD, Daniel I. Asher, MD, and Edwin G. Avery, MD

A 72-year-old male with severe three-vessel coronary artery disease, hypertension, dyslipidemia, diabetes, and obesity presents for coronary artery bypass surgery. The patient’s preoperative transthoracic echocardiogram (TTE) was notable only for low normal left ventricular systolic function (ejection fraction 45% to 50%) and impaired relaxation of the left ventricle. Following anesthesia induction that was conducted with midazolam, fentanyl, propofol, and rocuronium multiple doses of phenylephrine were required to maintain mean arterial pressures (MAP) above 70 mm Hg. Initial numbers from the pulmonary artery (PA) catheter revealed the following: PA systolic and diastolic 27 and 17 mm Hg, respectively, and a central venous pressure (CVP) of 17 mm Hg; the cardiac index was 1.7 L/min/m2. Once the transesophageal echocardiography (TEE) probe was dropped it was noted that the right heart structures were dilated, appeared sluggish in movement, and mild tricuspid regurgitation (TR) was noted. How will you further quantify this patient’s right ventricular function and what treatment approach, if any, may be needed? Important: The failing or failed right heart is NOT simply a passive conduit and shouldn’t be treated as such! If you were told this in medical school, please be advised that this isn’t true and never was true. Here are the basics of what you need to know about how to deal with the right heart.

Right Heart Anatomy Right ventricular dysfunction is known to predict poor outcomes in patients undergoing coronary surgery and thus its presence should not be taken lightly. One of the key difficulties in the assessment of right heart function is related to the asymmetric shape of the right heart which is often described as a cornu, or horn. Individuals with right atrial

minor axis dimensions greater than 50 mm and tricuspid valve (TV) medial to lateral dimensions greater than 38 mm as measured from the mid-esophageal four-chamber view should raise serious concerns of chronic right heart dysfunction. By the general eyeball test, the right ventricle (RV) should be approximately two-thirds the size of the left ventricle (LV), and the apex of the heart should come from the apex of LV, not the RV. The RV shares the muscular interventricular septum with the LV and, even though they are neighbors, they sometimes do not get along. The interventricular septum can bow toward the LV in diastole if the RV is volume overloaded in a failing state which could give the LV less real estate, thus decreasing LV filling.

Right Heart Dysfunction The importance of good RV function is undervalued by many clinicians, but a failing RV can take anyone out to the woodshed for a lesson. The RV’s main job is to propel deoxygenated blood through the normally low compliance pulmonary circulation for oxygenation and LV filling. A failing RV can impede adequate LV filling, impairing forward flow cardiac output. Quantifying RV function by visual estimation on TEE is complicated by its asymmetrical shape. However, tricuspid annular plane systolic excursion (TAPSE) is a relatively foolproof measurement of RV systolic and diastolic function. This measurement can be accomplished from a mid-esophageal 4-chamber view by simply measuring from just below the underside of the base of the anterior TV leaflet to the apex of the RV in both end systole and end diastole ( Fig. 241.1). The difference between these two values is greater than 15 mm in normal RV systolic function and no mathematical genius is needed to perform this calculation.

Figure 241.1. Illustration of an idealized transesophageal echocardiographic mid-esophageal fourchamber view at an omniplane of 0 degrees being used to calculate tricuspid annular plane excursion. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; TV, tricuspid valve; TAPSE, tricuspid annular plane excursion.

A PA catheter measures right-sided heart pressures and right-sided cardiac output by thermodilution and can, in conjunction with TEE, be helpful in making the diagnosis of RV dysfunction. For example, in our presented case above, the cardiac index is unacceptably and unexpectedly low. The PA mean pressure (diastolic is high) appears normal but the CVP and PA diastolic is on the high side—this is a big clue that we were dealing with clinical right heart failure. The low PA pressures and low PA pulse pressure are also clues that RV systolic function is poor; TEE visualization and a TAPSE of less than 10 mm will confirm the diagnosis. Direct observation of poor RV wall thickening during systole by TEE can also be helpful for qualitative measurement of RV function. Note that the mild TR observed in this patient is a bad sign in that the RV systolic function is so poor that even with a severely dilated tricuspid annulus the RV cannot generate much TR. We get it that this stuff is a little complicated, but, hey, if it were easy the surgeons wouldn’t need us to figure this all out. A standard intraoperative TEE probe cannot practically be used to continually monitor RV function in the ICU, but there are a few other options. In the intubated patient, one can use a miniature TEE probe (ClariTEE©) which provides an adequate diagnostic image in most patients to perform serial right heart examinations without the need for repeatedly removing and reinserting the TEE probe. This device can remain in

the patient for up to 72 hours which coincidentally is probably how many hours we all work in any single given week. TTE can also be used, but is limited in the postoperative period due to air, blood clots, or acoustic shadows in the chest or external dressings that can impede adequate visualization. Probably the most practical, though invasive, approach for continuous right heart monitoring is the PA catheter. Focusing on the ratio of the PA diastolic, mean, or systolic pressure to the CVP is a clinically useful way to serially assess right heart failure. When the PA:CVP ratio goes down (i.e., lower PA pressures and higher CVP) it is a sign that RV function is worsening in that it can no longer effectively pump blood into the PA. Both volume and pressure are backing up from the right heart into the venous circulation. An opposite change in the ratio of PA:CVP (i.e., higher PA pressures and lower CVP) is a favorable sign of good RV function. So a little more basic math goes a long way here in terms of keeping a watchful eye on RV function with our PA catheter.

Treating Right Heart Dysfunction So once we have established the diagnosis of RV failure using the quantitative and qualitative data from the PA line and the TEE, we need a good treatment plan. The Don’ts: In most situations, administration of more intravascular volume is not a good idea because it will further stretch the already dilated RV, pushing it off its Starling curve, and likely hastening complete RV failure. Giving volume to a fluid overloaded RV may remind us of the beer bong college days when it also turned out to be a bad idea to pound all that cold, foamy volume into the relatively small stomach. That activity was inevitably followed by uncomfortable physiologic reflexes as the through-put capacity of the system was overwhelmed. Intravenous administration of pure alpha-1 vasoconstrictors, like phenylephrine, is another bad idea as it will increase pulmonary arterial vascular resistance (i.e., right heart afterload) and reduce RV output. That being said, it’s true that increasing MAPs (i.e., usually to just above 80 mm Hg) can improve RV perfusion pressure and performance, just as long as the higher MAP doesn’t come along with a ton of increased pulmonary vascular resistance. We also recommend going easy on the positive end expiratory pressure (PEEP) as values above 5 mm Hg may functionally limit right heart filling and may further reduce overall cardiac output. The Do’s: The best drug cocktail for the failing right heart is what the late Rodney Dangerfield might call “The Triple Lindy” of supportive right heart moves and includes three drugs: intravenous milrinone for contractility, a selective pulmonary vasodilator (e.g., inhaled nitric oxide or inhaled epoprostenol), and vasopressin as needed to maintain a higher mean arterial pressure (e.g., 80 mm Hg). Vasopressin is made for this job because there are no vasopressin receptors in the pulmonary arterial vasculature

which helps to avoid unwanted increases in pulmonary vascular resistance. Other approaches in less severe RV failure may be to use epinephrine or dobutamine to increase RV contractility. One can also use a low-dose nitroglycerin infusion to help decrease PVR and increase RV perfusion. However, this is obviously limited by the need for adequate MAPs. Out of your league with drugs: Don’t call a personal injury lawyer; instead just note that in the most severe cases of RV failure, it may be necessary to leave the chest wall open to allow for optimal RV filling. This situation may be appropriate in our clinical case as RV failure may be expected to get better within 12 to 24 hours following coronary revascularization. Under the most dire circumstances, mechanical circulatory support devices must be considered and can include an intra-aortic balloon pump (IABP), venoarterial extracorporeal membrane oxygenation (VA-ECMO), dedicated right ventricular assist devices (RVAD) such as the Centrimag©, or a combination of them. The mechanical support device used will depend on the experience and preference of the cardiac surgeon and will differ from center to center. A caveat to keep in mind with RV failure is that use of an IABP will potentially worsen RV failure. The RV relies upon developed LV systolic pressure which creates a firm interventricular muscular septum to beat against in order to help propel blood into the pulmonary circulation. Because the IABP deflates during systole it creates a sort of vacuum in the aorta and hence reduces developed LV systolic pressure. Under these conditions the RV doesn’t have a firm muscular septum to beat against and RV output may fall. It’s a little bit like that dirty trick you may have played on your buddy when you’re on the see-saw (or your grandfather may have played on his buddies—this childhood prank seems eternal). That is, the physiology of the right heart, like a seesaw, relies on the law of opposing forces. Your buddy relies on your weight to keep them up in the air while you are down on the ground and if you abruptly jump off the see saw when they are up in air they lose the support needed to keep them up in the air and come crashing down on their tail bone, ouch! And so it is with the right and left hearts and the interposing septum.

Tricuspid Valve Regurgitation TR is most commonly functional in nature meaning that it is related to dilation of the RV and likely also the TV annulus. The mechanism of functional TR is when the RV chamber dilates it results in displacement of the RV papillary muscles which make up part of the TV subvalvular apparatus; the displaced papillary muscles pull the TV leaflets apart allowing regurgitation. TR can also be caused by infection-endocarditis, iatrogenic reasons, or external blunt or penetrating trauma which damages the TV apparatus. Severe TR is marked by a vena contracta width of greater than 0.7 mm in the

mid-esophageal four-chamber view. Secondary changes associated with severe TR are as follows: TV annular dilation, RA dilation, vena cava dilation, holosystolic flow reversal in the hepatic veins, and hepatic congestion-induced coagulopathy (i.e., there may be a prolonged partial thromboplastin time or International Normalized Ratio related to poor hepatic perfusion brought on by the high venous pressures). TR is best managed during anesthesia by not allowing the heart rate to decrease as this will result in an increase in the regurgitant fraction that will ultimately decrease RV output. Both chronotropic intravenous drugs or electrical cardiac pacing can prevent bradycardia-induced exacerbation of TR. Drugs or physiologic changes that can increase pulmonary vascular resistance can all be expected to worsen the degree of TR (e.g., alpha-1 vasoconstrictors or hypoventilation, hypoxemia, hypothermia, acidosis, etc.). We are starting to sound like our internist colleagues that tell us to avoid all of these things that are obviously bad, sorry about that, but we just can’t let it go unsaid. Since it is always easier to stay out of trouble than it is get out of trouble in cardiac surgical patients, we recommend running an intravenous dobutamine infusion prior to anesthesia induction in patients with severe TR to avoid bradycardia. The age-old decision to repair or replace the TV in the setting of moderate or worse TR should consider the degree of involvement of the subvalvular apparatus (i.e., TV ring annuloplasty repair will not be effective in rheumatic TV disease). Functional TR responds well to a ring annuloplasty repair and care should be taken to obtain trans-TV gradients following repair to rule out iatrogenic TV stenosis (i.e., mean gradients less 6 mm Hg with a normal cardiac index are desirable). TV endocarditis normally requires replacement of the valve. CAUTION: Note that under general anesthesia which can be accompanied by sympathectomy and unloading of the right heart that the degree of TR observed may significantly underestimate the amount of TR present when the patient is awake or in severe pain for whatever reason. In such cases acutely volume loading the right heart by placing them in steep Trendelenburg position may better reveal the patient’s actual degree of TR. Intravenous administration of an alpha-1 vasoconstrictor may also better reveal the actual degree to TR. It is also helpful to look for secondary signs of TR, like RA dilation, in the absence of an impressive TR jet to help make the decision of whether a TV repair is indicated.

Tricuspid Valve Stenosis TV stenosis is rare in most US-based clinical practices. It may be related to rheumatic disease, endocarditis, or carcinoid disease. Stenotic TVs are almost always replaced. Anesthetic goals are to maintain right heart preload, normal sinus rhythm, and midranged heart rate of approximately 70 to 90.

TAKE HOME POINTS Right ventricular dysfunction remains a significant cause of morbidity and mortality in patients undergoing cardiac surgery. Early identification of RV dysfunction may improve risk stratification and lead to early management of RV failure, so whatever you do don’t blow off assessment of the RV! Although RV assessment remains challenging secondary to its complex anatomy, the tricuspid annular plane systolic excursion (TAPSE) measurement provides a reasonable index of global RV systolic and diastolic function and you don’t need a PhD in physics or mathematics to master the technique. RV dilation can cause a leftward shift of the ventricular septum, modifying LV geometry. As a consequence, both LV distensibility and contractility may decrease resulting in reduced cardiac output. In the same manner, in patients requiring LVAD or IABP support, unloading of the LV alters RV size and shape and may lead to further RV failure which, like your dad may have said to you when you were growing up, “is exactly the situation we are trying to avoid.” In patients with a failing right heart, the top shelf drug cocktail is what we like to call “The Triple Lindy” of supportive right heart moves and includes: intravenous milrinone (i.e., increases RV inotropism and decreases pulmonary pressures), inhaled selective pulmonary vasodilators (e.g., inhaled nitric oxide or inhaled epoprostenol), and vasopressin (i.e., useful to increase mean arterial pressures greater than 80 mm Hg to promote better right heart coronary perfusion without increasing right heart afterload). Functional tricuspid regurgitation (FTR) is usually a prominent feature of RV dysfunction and may be the result of RV dilation and pulmonary hypertension. FTR generally responds well to TV ring annuloplasty so tuck this fact under your surgical cap. Because it’s easier to stay out of trouble than to get out of trouble in cardiac surgery, we recommend that a dobutamine infusion is run prior to anesthesia induction in patients with known moderate to severe, or worse TR. Suggested Readings Haddad F, Couture P, Tousignant C, et al. The right ventricle in cardiac surgery, a perioperative perspective: I. Anatomy, physiology, and assessment. Anesth Analg. 2009;108(2):407–421. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(7):685–713.

SECTION XII

OBSTETRIC ANESTHESIA

242 Introduction Christopher E. Swide, MD

Obstetric Anesthesia. It brings up memories of frequent pages, 24/7 coverage, urgent cesarean sections. But it is primarily a practice that involves two, and sometimes more, patients and other extremely involved participants. A mother and a child. A father-to-be. A concerned nurse. A worried obstetrician. It is a practice that one must manage outside of the “OR schedule.” To be available at all times to provide pain relief or safe patientand family-centered care. To be part of an important day in your patients’ lives. To appear in the baby book. To see the smile on a mom’s face when you relieve her pain or manage a complicated delivery. It is an honor and privilege to be part of such important moments. The chapters within this section will provide common sense approaches to challenges and patient management in the labor suite and delivery room. I hope you use these chapters to further enhance your practice to help women, babies, and their families.

243 Be Prepared for the Presence of a Doula in Both the Labor and Delivery Rooms Christopher E. Swide, MD

Doulas are becoming increasingly popular in the United States and are active on many labor suites across the country. DONA International is the oldest and largest of the doula organizations in the United States. It has more than 5,800 members, including 2,300 certified birth doulas in all 50 states. Many hospitals and health systems hire doulas directly, but it is also common for doulas to contract separately with the patient. The term doula is derived from Greek and refers to the most important female servant in the ancient Greek household. Today’s doulas are caregivers whose primary role is the emotional support of the mother during labor and delivery. Anesthesiologists and nurse anesthetists working on labor units will encounter doulas but are often confused about their role in the birth experience. It is important for them to have a general understanding of this caregiver’s role to facilitate optimal care for obstetric patients. Doulas are not licensed providers; therefore, there are no state requirements for doula education. However, DONA International offers a certification program that consists of completing a reading list; completing a workshop of a minimum of 16 hours; and documentation of previous experience in childbirth care by training in childbirth education or midwifery, work experience as a labor nurse, or observation of a childbirth preparation series. After completion of this program, the new doula must provide service to at least three clients and document the births with a 500- to 700word firsthand account of each experience. In addition, the new doula must provide evaluations from three clients, three primary care providers, and three nurses or midwives. Doulas do not provide clinical care to the mother. They do not make clinical decisions or offer opinions that might influence their clients’ decisions. A doula that is also a midwife, nurse, or another care provider, cannot function in those roles while serving as a client’s doula. Their primary role is emotional support of the mother, and facilitating positive communication between the mother, her nurses, midwives, and physicians. They maintain continuous presence during labor and help the mother’s

partner be part of the experience. Although many doula clients do not want regional anesthesia for labor, a significant number of patients still expect or decide to receive a labor epidural for pain relief. It is important for the anesthesia provider taking care of these patients to interact with the patient and the doula. Patients with doulas must consent to having the doula present for confidential medical discussions. The doula will expect to be in continuous attendance with the mother, and this should be respected unless there are medical or hospital policy rules that do not allow it. Doulas can be helpful to the anesthesiologists and nurse anesthetists, often comforting the mother during the placement of the regional block and maintaining communication patterns between the patient, the nurses, physicians, other caregivers, and the partner during labor. If a patient needs cesarean section, the doula should be included in the discussion and planning made to accommodate the doula in the operating room, if feasible. In the case of urgent cesarean section requiring a general anesthetic that precludes doula presence, the situation should be discussed with patient and doula, and all efforts made to preserve the team approach for delivery of the baby and to maintain respectful interactions. In summary, doulas can provide obstetric patients with excellent emotional support and increase the mother’s satisfaction with her birth experience. It is important for anesthesia providers to understand the doula’s role and incorporate the doula into the overall care plan, so that patients who choose doulas can have an optimal birth experience. TAKE HOME POINTS Take the time to understand the doula’s role in childbirth. Respect the mother’s choice in choosing a doula to participate. Introduce yourself to both the patient and the doula. Maintain respectful and professional interactions throughout the care of the patient. Learn the policy of your labor unit concerning doulas. If you are an OB anesthesia trainee, make sure to ask your teaching faculty about their experience and advice pertaining to doulas. Make patient care decisions and recommendations as you would with any patient in labor. Your standard of care does not change with patients using doulas. The parturient is the doula’s client, but your patient. And remember, be respectful always. Suggested Readings

Camann WA. Doulas—who are they and how might they affect obstetrical anesthesia practices? Society of Anesthesiologists Newsletter. 2000;64:11–12. DONA International website. Available at: www.dona.org. Accessed October 30, 2014. Meyer BA, Arnold JA, Pascali-Bonaro D. Social support by doulas during labor and the early post partum period. Hosp Physician. 2001;57–65.

244 Guests on the Labor Deck and in the Delivery Room—How to Manage It and Keep Your Professional Demeanor Christopher E. Swide, MD

The labor and delivery suite is one of the few places in the hospital where family and friends are almost universally present during procedures that are fraught with risk (the other being the induction of pediatric patients with the parent present). The obstetric anesthesiologist must have not only the clinical skills to deal with the medical management of parturients but also the social and communication skills to manage guests. In the obstetrics environment, the patient’s family and friends are often in the immediate vicinity. They can be distracting to care providers and may become stressed themselves by witnessing emergency care procedures. Unlike other chapters in this book that address anesthetic emergencies, this chapter focuses on methods for handling the potential repercussions of managing anesthetic emergencies in the presence of guests. And, as we discuss below, to be successful at this aspect of clinical practice, the anesthesia provider must view the obstetric nursing staff as true partners and valued allies for a good interaction with the patient and her guests. Every anesthesia provider must develop a practice model concerning guests. It is important that this model meet the needs of all “clients” (mothers-to-be, family and guests, the baby, the obstetrician, and the labor and delivery nurses) as well as his or her own needs. Fortunately, there is help available in handling these situations: 1) Follow institution policies. Hospital policies govern who can be in the delivery room or operating room (OR), and include processes of limiting access for medical cause as determined by the obstetric and anesthesia providers. Do not go outside your institution’s policies for any reason. 2) Communicate with the labor nurses. The nurses taking care of the patient often have a good understanding of the relationship dynamics of the patient’s family and friends. Thus, the nurses can provide excellent advice on how to best broach the subject of presence during procedures. It is also important that the nurses, physicians, and other

providers on the unit make a unified decision. 3) Communicate with the obstetric provider. The obstetric provider can be invaluable in helping the patient and her guests understand that the people she selected to be present at her delivery may be asked to leave the room if the care management plan necessitates it. 4) Communicate with the patient. Discuss the potential of asking guests to leave the room if necessary during a procedure as part of the basic patient interview. It is the author’s practice to always discuss this and to make sure the guests know that it is in the best interest of the patient. 5) Always remain calm and professional. Even in the midst of a real emergency or with an angry patient or guest, this is an important rule. If you must ask a guest to leave, try to frame it in terms of being able to best help the mom and the baby, rather than making it a contest of wills or control struggle. 6) Use the institution’s patient advocate . Patient advocates are trained professionals who are invaluable in dealing with stressed and angry patients, family members, and health care providers. These advocates can be used if the previous strategies are ineffective. This step almost always works to avoid utilization of the last step, which is activation of the security team. If all else fails, and if the anesthesia provider believes that guest presence puts the patient (or the provider) at risk, the last step is calling in the institution’s security team to escort the guests from the scene. Proper preparation and utilization of the other techniques almost always solves the problem before the need for security.

Helpful Hints for Managing Guests These tips are considered reasonable by most obstetric anesthesia providers. Before the start of care: You MUST check privately with the mother-to-be regarding her desire for guests in general as well as individual guests in particular. Remember that parturients are emancipated minors. So no matter what the patient’s age is and regardless of her cultural background or family situation or any other factor, she has the absolute legal right to a private conference with her care providers and to make an autonomous medical decision for herself about her care, including her guests. Private conversations with the mom-to-be should be witnessed by another medical provider.

Exceptions to this practice rule will be extremely rare, for instance in the unfortunate situation of a parturient who has a significant pre-existing cognitive disability. Try to ascertain how much medical knowledge the guest has. Sometimes guests with a degree of medical knowledge may have control issues. In discussion with guests, always mention that the pace can quicken even in routine deliveries and find out how people will feel about being asked to step out. There are warning signs that may predict for a difficult or disruptive guest: confrontational and angry interactions with staff, poor interactions with the patient, and poor communication skills. Do not allow these people in the room in the first place. Exercise caution in allowing “guests to support guests.” This situation sometimes arises with when the couple having the baby are themselves very young—for example, an older female family member might request to be in the room to support a teenaged father or the other very young mother. This is felt by obstetric anesthesia providers to be a somewhat gray area. Allow it only if you feel the extra person(s) will help the care team better care for the patient.

For the Labor and Delivery Rooms There is no real limit on the number of support people except for space. The nurses will often help provide crowd control in the labor rooms, so things do not get out of hand. Usually everyone except one person is asked to leave during procedures; however, anesthesia providers may reserve the right to have all guests leave the room if the epidural is anticipated to be difficult. Guests must sit! There are no exceptions to this. Guests must also remain in front of the patient, so that means that a guest should never act as the “holder” for an epidural. The sitting parturient may place her feet on the knees of the sitting support guest during epidural placement if that is comfortable for the patient and her guest.

For the OR Usually only one person is allowed in the OR for C sections, sometimes more if the anesthesia provider has met them and agreed beforehand to have them as guests. Guests may come and go from the OR only with an escort. Have a prearranged method to get a guest who gets woozy out of the delivery room. Remember that it is possible to faint from a chair—one of the editor’s brother fainted at the operative delivery of his third child, having sailed through the birth of his first two children without so much as a blink. After the baby is delivered, guests may approach the baby warmer only if the okay is given by the delivery team (including the pediatric team, if they are there). Usually no guests are allowed in the OR until the block is in and working. However, a

support person can occasionally be allowed into the room for the block, if the anesthesia providers believe that it may help them do their job more efficiently.

In General Guests must be a minimum of 18 years of age to be in the room for C sections (unless the guest is the father of the baby). There is no age minimum for labor and delivery rooms. Expect as you gain experience that your practices will both loosen and tighten. This author has loosened up on the number of people in the OR, provided they do not interfere with the tasks of the anesthesia team, but tightened up about moving guests out if needed and very much tightened up about only one support person for labor epidurals and no videotaping of procedures. The doula is a member of the patient’s care team and does not count as a guest. Cell phones are now everywhere in the clinical environment. At our institution, some practitioners encourage the spouse/partner to bring a cellphone into the OR to take pictures of the baby immediately after delivery. However, planned cellphone use should be reviewed before an operative delivery, as the obstetrician may have also had a discussion with the patient and her guest. A final note from F. Jacob Seagull, PhD : Successful obstetric anesthesia providers instinctively use a human factor approach for the management of guests in the obstetric suite. In other words, you will do well to create an environment in which expectations are clear, and plans are discussed in advance. Doing this means that when the time comes, you will be activating an existing plan, not explaining a new plan, managing expectations, explaining your actions or trying to calm worried guests. By discussing the actions beforehand, you can address any questions while everyone is calm. You can effectively “offload” the bulk of the tasks involved in getting people out of the labor and delivery rooms to your low-workload times. This offloading is what experienced anesthesia providers do in planning any difficult case, by preparing in advance for contingencies. Tell the guests that they may be asked to leave for a number of reasons pertaining to the ongoing management of the patient (noise level too high, arrival of extra care team providers, need to treat the patient for non–life-threatening events such as vomiting, a new peripheral IV, etc.), but that are not indicative of a true crisis. Guests will have a cognitive framework of the range of possible circumstances in which they might be asked to leave, and therefore may not assume the worst. They will be happy to “implement a plan” when the time comes; you will be happy that you don’t have to explain the situation. The goal is to try to arrange a win–win situation.

TAKE HOME POINTS Utilize as many sources as possible in developing your practice in managing guests on the Labor and Delivery deck and the OB operating room. Start with your hospital’s policies, always. Talk to and learn from senior colleagues and more experienced providers on the physician and nursing sides on how they have handled these situations—what has worked and what hasn’t. Acknowledge and accept that your practice will change as you become more experienced. The final decision is yours after consultation with the patient. The wishes of the other medical providers and the family come second. Don’t let a “problem” guest in the room to start with. Guests must sit and be escorted into and out of the room. Guests should never be pressed into the medical care of the patient. The “fainting stories” are not just folklore. All kinds of guests have been known to faint while supporting a parturient, even during epidural placement. This includes experienced medical professionals, combat veterans, and public safety personnel who have been present at many bloody trauma scenes, such as state police officers and firefighters. Unfortunately, lawsuits have resulted. Never lose your cool. Suggested Readings Altendorf J, Klepacki L. Childbirth education for adolescents. NAACOGS Clin Issu Perinat Womens Health Nurs. 1991;2(2):229–243. Kantor J. Move over, doc, the guests can’t see the baby . 2005, New York Times. www.nytimes.com/2005/09/11/national/11birth.html?.

245 Alternatives to Epidural Analgesia for Labor Pain—What to Consider, What You Might Be Asked Karen Hand, MB BS FRCA

Epidural analgesia is widely used in the United States and other developed countries, with approximately 60% of women overall receiving an epidural and even higher numbers for first babies. Neuraxial analgesia is generally very safe but there are circumstances in which its risks are increased or when it is contraindicated. Although neuraxial analgesia is generally popular among laboring women, many wish to use alternative methods of analgesia. Providing safe and effective analgesic techniques for women not desiring, or unable to have an epidural, may improve maternal satisfaction with labor analgesia. Having effective alternative techniques may also reduce the temptation to take risks with epidural analgesia. If your bottom line for platelet count is 75, what do you do with a platelet count of 70? If you know your patient has Harrington rods down to L5 are you going to try a neuraxial technique? It’s good to have an alternative. There is a range of very low-risk approaches to labor analgesia including psychological techniques such as emotional support, meditation, and breathing techniques. The water bath, massage, and aromatherapy may also be used. Midwives use interventions such as sacral saline injections and TENS stimulation. However, this chapter will focus on three techniques which may be considered intermediate in terms of potential efficacy, labor intensity, and medical involvement—remifentanil patientcontrolled analgesia (PCA), nitrous oxide analgesia, and acupuncture.

Remifentanil PCA Remifentanil is an ultra–short-acting synthetic opioid. It is generally given by infusion. However, for labor analgesia it may be administered via PCA as a small bolus dose, either with or without a background infusion. It has become the opioid of choice in many centers for use with a PCA when an epidural is contraindicated. Opioids have been the mainstay of labor analgesia in the past having the advantages

of being cheap and readily available. Their disadvantages include their limited efficacy for labor pain and side effects for both the mother and baby, particularly respiratory depression. To avoid respiratory depression in the neonate, opioids must be limited close to delivery. Meperidine has traditionally been the opioid of choice for labor analgesia, with less risk of respiratory depression, although as an alkaline drug there is a risk of ion trapping and accumulation in a distressed, acidotic fetus. Labor pain in the first stage is experienced primarily during contractions. Remifentanil PCA may effectively treat the pain of contractions without the risks of longer-acting opioids, particularly accumulation in the fetus. It has the advantage of offering the mother an element of control over her pain. Remifentanil PCA is administered as a bolus dose of, for example, 0.25 to 0.5 mcg/kg with a lockout period of 2 minutes. A background infusion can be added, with rates of, for example, 0.025 to 0.05 mcg/kg/min. An infusion may increase the efficacy of remifentanil but may also increase the risks. The risks of remifentanil infusion include maternal bradycardia and respiratory depression. Maternal deaths have been reported, as has neonatal respiratory depression. Remifentanil PCA requires careful monitoring and staff training. It is generally considered as an alternative when neuraxial analgesia is contraindicated, rather than as an attractive option in itself. It has been described negatively as “a poor man’s epidural.”

Nitrous Oxide Nitrous oxide is an anesthetic gas which is widely used worldwide in subanesthetic concentrations for labor analgesia. Its use is reemerging as an option for labor analgesia in the United States. It is popular among midwives and their patients. It is perceived as a safe and relatively simple option. For women desiring an “unmedicated birth” it may be viewed differently from other drugs. Nitrous oxide for labor analgesia is administered by face mask or mouthpiece as a 50% mix with oxygen, utilizing a demand valve opened by inspiratory effort. The mother is instructed to take deep breaths at the onset of the contraction as she feels it begin to build, because the analgesia is slightly delayed. It is important that she stop inhaling nitrous oxide between contractions and that she holds the mask herself. Advantages of nitrous oxide include that it is relatively safe in the 50:50 mix, with little risk of sedation. It is relatively cheap and easy to administer. It has a quick onset and offset of action, so can effectively treat the pain of contractions without accumulating in the mother or fetus. It offers the woman a sense of control over her own analgesia. There are some contraindications to nitrous oxide analgesia. Nitrous oxide is more

soluble than nitrogen so accumulates and expands air-filled spaces, so must be avoided in a woman with, for example, a pneumothorax, or some types of recent eye or ear surgery. A woman who cannot hold the mask herself should not use nitrous oxide. Nitrous oxide interferes with B12 metabolism so should be avoided in a woman with confirmed B12 deficiency. Nitrous oxide has some disadvantages. It’s efficacy for labor analgesia is limited compared to neuraxial analgesia. It is probably best compared to opioids in terms of analgesia; however, this may be adequate for many women. Nitrous oxide may exacerbate hypoventilation and desaturation between contractions. Nitrous oxide may be less helpful than epidural analgesia for the woman desiring an unmedicated birth who becomes exhausted. For women at high risk of cesarean section or at high risk of complications, if general anesthesia is required, an epidural has the advantage that it can be used for anesthesia. Nitrous oxide is a potent greenhouse gas, with an effect on the atmosphere 100 times that of carbon dioxide. There are also concerns about its potential adverse effects on hospital staff. There have been reports of increased rates of abortion in exposed hospital staff, although studies have not confirmed this. Nitrous oxide must be effectively scavenged. It may be expensive to install built-in scavenging to a labor and delivery suite. There are nitrous oxide and oxygen delivery devices available which utilize standard wall suction for scavenging. Despite its widespread use worldwide, there are few randomized controlled trials of nitrous oxide labor analgesia and no studies of its long-term effects on the fetus. Apoptosis of developing neurons as a result of exposure to anesthetic agents is a current concern under investigation. A detrimental effect of fetal exposure to nitrous oxide during labor cannot currently be excluded.

Acupuncture Acupuncture is a complementary medical modality, which is widely used in the United States and Europe, as well as in China, its historical home. Acupuncture has a growing body of research behind it. It is very popular, with 6% of the US population having used it for various ailments. Theoretically, acupuncture is an ideal adjunct for analgesia in labor because it is relatively free of side effects and may have beneficial effects on the progress of labor, although in the framework of Western medicine, the placement of needles at points seemingly unconnected to the neuroanatomical pain pathways may seem bizarre. Acupuncture involves placing fine needles at specific anatomical points, with a view to influencing the circulation of “chi” or “qi.” “Qi” is a term used in traditional Chinese medicine which does not have an equivalent in Western medicine, but is something like

life force, or energy, which circulates in specific channels or meridians. Diagnosis and selection of acupuncture points can be taken to a high art. However, at a basic level, a limited number of points known to be beneficial in labor can be used effectively. The research data on acupuncture for labor analgesia are mixed. A Cochrane review of labor analgesia placed acupuncture and acupressure in the “maybe” group in terms of evidence of efficacy. However, there is high-quality evidence supporting the efficacy of acupuncture for some other indications of interest to anesthesiologists, particularly prevention of postoperative nausea and vomiting, which suggests that further research for acupuncture in labor is warranted. Acupuncture research is hampered by our lack of understanding of how acupuncture works. Studies often include a “sham” arm, although there is a lack of agreement on how to use “sham” acupuncture in a way which will clearly delineate placebo effects. Some will argue that there is already sufficient evidence that acupuncture is more than placebo, and that study of acupuncture in comparison with other accepted treatments is more helpful. Studies vary in terms of the acupuncture points chosen, whether or not electrical stimulation is used, the duration of treatment, and the setting and personnel providing the treatment; so it is hard to evaluate the sum of evidence. For labor analgesia, pain scores may not tell the full story. Maternal satisfaction and coping scores may be more helpful. What we do know is that acupuncture affects release of endogenous opioid, as well as oxytocin. There is evidence that acupuncture delays the time to request for epidural analgesia, and that women using acupuncture would choose to do so again. Acupuncture was found to be inferior to sacral saline injections, although this technique may actually be acting on sacral acupuncture points. There are various ways to provide acupuncture for labor analgesia in the hospital setting. In the United States, most acupuncture in the community is performed by specialists in Traditional Chinese Medicine, known as licensed acupuncturists. Many women utilize the services of licensed acupuncturists during pregnancy, whether for nausea, carpal tunnel syndrome, breech presentation, or initiation of labor. In some settings it may be possible to enable women to have their licensed acupuncturist accompany them into the delivery suite, in the same way that they are accompanied by their chosen doula. Other hospitals may employ licensed acupuncturists to provide a similar service. In the United States, in most states, physicians are able to train to provide acupuncture, with a minimum of 200 hours of additional CME training. However, most of us who have done this training don’t find it practical to be on-call for acupuncture for labor analgesia. This will not usually be a cost-effective way of utilizing the skills of an anesthesiologist, and the financial remuneration is far less than for anesthesia services. In our hospital we have an innovative program which allows

anesthesiologists to train and be accredited in very limited, single-point acupuncture for the prevention of postoperative nausea and vomiting. We have ongoing studies of simple one- or two-point acupuncture for a variety of perioperative indications. A training and accreditation program allowing staff who are already present on the labor and delivery suite to provide a limited acupuncture service may be a practical option, whether that is the obstetric anesthesiologist, or if regulations allow, midwives or nursing staff.

Figure 245.1. Acupuncture at the LI 4 point.

For a simple approach to acupuncture for labor analgesia there are two points which are commonly used: LI 4 (Hegu): This point is located at the base of the anatomical snuff box—on the dorsum of the hand, between the first and second metacarpals, approximately in the middle of the second metacarpal bone on the radial side (Fig. 245.1). The needle is inserted to a depth of 0.5 cm. SP 6: This point is located on the spleen meridian and is an empirical point located about one hand-breadth above the medial malleolus. It is especially useful in difficult labor. It may also aid in cervical dilatation. It is needled with a perpendicular or oblique proximal insertion.

Acupuncture is relatively low risk but is not without complications, including the risk of infection and damage to underlying structures such as the pleura, bowel, and nerves, depending on point location. TAKE HOME POINTS Many women can’t or won’t consider epidural analgesia for labor. This is sometimes caused by a previous negative experience. Women are informed consumers of labor analgesia—assume that your patients would have read about and talked to women who have received a number of different complementary and alternative treatments for labor pain. Many of these treatments will provide only low-level relief. Remifentanil PCA, nitrous oxide, and acupuncture may all be welcome alternatives to labor analgesia for some women. Remifentanil is given in small boluses as a PCA modality. Risks include maternal hypoventilation and death, and fetal bradycardia and respiratory depression. Nitrous oxide is given via mask at the start of a contraction. The patient must be able to hold the mask herself. Scavenging of waste nitrous oxide is required. Risks include hypoventilation and desaturation between contractions, unknown fetal sequelae, and risks to the exposed hospital staff. Acupuncture is a modality that is now firmly established within the confines of Western medicine especially as a complementary technique. Two points that are of special efficacy for the laboring parturient are the hand point LI 4 (Hegu) and the ankle point S6. Make sure you have posed the appropriate questions about these modalities to your institution before the patients pose them to you. You don’t want a patient to come in and tell you about what’s new in labor analgesia. Suggested Readings Jones L, Othman M, Dowswell T, et al. Pain management for women in labour: An overview of systematic reviews. Cochrane Database Syst Rev. 2012;(3):CD009234. Likes FE, Andrews JC, Collins MR, et al. Nitrous oxide for the management of labor pain: A systematic review. Anesth Analg. 2014;118(1):153–167. Muchatuta NA, Kinshasa SM. Remifentanil for labor analgesia: Time to draw breath? Anaesthesia. 2013;68(3):231–235.

246 Epidural Labor Analgesia: Does It Prolong Labor? Remigio A. Roque, MD and Brandon Michael Togioka, MD

Epidurals are a popular and effective choice in the management of labor pain. Various forms of neuraxial analgesia have been used in childbirth since the late 19th century. One of the first described neuraxial anesthetics involved intrathecal injection of cocaine to produce total anesthesia of the lower body. Since that time, the practice has evolved greatly. Advancement in both technique and local anesthetic formulations has provided safer, better-controlled, and more effective epidurals, a fact reflected in their increased use. However, despite their popularity and common use, several questions remain. How do epidurals affect the progression of labor? Do epidurals increase the rate of cesarean and instrumental delivery? Does it matter when epidural analgesia is administered or what concentration of local anesthetic is used? Labor is defined as regular uterine contractions that bring about demonstrable effacement (i.e., thinning) and dilatation of the cervix. While it is not usually difficult to determine if someone is in labor, it can be quite hard to know exactly when labor started and thus challenging to determine the duration of labor. Labor is defined by three stages. The first stage of labor encompasses the period of cervical effacement and dilatation. It can be further divided into two phases—a latent phase, in which regular uterine contractions start to cause cervical thinning and dilation, and an active phase when the rate of cervical dilation speeds up. Previously, the transition from latent to active labor in the United States was set at 4 cm, but in an effort to decrease the number of cesarean sections called for failure to progress, the transition point was moved to 6 cm. The active phase of the first stage of labor ends when the cervix has fully dilated to 10 cm. The second stage of labor encompasses the period of fetal expulsion—beginning when cervical dilatation is complete and ending with delivery. The third stage of labor encompasses the time following delivery during which there is placental separation and expulsion. Determining the impact of epidurals on the stages of labor is difficult. There is a clear association between the use of neuraxial anesthesia and prolonged labor, cesarean

delivery, and instrumental vaginal delivery (i.e., using a vacuum or forceps to deliver a baby). However, a causal relationship is not clear. The unpredictable and individualized nature of labor makes it difficult to design and perform randomized controlled trials (RCTs). Ideally, an RCT studying the effect of epidurals on labor would contain a control group that did not receive any analgesia, a requirement that would not get IRB approval. Additionally, study groups are hard to maintain as crossover rates are high—both from the control group to the epidural group (e.g., worsening pain, dystocia) and from the experimental group to the control group (e.g., rapid labor that does not allow time for an epidural). Double-blinding is also near impossible as epidurals have repeatedly been shown to offer superior pain control and often some degree of leg weakness making it fairly obvious which intervention a patient has received. To this extent, there may not be a definite answer with regard to the effect of epidurals on labor, but there is still much that we can tell our patients. There are no RCTs examining the effect of labor epidurals in which the primary outcome is the duration of the first stage of labor. When RCTs looked at the duration of the first stage of labor as a secondary outcome prolongation was generally seen. While the mechanism for epidurals prolonging the first stage of labor is still unknown many experts believe it has to do with an imbalance in the autonomic nervous system. It is postulated that epidural analgesia may slow labor by blocking parasympathetic (laborpromoting) outflow without fully interrupting the sympathetic (tocolytic) innervation to the uterus. At this point, it can only be said that epidurals may prolong the first stage, and the effect is likely to be modest—around 30 minutes. In contrast, there is little doubt that epidural analgesia extends the second stage of labor. The American College of Obstetrics and Gynecology (ACOG) allows for an extra hour of pushing to occur in patients who have received an epidural before diagnosing a prolonged second stage of labor. Similar to studies on the first stage of labor, it is impossible to complete an ideal study on the second stage of labor. In an ideal study, the epidural would be placed at 10-cm dilatation so as not to have a carryover effect from the first stage, there would be a control group without any analgesia, and oxytocin usage would be kept similar between study arms. Again, despite imperfect science it appears that the average prolongation is around 15 minutes when compared to patients receiving systemic opioids. The mechanism behind this protraction is not known, but several possibilities have been suggested. It may be that having complete analgesia during the second stage decreases maternal pain to the point that it decreases the urge to bear down and push. Additionally, if high concentrations of local anesthetic are used in the epidural the abdominal and pelvic floor musculature are weakened leading to impaired maternal expulsive efforts and impaired fetal rotation during descent. The delay in second stage has not been shown to be harmful to either

mother or baby as long as routine monitoring and labor management are continued. With respect to the last stage of labor, epidurals do not increase the time for delivery of the placenta. In situations of spontaneous or expressed placental delivery, there appears to be no difference in the duration of the third-stage labor. However, in cases where manual extraction is required, use of epidural anesthesia shortens the process by several minutes. It may be that use of epidurals in these cases provides a permissive effect, allowing providers to intervene earlier under the safeguard of good perineal analgesia. With these aforementioned consequences of epidural use on labor progression, it would be reasonable to presume that epidurals might also impact the mode of delivery. The first studies on this topic showed an association between neuraxial anesthesia and increased rates for both instrumental and cesarean delivery. As previously discussed, optimal studies are hard to design and are limited by several factors. In this case, the association of dystocia (difficult labor) with higher rates of cesarean and instrumental delivery cannot be overlooked. The intensity of labor pain has been shown to impact the rate of cesarean delivery. Lower rates of spontaneous vaginal delivery and higher rates of cesarean delivery have been observed in women who required higher doses of IV analgesia throughout their labor. Additionally, these women rated their pain subjectively higher prior to the administration of analgesia, and the indication for progressing to cesarean section was more often for dystocia. It has also been observed that women with more breakthrough pain, despite receiving epidurals, are at increased risk of operative delivery. To this extent, a request for an epidural may serve as a marker for the severe pain associated with dystocia, which is itself a risk factor for having a cesarean or instrument-assisted delivery. No RCTs have been designed to specifically look at the effect of epidural analgesia on the rate of instrumental delivery as a primary outcome. Furthermore, most studies that have been completed do not define the criteria used for proceeding with instrumental delivery, making it difficult to discern if obstetrician bias may have effected the decision to use forceps or a vacuum. The available data are conflicted, with some studies showing increased rates of instrumental delivery with an epidural and others showing no difference. This discrepancy may be explained in part by differences in the concentration of local anesthetic used. Epidurals with higher concentrations of local anesthetic produce a denser block that results in more complete analgesia in the second stage which can decrease the urge to push. Higher local anesthetic concentrations will also cause more abdominal and perineal muscle weakness which can slow down fetal descent. Thus, it is not surprising that studies involving epidurals containing higher concentrations of local anesthetic are more likely to show that epidurals increase the rate of instrumental delivery.

The question pregnant women are often most interested in is whether epidurals increase their chances of having a cesarean section. Early studies demonstrated significant increases in the rate of cesarean delivery when women were given an epidural. However, large meta-analyses have since shown this not to be true. Initial studies also suggested that the risk of cesarean was higher when epidurals were administered during the latent phase of the first stage of labor (i.e., at a cervical dilation less than 4 cm). As a result, previous statements by ACOG recommended for practitioners to delay administration of epidural anesthesia until cervical dilatation reached 4 to 5 cm. Multiple well-conducted studies have now shown that early epidurals (i.e., epidurals placed before a woman is 4 cm dilated) do not increase a woman’s risk of having a cesarean section. ACOG has since adjusted its statement, concluding that: “Neuraxial analgesia techniques are the most effective and least depressant treatments for labor pain.” “There is no other circumstance where it is considered acceptable for an individual to experience untreated severe pain, amenable to safe intervention, while under a physician’s care. In the absence of a medical contraindication, maternal request is a sufficient medical indication for pain relief during labor.” “The fear of unnecessary cesarean delivery should not influence the method of pain relief that women can choose during labor.” TAKE HOME POINTS Epidurals are a popular, safe, and effective choice for managing labor pain. There are clear associations between use of neuraxial anesthesia and both prolongation of labor and higher rates of instrumental and cesarean delivery. It is very difficult, however, to make causal statements regarding these effects. Epidural use may prolong the first stage of labor by 30 minutes and the second stage of labor by 15 minutes. This delay by itself has not been shown to worsen maternal or fetal outcomes. If manual extraction of the placenta is needed, having an epidural makes the process faster. The request for an epidural may serve as an indicator of dystocia which by itself increases a woman’s chances of having an instrumental or cesarean delivery. Epidurals may increase the rate of instrumental delivery. The effect of an epidural on risk for instrumental delivery is likely dependent upon the concentration of local anesthetic run through the epidural. Epidural use does not impact the rate of cesarean delivery, regardless of when it is administered.

According to ACOG, maternal request is a sufficient indication for pain relief during labor in the absence of other medical contraindications. Suggested Readings Alexander JM, Sharma SK, McIntire DD, et al. Intensity of labor pain and cesarean delivery. Anesth Analg. 2001;92(6):1524–1528. American College of Obstetricians and Gynecologists Committee on Obstetric Practice. ACOG committee opinion. no. 339: Analgesia and cesarean delivery rates. Obstet Gynecol. 2006;107(6):1487–1488. Leighton BL, Halpern SH. The effects of epidural analgesia on labor, maternal, and neonatal outcomes: A systematic review. Am J Obstet Gynecol. 2002;186(5 Suppl Nature):S69–S77. Leighton BL, Halpern SH, Wilson DB. Lumbar sympathetic blocks speed early and second stage induced labor in nulliparous women. Anesthesiology. 1999;90(4):1039–1046. Marucci M, Cinnella G, Perchiazzi G, et al. Patient-requested neuraxial analgesia for labor: Impact on rates of cesarean and instrumental vaginal delivery. Anesthesiology. 2007;106(5):1035–1045. Rosaeg OP, Campbell N, Crossan ML. Epidural analgesia does not prolong the third stage of labour. Can J Anaesth. 2002;49(5):490–492. Sharma SK, McIntire DD, Wiley J, et al. Labor analgesia and cesarean delivery: An individual patient metaanalysis of nulliparous women. Anesthesiology. 2004;100(1):142–148; discussion 6A. Wong CA, Scavone BM, Peaceman AM, et al. The risk of cesarean delivery with neuraxial analgesia given early versus late in labor. N Engl J Med. 2005;352(7):655–665.

247

We Were Taught Once a C-section, Always a C-Section … What to Do When Your Hospital Now Wants to Provide Trial of Labor After Cesarean (TOLAC) Services Jordan B. Johnson, MD and James S. Hicks, MD MMM

Providing anesthesia services in the obstetric setting is a necessary and virtuous endeavor. The peripartum period for women is a time filled not only with intense emotional experiences but also with decisions regarding their birth process and the medical implications of labor and delivery. For many women and their families the peripartum period is straightforward, allowing for a pleasant patient–anesthesia provider relationship involving primarily labor analgesia. However, for some patients, personal preference and medical risk factors influence the patient–anesthesia provider relationship to an unexpected and significant degree. These outside-the-average situations can involve consideration of surgical anesthesia and resuscitation and even force the clinical and administrative reviews of each hospital’s capability to provide certain services. The marketing of hospital services has become an increasingly obvious phenomenon in recent years. Obstetric services in particular have often held the spotlight given their potential to produce happy patients and multigenerational allegiance. Posh facilities with luxurious amenities, excellent anesthesia coverage, and “walking” epidurals typify the lengths to which hospitals go to attract patients. Increasingly, the ability to provide a trial of labor to patients who have had a previous cesarean section (TOLAC) has become another service that administrators (and sometimes, but not always, obstetric providers) wish to offer. Recent published work has shown that, in certain high-risk populations of women who had a previous cesarean section, over 80% of them elected to have a repeat cesarean section. But, of course, this means that up to 20% of these high-risk, previous cesarean patients choose to undergo a trial of labor. Importantly, only two-thirds of these patients attempting a high-risk trial of labor were successful, at having a vaginal birth after cesarean (VBAC). The most recent practice bulletins for TOLAC issues by the American Congress of Obstetricians and Gynecologists were in 2010. These bulletins emphasize ACOG’s recommendations regarding the patients for whom TOLAC is appropriate as well as risk factors for an unsuccessful trial. ACOG strongly recommends (level A) that most women who have had a single previous low transverse cesarean delivery should be offered and counseled regarding TOLAC and VBAC. They also identify multiple other clinical risk factors for decreasing the likelihood of a successful TOLAC, with which

anesthesia providers should be familiar: multiple previous cesarean deliveries, fetal macrosomia, >40 weeks of gestational age, previous low vertical incision, maternal obesity, non-white ethnicity, short interpregnancy interval, and pharmacologic induction with prostaglandins. There must be a system in place for identification and recognition of these factors in patients attempting TOLAC so as to be prepared to provide surgical anesthesia in a safe and timely manner. This is necessary because a greater risk of major maternal morbidity, including uterine rupture, associated with TOLAC is most often manifested at the time that TOLAC has failed and a repeat cesarean delivery is required. TOLAC is one example of a clinical scenario at the focus of a joint statement from both the American Society of Anesthesiologists (ASA) and ACOG. They recognized the need to have established Optimal Goals of Anesthesia Care in Obstetrics, originally published in 2007 and amended in 2010. These goals are summarized as follows: 1) A credentialed anesthesia provider needs to be available to administer an obstetric anesthetic when necessary. 2) A credentialed anesthesia provider needs to be available at any time to support vital functions in the event of an obstetrical emergency. 3) Credentialed anesthesia and surgical providers need to be available to begin a cesarean delivery within 30 minutes of the decision to do so. 4) Because of the increased risk of major morbidity (e.g., uterine rupture) associated with TOLAC, appropriate facilities and personnel should be immediately available, and when these are deemed not immediately available the decision to move forward with TOLAC should only be made after the patient has been informed of the risks. 5) An appointed physician in anesthesia should be readily available for all anesthetics administered. For larger centers having high obstetric volumes, the requirement for immediate availability is often easily met by current practice in which anesthesia and obstetric providers are always in-house. For lower volume facilities, however, maintaining immediately available anesthesia and obstetric capabilities over the course of an extended labor can prove practically and financially infeasible. Language in Optimal Goals of Anesthesia Care in Obstetrics is not prescriptive for the manner in which such hospitals elect to meet these recommendations, acknowledging that individual circumstances must dictate when a TOLAC approach is safe and practical.

TAKE HOME POINTS Many women who have had a previous low transverse cesarean section can have a successful trial of labor resulting in vaginal delivery, and may choose this as their preferred labor method. Hospitals should remain sensitive to requests by individual patients for TOLAC and attempt to accommodate these requests whenever possible. Certain risk factors should be identified that predispose patients to having a failed TOLAC, which carries a higher risk of major morbidity. The decision by hospitals and patients to attempt a TOLAC should be made only after both parties understand the individual hospital’s capability to fulfill the provisions in Optimal Goals of Anesthesia Care in Obstetrics. One of the staples of a well-functioning obstetric anesthesia program is the ability of qualified anesthesia providers to work alongside the obstetric physicians and nurses to timely provide surgical anesthesia. In addition, the teamwork approach involving coordinated identification of patients with risk factors which increase the likelihood of requiring surgical anesthesia is paramount. Suggested Readings American Congress of Obstetricians and Gynecologists. Practice Bulletin. Vaginal Birth After Previous Cesarean Delivery. Number 115, August 2010. ASA House of Delegates. American Society of Anesthesiologists Optimal Goals for Anesthesia Care in Obstetrics. Park Ridge, IL: American Society of Anesthesiology; Approved by ASA House of Delegates October 17, 2007 (last amended October 16, 2013). Macones GA, Peipert J, Nelson DB, et al. Maternal complications with vaginal birth after cesarean delivery: A multicenter study. Am J Obstet Gynecol. 2005;193:1656–1662. Regan J, Keup C, Wolfe K, et al. Vaginal birth after cesarean success in high-risk women: A populationbased study. J Perinatol. 2015;35:252–257. Epub ahead of print. 23 October, 2014.

248 Should We Place a Spinal for a Version? Anesthesia for External Cephalic Version Angela Pennell, MD and Brandon Michael Togioka, MD

Breech presentation affects 3% to 4% of term pregnancies. Because a fetus is more likely to be safely delivered vaginally from the vertex position, external cephalic version (ECV) is a technique used by obstetricians to change the presentation of the fetus from breech to vertex. The procedure is performed as follows: The obstetrician will apply something over the abdomen (corn starch or gel) to facilitate smooth sliding of their hands over the patient’s abdomen. The obstetrician will then place their hands behind the mother’s pubic symphysis to pull the baby out of the pelvis. The obstetrician will then attempt to change the baby to a head down position through either a forward or backward somersault. Periodic assessment of fetal well-being either with ultrasound or a Doppler is performed every few minutes. The obstetrician may make multiple attempts at successful version, but their efforts are usually limited to no more than a few attempts. Significant fetal bradycardia and substantial patient discomfort (important for anesthesia) are signs that the ECV should be abandoned. Every attempt at an ECV is essentially a balancing act between the potential advantages allotted from a vaginal delivery and the risks of placental abruption, cord prolapse, rupture of membranes, and fetomaternal transfusion (i.e., fetal blood cells coming into contact with the maternal circulation). Depending upon the study, the success rate from ECV is quite variable from as low at 16% to as high as 100%, with success rates of 50% to 60% commonly quoted to patients. Both obstetric and anesthesia staff acknowledge that the success of an ECV may depend to a considerable degree on the skill and experience of the obstetrician combined with the level of pain tolerated by the patient. That being said, the following factors may be associated with higher rates of ECV failure: maternal obesity, nulliparity, advanced cervical dilation, low station (i.e., a baby that has descended further into the pelvis), and an anterior placenta. The question of whether neuraxial anesthesia (spinal or epidural) facilitates successful ECV has been controversial. However, there is now accumulating evidence

that neuraxial anesthesia likely improves the chance for a successful ECV. There are several prospective trials, retrospective studies, and meta-analyses that have investigated this topic. A Cochrane review from 2015 showed that ECV was more successful when neuraxial anesthesia was combined with a tocolytic versus tocolytic alone. A very recent meta-analysis by Magro-Malosso et al. in the American Journal of Obstetrics and Gynecology found a statistically significant increase in the rate of successful ECV when neuraxial anesthesia was used. Despite these findings, a February 2016 American College of Obstetricians and Gynecologists Practice Bulletin recently stated: “data are insufficient to conclusively…make a recommendation favoring spinal or epidural anesthesia during ECV attempts.” In this manner, the rate of neuraxial blockade for ECV was found to be quite variable across the country with some hospitals noting use of neuraxial anesthesia for all attempts while others stated they never used neuraxial anesthesia for ECV. We believe some of the controversy may be because studies involve different local anesthetic types and concentrations. Interestingly, in the above-mentioned meta-analysis by Magro-Malosso et al., the studies that showed no benefit from neuraxial anesthesia used less dense blocks than the studies that showed benefit. The denser blocks may have allowed for more abdominal muscle relaxation and less maternal pain leading to less guarding and a higher rate of ECV success. So one may ask, why not give everyone a dense block? Well, some obstetric providers hold the belief that a dense neuraxial block can mask the pain that sometimes accompanies a placental abruption leading to delayed recognition and potentially a worse fetal outcome. Furthermore, removing pain as a limiting factor in the procedure may also increase the potential for a greater number of maneuvers and more aggressive attempts. In addition, neuraxial anesthesia carries its own risks: hypotension, infection, paresthesias, bleeding/epidural hematomas, and postdural puncture headaches. If you are told about an ECV, the first question that you should ask is the gestational age of the mother, as this will greatly affect your anesthetic plan. The American College of Obstetricians and Gynecologists recommends offering an ECV to women starting at 37 weeks of gestation. Thirty-seven weeks is recommended because the baby is full term (in case of complications necessitating an emergent cesarean section) and if the ECV is successful a spontaneous reversion back to breech presentation is less likely at later gestations. In addition, amniotic fluid seems to peak at around 34 weeks and some studies show higher rates of ECV success with larger amniotic fluid volumes. At our institution, women at 37 weeks often receive an ECV attempt in a labor room without anesthesia involvement. Women can request a spinal for ECV at 37 weeks, but this decision shifts their procedure to the operating room and significantly prolongs their time in the hospital. For these reasons, most women elect for an anesthesia-free ECV at

37 weeks. If the 37-week attempt is unsuccessful, women are offered a second attempt at 39 weeks with combined spinal–epidural anesthesia in the operating room. If the 39week attempt is successful, the pregnant mother is moved to the labor floor and uses the epidural for analgesia. If the ECV is unsuccessful, we proceed with a scheduled cesarean section. In both cases, tocolysis with terbutaline is considered as ECV success rates have been shown to be higher with tocolysis than without. Any time an ECV is performed, with or without a block, it is prudent to be prepared for an emergent cesarean section. For this reason, ECVs should generally be performed during the daytime when staffing levels are higher and all patients having an ECV require peripheral intravenous access. Remember to have a nonparticulate antacid such as citric acid/sodium citrate, a device to provide left uterine displacement, a smallerdiameter endotracheal tube, and emergency airway equipment available. Most of the time when anesthesia is not on board at the time of a called emergent cesarean section, general endotracheal intubation is necessary; however, it is always worth having a conversation with the obstetricians and potentially checking one last fetal heart rate before proceeding with a cesarean section under general anesthesia. TAKE HOME POINTS ECV is typically performed in term parturients and has a highly variable success rate. Always prepare for an emergent cesarean section when an ECV is being performed, regardless of whether anesthesia will be utilized. We will say this again—don’t assume that an ECV proceeding to an emergent operative delivery is a theoretical concern only. It isn’t. For this reason, even if there isn’t a plan to perform neuraxial anesthesia for the ECV, many institutions have a practice policy that mandates placing decent IV access before starting the ECV procedure. The editors have also trained and worked at institutions that would only undertake ECV if the anesthesia staff was observing the procedure or in the immediate vicinity. There is accumulating evidence that neuraxial anesthesia facilitates successful ECVs. Widespread adoption of ECVs under regional anesthesia has been hindered by concerns that neuraxial anesthesia may mask and possibly predispose toward complications such as placental abruption. The decision to place a spinal or epidural for ECV should be made in concert with the obstetric team and patient after a thorough discussion of risks and potential benefits. Suggested Readings

American College of Obstetricians and Gynecologists (ACOG). External cephalic version. ACOG Practice Bulletin No. 13. Obstet Gynecol. 2016;127(2):e54–e61. Brace RA, Wolf EJ. Normal amniotic fluid volume changes throughout pregnancy. Am J Obstet Gynecol. 1989;161(2):382–388. Cluver C, Gyte GM, Sinclair M, et al. Interventions for helping to turn breech babies to head down presentation when using external cephalic version. Cochrane Database Syst Rev. 2015;(2):CD000184. Kok M, Cnossen J, Gravendeel L, et al. Clinical factors to predict the outcome of external cephalic version: A metaanalysis. Am J Obstet Gynecol. 2008;199(6):630.e1–e7; discussion e1–e5. Magro-Malosso ER, Saccone G, Di Tommaso M, et al. Neuraxial analgesia to increase the success rate of external cephalic version: A systematic review and meta-analysis of randomized controlled trials. Am J Obstet Gynecol. 2016;215(3):276–286. Sultan P, Carvalho B. Neuraxial blockade for external cephalic version: A systematic review. Int J Obstet Anesth. 2011;20(4):299–306. Weiniger CF, Sultan P, Dunn A, et al. Survey of external cephalic version for breech presentation and neuraxial blockade use. J Clin Anesth. 2016;34:616–622.

249 Management of an Accidental Dural Puncture in the Laboring Patient “When the Hanging Drop Becomes a Flowing River …” Dustin McGirr, DO

A 158-kg parturient requests an epidural for labor analgesia. Painful contractions hinder the patient’s ability to remain still during lumbar epidural placement. The procedure is further complicated by difficulty palpating the bony anatomy. After multiple attempts at epidural placement, you finally achieve “loss of resistance” (LOR). Following removal of the LOR syringe, cerebrospinal fluid pours out of the Tuohy needle. What are your options for providing labor analgesia in the setting of an accidental dural puncture (ADP)? What are the specific risks and potential benefits in providing neuraxial anesthesia following an ADP? An accidental dural puncture (ADP) complicates ∼1% of epidural placements in laboring patients. Following recognition of a dural puncture, the practitioner has two options: (1) replace the epidural catheter at the same or (preferably) alternative interspace; or (2) provide continuous spinal analgesia through a catheter threaded into the subarachnoid space. The most appropriate management of an ADP in a laboring parturient is currently unclear. In a recent survey of North American obstetric anesthesiologists, 75% of respondents reported replacing the epidural following an ADP; whereas, 25% placed an intrathecal catheter. Concerns involving central nervous system (CNS) infections and neurotoxicity have hindered universal acceptance of continuous spinal analgesia. Placing a catheter into the intrathecal space provides a direct conduit from the outside environment to the CNS, theoretically increasing the risk of both neurologic infection and injury. In 1992, the United States Food and Drug Administration mandated the withdrawal of intrathecal microcatheters (27G or smaller) due to several cases of cauda equina syndrome. Subsequent investigations suggested that the neurologic injury was a result of direct CNS exposure to large doses of concentrated local anesthesia, specifically, greater than

100 mg of 5% hyperbaric lidocaine. The slow flow rate of hyperbaric solutions through small-bore catheters likely resulted in the pooling of highly concentrated local anesthesia onto nerve roots in the sacral area. More recently, Arkoosh et al. demonstrated that intrathecal catheters can be used safely and effectively in the parturient. Labor analgesia was provided for 329 parturients using a combination of isobaric bupivacaine (0.25%) and sufentanil (5 mcg). No CNS infection or permanent neurologic changes were reported. Patients receiving continuous intrathecal analgesia reported higher maternal satisfaction, less motor blockade, and earlier ambulation. In addition to the benefits demonstrated in Arkoosh et al.’s study, there are several other reasons to consider placement of an intrathecal catheter in the setting of an ADP. Spinal anesthesia offers more rapid onset (2 to 3 minutes versus 10 to 15 minutes for epidural analgesia) and greater control of analgesia. An intrathecal catheter avoids the risk of a patchy or unilateral block which may occur with a labor epidural. In addition, the lower dose requirement of local anesthesia used in spinal anesthesia virtually eliminates the risk of toxic systemic effects. Furthermore, refraining from subsequent epidural attempts obviously avoids the risk of additional dural punctures, especially in patients with lumbar anatomy that is abnormal or difficult to palpate. Finally, evidence from several sources report a small but significant decrease in postdural puncture headache rates with intrathecal catheter placement in the setting of an ADP. Table 249.1 ■ Suggested Patient-Controlled Spinal Analgesia (PCSA) Settings Local Anesthetic

Bupivacaine Ropivacaine Opioid

Fentanyl Sufentanil

Loading Dose (mg) 1.0–3.0 2.0–4.0

Infusion (mg/hr)

Bolus (mg)

0.5–3.5 1.0–4.0

0.5–1.25 1.0–2.0

Loading Dose (mcg) 10–20 1–5

Infusion (mcg/hr)

Bolus (mcg)

2–10 1–5

2–5 1–2

Vigilance must be exercised in the management of a spinal catheter. Placement of a catheter in the intrathecal space allows direct contact with components of the CNS. As such, the catheter should be threaded into the subarachnoid space a distance of only 2 to 3 cm. Spinal analgesia can be initiated and maintained with a combination of low-dose isobaric local anesthesia and/or lipophilic opioids (Table 249.1). After a loading dose, the infusion should be initiated at a low rate and gradually titrated to the patient’s analgesic requirements. The patient-controlled spinal analgesia (PCSA) function can be disabled or set to a conservative lockout rate (i.e., small boluses every 30 minutes). Avoiding unnecessary disconnections of the infusion system minimizes the risk of contamination and drug error. The catheter and pump should be clearly labeled, so that all healthcare providers are aware the catheter is located in the intrathecal, not epidural, space (Fig. 249.1). Finally, the sensory level and intensity of motor blockade should be monitored frequently to avoid inadvertent high spinal anesthesia.

Figure 249.1. Proper labeling of the catheter, infusion tubing, and pump following placement of an intrathecal (aka “spinal”) catheter.

If the practitioner elects to replace the epidural rather than use an intrathecal catheter, additional care must be exercised. Local anesthesia or opioids injected through the epidural catheter may pass through the dural puncture site and into the subarachnoid

space. Epidural boluses should be initially limited to 5 mL to avoid an unexpected high neuroblockade. Regardless of whether an epidural or intrathecal catheter is used following an ADP, it is important to recognize that a complication, albeit common, has occurred. As such, the patient’s post-delivery course should be followed closely and documented in their medical record. TAKE HOME POINTS Intrathecal catheters can be used safely and effectively after ADP. Intrathecal catheters and pumps should be clearly labeled to avoid being misidentified as epidural. Benefits of continuous spinal anesthesia include rapid onset, uniform distribution of intrathecal medications, and avoidance of additional ADPs. Potential risks of intrathecal catheters include CNS infection, CNS injury, and inadvertent high motor blockade. There is the potential for epidural medications to diffuse into the intrathecal space following an ADP. Suggested Readings Arkoosh VA, Palmer CM, Yun EM, et al. A randomized, double-masked, multicenter comparison of the safety of continuous intrathecal labor analgesia using a 28-gauge catheter versus continuous epidural labor analgesia. Anesthesiology. 2008;108(2):286–298. Ayad S, Demian Y, Narouze SN, et al. Subarachnoid catheter placement after wet tap for analgesia in labor: Influence on the risk of headache in obstetric patients. Reg Anesth Pain Med. 2003;28(6):512– 515. Baysinger CL, Pope JE, Lockhart EM, et al. The management of accidental dural puncture and postdural puncture headache: A north American survey. J Clin Anesth. 2011;23(5):349–360. Choi PT, Galinski SE, Takeuchi L, et al. PDPH is a common complication of neuraxial blockade in parturients: A meta-analysis of obstetrical studies. Can J Anaesth. 2003;50(5):460–469. Cohen S, Amar D, Pantuck EJ, et al. Decreased incidence of headache after accidental dural puncture in caesarean delivery patients receiving continuous postoperative intrathecal analgesia. Acta Anaesthesiol Scand. 1994;38(7):716–718. Pan PH, Bogard TD, Owen MD. Incidence and characteristics of failures in obstetric neuraxial analgesia and anesthesia: A retrospective analysis of 19,259 deliveries. Int J Obstet Anesth. 2004;13(4):227–233.

250 “We Have an Urgent C-Section!” The Pitfalls of Intrapartum Monitoring of the Fetus Richard C. Month, MD FASA

You are approached by the on-call obstetrician who states she must proceed with an urgent Cesarean delivery for one of the patients on the labor floor. The patient is a 29year-old G2P1001 at term. She has been laboring for more than 9 hours and is on a magnesium infusion for severe preeclampsia. Her magnesium level is therapeutic. Continuous fetal monitoring shows: Baseline: 110 beats per minute Variability: Minimal Accelerations: Absent Decelerations: Persistent late decelerations The obstetrician states that due to the poor fetal heart rate tracing an urgent Cesarean delivery is indicated, and that any delay may harm the fetus. While you proceed with the delivery, you ask yourself the following: 1) What is the likelihood that this neonate will require resuscitation in the delivery room? 2) Does the fetal heart tracing above truly require an urgent delivery? 3) Can any of the intrapartum interventions attempted cause detrimental-appearing changes to the fetal heart rate tracing?

Introduction There are approximately 100 million attended births worldwide each year. Of these, 10% of neonates will require some resuscitative effort, and 1% will require intensive support. Since the anesthesiologist may, in many circumstances, be the most available critical care-trained physician to the neonate at the time of delivery, identifying the neonates at risk for resuscitative need is extremely important. Thus, it is hoped that effective monitoring of the fetus will identify those neonates at risk. The current gold standard in intrapartum evaluation of the fetus is electronic fetal

heart rate monitoring (FHR), also known as cardiotocography. This combines monitoring of the fetal heart rate with monitoring of the uterine contractions. Monitoring the fetal heart rate and its response to uterine contractions correlates highly with wellappearing neonates. That is, a “reassuring” FHT carries a 90+% correlation with a 5minute Apgar score greater than 7. However, due to treatment and medication interactions, limits of the examination, and normal variation between infants, the false positive rate is as high as 50%.

Basics of Fetal Heart Rate Monitoring Fetal heart rate monitoring consists of a continuous measurement of both the fetal heart rate and the strength and timing of uterine contractions. These two measurements are graphed together and described in terms of four parameters: baseline, variability, accelerations, and decelerations. In combination, a final determination is made regarding the status of the fetus, and interventions are taken.

Baseline Fetal heart rare baseline is an attempt to measure the fetal heart rate while ignoring accelerations and decelerations (described later). It is defined as the mean fetal heart rate in any 10-minute window. It is typically rounded to the nearest 5 beats per minute. Normal baselines range from 110 to 160 beats per minute, with higher heart rates considered fetal tachycardia and lower heart rates considered fetal bradycardia.

Variability Variability is a measure of the normal interplay between the immature fetal sympathetic and parasympathetic nervous system. It is a measure of fluctuations in the baseline fetal heart rate both in amplitude and frequency measured over a 10-minute window. Normal, o r moderate, variability is fluctuation from 6 to 25 beats per minute from baseline. Fluctuations more pronounced than this are called marked, while detectable fluctuations less than this are called minimal. Undetectable fluctuations are called absent.

Accelerations Fetal heart rate accelerations correlate well with fetal central nervous system wellbeing. They are defined as a visually apparent abrupt increase in fetal heart rate of at least 15 beats per minute for at least 15 seconds for a fetus of 32 weeks of gestation or older.

Decelerations

Decelerations are the most watched component of fetal heart rate tracings. They are defined much as an acceleration: a visually apparent abrupt decrease in fetal heart rate of at least 15 beats per minute for at least 15 seconds. They are further defined morphologically as follows. Early Decelerations: Usually symmetrical, gradual decrease and return of the FHR. The nadir of deceleration occurs at the same time as the peak of the contraction. Associated with fetal head compression and a fetal vagal response. Usually considered benign. Late Decelerations: Usually symmetrical, gradual decrease and return of the FHR. The nadir of the deceleration occurs after the peak of the associated contraction. Associated with a fetal chemoreceptor response to acidosis, secondary to uteroplacental insufficiency. Always considered pathologic. Variable Decelerations: Abrupt decrease in FHR, with equally abrupt return to baseline. When associated with contractions, onset, depth, and duration will vary with successive contractions. Associated with a fetal baroreceptor reflex, secondary to umbilical cord compression, causing an increase in fetal systemic vascular resistance. May be benign or pathologic depending on the situation. Prolonged decelerations, like prolonged accelerations, are between 2 and 10 minutes in length; any acceleration or deceleration of more than 10 minutes is considered a change in baseline. Intermittent decelerations occur with less than half of the contractions over a 20-minute period, while persistent decelerations occur with half or more.

Pitfalls With FHR Monitoring Inter-observer Variability All fetal heart rate measurements are done with some degree of subjectivity. In an effort to decrease this effect, a three-tiered system was developed to group fetal heart tracings into meaningful categories. These categories are outlined below.

Category I

Description

Interpretation

Must include ALL of the following: • Baseline: Normal • Variability: Moderate • Accelerations: Present or absent • Decelerations: Absent,

Normal, or reassuring. Associated strongly with fetal wellbeing and normal fetal acid–base status

Category II

Category III

except early decelerations may be present Include all tracings not Indeterminate, equivocal, identified as Category I or suspicious, or atypical. Not Category III. These immediately predictive of account for the vast positive or negative fetal majority of fetal heart rate acid–base status. Per tracings. guidelines, “such tracings require constant reevaluation and surveillance.” Either: Abnormal or nonreassuring. • Absent variability with any Associated strongly with of the following: fetal acid–base • Recurrent late abnormalities at the time decelerations of observation. Efforts to • Recurrent variable resolve the acid–base decelerations disturbance, up to and • Fetal bradycardia including urgent delivery, • Sinusoidal pattern (FHR should be taken with a sine-wave like immediately. undulating pattern of 3–5 cycles per minute lasting 20 minutes or more.

Even with the three-tiered system, inter-observer variability is still a significant problem, as each tier is directly dependent on a combination of observations all of which are associated with varying degrees of variability; poor inter-observer correlation is noted with fetal bradycardia, decreases in variability, recurrent and/or prolonged decelerations, and variable decelerations. This is a likely cause of the large number of false positive fetal heart rate tracings.

Effects of Treatment on the Fetal Heart Rate Many of the interventions, specifically medications, undertaken through the course of labor and delivery are associated with changes in the fetal heart rate. Most medications readily cross the placenta and thereby have a direct effect on the fetus. Magnesium acts as a central nervous system depressant and readily crosses the placenta. This

causes a decrease in fetal heart rate, a reduction in variability, and a loss of accelerations if previously present. These would cause deleterious-appearing changes to the fetal heart rate tracing without worsening fetal outcome or indicating fetal acidosis. Similar effects are noted with opioids, benzodiazepines, and certain classes of antiemetics. Conversely, certain drugs may affect fetal acid–base status iatrogenically, while not indicating a perfusion issue and not leading to poor fetal outcomes. These include ephedrine, atropine, and scopolamine, all of which readily cross the placenta. All three may contribute to fetal tachycardia, and atropine has been shown to eliminate fetal heart rate variability.

Conclusion While FHR monitoring has become the gold standard in intrapartum fetal monitoring, it is not without significant concerns for error and misinterpretation. Interpretation of fetal heart tracings should therefore never be made without consideration of other fetal and maternal factors, nor should it be made without understanding of its limitations. TAKE HOME POINTS The current gold standard in intrapartum evaluation of the fetus is electronic fetal heart rate (FHR) monitoring. Normal, or reassuring, FHT carry a 90+% correlation with a 5-minute Apgar score greater than 7. However, the false positive rate is as high as 50%. Fetal heart rate monitoring consists of a continuous measurement of both the fetal heart rate and the strength and timing of uterine contractions. These two measurements are graphed together and described in terms of four parameters: baseline, variability, accelerations, and decelerations. In combination, a final determination is made regarding the status of the fetus, and interventions are taken. All fetal heart rate interpretations are subject to significant inter-observer variability. In an effort to decrease this, FHR tracings are grouped into Category I (normal/reassuring), Category II (indeterminate), and Category III (abnormal/nonreassuring). Even with these categories, large inter-observer variability persists. Nonetheless, anesthesia providers should be knowledgeable and practiced in interpreting the FHR tracing and should do so as part of the basic provision of care. Numerous common medications and interventions can affect the fetal heart tracing in ways that appear deleterious, but may, in fact, be benign. Suggested Readings

American Heart Association; American Academy of Pediatrics. 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: neonatal resuscitation guidelines. Pediatrics. 2006;117(5):e1029–e1038. Beard RW, Filschie GM, Knight, CA, et al. The significance of the changes in the continuous fetal heart rate in the first stage of labour. J Obstet Gynaecol Br Commonw. 1971;78:865–881. Chauhan SP, Klauser CK, Woodring TC, et al. Intrapartum nonreassuring fetal heart tracing and prediction of adverse outcomes: Inter-observer variability. Am J Onstet Gynecol. 2008;199:623.e1--623.e5. Hughes S, Ward M, Levinson G, et al. Placental transfer of ephedrine does not affect neonatal outcome. Anesthesiology. 1985;63:217–219. Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of Child Health and Human Development workshop on electrical fetal monitoring: Update on definitions, interpretation, and research guidelines. Obstet Gynecol. 2008;112:661–666. Murad S, Conklin K, Tabsh K, et al. Atropine and glycopyrrolate. Hemodynamic effects and placental transfer in the pregnant ewe. Anesth Analg. 1981;60:710–714.

251 Stat C-Section—The 30-Minute Rule and Beyond Karen Hand, MB BS FRCA and Christopher E. Swide, MD

Nearly one-third of all births in the United States today are by Cesarean section (Csection), a dramatic increase from 5.5% of births in 1970. Traditionally, these deliveries have been classified “elective vs. urgent.” A considerable number of Csections fall into the urgent, or even emergent, category. It is imperative that the anesthesiologists caring for these patients understand that the parturient presenting for non-elective C-section brings with her unique anesthetic challenges. It is also imperative that we understand that the health, safety, and well-being of the mother always take priority over that of the fetus. In some cases both the mother and the baby are equally in jeopardy, however, in many cases there is an increased threat to either the well-being of the mother or to the well-being of the fetus alone. Refinements to the classification system for urgency of Csection may improve communication around urgent need for delivery, and perhaps improve safety for both mother and baby. Historically, the “30-minute rule.” was adopted 25 years ago by the American Congress of Obstetricians and Gynecologists, and subsequently endorsed by other bodies such as the ASA and The Joint Commission. In the United States, the 30-minute rule mandates that obstetric units must be able to provide for a decision-to-incision time of 30 minutes or less for urgent cases. Unfortunately for everybody, there is surprisingly little scientific evidence in support of the 30-minute timeline. What data there are even suggest a worse outcome for babies delivered most rapidly—although of course this probably reflects a need for the fastest deliveries for the sickest babies. There is some evidence that suggests worsened outcomes after 40 minutes or even after 75 minutes. Taken outside the clinical context, these data are hard to apply concretely to our clinical practice—75 minutes seem like an awful long interval for decision-to-incision. On the other hand, for some babies a decision-to-incision interval of 15 minutes is too long and will result in severe fetal morbidity or mortality.

How do you devise a path of safety for your patients through these urgent and emergent situations? First of all, as we have stated elsewhere, the most skilled, experienced, and successful OB anesthesiologists know a lot about obstetrics per se. We recommend that you become and remain comfortable in understanding and distinguishing irreversible causes of fetal compromise, such as cord prolapse, severe placental abruption, uterine rupture, and terminal fetal bradycardia. These emergent conditions require delivery as rapidly as possible, and the inflection point on the risk–benefit ratio is at a very different point in the anesthetic care plan from scenarios such as arrest of labor or nonreassuring category II fetal heart rate tracing. Communication between the obstetrician and anesthesiologist about the urgency of Csection can be challenging and, unfortunately, is often limited to “Have we got time for a quick spinal?” However, new classification systems may help improve communication regarding urgency. The Lucas classification system was first described in 2000. It is widely used in Europe, having been adopted by the Royal College of Obstetricians, for example. In this system there are four categories of urgency: Category 1: Emergency. An immediate threat to the life of the mother or fetus. Category 2: Urgent. Maternal or fetal compromise requiring prompt delivery. Category 3: Needing early delivery but maternal or fetal compromise is absent. Category 4: Elective. Can be scheduled at a time to suit mother and staff. A Lucas category 1 C-section is usually understood to require general anesthesia, unless there is a labor epidural in place which can be extended rapidly, or unless general anesthesia poses an unacceptable risk to the life of the mother. For a Lucas category 2 Cesarean section it will usually be possible to avoid general anesthesia with its attendant risks. Other similar classifications, such as the “traffic light system,” have been proposed. This classification assigns green for elective and nonurgent C-sections, yellow or orange for urgent but there is some for regional anesthesia, and red for emergent operative delivery and baby needs delivery now. There are no specific data to support this system nor are we, the editors, aware of national standardization of the traffic light classification. The disadvantages of the Lucas and other systems occur because of the variability of opinion between providers as to category for particular scenarios, although in testing the Lucas system was found to achieve the most consistent level of agreement between providers.

In the United Kingdom, the National Institute of Clinical Excellence reported on the use of the Lucas classification system in 2011. It was emphasized that although units must be set up to able to deliver a fetus within 30 minutes, that is not always necessary or desirable, and that decision-to-delivery interval should be used as an audit standard rather than to judge interdisciplinary team performance for any individual C-section. A recent study apparently demonstrated improvement in neonatal outcomes with a dedicated effort to reduce the time for decisions-to-delivery intervals, but at the expense of an increase in the number of general anesthetics administered to the mother. An accompanying editorial urged caution in increasing risks to the mother. For the anesthesiologist attempting to balance the safety of both mother and baby this is all well and good, but what do you actually DO in the various stages of obstetrical clinical emergency? First of all, you quickly review in your mind how you would do an urgent or emergent delivery for each patient you meet on the labor deck when you meet her. And you ask the relevant questions such as the urgency of previous deliveries. Feel free to form opinions within your own mind as to how likely the patient is to have an uncomplicated labor and delivery—look comprehensively at your patient including her body habitus, her other medical problems, and her psychological and emotional state. If you think you might be heading toward an urgent or emergent delivery in later hours, get the epidural in and get it working. Secure decent IV access, this is no time to scruple about putting in an 18-gauge cannula. Keep a close assessment of where the labor block is and don’t let it wear down. For every level of clinical urgency, whether you organize it in your mind into Lucas categories or another classification (e.g., 5 minutes until incision, 10 minutes until incision, 20 minutes until incision, and so forth) you should develop and know handsdown what you are going to do. You need a tried and true method for each category. The authors and editors have practiced OB anesthesia for many years and here are some of our own practice parameters: First, never neglect standard ASA monitors —call for help in placing these or have the nurses or medical students do this. When the case is reviewed, you do not want to spend any time explaining why the monitors weren’t on. And remember, universal precautions—always! Urgent operative delivery with low or medium epidural level: 20 cc of 3% chloroprocaine after standard test dose with patient positioned on operating room table. Also, for supplementation of the “nonperfect block,” we use ketamine 40- to 50mg bolus to start, then a 10- to 20-mg bolus, titrated to nystagmus.

Urgent operative delivery with significant epidural labor block: 10 cc of 3% chloroprocaine after standard test dose with patient positioned on operating room table. Urgent operative delivery without epidural and when general anesthesia is contraindicated: use spinal anesthesia with hyperbaric bupivacaine. There is a slight range of doses recommended. The editors teach and use 12 mg of 0.75% hyperbaric bupivacaine (1.6 cc) for a parturient of average height for these clinical situations. If the patient is short or there are concerns about the potential and sequelae of a high block, use 10 mg of 0.75%. This dose range should give a reliable surgical block that is familiar and relatively easy to manage. Also when minutes or seconds count, this is a quick and easy dose to draw up. Ketamine can be used to supplement as noted above. The editors also use a 25-gauge Whitacre for both urgent and nonurgent spinals. We will occasionally use a bigger spinal needle, such as a 22-gauge Whitacre needle, if we have assessed an increased difficulty of placement, such previous back surgery or prepregnancy morbid obesity. Keep in mind that use of a 22-gauge spinal needle for a parturient significantly increases the risk of postdural puncture headache. This risk is accepted with the view that spinal headaches can be very painful but are not dangerous in the way that a delayed emergent delivery is painful. Although larger needles are sometimes used, it should not be inferred that a 22-gauge needle is standard of care for urgent C-sections or reflective of common practice. Emergent operative delivery: keep in mind that these are rapid sequence inductions! We use etomidate 0.3 mg/kg as a mainstay of our urgent or emergent general anesthetics. For asthmatics we use ketamine 1- to 2-mg/kg induction bolus. For neuromuscular blockade, we use succinylcholine 1 mg/kg or rocuronium 1 mg/kg if succinylcholine is contraindicated. We don’t use vecuronium for a stat C-section because the onset is too slow, but in the case of drug shortage or some other situation when that is the only option, we would give vecuronium 0.3 mg/kg to speed the onset of neuromuscular blockade. It is generally agreed that the quickest way to prepare the mother for rapid delivery of the fetus is with general anesthesia. However, during pregnancy there are numerous physiologic changes which occur by the third trimester which potentially make general anesthesia more hazardous. The anesthesiologist must be familiar with the major physiologic changes that occur with pregnancy and their anesthetic implications (Table 251.1).

Table 251.1 ■ Physiologic Changes Associated With Pregnancy

System

Physiologic Changes at Term Gestation (Compared With Prepregnant Values) Anesthetic Implications

Respiratory

30–40% increase in oxygen consumption 20% decrease in FRC 45% increase in minute ventilation Increased airway edema and mucosal friability Cardiovascular 50% increase in cardiac output 20% decrease in SVR Possible aortocaval compression by gravid uterus 55% increase in plasma volume 45% increase in blood volume Gastrointestinal Anatomic displacement of stomach cephalad and left Decreased lower esophageal sphincter tone Delayed gastric emptying Increased gastric acid secretion Nervous Increased sensitivity to IV anesthetics MAC of volatile agents reduced 15–40%

Rapid development of hypoxemia during apnea, potentially difficult intubation

Miscellaneous

Difficult laryngoscope insertion, reduce dosages of NDMR

Engorged breasts Increased sensitivity to nondepolarizing MR

Aortocaval compression → decreased preload → hypotension in supine parturient → uteroplacental insufficiency

Increased risk for aspiration (Mendelson syndrome)

Adjust doses accordingly

FRC, functional residual capacity; IV, intravenous; MAC, minimum alveolar concentration; MR, muscle relaxant; NDMR, nondepolarizing muscle relaxant; SVR, systemic vascular resistance.

Data from the triennial reports into maternal mortality from the United Kingdom have consistently shown increased mortality in women undergoing general anesthesia in pregnancy compared with regional, with the majority of deaths attributed to anesthesia being related to the airway and difficulties with intubation and ventilation. Data from the United States from the 1990s suggested a 16.7-fold increased mortality with general anesthesia. More recent data have improved, but with mortality associated with general anesthesia still nearly double that with regional anesthesia. In addition, more recent data emphasize the risk of airway complications during emergence and recovery, with half of airway-related deaths occurring during this period. One final note: These cases are also situations that call for close and direct supervision of the resident or fellow who might be placing the block or managing the airway. We believe that the only way a trainee can gain the judgment and experience needed to become consultants is to participate as full providers in these challenging cases. However, the senior anesthesiologist or attending must stay actively involved. This active involvement can be placing the block or allowing the resident to place the block, depending on the situation. The attending anesthesiologist is ultimately responsible for his or her decisions. Suggested Readings Chestnut DH. Obstetric Anesthesia Principles and Practice. 3rd ed. Philadelphia, PA: Mosby; 2004:421–459. Hawkins JL, Chang J, Palmer SK, et al. Anesthesia-related maternal mortality in the United States, 1979– 2002. Obstet Gynecol. 2011;117(1):69–74. Hawkins JL, Koonin LM, Palmer SK, et al. Anesthesia-related deaths during obstetric delivery in the United States, 1979–1990 [Clinical Investigation]. Anesthesiology. 1997;86(2):277–284. Lucas DN, Yentis SM, Kinsella SM, et al. Urgency of caesarean section: a new classification. J R Soc Med. 2000;93:346–350. Mhyre JM, Riesner MN, Polley LS, et al. A series of anesthesia-related maternal deaths in Michigan 1985– 2003. Anesthesiology. 2007;106(60):1096–1104. Munnur U, de Boisblanc B, Suresh M. Airway problems in pregnancy. Crit Care Med. 2005;33(10):s259– s268. Nageotte MP. The 30-minute standard: how fast is fast enough? Am J Obst Gyn. 2014;3:177–178. Soltanifar S, Russell R. The National Institute for Health and Clinical Excellence (NICE) guidelines for caesarean section, 2011 update: implications for the anaesthetist. Int J Obst Anes. 2012;21:264–272. Tolcher MC, Johnson RL, El-Nashar SA, et al. Decision to incision time and neonatal outcomes. A systematic review and meta-analysis. Obstet Gynecol. 2014;123(3):536–548.

TAKE HOME POINTS The urgent or emergent C-section case is one of the highest-risk clinical situations

you will encounter in your practice, right up there with patients with ruptured aortas, epiglottitis, head trauma, and penetrating trauma. You must maintain clinical competency and currency in this area if you are an obstetrical anesthesia provider. If you do not routinely do OB anesthesia, keep in mind that you may be called to the labor and delivery deck to help in an emergent situation. It’s okay to develop a clinical suspicion that you might be facing in an urgent or emergent section for a particular patient. Get a decent epidural and IV in before you need them and keep a close eye on them. The medical situation of the parturient will provide enough uncertainty—you don’t want to be wondering if a tenuous 22-gauge IV is going to get the patient and you through an operative case. There are situations such as cord prolapse, severe abruption, and uterine rupture where rapid delivery is likely to be beneficial to a compromised fetus, but there are other situations where this is not clearly the case. Stay current on your OB knowledge. Classification of urgency of C-section may aid communication. Stay current on these, but always think about how the current classification relates to what you are actually going to do and give. The classification of the clinical situation almost always translate to a time interval—5 minutes, 10 minutes, etc. Don’t ask the surgeon if you have time for a spinal, ask what is the target time for incision and then make your clinical decisions. Efforts to improve decision-to-incision intervals should not come at the cost of unnecessarily increased risk to the mother. The mom and the baby deserve full ASA monitors! Do not underestimate the potential difficulty of the airway! These acute situations may call for the most experienced clinician to do the airway or the block. Every single aspect of these clinical situations will be easier to review and discuss on a post hoc basis if the health of the mother and baby has been preserved. Malpractice litigation that arises from the urgent or emergent section can be especially devastating for the anesthesia provider. Unfortunately and sadly, the editors have personally talked with malpractice attorneys who actively look for cases of urgent or emergent operative delivery with poor outcomes, especially if a trainee or junior anesthesiologist made several unsuccessful attempts to initiate the anesthetic. As discussed above, it’s okay to take steps to make sure that you and your staff come through safely, after doing everything medically and legally mandated and appropriate to secure the health and safety of the mother and baby.

252 Postpartum Hemorrhage: Don’t Forget That Having a Baby Is Major Surgery Alexander Y. Fu, MD and Brandon Michael Togioka, MD

Postpartum hemorrhage (PPH) (i.e., >500 mL blood loss after vaginal delivery or >1,000 mL blood loss after cesarean delivery) occurs in up to 4% of parturients and is on the rise in many developed countries including the United States and Canada. Fortunately, the maternal physiology seems to be prepared for this blood loss. At term, plasma volume is increased by 45% while red blood cell volume is increased by 20%, thereby causing dilutional anemia. For most women, this translates to an increase in blood volume of 1,000 mL to 1,500 mL. Furthermore, pregnancy is associated with a hypercoagulable state in which fibrinogen and factors VII, VIII, IX, X, and XII concentrations increase, which may help to limit blood loss. On the flip side, platelets can decrease and fibrinolysis can become accelerated in the third trimester potentially leading to more bleeding. Patients may have a chronic coagulopathy or develop an acute coagulopathy as a result of massive hemorrhage, HELLP syndrome (i.e., hemolysis, elevated liver enzymes, low platelets), acute liver failure of pregnancy, or disseminated intravascular coagulation (DIC). To this extent, one can see that pregnancy is a complex interplay of physiologic changes that influence bleeding associated with delivery.

Uterine Atony The number one cause of PPH is uterine atony (i.e., a lack of uterine muscle contraction after delivery), making up 80% of all PPH events. Risk factors include a retained placenta, abnormal placentation, a distended uterus (e.g., multiple gestations, fetal macrosomia, polyhydramnios), chorioamnionitis, prolonged labor, and general anesthesia. Bimanual uterine massage (i.e., kneading the uterus with one hand in the vagina and the other hand on the abdominal wall) is the first-line therapy for atony. It promotes uterine contraction and reduces bleeding even while the uterus remains atonic. The mainstay of pharmacologic treatment for uterine atony is oxytocin. Like all other medications used to treat atony, oxytocin stimulates uterine contraction. Rapid

intravenous injection of oxytocin can cause tachycardia, chest tightness, and hypotension; so it is usually diluted 30 to 40 units into 1 L crystalloid and administered via drip. Anecdotally speaking, we have yet to see chest tightness that does not resolve after decreasing the rate of oxytocin administration. Methylergonovine is a synthetic ergonovine analogue that can have LSD-like actions above 2 mg. The dose for uterine atony is ten times lower at 0.2 mg per intramuscular/intramyometrial injection. It can be redosed at most every 2 hours to a maximum of 5 doses. Methylergonovine can cause hypertension through vascular smooth muscle constriction and is therefore relatively contraindicated in patients with hypertension or preeclampsia. Exercise caution while using in conjunction with CYP 3A4 inhibitors such as macrolide antibiotics, HIV protease or reverse transcriptase inhibitors, or azole antifungals, as they may prolong or enhance the effect on vascular smooth muscle. Of note, though off label, in a pinch some clinicians will dilute methylergonovine to 20 µg/mL for patients with a relative contraindication to the drug and given it intravascularly 1 mL at a time with a blood pressure reading after each dose. Anecdotally speaking, this technique appears to work without uncontrolled increases in blood pressure. Carboprost is a synthetic Prostaglandin2α analogue that is administered 0.25 mg per intramuscular/intramyometrial injection. Carboprost should be avoided in patients with asthma given case reports of bronchospasm after administration. Misoprostol is a synthetic prostaglandin E1 analogue that can be used for induction of abortion, treatment of ectopic pregnancy. For treatment of uterine atony, misoprostol is administered as a single dose of 400 to 1,000 µg sublingually or per rectum. Earlier in our personal practice, we gave this drug by placing the tablets sublingually and noticed that 30 minutes later most of the drug had not been absorbed. We now routinely crush the tablets before administering them sublingually and have yet to see any side effects other than diarrhea. Of note, patients don’t seem to complain about the taste. When pharmacologic therapy for uterine atony is unsuccessful, more invasive options are available. Uterine artery or internal iliac artery (formerly known as the hypogastric artery) embolization is highly effective at controlling bleeding from uterine sources. The uterine artery provides 90% of the blood flow to the uterus. If a patient is stable enough to undergo an angiographic procedure and radiologic support is available embolization may be considered as an alternative to exploratory laparotomy. During an exploratory laparotomy, surgical ligation of these arteries can also be performed to achieve the same effect as embolization. Uterine compression sutures are another option for controlling PPH due to atony. There are several techniques, including the B-Lynch, Hayman, and Pereira sutures, but each has the purpose of mechanically compressing the uterus.

More recently, intrauterine balloon tamponade has been used as a minimally invasive treatment option that can preserve fertility. Intrauterine balloon tamponade exerts inward to outward pressure against the uterine wall. Balloon tamponade can be performed with a number of devices, but only the Bakri balloon and the BT-cath balloon are FDA approved for this application. If ligation, embolization, compression suture, or balloon tamponade are unsuccessful, then hysterectomy is required. Aortic cross-clamping may be necessary if bleeding cannot be controlled initially. In summary, treatment of uterine atony should commence with bimanual massage and oxytocin followed by methylergonovine, carboprost, or misoprostol. If the patient is unstable exploratory laparotomy with likely hysterectomy must be performed. If the patient is stable with a slow bleed and previous interventions were ineffective uterine artery embolization or balloon tamponade can be attempted.

Lacerations Another primary source of PPH is obstetric laceration. Laceration should be suspected whenever the uterus is firm (not atonic) and there is still bleeding. Vaginal bleeding can arise from laceration of the vaginal artery during pushing. Risk factors include nulliparity, advanced maternal age, and fetal macrosomia. The vaginal artery can originate from either the internal iliac or uterine artery. If, during an operation, there are signs of bleeding out of proportion to what is seen on the surgical field, the anesthetist should check under the drapes. We have done this on numerous occasions on the labor floor (and in the operating room) and have found insidious bleeding on a number of occasions. Vulvar hematoma can arise from laceration of branches of the pudendal artery. Vulvar hematoma is usually associated with severe pain. If the hematoma is small, it may be treated with ice packs and analgesics. If the hematoma is large, a second IV should be placed, and the patient should be brought to the operating room for surgical intervention. Retroperitoneal bleeding is often missed and as such has led to some of the worst outcomes we are aware of—and this unfortunately includes a patient death. Retroperitoneal bleeding results from laceration of a branch of the internal iliac artery. Bruising of the flanks (Grey Turner’s sign) is pathognomonic, and hematuria can also result from the bleed. Retroperitoneal hematoma should be considered if the patient is showing signs of hypovolemia, but there is no bleeding on the field or under the drapes. If suspected, it is my personal practice (Dr. Togioka) to recommend to the obstetricians that we page general surgery, gynecology-oncology, or trauma surgery to assist in surgical exploration.

Other Causes of Postpartum Hemorrhage Another common cause of PPH is a retained placenta, which is a placenta still in the uterus 30 minutes after delivery. A retained placenta prevents the uterus from contracting properly allowing blood vessels inside the uterus to continue to bleed. It is now controversial whether the umbilical cord should be pulled in an attempt to help the placenta separate. If a retained placenta is causing significant bleeding the obstetric provider will enter the uterus with their hand and attempt to remove it. Uterine relaxation with tocolytic medication aids the obstetrician in removing the placenta. Inhalational anesthetic agents, low-dose nitroglycerine, terbutaline sulfate, and magnesium may be used for this purpose. Abnormal placentation occurs when the placenta attaches abnormally to the myometrium. The three categories of abnormal placentation are placenta accreta (attachment to the myometrium), placenta increta (invading into the myometrium), and placenta percreta (invading through whole thickness of myometrium). Abnormal placentation is associated with heavy blood loss of at least 2.5 to 5 L. Therefore, delivery is usually by way of cesarean section with general anesthesia, an arterial line, and large-bore intravenous access or a central line. Disseminated intravascular coagulation (DIC) is a condition characterized by massive activation of the clotting cascade, widespread thrombosis, and consumption of clotting factors/platelets leading to massive bleeding and multiorgan failure. DIC had a prevalence of 12.5 per 10,000 deliveries and accounted for one-quarter of maternal deaths in the United States from 1998 to 2009. Ironically, peripartum hemorrhage itself is a common cause of DIC. Other causes include amniotic fluid embolism, sepsis, and intrauterine fetal demise. One should make sure to inspect IV sites for bleeding to trigger suspicion for DIC.

General Response to Bleeding The initial management of a patient with unexpected PPH can be challenging as they will most likely present with limited IV access and an unprotected airway. The first line of action should be to call for help. Next, call for blood products and establish additional intravenous access. Consideration should be given to placing an arterial line to help guide transfusion therapy. Arterial line placement is in the basic skill set for anesthesiologists—you don’t ever want to be in the position of trying to explain why you didn’t do something that you have done hundreds of times or more for other types of patients. Also, don’t forget about the airway! Intubating the patient may be necessary to protect the airway as significant bleeding can lead to airway edema or an altered mental status. Don’t wait too long to secure either the arterial line or the airway. Some providers suggest activating the massive transfusion protocol if estimated

blood loss is greater than 1,500 mL. Massive transfusion protocols generally suggest giving a ratio of blood product that mimics transfusing whole blood. Packed red blood cells (PRBC) and fresh frozen plasma (FFP) are usually given in a 1:1 ratio. For every 6 units of PRBC and 6 units of FFP that are given, 1 unit of platelets is given. These protocols are based mainly upon retrospective studies involving trauma victims in the military. There is no study in the obstetric setting showing improved maternal outcomes when transfusion is performed with a high FFP:PRBC ratio. Furthermore, there are risks with giving more FFP: increased incidence of infection, higher incidence of organ failure, and risk for acute respiratory distress. To this extent, we don’t hold steadfast to the 1:1 ratio. Usually, we start by transfusing PRBC only and if bleeding continues, we then start to add in FFP. By the end of the case, we are usually happy if my ratio of FFPto-PRBC is between 1:2 and 1:1 (i.e., we don’t think it is advantageous to give FFP faster than PRBCs to play catch up). A hemoglobin concentration, calcium level, and coagulation panel (aPTT, PT, fibrinogen, platelet count) should be sent regularly to monitor the progress of transfusion. Cryoprecipitate is usually given in response to a low fibrinogen level. Another important aspect of resuscitation is the maintenance of a normal blood pH, as patients with a pH