Basic Anaesthesia Handbook [6 ed.] 9789673633135

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I A< I ( ANAESTHESIA • I

adia Honom Ishak

PENERBIT � PRE S

lJNM!RSm 'l'EKKOLOOI MARA

Second Print 2016 Third Print 2017 Fourth Print 2018 Sixth Print 2019

© UiTM Press, UiTM 2015

All rights reserved. No part of this publication may be reproduced, copied, stored in any retrieval system or transmitted in any form or by any means; electronic, mechanical, photocopying, recording or otherwise; without prior permission in writing from the Director of UiTM Press , Universiti Teknologi MARA, 40450 Shah Alam, Selangor Darul Ehsan, Malaysia. E-mail: [email protected] UiTM Press is a member of MALAYSIAN SCHOLARLY PUBLISHING COUNCIL

Perpustakaan Negara Malaysia Cataloguing-in-Publication Data Nadia Hanom Ishak BASIC ANAESTHESIA HANDBOOK / Nadia Hanom Ishak. ISBN 978-967-363-313-5 1. Anesthesia--Handbooks, manuals, etc. 2. Anesthesiology--Handboks, manuals etc. I. Title. 3617.96

Printed in Malaysia by : UiTM Printing Centre Faculty of Art & Design Universiti Teknologi MARA 40450, Shah Alam, Selangor.

CONTENTS PREFACE ACKNOWLEDGMENTS ABBREVIATIONS

HISTORY OF ANAESTHESIA PREOPERATIVE ASSESSMENT CORE AIRWAR MANAGEMENT ANAESTHETIC TECHNIQUES CORE ANAESTHETIC DRUGS PERIOPERATIVE MONITORING PERIPERATIVE FLUID AND ELECTROLYTES PERIOPERATIVE BLOOD COMPONENT TRANSFUSION POST-ANAESTHESIA CARE ACUTE PAIN MANAGEMENT INTRODUCTION TO CRITICAL CARE

INDEX

Preface "The best thing about modern living is anaesthesia" - Meg Ryan, American actress and producer. Anaesthesia has emerged as an important facilitatory and supportive clinical discipline in our healthcare system. It is almost impossible to imagine today's health care without surgery. However it is equally impossible to imagine a surgery without anaesthesia. It plays a pivotal role in a variety of surgical disciplines (i.e. general surgery, obstetrics gynaecology, paediatric surgery, orthopaedics, maxillofacial etc.) and diagnostic studies. Physiology and pharmacology are dry subjects when they are taught in medical schools but are brought to life in the practice of anaesthesia. They link together basic sciences and clinical practice. Furthermore, there had been a vast evolution in anaesthesia, critical care and pain medicine for the past 150 years. Medical students undergoing anaesthesia postings or rotations may find it difficult to find a reference book that is not 'too detail' for their short (usually 2-4 weeks) but important posting. Hence, this book serves as an alternative reference for those who wish to have the gist of anaesthesia without having to commit to long reading hours or even days. The main aims of anaesthesia teaching in undergraduates are for the students to be able to grasp the principles of resuscitation (airway, fluid management, drug choices), basic knowledge of safe perioperative anaesthesia, management of acute pain perioperatively and its vital role in critical care services. The topics covered in this book are relevant for housemen, medical officers and nurses who are new in the anaesthesia department as it provides quick overview on the principles of anaesthesia. We would like to thank all contributors for their valuable time and endless effort in writing and completing this handbook. It is hoped that this book will enlighten those who are clueless about what anaesthesia is all about during clinical years in medical school and provides invaluable knowledge for patient care in all fields of medicine in their future career. May there will be more housemen and medical officers be aspired to join our anaesthesia community. Nadia Hanom Binti Ishak MB BCh BAO (Ireland), M.Med (Anaesth) (UKM) Senior Lecturer in Anaesthesiology & Critical Care For enquiry/feedback: [email protected]

Acknowledgements I am grateful, blessed and thankful to Allah Almighty on the birth of this handbook after it had suffered a long hiatus and many technical challenges since 2011. My utmost gratitude is to my husband (Hilmey Mahyiden), son (Zaim Adam; you were the reason for the long hiatus), parents (Sabariah Ahmad and Ishak Shamsudin) and siblings (late Kak Nim, Irina Hanis, Zain Azraai) for their undivided and continuous supports throughout my life and career. I am extremely thankful to Professor Dr. Arif Osman from Kulliyyah of Medicine, International Islamic University Malaysia for throwing this brilliant idea of producing a simple but practical handbook of anaesthesia tailored for medical students undergoing their anaesthetic posting or rotation.

Special thanks to Professor Dr. Karis Misiran (my dedicated teacher during Master's Programme in Universiti Kebangsaan Malaysia, mentor, editor, father­ figure, friend) for giving me the encouragement, support and advice into completing this handbook. Thank you for believing in me.

This handbook would not have been completed or possible without the contributions from my fellow anaesthetists (Rusnaini Mustapha Kamar, Siti Aznida Ab Karim, Khairul Azman Ibrahim, Mafeitzeral Mamat). Illustrations were personally and beautifully drawn by Khairul Azman and Siti Khadijah Mohd Rasli (UiTM medical laboratory technician). I would also like to send our sincere appreciation to UiTM Press (Penerbit UiTM) for their support in publishing this handbook. Not forgetting, my sincere gratitude to the authors, local or international bodies, publishers whom had granted me the copyright permission for their original work to be reproduced in this handbook. They are: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

American Society of Anesthesiologists (ASA) Association of Anaesthetists of Great Britain & Ireland (AAGBI) Blackwell Publishing Limited British Medical Journal (BMJ) Publishing Group Limited Connie M. Baker, MS, Wong-Baker FACES® Foundation Dr. Kerry Brandis, Australia Elsevier Limited Institute for Healthcare Improvement (IHI) John Wiley and Sons Ministry of Health Malaysia Malaysian Society of Anaesthesiologists Malaysian Society of Intensive Care

13. National Blood Authority, Australia 14. Professor Dr. Mohamad Said Maani Takrouri, Pan Arab Anaesthesia Group 15. Sandra I Merkel, MS, RN (Clinical Nurse Specialist, C.S Mott Children's Hospital) and The Regents of the University of Michigan 16. Wellcome Library, London 17. World Health Organization

Many thanks to all general OT, ICU, CICU, CCU, HOW staff and patients in Cardiovascular and Thoracic Centre, Clinical Training Centre UiTM and Sungai Buloh Hospital whom were directly or indirectly involved in the process of this project. Last but not least, my sincere thanks to my past and current teachers, friends and students who have inspired, thought and made me who I am today.

Abbreviations ABG : arterial blood gases ACC : American College of Cardiology ACh : acetylcholine AFOI : awakefiberoptic intubation AG : anion gap AHA : American Heart Association ak a : also known as AO : atlanto-occipital APO : acute pulmonary oedema APS : Acute Pain Service ARDS: acute respiratory distress syndrome ASA : American Society of Anaesthesiologist ASPAN: American Society of Parenteral and Enteral Nutrition BVM : bag-valve-mask BP : blood pressure bpm : beats per minute CCU : Coronary Care Unit CDC : Center of Disease Control CICU: Cardiothoracic Intensive Care Unit CICV : can't intubate, can't ventilate CL : Cormack Lehane Cl- : chloride cLMA : classic laryngeal mask airway cm : centimeter CMV: cytomegalovirus CN : cranial nerve CNS: central nervous system CO : cardiac output CO2 : carbon dioxide COAD : chronic obstructive airway disease CPAP: continuous positive Airway pressure CPET: cardio-pulmonary exercise testing CPP : cerebral perfusion pressure CPR : cardio-pulmonary resuscitation CRBSI: catheter-related bloodstream infection CSE : combined spinal epidural eve : central venous catheter CVP : central venous pressure CVS : cardiovascular system CXR : chest x-ray

DBP : diastolic blood pressure DIVC : disseminated intravascular coagulation DM : Diabetes Mellitus DSM : Diagnostic and Statistical Manual of Mental Disorders DVT : deep venous thrombosis EBV: estimated blood volume ECF : extracellular fluid ECG : electrocardiography EEG : electroencephalography e.g. : example EMLA : eutectic mixture of local anaesthesia ESPEN : European Society of Parenteral and Enteral Nutrition ETC02: end tidal carbon dioxide ET02 : end tidal oxygen ETT : endotracheal tube etc. : et cetera (and other things/and so on) fb : fingerbreadth FBC : full blood count FEMG : frontal electromyography FFP : fresh frozen plasma Fi02 : fraction of inspired Oxygen FRC : functional residual capacity G : gauge GA : general anaesthesia GCS : Glasgow Coma Scale GEB : gum elastic bougie GIT : gastro-intestinal tract GORD : gastro-oesophageal reflux disease Hb : haemoglobin HC03- : bicarbonate HDU : High Dependency Care Unit HES: hydroxyl-ethyl starch HIV : Human Immunodeficiency Virus HPT : hypertension hrs: hours ICF : intracellular fluid ICP : intracranial pressure ICU : Intensive Care Unit i.e. : that is IHD : ischaemic heart disease IHI : Institute for Healthcare Improvement iLMA : intubating laryngeal mask airway IM : intramuscular INR: international normalized ratio

IOP : intraocular pressure IPPV : intermittent positive pressureventilation IV : intravenous IVDU : intravenous drug user IVRA : intravenous regional anaesthesia K+ : potassium LA : local anaesthesia LAST : local anaesthetic systemic toxicity LMA : laryngeal mask airway LOR : loss of resistance LR : lactated Ringer's MAC : monitored anaesthesia care MAP : mean arterial pressure MDR-GNB : multidrug resistant Gram negative bacilli METs : metabolic equivalents MH : malignant hyperthermia MHz : mega Hertz Ml : myocardial infarction mins : minutes MOH : Ministry of Health MLT : microlaryngeal tube mm : millimeter mph : miles per hour MRO : multidrug resistant organism MRSA : methicillin resistant staphylococcusaureus MSA : Malaysian Society of Anaesthesiologists MSIC : Malaysian Society of Intensive Care MTP : massive transfusion protocol N : Newton N2 : nitrogen N20 : nitrous oxide Na+ : sodium NGT : naso-gastric tube NMB : neuromuscular blocking NSAIDs: non-steroidal anti-inflammatory drugs 02 : oxygen oC : degree Celcius CSA : obstructive sleep apnoea OT : operating theatre PACU : Post Anaesthesia Care Unit PA02 : alveolar oxygen tension Pa02 : arterial oxygen tension PaC02 : arterial carbon dioxide tension

PAP : pulmonary artery pressure PAWP : pulmonary artery wedge pressure PCA : patient-controlled analgesia PCEA : patient-controlled epidural analgesia PCM : paracetamol pCO2 : partial pressure of carbon dioxide PEEP: positive end expiratory pressure pg. : page PICU: Paediatric Intensive Care Unit PO2 : partial pressure of oxygen PO42- : phospate PONV : post-operative nausea and vomiting PPV : positive pressure ventilation PRBCs : packed red blood cells PRIS : propofol infusion syndrome PTC : post-tetanic count RA : regional anaesthesia RAE : Ring Adair Elwyn RBC : red blood cells RE : response entropy RSI : rapid sequence induction SAMBA: Society of Ambulatory Anesthesia SBP : systolic blood pressure SC : subcutaneous SE : state entropy sees : seconds SGA : supraglottic airway SpO2 : 02 saturation SvO2: mixed venous oxygen saturation TBW : total body water TMD : thyromental distance TMJ: Temporomandibularoint TIVA : total intravenous anaesthesia TOE : transoesophagealechocardiography TOF : train of four URTI : upper respiratory tract infection VRE : vancomycin resistant enterobacteriaceae vs.: versus WHO : World Health Organization µm : micrometer > : more than < : less than = : approximately

1 HISTORY OF ANAESTHESIA Anaesthesia was a dangerous medical art which balanced between life and death until about 100 years ago or so, when the advancement in anaesthesia was drastic until it became relatively safe to anaesthetise just about anybody. It is a gift to mankind and its milestones are briefly outlined in this topic.

Among the earliest to practise anaesthesia were the Muslim physicians from as early as the 12th century. The Arabs devised the soporific sponge (Figure 1.01) which was the starting point of modern anaesthesia; a sponge soaked with hashish, opium, papver and other aromatic herbs which were dried under the sun. Upon usage, it will be humidified and held over the patient's nostrils where it gets absorbed via mucous membrane inducing sedation or unconsciousness for surgery to take place. This was described in detail by lbn al Quff in his book al Umdah Fi Sinaat Al Jirahah where sleep and insensibility inducing substances were contributed by opium, mandrake, Hyocymus a/bus, belladonna, Cannabis sativus, C. indica and wild lettuce. He also mentioned about the dangers of the drugs and stressed that they should only be used in major procedures.

J

A'.' fl/lif f h1 !1,

---..;__-

Figure 1.01: Artistic impression of an Arabic anaesthetist (reproduced with the kind permission of Pan Arab Anaesthesia Group)

Subsequently, the Europeans practised the same concept but using slightly different ingredients. They used the mandrake plant which its benefit was unclear and also hemlock which was a poisonous alkaloid that could kill along when combined with the ever popular opium.

There was no significant advancement until a maverick chemist, Humphrey Davy conducted physiological experiments with the then newly discovered laughing gas; nitrous oxide (N2 0). Forty five years later in 1844, Horace Wells; a dentist, invited a travelling scientist; Gardner Colton to administer N2 0 during wisdom tooth extraction of his patient. Then, William Thomas Green Molton; another dentist who have worked with Horace Wells before, started using ether soaked handkerchief to anaesthetise his patients (Figure 1.02). This first ether anaesthesia using Morton's Inhaler was publicly demonstrated in 1846 at the Massachusetts General Hospital, Boston for a removal of tumour from the jaw. A year later, ether anaesthesia then progressed to chloroform anaesthesia which was popularised by Dr James Young Simpson who was the Professor of Obstetrics in Edinburgh. However, chloroform had certain drawbacks as it could potentially cause severe liver damage and precipitate sudden death even though it was more potent and much easier to handle.

Figure 1.02: An oil painting by Ernest Board on the first use of ether as an anaesthetic agent in 1846 by the dental surgeon William T.G Morton (reproduced with the kind permission of Wellcome Library, London)

For a long time, it was ether-chloroform and back to ether until the revolutionary inhalational/volatile agent; halothane was introduced in 1956 in USA. Despite Halothane causing hepatitis, it remained the best choice until isoflurane was introduced in 1980. However when sevoflurane was introduced in 1994, halothane was left to the third world country. In 1930's, John Lundy of the Mayo Clinic described thiopentone use as an IV anaesthetic agent in detail which later popularised the concept of balanced anaesthesia (pg. 111). The most popular IV anaesthetic agent; propofol was introduced clinically in 1977 and since then had gained popularity as an induction

agent. Etomidate, which was the "propofol of 70's", was put to rest after it was confirmed that patients on etomidate had doubled mortality compared to those who weren't.

On the innovations in techniques of general anaesthesia (GA); The first endotracheal intubation in an animal was reported by Vesalius in 1543. Later 1878, the first elective endotracheal intubation was performed by Macewen. During the World War I, there were wide usage of tracheostomy and intubation. In 1913, Chevalier Jackson invented the first laryngoscope and was further improvised by Magill, Miller and Macintosh. In 1943, curare (poison used by the South American indigenous people in their arrow or blowgun darts as paralysing agent) in the form of tubocurarine was introduced as a muscle relaxant for abdominal relaxation during GA and endotracheal intubation. The first prototype of laryngeal mask airway (LMA TM) was introduced by Archie Brain, a British anaesthetist in 1981 for an elective inguinal hernia repair. Since then, there has been a vast usage of this supraglottic airway device in elective anaesthesia and emergency airway management. Subsequent innovations had also took place based on this invention.

On the innovations in techniques of regional anaesthesia (RA); In 1885, James Leonard Corning (neurologist in New York) was experimenting cocaine on the spinal nerves of a dog but had accidentally pierced the dura mater inducing spinal anaesthesia. Later, in Kiel, August Bier electively performed the first spinal anaesthesia on man in 1898 by which he used 3.0 ml of 0.5% cocaine solution. Any account of the history of anaesthesia would not be complete without mentioning the first field block on the eye using cocaine by Carl Koller (1884 ). Koller was a friend of the famous Sigmund Freud through whose influence led him to experiment with cocaine. He was considered the first to clinically use the local anaesthetic effect of cocaine. This discovery enabled William Halsted to perform the first brachia! plexus block a year later (1885). In 1921, Fidel Pages; a Spanish surgeon developed the techniques of epidural anaesthesia. REFERENCES AND FURTHER READING

1. AI-Fallouji M. Arabs were skilled in anaesthesia. BMJ 1997; 314: 1128. 2. Mohamad SMT. Historical essay: An arabic surgeon, lbn al Quff's (12321286) account on surgical pain relief. Anesth Essays Res 2010; 4: 4-8. 3. History of Anaesthesia. Available at: http//www.goldcanyon.com. Accessed on 15/2/14. 4. Diemente D, Campbell R. Sir Humphrey Davy. Available at: http:// www.woodrow.org 5. Ezri T, Evron S, Hadad H, Roth Y. Tracheostomy and endotracheal intubation: a short history. Harefuah 2005; 144(12): 891-893. 6. Curare. Medical Discoveries. Available at: http//www.encyclopedia. corn.

Accessed on 28/6/14. 7. Little DM, 1985. Classical anesthesia file: Survey in Anesthesiology. Waverly Press Inc;. 8. Van Zundert TC, Brimacombe JR, Ferson DZ et al. Archie Brain: celebrating 30 years of development in laryngeal mask airways. Anaesthesia 2012;67(12): 1375-85. 9. Marx GF. "The first spinal anesthesia. Who deserves the laurels?"Regional Anesthesia 1994; 19(6): 429-430. 10. Brill, S, Gurman GM, Fisher A. "A history of neuraxial administration of local analgesics and opioids". European Journal of Anaesthesiology 2003; 20(9): 682-689.

2 PREOPERATIVE ASSESSMENT WHAT IS PREOPERATIVE ASSESSMENT?

1. It is a process of clinical assessment prior to the commencement of anaesthetic care for surgical and non-surgical procedures 2. This process involves:

(a) Performing anaesthetic assessment (history and examination)

(b) Estimating risk (risk assessment tools: ASA scoring system, concept of

MET's for non-cardiac surgery and bedside airway test) for the particular patient

(c) Reviewing or requesting appropriate basic and advanced investigations (d) Planning risk reduction strategy: (i) Preoperative optimization (if required)

(ii) Planning and discussing the appropriate modes of anaesthesia and analgesia with the patient or next-of-kin and surgeons involved (iii) Prescribing relevant preoperative drugs (aka premedication) (iv) Rationalizing patient's own regular medication (whether to withhold, adjust or continue) (v) Fasting guidelines

(e) Planning postoperative care (f) Providing information and answering questions from the patient or caretaker/

guardian 3. Preferably performed by the anaesthetist whose going to conduct the anaesthesia or can be done by other anaesthetist and the assessment is to be conveyed to the anaesthetist in charge

4. Performed prior to surgery either in the pre-anaesthetic clinic or as an inpatient (general ward, ICU, emergency department) at an appropriate time to allow preoperative preparation and optimization (if needed)

OVERALL AIMS

1. Anticipating potential difficulties and formulate a suitable perioperative plan to avoid or minimize crisis hence improves patient's safety

2. Ensuring that the patient is medically fit and stable for the surgery and anaesthesia via preoperative optimization

3. Being able to weigh the risks vs. benefits of anaesthesia if the patient is to undergo planned surgery

4. Improving patient outcomes postoperatively 5. Deciding the appropriate equipment, numbers and seniority of staffs who will be needed during administration of anaesthesia related to individual

pre/co-morbidities and types of surgery 6. Achieving a fully informed patient and to obtain consent regarding planned

anaesthetic technique 7. Providing the opportunity for patients to ask questions and clarify matters concerning anaesthetic care (to allay anxiety among patients)

8. Minimizing the risk of late cancellations in elective surgeries 9. Establishing a rapport with the patient

ANAESTHETIC ASSESSMENT A. History

1. A focused history in relevance to anaesthesia is performed rather than a general history 2. It can be taken from the patient itself, relatives/ guardian/ caretaker or

previous medical records 3. It is important to determine: (a) the presenting condition and the urgency of the planned surgery

(b) co-morbidities (HPT, IHD, DM, GORD, asthma etc.) and their current status (c) the degree of functional reserve (capacity is evaluated by MET's)

(d) classification of physical status (ASA scoring system: Table 2.1) (e) previous anaesthetic and surgical history (check on previous anaesthetic notes/charts: presence of difficult intubation or regional anaesthesia, sequelae such as PONV, postoperative ICU admission or prolonged ICU stay etc)

(f) drug history (types, dose, compliance), herbal or dietary supplements

intake (pg. 161), allergies (presentation and treatments used to revert the allergy)

(g) smoking habits (risk of increase in mucus secretion, hypoxaemia and

bronchospasm) (h) alcohol consumption:

i) Acute intoxication causes decreased consciousness (uncooperative)

and gastric emptying (risk of vomiting and aspirating) ii) Chronic alcohol consumers are known to be hepatic enzyme inducers in which it may cause increase in the metabolism of GA agents leading to usage of higher doses and risk of cardiovascular

instability (i) hereditary conditions relevant to anaesthesia (dystrophia myotonica, malignant hyperthermia, porphyria: pg. 148 etc.)

(j) presence of recent or active URTI. Non-urgent surgery should be

postponed few weeks until patient recovered as they are at isk of bronchospasm perioperatively

(k) time of last oral intake

B. Examination 1. In addition to a thorough general and clinical examination, the anaesthetist

must: (a) perform bedside airway assessment (pg. 38) and identify any features of difficult airway

(b) inspect the peripheries to determine the possibility of difficult IV access (obese, Down's syndrome and IVDU)

(c) inspect the bony landmarks and suitability of areas for RA (if relevant)

(d) document any pre-existing neurological deficit if present (in case unexpected morbidity arises postoperatively e.g. prolonged sensory or motor blockade after an epidural anaesthesia)

C. Risk Assessment There are three (3) risk assessment tools which will be discussed here: 1. American Society of Anesthesiologists classification system (Table 2.1)

(ASA)

physical

status

(a) Relates to the patient's general health upon presentation for a surgical procedure

(b) Widely used as it allows a uniform and an easy way of communication

among anaesthetist, but it is non-specific

(c) "E" is appended to any grade of the ASA physical status in the event of emergency surgery

(d) Limitations: (i) there is no moderate systemic disease between ASA II and Ill which is neither mild or severe (ii) there is no clear class for patient with more than 2 systemic disease of different degree of severity

Table 2.1: American Society of Anesthesiologists (ASA) physical status

classification system (excerpted from Relative Value Guide®/2014 of the American Society of Anesthesiologists. A copy of the full text can be obtained from ASA, 1061 American Lane, Schaumburg, Illinois 60173)

Categ ory I

Ill

111

Descri ption of 'P afie n

A no m1al hea hy pa tie nt

A patient wrth m·1 d system ic d isease wittiout funct1i o na1 imitation A patient wi, th severe system]c d isease with defi nite fu nctiona l

imi ation

IV

.A patient wi h seve e s,y stemic d isea s e tha t is a constant th rea o life

V

A m or bund patien expec ;ed to su rvi ve surg,e ry

VI

ho is nor

Examp,le

I Mild d iabetes (contro l led with o ra medications) Hy pe,rt e ns ion ( contra lled ) C h o ni c bronchif s Anaem ia

Diabetes (control led with i nsur n ) Stable a n g ina Asth ma (0111 �reatment) Mode rate pulmonary insumc·e ncy M o.m id obesity l m m u mosupp ressed Unstabl, e angina Myoca rditi s Y Pu lmona1, hepa tic , endo c in e or re na I in su ffi c • e ncy

ithout

A dee ared bra in- dead patient hose organs are being re m oved for donor pu rposes

2. METs scoring system

(a) The American Heart Association (AHA) and American College of Cardiology (ACC) recommend using metabolic equivalents (METs) in assessing and classifying the functional capacity (Table 2.2)

(b) A MET is used to quantify the 02 consumption by the body during physical activity

(c) One(1) METs is assumed to be 3.5ml/kg/minute of 02, consumed by a 40 year old 70 kg man at a resting state.

Table 2.2: METs Scoring System

M ETs 1 -4

4-7 7- 1 0 > 1O

METs Activity

C l assifi cati o n

M ovi n g furnitu re, di gg·ng, spadin g, go l f, re c reati o n a l swi m ming , badm i nton , b icy dii ng ( lei s u r,e ) , ten ni s (d o u b les )

Moderate

B icycli n g (racing ). sq ua sh . run n i ng! (crnss cou ntry}. m a rti a I a 11s (ka rate , boxi ng), footbal l (com petit ive), h eavy 1abou r

Excelle nt

Sweep i ng carpet or fl oors, talki ng and eating o:nly,. bathing , sitti ng. th in ni ng ga rden , ironi ng , rid ing in a car/ bus, stai r ci imbing (slow pace ), bowling

S tai c l i mbi ng (fast pace) te n ni s (si ng l es ) , jogging, ra ce wal king, aembics

Poor

Good

(d) Patients with a score of < 4 METs has been identified as the level at which a patient have poor outcome following major surgery (e) The assessment based on METs classification which depends on the 'subjective' reporting of exercise capacity by the patient which may lead to inaccuracies (high risk individuals may be incorrectly identified and

vice versa)

(f) Objective assessment such as a well conducted cardio-pulmonary exercise testing (CPET) is recommended instead to assess the true exercise capacity (A full overview of CPET is beyond the scope of this handbook)

3. Bedside airway assessment (pg. 38) D. Review or request appropriate basic and advanced investigations 1. Generally, there should be no routine investigation, it should be selectively

performed to either quantify or confirm the degree of abnormality suggested in the patient's history, examination and proposed surgical/ non-surgical procedure 2. Requesting unnecessary investigation is neither useful nor costeffective

3. Investigations may be indicated in:

(a) identifying or verifying a disease/disorder (b) evaluating the extent of the current disease/disorder

(c) formulating which anaesthetic technique or alternatives for the patient

4. Basic investigations: FBC, urea, creatinine, blood glucose, INR, ECG and CXR 5. In specific circumstances, advanced investigations may be required and this is dictated by the findings from the physical assessment (pulmonary function test, echocardiography, lateral view of cervical spine - to exclude atlanto-axial instability in rheumatoid arthritis). In this case, these relevant investigation results may affect anaesthetic management and outcome

E. Risk reduction strategy 1. Optimizing the patient's medical condition

(a) If time permits, referrals within or to another healthcare team/discipline will allow optimization of pre-existing medical condition (b) A proper consultation and intervention might be needed to improve the patient's health condition before subjecting them into anaesthesia care

and surgery (c) Ideally this must not be done at the very last minute in order to avoid suboptimal management preoperatively

2. Planning and discussing the modes of anaesthesia and analgesia

(a) The planning strategy and process must take into account a thorough understanding of the:

i) related surgical procedure ii) patient's co-morbid status

iii) advantages and disadvantages of the anaesthetic techniques

iv) patient's wishes (b) Technique of discussion and explanation of the pros and cons of why a certain mode of anaesthesia or analgesia is preferred, usually will lead

or guide the patient into approving the proposed anaesthetic plan 3. Prescribing preoperative drugs (premedication) (a) Primary aim: Relief anxiety, alleviate pain and improves cooperation

(b) Secondary aim: Reduction in the usage of induction and inhalational agent

(c) Indications are often referred to as the 7A's;

(i) Anxiolysis • Benzodiazepine is generally prescribed preoperatively to alleviate anxiety and reduce stress-induced physiological changes in scheduled surgical patients and in children with

learning disability

• Establishing a good rapport with the patient by discussing the anaesthetic techniques and answering questions promptly are also an important component of anxiolysis

• Avoid sedative drugs preoperatively in ill, septic, elderly, premature babies, neonates, infant < 6 months and patients with potential airway problems (obese, OSA, previous history of difficult intubation)

(ii) Amnesia • Benzodiazepines are most commonly used for this purpose (midazolam has the most marked effect) • It is beneficial in patients undergoing invasive procedures prior to anaesthesia.

(iii) Analgesia: In paediatric practice, EMLA cream (pg. 158) is used as a topical anaesthesia and applied 45 minutes to 1 hour prior to venipuncture (iv) Anti-emesis: This is targeted to specific groups of patients with high risk of PONV (pg. 237)

(v) Antacid

• Purpose of prescribing antacids is to alter the gastric secretions

rendering it to be less acidic and less in volume • It also serves as prophylaxis against gastric acid aspiration • Indicated in all obstetric, obese patients, known history of hiatus hernia and reflux oesophagitis • 4 types of commonly used drugs are: - H2 receptor antagonist (ranitidine) - proton pump inhibitor (omeprazole)

- non-particulate antacid (sodium citrate) - gastrokinetic agent (metoclopramide)

(vi) Antisialogogue • It is an anti-cholinergic (glycopyrrolate: pg. 159) commonly given about 30 minutes prior to fiberoptic intubation • It reduces salivation and facilitates fiberoptic intubation by providing better visualization

(vii) Additional: Antibiotics, steroids and nebulized J3-adrenergic

4. Justifying the patient's own regular medication (a) Patients may be taking regular medications/herbal supplements (pg. 161) that could interact with anaesthetic drugs

(b) It is pivotal to decide and choose which drugs are to be continued, adjusted or withhold

(c) Examples: • warfarin need to be changed to heparin in time so that the INR level

can reduce to an acceptable operative levels • prolonged {> 3 months) or high-dose {> 10 mg/ day) corticosteroid

treatment warrants perioperative corticosteroid supplementation • oral hypoglycemic agents should be stop on the day of surgery

(insulin sliding scales infusion may need to be started for those on

insulin or when prolonged fasting is anticipated) 5. Fasting Guidelines

(a) Adequate fasting is important as it minimizes the risk of regurgitation and pulmonary aspiration of gastric contents while providing anaesthesia (in particular during the process of GA) (b) Gastric emptying is faster for liquid compared to solids (carbohydrate >

protein > fat) (c) Rate of gastric emptying influences the risk of PONV. It is determined by few factors:

• slowed by: anxiety, pain, mechanical obstruction, labour, drugs (opioids, anti cholinergics)

• increased by: gastric distension, drugs (metoclopramide)

(d) Below are the recommended minimum fasting periods based on the ASA guidelines:

• six (6) hours for solid food, infant formula or other milk • four (4) hours for breast milk • two (2) hours for clear non-particulate and non-carbonated fluid (small volumes of 10 ml/kg have been shown to reduce the

volume and acidity of gastric content) 6. Planning postoperative care

(a) Modes of analgesia should be planned and explained to patient during

this preoperative visit (b) Decision for postoperative care in general ward, HOU or ICU are determined by the premorbid status

r

L

✓ It is worth to , c ommunicate a.nd1 discuss with the surgeon on the nature, extent and a nticipated d urnti on o,f surgery in order to formu I ate the most a ppro,p ri ate a naestti eti c plan for the p1a Uent ✓ It is i m portant tha t plans are being con veyed to s u rgeons, nurses and other a n aesthetic staff where relevant ✓ Anaesthetic assessment and premedication orders should be written legibly i n the preoperative: form (Appendix 1 ) to avoid confusion ✓ R is 1k disclosur,e assodated with the chosen anaesthesia are done for those that are more serious and likely to occu r (Appendix 3) ✓ It is important to document discussions regarding the planned anaesthesia and consent should be signed as well as witne, s sed (Appendix 4) ✓ T h ,e u l timate g,oa l l of preope rative assess ment is to provide s afe anaesthesia care and min i mize the periopera ive morbid.ity/mortal �fy as much as possf ble

,

..J

REFERENCES AND FURTHER READING 1. Gwinnutt CL. Lecture Notes: Clinical Anaesthesia (2nd edition). Oxford:

2. 3. 4. 5.

6.

Wiley-Blackwell Publishing; 2004. Spencer R, Mcindoe AK. Preoperative assessment. Anaesthesia and Intensive Care Medicine 2003 : 3 19-323. Minchom A. Preoperative assessment. Anaesthesia and Intensive Care Medicine 2006: 437-44 1. Lee CY. Manual of Anaesthesia (2nd edition). Singapore: Mc Graw-Hill; 2006. Ainsworth BE, Haskell WL, Herrmann SD, Meckes N, Bassett Jr DR, Tudor-Locke C, Greer J L, Vezina J, Whitt- Glover MC, Leon AS. 20 1 1 Compendium of Physical Activities: a second update of codes and MET values. Medicine and Science in Sports and Exercise 20 1 1 ; 43(8): 1575158 1. FJ Garda-Miguel, PG Serrano-Aguilar, J Lopez-Bastida. Preoperative assessment. Lancet 2003; 362: 1749-1757. Basic

7. Cote CJ. The upper respiratory tract infection (URTI) dilemma: fear of complication or litigation? Anesthesiology 2001; 95: 283-285.

8. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy

patients undergoing elective procedures. Anesthesiology 2011; 114: 495-511.

3 CORE AIRWAY MANAGEMENT Throughout ones medical career, airway challenges may be encountered during an emergency event. Airway refers to the upper airway structures; nasal, pharynx, larynx, trachea and bronchus. Principles of managing the airway is core

knowledge and skill which should be acquired by every medical practitioner and are deemed an invaluable tool throughout ones practice. Maintaining a patent airway is pivotal in providing adequate oxygenation and ventilation. Failure in maintaining an airway even for a brief period of time can be life threatening.

There are four (4) important considerations in this topic: 1. Applied airway anatomy & physiology

2. Airway evaluation 3. Airway management 4. Difficult airway

APPLIED AIRWAY ANATOMY AND PHYSIOLOGY

The aim is to highlight relevant anatomy and physiology of practical importance in core airway management. Having this knowledge will make us understand why we do some of the things we do.

Nose 1. Nasal airway is the primary channel for normal breathing which is structurally supported by bone and cartilage

2. Nasal septum (Figure 3.01) is the wall which separates the left and right nostril. A deviated septum (Figure 3.02) can cause upper airway obstruction which poses

potential difficulty in maintaining airway in conditions like: (a) mask ventilation: use the oropharyngeal airway to overcome this

(b) nasotracheal intubation: might need to use the other patent nostril o insert the nasal ETT either directly or fiberoptically

Nasal1 septum

Fig u r•e 3. 01 1 : N o rmall septum (frontal! section of nasall cavity )

fig11Jre· 3. 1 0 2:� Deviated se ptum

3. Presence of turbinates (narrow passages that are covered with moist nasal respiratory mucosa with rich vascular capillary bed directly beneath it) on the

lateral wall of each nasal cavity serves as an air conditioning function in which it filters (particles > 4 mm are removed in the mucus), warms and humidifies the inspired gases (Figure 3.03)

4. When the nostrils are bypassed (in cases where patient is intubated with ETT or supraglottic airway is used), cold and dry gas will reach the lower airways and disrupts the ciliary activity causing retention of mucus leading to micro-atelectasis.

Therefore, it is recommended to use heat and moisture exchangers (HME) which will be usually mounted between the ETTi supraglottic airway and the breathing circuit 5. Nasal mucosa easily absorbs many medications directly into the venous circulation giving its therapeutic effect. This is important in situations where awake

fiberoptic intubation (AFOI) is being considered by which the upper airway has to be anaesthetized with LA prior to the procedure

Naso pharynx

Oroph rynx

Figure 3.03: Sagi�I section of upper resp iratory tract

Pharynx

1. Pharyngeal airway is the airway passage between the posterior part of the nasal cavity and superior part of larynx 2. Anatomically and functionally it can be divided into (Figure 3.03):

(a) nasopharynx: lies above the soft palate and behind the nasal cavities (b) oropharynx: lies from the inferior aspect of soft palate to the dorsal border of tongue and superior aspect of the epiglottis (c) laryngopharynx: lies between superior border of epiglottis and inferior border of cricoid cartilage

3. Pharyngeal airway is supported and kept patent by the presence of soft tissues

and tension of the muscles of swallowing (genioglossus, geniohyoid, sternohyoid, sternothyroid and thyrohyoid)

4. Pharyngeal airway is vulnerable to collapse when the muscle tone surrounding

the pharynx becomes depressed or paralyzed (during GA). The common sites of obstruction is the soft palate, epiglottis and the tongue

5. To relieve the obstruction, basic airway manoeuvre can be applied (head tilt, chin lift and jaw thrust: pg. 49). This will tense the muscles of the floor of the mouth causing the larynx and hyoid to be lifted away from the posterior pharyngeal wall 6. Patients who are at risk of pharyngeal airway collapse (Table 3.1) should be identified during preoperative bedside airway assessment

Table 3.1 : Causes of airway obstruction Cond iti on

M echa n· ca I Obstru ction

Exampl,e s

Nasal obstruction Pllaryngea' I o bs rucfon La1fY11gea obslm ction

Syn d ro m ic diseases a nd cran i,o faci al abno rma li t es

Downs, p·erre Ro !J i n , acrnmegaly, Treacher Collin s, C ouzon s, Goldenhaar, achondrnp las ia

N e uromuscular disorde r

M uscula r dystro hy, myoton ic dystrophy, Gullai nB.a rre , yast h enia gravis, poliom yelitis

Obes i ty

Othe rs

O besity sleep apnoea ,( OSA) , Prader-Will i

Ageing

Patho physio logy

j

Devia, ed .se ptum , chron ic 11asal congestion , fore- i gn bo : y

I

tu mou li ha e ma oma , foreign body

I Adenotonsi l la r hypertrnphy

Laryngomala c ia umour, , oedema , go iter, fo reig n body Macrog oss ia , m icmgna thia, maxillary hy,popla s ia Pharyn geal soft tis sue s hype rtmp hy

I muscles

Deterio rat ion of plh aryngea l

7. Oropharyngeal and nasopharyngeal airways are useful adjuncts to improve and

maintain airway patency

8. In difficult airway condition, LMA can be inserted to maintain the airway and oxygenate the lungs

9. Glossopharyngeal nerve block can be performed by:

(a) applying tongue depressor to the lateral surface of buccal mucosa and

spraying LA to the tonsillar fossa bilaterally (b) asking the patient to gargle the LA to maximize the spread of block (useful to supplement airway block prior to AFOI: pg. 65) Larynx

1. It is an organ of phonation and commonly known as the 'voice box'/vocal cord/glottis 2. Lies between the level of C3-C6 vertebrae (newborns: C2-C3) 3. Vocal cord is the narrowest portion of the airway in adults and acts as a sphincter or valve that protects the lower airways from aspiration of gastric contents during swallowing 4. Innervated by 2 branches of each CN X (vagus nerve); superior laryngeal and recurrent laryngeal nerves

5. Laryngeal structures (Table 3.2) can simply be divided into:

{a)

Cartilage

- solitary cartilage {epiglottis, thyroid cartilage, cricoid cartilage) - paired cartilage {arytenoids, corniculate, cuneiform)

{b)

Membrane

- thyrohyoid membrane, cricothyroid membrane

{c)

Bone

- hyoid

{d)

Muscles

- external muscles of larynx - internal muscles of larynx

e!

Iii

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Table 3.2: Luyngeal structures

scopy determines the success riagement f sBURP" and "bimanual olves manipulation of 'thyroid

Laryngeal structure 1 . Solitary carti lage

Anatomical desaiption

Clinical application

i. Epiglottis {Figure 3.04) .JI i. ': :'

Hyoid bone Epiglottis

-----Thyroid lamina Thyroepiglottic ligament

Figure 3.04: Cross section of the larynx P technique

and index finger on the patient's d and Rightward Bressure' �lion at which 1he >est laryngeal view

• • • • • •

Leaf like shape It stands ob6quely posterior to the base of tongue and hyoid body, anteriorly to the la,yngeal inlet It's free end is broad and sfightty notched in the middle It's attached end is loog, narrow and oonnecled by thyroepiglottic ligament It's sides are bilateraly pined to the arytenoids by a,yepiglottic folds fOfflling the laryngeal inlet Vallecula: is a depression formed by 1he glossoepiglottic fold (mucous membrane that covers the anteoor part of epiglottis and pharyngeal surface of the tongue)

Figure 3.05: Blade tip p •

During swallowing, larynx wiD l epiglottis posteriatf to dose o preventing aspiration of gastri( • During laJyngoscopy, the blade is placed in the vallecula in oo: visualization of the glottis (Figt • Jn infant/children: epiglottis is k • The epiglottis serves as a :refei Lehane Grading (pg. 55)

Laryngeal structure J'o:ne by the laryngps-eopist � 3 .09}

Solitary cartilage

Anatomical description

Cl inical appfication

ii. Thyroid cartilage (Figure 3.06 and 3 .07)

•

•

•

A full laryngeal view during laryngo of tracheal intubation in airway ma, Laryngeal view can be improved b) laryngoscopy" technique which in'll cartilage

I.

BURP technique

• • • • •

: Th.yroid c artil l.11g:e ln by laryng:oscop ist istant wil l take over 1he tryrl!Joscopist and tracheal

Largest laryngeal cartilage and shaped like a shield (serves to protect the vocal cord structures) Consist of 2 lamina that fused together at its lower 2/3 foming laryngeal prominence Superiorly, the lamina separates and has a V shape which foons the lhyroid notch Posteriorly, it has 2 superior and 2 inferior horns (oomua) Bilateral inferior oomuas will connect to cricoid cartilage by cricothyroid ligament Glottic opening lies directly behind this cartilage

TT

_ _ _ ¾4

Hyo id bone

Th� cart,

_../

Thyroid cartilage • � 3. 1 0: Ass istant in g l aryng,eal pressu re aryn goscop ist g:e ts an al v iew

Cricoid carnlage

Figure 3.06: Oblique view of the thyroid cartilage

Figure 3.07 : B U RI • • •

Described by Knil in 1 993 An assistant will place lheir thumb thyroid cartilage They will exert a '.!;la ckward !!.pwar {patient's right) and sustain the po! laryngoscopist is able to have the t

norm ing cri coid q, id sequence fain t/children

Laryn geal structure Solitary ca rlii lage

An atonn i c. a l des c ili ptiori

C l ini cal a,ppl ication I I . B i m an ual lal)ln goscopy Bpiglottis

Greater oomu of hyoi d bone

•

Mani pulation of the thyroid carti lage iis c themselves du ring1 laryngoscopy {Fig ;un

J_e,s ser conn.11 of hyo i d bone _ T lhyro h yoidl memb r ane

·�

r---

Cricoflh yn1i d mem b1m ne ,___ C rioo i d ciirtilage

ure

• s

liZJ!fl-«

Figure J, . ll9 man i pu l atil •

After an optimal laryng,e al view, the assi position that heliS Deen detem1rned by l.i intubation pursued (Figure 3. 1 0)

Tracheal cartilage

Fig1ufe 3.llilk Fro ntal v i ew of the thyroid carti lage

Fig u n applyi after I , optim

subluxatio:n or

. mexpenen ce : jutting1 out ifro m 1ic diooases mess of voice,

Laryngeal structure Solitary ca rti lage

Anatom ica l, desc. r i ption

i i i . Crico id , c arti la�re {Fig ure 3_06, 3 .08) • A sig n et ri ng shape that forms s1 complete ring at th. e base of laryrn ( Figu re 3_ 1 1 ) and lies below lhe thyrord c a rtr lag:e at the level of GEi • Ainteriorfy, the cartl lag;e heig ht is 1 crn a nd postel"iorty it rs 2 cm extending [11 a c ephalad di redion (forms lhe posterior wal l o f l arynx at th e level o f th e cricothyroid membrane and thyroid cartila g e ), • Cricotrad1ea! ligament wi ll s tJspe!11d tile tmcilea from the oricoid carti lage • Laryng;e al i nlet extends firom the epigtottiis to tile lower borders of cri coid cartilage ..-n!II 1.";1,t

11

• •

Th is, carti lag,e is .m i m pornmt structure i n p-e1 pressure (Fig;u re 3 . 1 2 and pg1 • 1 1 8) d u ring ra ind'uction i111 emergency ilfa cheal in�ubatio :n It is the 11arrowest porlio:n of the airrway in inl

-----� '� tJJ---r2--'

t � (\

•

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Hyoid bone t.p ! glottis

Vesti bu hn fold • (fa lse cord �

Voca l cord ,, --- Thyroid! c ..uti l�ge

•

C l in i cal app! 'ication

C·ri coid ca rti lage

Trachea l cmtilage

F ig u re 3 . 1 1 : C riooid ca rt i la ge (sa gitta l view)

Figure 3 . 11 2' : C rico i d prnss,

Laryn geal structure LA via th i;& 1d tracheal!

Anato:mkal description i.

Trnche.a

:.xcitement

saliva/blood/ 1i ng of a irway

•

I;_

Com icu m ate �- . . cani l,a ge

situatio111 e farynx) . It i ,s ;ecrni ng tfie

riai i nfold i:ng local ruent

Aryten oids

Epig'.lottis

Vocal cord ----,,.� � �¥ .;,

g LA tram;1 blodk i n

b ilatera l

C lin ical appl icatio n

• •

'\' I

• •

1

Cu :ne ifo:rm calltilage

This cartilage is very frag ile and prone to rnju ry (: dislocation) Risk factors associated viith this injury inclu des: i anaesthetist, direct pressure from the ETT, stylet the ETT. traumatic imubalion and several system (rheumatic. arthritis, acrorne91aJy) Posfi-extubatfon patients wCTI present with hoarse• SO[e throat, dyspoogia or i nspir:ato ry slrido. r

Fig u re 3. 113: Vocal cord

Paired and triangular-shaped carnlage Articulates poste:rosupenorly to the border of aicoid ,�ge at cri comytenoid joint via cri coorytenoid ligament • Site of attachment for vocal ligament and intrinsic muscles of vocal card • P1l ays a major role fo r the piooiition of vocal cmd {wlilen the vocal: ligament tenses) i i. Com i c:ulate • Hom-shaped • Fused with lhe apex of arytenrnd camlage and fos. posterior to the aryep1gloffic fold i i i. Cu 11it e;i fom11 • Wedgfr.-Shaped • Lies within the aryepiglottic fold amj ante.ii(r to the oomLc.ulate canilage • Forms the lateral aspects of the epiglottis

I•

Supports the v,ocal f;old

I•

Supports too vocal fold

Laryngeal structure

Mem bran e

An atomi c .ai l des,c ri ption

i . Thyro hyoid (Fig; ure 3 .08}

• •

i i. Cricothyroid (FJg; ure 3 .08} • Avascufar yellow e Imme ti ssue membra11e that joins the 1 uppe:r bord'e:r of cricoid eartiJag;e and lower bmd'e ir of th!(ifoid cartil age • Approxi m ately 1 0 mm (heig ht} x 22 mm (wrdth} • It lies 11- 1 _5 fb below the thyfOid notch • Vocal oords are approximately 1 cm above lhe clicothyiro id mernbra11 e (less like:ly to be damaged d uring cri' oothyrnto my)

� -[he roi >en l!he i

sa[ival 1p dle

M embrane th at joins the upper oorder of thyroid cartilage and hyoid bone Inter nal laryngeal nerve (sensory branch of superior f .,iryngeal nerve) pierces th is m embran e

B 011e

; of

cal ise ilie � [I M lf.scles

H yo i .d ( Figure 3_08) • Horseshoe shaped bo11e , ro cated a,t the a nte.rirnr m idl ine of the1 111eck • It has a central body and 2 pairs of oom 1L1 o1 (g reater and lesser comu) • lhe internal laryng eal nsrve (sensory bra11 ch of s uperior lai-y11geal nerve} iPierces the thyrohyoid membrane app:rox:imately 1' cm i nferi or to the greater comu Externa l m u scles of larynx (passing between the l.uyro: a11d surrou ndi ng stru. clure }: I.

Suprallyoid g, mup • Stylohyoid • M ylohyoid • Ge11 iohyo id D igastri.cs

..

C l ini cal .J pp ! ication

•

I

•

Superio r lmyng,e al nerve b lock can be do ne by givi ng mem brane (su!);plements the .iif\'ll'ay block in AFO I a1' ste,nti ng as it abor is hes the gag 1reflex) Recurrent la ryngea l nel'Ve blod can be done by g iviITTJ tmcheal ly via tllis membran e (su ;p ;ple.rnents the a:i rwa) AFO I, awake taryng, osoope or retrograde intubati'on} Site fm cri rnthyrotomy (pg1_ 167) in 'emergen cy airway' (when the le'lel of a irway ol1stru ction is a bove or at tlhi oonsideredi as the last resort when other methods of � .air:way and maintaining oxygenation has fair ed

•

S uperio r lmyng.e al neJ¥ie b lock c.an be done using the gre.iiter c.o m u of hyoi:d bon e as a landmait.: membranE (supplernelllts the a irway bl'od in AFOI}

•

Laryngospasm is a fo:roed closu re of the vocal cordls , of the mytenoids and aryepig lottic folds seooncl. ary to sti 111 1U lation to the vocal cordls, made worse by su bseq coverag e by the epigtotti is Vul'nerably ca n occur duri ng stage II of anaesthesia (E stage) Risk factors: niranrpula:tron of airway a11d pre.se11 ce of : vom irus duri11g lig 'ht pf,me of anaesthes ia, rmlposition device, G O RD and aspi rntion

•·

•·

v ngeal 1cture

An.atom i:eal descri pti , o n

Cl in ical' app]icatiot i

11_ l nfrahyoidl group • Stemothyroid •· Stemohyoid • Thyrohy oid • Omohyo id

•

Intrin s i c m usc�es of 1 1 �u)i'n:x (musdes ccn fi ned to ihe la rynx ): • l ntera rytenoid • Lateral cri ooarytenoidl • Posterior aicoaryt.e noid • Criculhyro1d • Th�omytenoid

.. •

A fiirm and sustained! jaw lhrust (pg _ 49) can someti mes br:e lruyngo�asm wilhil"I ·1 -2 brealhs. This is possibfe .as Ille hy bone wi ll be elevated and ep ig lottis become stre1ched tio o� aryepig1otti c fol , d s hence opens up !he vocal colds Ollher tmatme. r1t to owmome laryngoopasm: removal of the bloodf'vornitus, CPA.P, deepen the anaesthesia by dialling u vdlame agent and usage of muser e relaxant Recurrent laryrigeail1 11e1Ve siuppl ie..s al.I the trntrinsic muscles larynx (except fur cricothyroTd), rie rve inj ury may fead to vo curd! dysfuri cti:on . Unil ateral nerve iHjll'ry may not compromi a irway function btit m1y impair th. e. poot, e ctive a 1rway renexe ,renling aspirruioo

Trachea

1. Commonly known as the 'wind pipe'. It is a midline structure although in the thorax it may be slightly deviated to the right by the presence of the

arch of aorta and can be further divided into upper extrathoracic and lower intrathoracic part 2. In adult, it's length measures approximately 10-12 cm and its internal diameter is about 2-2.5 cm

3. Extends from below the cricoid cartilage (C6 level) to the carina and ends by dividing into right and left mainstem bronchus (T4/T5 level)

4. Formed by a series of 15-20 C-shaped cartilages which forms the anterior and lateral walls of the trachea

5. The cartilage deficient part at the posterior is completed by two layers of smooth muscles (transversely placed trachealis muscle and an inner superficial longitudinal layer) and fibrous tissues that runs along the length

of the trachea 6. Tracheal cartilages are covered with mucosa and respiratory epithelium

which is pseudostratified ciliated columnar epithelium which the cilia

movement helps to expel foreign particles and mucus 7. Goblet cells are situated between these epithelial cells and secretes mucus to moisten and warm the trachea as well as to trap and remove foreign particles from the airway

8. Important structures (Figure 3.14) that are related to the trachea are the recurrent laryngeal nerve posterolaterally (in the trachea-oesophageal groove), esophagus posteriorly, isthmus of the thyroid gland (lies over 2nd to 4th cartilage) and thyroid veins anteriorly

Vag us n e rve -� nerve

vei n s tsthmus f thyroid nd

9. Differences between children and adult's trachea are as below: (a) children's trachea is smaller and in early life, its size and diameter corresponds more to body weight than height

(b) more deep lying, mobile and bifurcates at a higher level compared to in adults (T4/T5 levels)

(c) there's a discrepancy between the subcricoid and carina diameter which makes the trachea funnel shaped and later, this will diminish to become

more cylindrical shaped 10. Clinical application:

(a) during bronchoscopy, the posterior part of the trachea where the longitudinal smooth muscle is seen running is identified and helps to determine the right and left mainstem bronchus

(b) prolonged intubation with high cuff pressure can cause vocal cord palsy

by exertion of pressure on the recurrent laryngeal nerve (c) as the diameter of trachea in children is much narrower (7-15mm), thus a slight oedema of 1 mm thickness will cause very significant narrowing of the tracheal diameter leading to airway obstruction (d) smoking causes increased secretion of hyperviscous mucous (ciliotoxins) that can inactivate and destroy the cilia which later impairs the tracheobronchial mucous clearance. Besides that, irritants in the smoke can also disrupt the integrity of the (a) epithelium. Incidence of respiratory events during anaesthesia in smokers almost double than that of non-smokers (5.5% vs 3.3%) (e) bedside percutaneous tracheostomy is a popular option chosen in the critical care compared to open surgical tracheostomy with regards to patients with prolonged mechanical ventilation. Its incision landmark is between the 1st and 2nd cartilage. However, there is a possibility of damage and bleeding if the thyroid gland is enlarged or the neck is short due to anatomical displacement of the neighboring structures Bronchus 1. Trachea ends at the carina by bifurcating to the right and left mainstem

bronchus which forms a subcarinal angle approximately between 40-1050 (Figure 3.15) 2. The right and left mainstem bronchus differs anatomically in terms of length, orientation and angle that it forms with the central axis (Table 3.3) 3. lnadvertant endobronchial intubation might occur due to the vertical orientation of the right mainstem bronchus if the ETT is advanced too much leading to collapse of the contralateral lung and hypoxia

Table 3.3: Anatomical difference be twe, e n right and l left mainstem bronch us f

M a i n B ron c h us

Ri g h t

Le t

Length (cm)

2-2.5

4-4.5

Angl,e

20-30°

40-4 6°

Orienta tion

More vertical

More hori�ontal

Dista nce between · c arina and upper bronchus (cm)

1 .5-2.0

4.5-5.0

Ri i g ht main bronch us

Tracheal bifurcati on Left mai n bronch us

0 11

I I I I I

_.

> 35

. 0

Figure 3.15: Right and left mainstem bronchus

AIRWAY EVALUATION

A comprehensive airway evaluation is important in predicting and detecting a

potential difficult airway. This is best divided into history, bedside airway examination and special investigation related to airway. History

Extract any history regarding: 1. Previous difficult intubation or mask ventilation (patients will usually be

informed by their anaesthetist or attending doctor regarding this incident if there is any)

2. Airway related events (previous broncho/laryngospasm, change of voice, surgical/radiation at the head and neck area) 3. Airway related disease or symptoms (asthma, goitre, URTI, OSA, congenital/acquired syndromes, noisy breathing, shortness of breathing) Bedside Airway Assessment Assess general airway physics:

1. General appearance (obese, pregnant > 12 weeks, syndromic features with potential difficult airway (syndromes): Down's, Pierre-Robin, Treacher-Collins, Goldenhaar, Beckwith, Hurler's/ gargoylism)

2. Signs of airway obstruction/distress (hoarse voice, strider, retraction of suprasternal/ supraclavicular/intercostal space, tracheal tug, restlessness,

cyanosis) 3. Anatomic features associated with difficult airway management (receding chin, short muscular neck, micrognathia, protruding maxillary incisor and

jaw, high arched palate, deviated trachea) 4. Pathological: infections (retropharyngeal abscess, croup, epiglottitis),

arthritis of the neck (ankylosing spondylitis, rheumatoid arthritis), swelling of the head and neck (gaiter, cystic hygroma, nasopharyngeal carcinoma)

and facial trauma/bums 5. Nose: assess the symmetry (deviated nasal septum) and patency of nares (polyps)

6. Teeth: prominent, chipped or capped teeth, loose tooth, edentulous, dentures

Performance of bedside airway test:

1. Combination of bedside airway tests are more meaningful in predicting

difficult airway compared to individual bedside airway tests 2. Sometimes these tests may over or under predict the likelihood of difficult

airway 3. Individual tests are: (a) Mallampati test

(b) inter-incisor gap and temporomandibular joint (TMJ) (c) mandibular protrusion test (d) thyromental distance (TMD) or Patil's test (e) sternomental distance or Savva test (f) atlanto-occipital (AO) joint extension A. Mallampati test

1. Patient is remained seated with the neck at a neutral position 2. They are asked to open the mouth widely and protrude the tongue as far out as possible (without phonation) 3. Then inspect the oropharynx and determine the Mallampati class based

on findings in Figure 3.16 4. Class Ill and IV predicts the difficulty in direct laryngoscopy and attempt of intubation (but a poor predictor in difficult bag mask ventilation)

5. Based on this, it is better to combine Mallampati test with other bedside airway tests to sufficiently assess and predict a difficult airway

.

•

1

-..... ,_ .

Soft pa late

_ _ , .w--

-'--- si ! ll ar

__.......,� ...__ ;:

✓--- � '

1...-8"'7--._

. �-

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Ill

Figure 3.1 6: Mallampati class

IV

r------------------------------I crass I: Soft palate, uvu la and tonsillar pillars seen I Class H: Soft patate and uvula seen . Tonsillar pillars not seen I Class Ill: Only soft palate and base of uvula seen (possible to intubate I I with some difficulty) I Class IV: Soft pa late not seen (most at risk of d ifficult intubation) I ·-------------------------------

• • • •

Sou rce : 1. Mallampati SR, Gatt SP, Gugino LD, et al. A clinical sign to predict difficult

tracheal intubation: a prospective study. Canadian Anaesthetists ' Society Journal 1985; 32(4 ): 429-434 2. Samsoon GLT, Young JRB. Difficult tracheal intubation: a retrospective study. Anaesthesia 1987; 42: 487-490

B. Inter-i ncisor gap and temporomand ibu lar joint (TMJ) 1. Patient is asked to open their mouth widely, the distance between upper and lower incisors is measured (Figure 3.17) 2. Normal distance is 4-6 cm (3 fb)

3. Reduced ability to open the mouth indicates reduced mobility of the TMJ and impaired access to the patient's airway

4. Measurement of < 2 cm (1 fb) predicts a difficult laryngoscopy and

insertion of supraglottic airway 5. Restricted movement can be due to ankylosis/ fibrosis, tumors etc.

� I I I I I I I ·

Figure 3.17: Inter-incisor gap measurement

C. Mandibular protrusion test

1. Patient is asked to protrude the mandible as far as possible and the

capacity to bring forward the lower incisors beyond the upper incisors are classified to 3 classes (Figure 3.18) 2. This test predicts the adequacy to visualize the larynx during direct laryngoscopy

Figure 3.18: Mandibular protrusion test

r-- - - - - -------- - - -- --------- ---I I C lass A: Lower inci sors or mandi ble able to be protruded or advanced I beyond the upper incisors I C lass B : Lower incisors or mandible i s edge to ,e dge with upper incisors I o I C llas : s C : Unable to pr trude mand ible at all or owe r incisors cannot go I beyond the upper incisors (pred icts diffi.cult laryn goscopy) I

• I I I I I I I I

� - - - - - -- - - - - - - - - - - - - - - - - - - - - - - - - ·

D. Thyromental distance (TMD) or Patil's test

1. Request the patient to fully extend the neck, the distance between tip of thyroid cartilage (notch) to the tip of the chin (mental prominence) is measured (Figure 3.19A) 2. This distance estimates the potential space into which the tongue can be displaced during laryngoscopy 3. Measurement of < 6 cm (3 fb) predicts a difficult laryngoscopy

F i g u re 3_ 11 9:

A - T hyrom e ntai distan ce (ti p of til e t hyroid ca rtilage to th e 1i p of m , e mil:u m)

B - Ste r ri o m e ntal dista n eie (uppe, r border of th e m a 11 u briu m to 1 he tip o f m e nt iu rn )

E. Sternomental distance or Savva test

1. Request the patient to fully extend the neck, the distance between the upper border of manubrium sterni and the tip of the chin (mental prominence) is measured (Figure 3.198)

2. Measurement of < 12 cm predicts difficult airway Basic F. Atlanto-Occipital (AO) joint extension

1. Patient will face directly to the front, head erected and neck extended as maximum as possible with the mouth open

2. Visual estimation on the angle traversed by the occlusal upper teeth will

predict the feasibility of the patient to perform the "sniffing the morning air" or Magill position (Figure 3.21)

3. Visual estimation in the reduction of AO joint extension is usually made and graded as in Figure 3.20, for accurate measurement a goniometry can be used 4. This test reflects the possibility of the patient to align the 3 anatomic axes, namely the oral, pharyngeal and laryngeal axes (Figure 3.21)

5. When the AO joint cannot be extended, attempts to do so causes the convexity of the cervical spine to bulge anteriorly, pushing the larynx more anterior

6. Grade Ill and IV predicts difficult laryngoscopy

·------------· Grade I: > 35 � (N orm a l an gle of extension ) Grade Ill : 22" -34 ° G rade m : 1 2� -21 " G rade IV: < 1 2" 1

I I I I I I

S ourc e : Bell h ouse CP, Dove C . C riteri a for estimatin g l i kel ihood of difficulty of ,e n d otrach e a l i ntu bati on wm th, e Maci ntosl h l aryn gosoope . Ana esth Intensive care 1 9 88; 1 6: 32 9-33 7 Figure 3.20: Atlanto-occipital joint extension (angle of extension)

Special Investigations

Relevant X-rays of the neck and cervical spine should be performed if time

permits:

1. Lateral cervical X-ray (head in neutral position)

(a) This allows several measurements which predicts difficult laryngoscopy

(mandibulo-hyoid distance, anterior/posterior depth of mandible, C1-C2 gap, atlanto-occipital gap) (Details of the measurement is beyond the

scope of this handbook)

2. Computed Tomography/ MRI

(a) Able to delineate level and degree of airway obstruction

(b) Estimation of size of the mass which is causing the airway obstruction * If there are any risk factors showing an anticipated difficult airway and BMV, AFOI should be considered instead of undergoing induction procedure prior to intubating the patient

AIRWAY MANAGEMENT 1. Airway management are often encountered during resuscitation and surgical procedures for delivery of assisted ventilation (elective or emergency)

2. Clinical management of the airway can be simply divided into: (a) Preparation of the patient

(b) Airway maintenance and ventilation

(c) Endotracheal intubation and extubation (d) Difficult airway management Preparation 1. Equipment

(a) Apply MMAALESSSS rule (pg. 115) (b) Choose the appropriate size of ETT and blade (pg. 88). Check the ETT cuff (ensure no leak) and the adequacy of laryngoscope light source

(c) Place the stylet in ETT for all urgent and emergent intubations (Figure 3.59B)

(d) Prepare drugs (opioids, induction, NMB agent) (e) DO NOT FORGET RESUSCITATION DRUGS (atropine, ephedrine, ± phenylephrine, ± adrenaline)

2. Patient: (a) Attach the essential standard monitoring (pg. 166) and obtain baseline vital signs (ECG, non-invasive BP device, pulse oximetry) (b) Position the patient in the "sniffing the morning air" or Magill position

(Figure 3.21) with the neck flexed and extension of AO joint in order to align the laryngeal structures (Table 3.2)

Figure 3 . 2 1 : 1 '' S n iffi ng the m o rn ing a i r" or MagUI po1 sitton 1( alig nm e n t of ora l 1 phary n g e a l and la ryngeal axe s )

Sourc, e : Cormack RS, Lehane J. D ifficult tracheal in tubati on in obstetrics. Anaesthesia 1 984; 39 : 1 1 05-1 1 1 1 (reproduced with the kind permission of Joh n Wiley and Sons) (c) "Ramping" position (Figure 3.22) can be applied in obese patients with short neck in which towels are placed in between scapula to gain a

horizontal alignment between the external auditory meatus and the suprasternal notch (from lateral view)

A-Su pi ne witho ut ram ping pos ii' t ion

B-Supi ne• with rampi ng pos,i tion 1

F i g u re 3 . 2 2

(d) Troop elevation pillow (Figure 3.23A) is a special device that mimics 'ramping' or 'stacking blanket' technique and addresses the stability issue associated with them (Figure 3.238) (e) Both method aims to achieve a horizontal alignment between the external auditory meatus and the suprasternal notch by elevating the head and upper torso resembling semi-recumbent position

(f) This semi-recumbent position will cause downward displacement of fat and abdominal content which later minimizes the effect on diaphragmatic and

intrathoracic pressure allowing better preoxygenation, ventilation and direct

laryngoscopy

(g) Remove or suction any foreign materials from patient's mouth (h) Preoxygenation (pg. 116)

Figu r,e 3 . 23A : liroo p eleva tion p Ulow

Fi,g u re 3.23B : Patie n t lyi n g o n tro o p elevation pillow

Airway Maintenance

Techniques to maintain a patent airway:

1. Remove any visible obstruction from the patients mouth (dislodged dentures, foreign body, food) 2. Suction the oropharynx (if suspect there's any blood, vomitus, secretions etc.)

3. Perform basic airway maneuvers to ensure a patent airway: (a) Head tilt (Figure 3.24A)

i. Hand is placed on patient's forehead and firm backward pressure is applied

ii. This relieves minor obstruction (b) Chin lift (Figure 3.24B)

i. With the other hand, the chin is gently lifted to displace the tongue anteriorly

fig u ire 3 .24: A-Hea d rn t B _JC h i n l"ft

F i g1u re 3 . 2 5 : Jaw th 1 rus1

(c) Jaw thrust (Figure 3.25)

i. Patient's bilateral ascending rami of the mandible just beneath the ear lobes are firmly grasped and pulled forcefully upward

(anteriorly) with both hands ii. This will make the lower teeth reside in front of the upper teeth iii. Principally this resembles the triple airway maneuver (mandibular advancement, head extension and mouth opening)

iv. Jaw thrust provides tension to the hyoid bone anteriorly, which in turn draws the epiglottis away from the posterior pharyngeal wall (opens the pharynx) and pulls the tongue away from the palate (opens the oropharynx)

v. This maneuver improves airway patency and ventilation 4. Perform airway maneuvers for mask ventilation: (a) One handed EC-clamp (holding the mask: Figure 3.26) i. Operator will be at the head end of the patient

ii. Mask's cuff must fit and cover the patient's bridge of the nose and mouth iii. Place the left thumb and index finger around the port or chimney of the mask (C portion)

iv. Lower 3 fingers are spread to hold the patient's mandible and its inferior angle (E portion) while concurrently giving an upward force against the anaesthesia face mask

v. Perform a downward tight seal (clamp portion) of the anaesthesia face mask to ensure there's no leak under the cuff while the right hand squeezes the anaesthetic/Ambu bag for ventilation

Fig m,e 3.2 6 : One ha n ded !EC-c l am p

Fig l.ll r, e. 3.27: Two -hand j a w t h m st a n d m a s k v entilati on

(b) Two-hand jaw thrust and mask ventilation (Figure 3.27)

i. Usually reserved for difficult cases (obese, edentulous, bearded) ii. A second operator will squeeze the anaesthetic/Ambu bag for ventilation

·------------------ ------·

I I I I I I I I

S. i g n s of s u c c e s sfu l l sea l and ve nti l atio n : ✓ ✓ ✓ ✓

A fogg1 y I ma. sk

Chest rise with def ve ry of PPV B re a th so unds on a uscu ltat io n A firm/tau UfiuH bag R e• tu 0. 1 n e. xha.· l ation . . r n of CO2 . . . . . . C. ap no. g· , ra p h, .y

I I I I I I I I

·------------------ ------·

Ventilation

C

·c

1. Bag mask ventilation (BMV) is usually used to deliver inhalational

anaesthetic/volatile agent to an unconscious patient after induction process

in order to achieve a good plane of anaesthesia before placement of advanced airway adjunct 2. However, mask ventilation is contraindicated in patients with full stomach or those at risk of aspiration (except in emergency situation like desaturation, mask ventilation can be performed with application of cricoid pressure) 3. Ventilation can be assisted via available airway adjuncts which can be further classified as:

(a) Basic airway adjunct

i. Oropharyngeal airway (pg. 71) ii. Nasopharyngeal airway (pg. 72) * Both provide an artificial route or passage for air to flow to the

hypopharynx (upper airway)

(b) Advanced airway adjunct i. ETT (pg. 87)

ii. LMA (pg. 75) (c) Subglottic airway management i. Tracheostomy

- done when the upper airway patency or protection is not assured - can be done either by an open (surgical) approach or percutaneous dilatational technique (done bedside in critical care setting)

ii. Cricothyrotomy - airway access via the cricothyroid membrane

- done in 3 situations: • Procedural: allowing surgical access in elective laryngeal surgery • Precautionary: when airway management is anticipated to be difficult (obvious maxillofacial injury or turner)

• Rescue effort: when all forms of airway control have failed Endotracheal Intubation

1. "Introduction of an ETT into the trachea for means of ventilation" 2. Indications for intubation as in Table 3.4

Table 3.4: Indications for intubation

Anaesthetic Ai1rN ay protection from soiling by b lood, gastric contents (e .g . denta l, ENT, emergency surg, e ry ),

Apnoea and impendrng respiratory a 11est (progressive re sp irntory acidosis cardiovascular instability, altered mental state)

Restricted access t o patient (e.g. prone, head and neck surgery)

Pulmonary toileting (al low aspiration of s:putum and secretions)

Muscle re , l axation required (e.gI . abdominal1 surgery)

To se,c ure ai rvi/ay (e. g . unconscious. ail"'Nay obstrudion, impaired lary ngeal reflexes)

Thoraootomy/ intra-thoracic surgery

Facial and upper airNay abnormality

w·m impending obstiruction (burns, tra u ma)

Obesity

Failed triall of non-invasive ventilation ,( pg. 287)

Failure of MA insertion

CPR

3. Technique of laryngoscopy and intubation (a) place the patient in "sniffing" position (Figure 3.21) and preoxygenation (pg. 1 16)

(b) Induction of GA (pg. 1 12)

(c) once paralyzed (assessed by the presence of jaw laxity with no (d) (e) (f) (g)

resistance to mouth opening), direct laryngoscopy is performed if there is difficult airway issues and paralysis was not given, direct laryngoscopy can still be performed in a spontaneously breathing patient as long as they are maintained with volatile agents direct laryngoscopy involves alignment of 3 anatomic axes into an arbitrary straight line (oral, pharyngeal and laryngeal axes -Figure 3.21) mouth are opened with the right thumb and index finger or tongue and jaw can be pulled downward to create space for insertion of the laryngoscope blade hold the laryngoscope with the left hand and the handle should be pointing at the patient's feet (Figure 3.28)

(h) insert the laryngoscope blade into the right corner of the mouth (avoid putting force on the upper incisors) (i) curve of the blade will sweep the tongue towards the midline (Figure 3.28) and tip of the laryngoscope is placed in the vallecula (base of

tongue) as the blade is advanced 0) epiglottis edge is lifted off from the pharyngeal wall by applying lifting force on the handle in the direction of upward and forward (Figure 3.29) thus exposing the glottis (vocal cord)

Figure 3.28 : Insertion of laryn goscope

Grade I

Figure 3 .29: Placement of laryngoscope in val lecula and force app lied on the laryngoscope handle for opti mum glottis exposure

Grade II

Figure 3.30 : Cormack Lehane (CL) Grades

..- ------

Grade Ill

Grade IV

Grade I

Most of the glottis is see n

Grade Ila

Only posterior half of the glottis is seen

Grade llb

Only posterior quarter of the glottis is seen

Grade Ill

Only epiglottis seen (none of glottis seen -> difficult laryngoscopy)

Grade IV

Neither epiglottis nor glottis can be seen {d ifficult laryngoscopy)

(k) exposure and opening of the vocal cords during laryngoscopy are described by Cormack and Lehane (CL) grades (Figure 3.30)

(I) if there are secretions at the glottis and posterior pharynx, remove it with a Yankauer suction catheter (m) once vocal cords view are clear, insert the ETT containing a pliable stylet

from the corner of the right side of the mouth and advance it in between the cords into the trachea until the black mark disappears or insert cuff 1-2 cm

past the vocal cords

(n) hold the tube, remove the laryngoscope then the stylet and lastly inflate the ETT cuff to create seal during manual ventilation/PPV (o) begin manual ventilation (either with the Ambu-bag connected to ETT or

with reservoir bag if the breathing circuit from GA machine is attached to the ETT)

(p) if cricoid pressure (Figure 4.04: pg. 118) is applied, it should be continued until ETT placement is confirmed (pg. 120)

(q) all patients involved in major trauma are presumed to have cervical injury until proven otherwise (radiologically or neurologically), therefore all of them would have a cervical hard/rigid collar in situ

(r) manual in-line stabilization will reduce cervical movement by up to 60% and this must be performed during the process of direct laryngoscopy and

intubation to avoid further risk of cervical cord injury (s) manual in-line stabilization: i. Front part of the cervical hard/rigid collar should be removed to ease intubation

ii. The assistant (doctor or staff nurse) will stand behind the supine patients' head (Figure 3.31A) or the side from in front of the patient (Figure 3.31B) and hold the head by ensuring their

fingertips pressed on each mastoid process

iii. Thumbs pressed firmly on the temple

iv. Both arms will be stabilized and elbows are locked firmly on the trolley

v. Main goal is to maintain a neutral position for the head to be aligned with the body, thus preventing any cervical movements during laryngoscopy and intubation

Figure 3.31: Manual in line stabilization

4. Optimization for intubation (a) position the pillow to allow neck flexion to the chest (approximately 35 ° ) and head extension on the neck (15 ° below horizontal line) (b) external laryngeal pressure (apply BURP: pg. 28) (c) consider using McCoy blade (Figure 3.53: pg. 82) if only epiglottis is visible

(d) consider using straight blade (Figure 3.52B: pg. 81) if patient has receding chin, prominent incisor or long epiglottis

5. Adverse effects of direct laryngoscopy

(a) parasympathetic stimulation in infants (profound bradycardia) and adult (bronchospasm) (b) sympathetic stimulation in adults i.e. tachycardia, HPT and raised ICP

6. Complications of intubation (a) Early: - jaw dislocation

- laryngeal injury - epistaxis (nasal intubation)

- obstruction, dislodgement or kinking of ETT (b) Late:

- aspiration following extubation

- tracheal stenosis - laryngeal stenosis - vocal cord ulcer and granulomata * Insertion of LMA can be done when patient has been induced and breathing spontaneously. Muscle relaxants can optionally be given when an LMA is used. Application of LMA is explained further at pg. 76 Endotracheal extubation/ LMA removal 1. Purposeful removal of the ETT/LMA from the nasopharyx or oropharynx

2. The stress response during emergence (pg. 122) from GA and extubation will not differ from the stress response during intubation 3. It can be done either patient is: (a) Awake: i. performed when airway reflexes returned, eyes open upon instruction, able to lift up the head and presence of spontaneous ventilation ii. may demonstrate hypertension, tachycardia, coughing/bucking due to the awareness of ETT in-situ iii. respiratory complications (airway obstruction and microaspiration post-extubation) are minimized via this method (b) Deep: i. performed when patient is still anaesthetized (end-tidal sevoflurane concentration > 3%), presence of spontaneous i. ventilation but no return of airway reflexes ii. this method decreases CVS stimulation (hypertension, tachycardia) and reduces the incidence of coughing/bucking on the ETT but there is a greater incidence of iii. respiratory complications such as laryngospasm/airway obstruction (due to pooling of secretions and relaxed tongue) and micro­ aspiration post-extubation (due to late iv. return of pharyngeal reflex) 4. Position during extubation may also vary according to the patients clinical condition and type of procedure done (a) Supine (favored in uncomplicated airway) (b) Left lateral this position will keep the tongue away from posterior

pharyngeal

(c) Head-down wall thus keeps the airway patent and minimizes risk of aspiration (d) Semi-upright (done in obese or those who are anticipated to be at risk of

respiratory compromise, this facilitates spontaneous ventilation and diaphragmatic excursion which will improve the FRC)

5. Extubation performed after patient has been adequately reversed (pg.123) 6. Steps for ETT extubation:

(a) administer 100% 02, inhalational/volatile agent is stopped at the end of operation (if planning for awake extubation) (b) suctioning of oropharynx to keep the airway patent (gently done to avoid trauma to the pharynx and airway structure)

(c) insert bite block or oropharyngeal airway (to avoid biting of ETT during emergence which can hinder oxygenation and increase the airway pressure) (d) deflate ETT cuff

(e) simultaneous application of positive pressure to the reservoir bag and removal of ETT (f) suctioning of any residual oral secretions (may cause airway obstruction and trigger laryngospasm if it is not sucked) (g) apply high flow 02 via mask

(h) in deep extubation, inhalational agent is stopped after extubation, gentle handling of the patient is paramount to ensure a smooth recovery from

anaesthesia (especially in children, they easily get laryngospasm secondary to vigorous movements and oral secretions during light plane

of anaesthesia or recovery) (i) observe and look for any airway compromise post-extubation (anticipate

in those who have difficult airway management during intubation or placement of SGA device) 7. Principles of LMA removal is the same as ETT extubation, the only difference is

that the LMA cuff doesn't need to be deflated as any residual secretions that pooled above the LMA cuff can be removed simultaneously with the LMA once ready

8. Complications with ETT extubation: glottis or subglottic oedema, hoarseness of

voice, subglottic or tracheal stenosis, vocal cord granuloma and paralysis

* Refer Appendix 5, 6, 7 for the algorithm in managing extubation in different

situations based on the consensus given by the Difficult Airway Society, 2012. DIFFICULT AIRWAY

"A clinical situation by which a conventionally trained anaesthetist and well versed

in alternative methods experiences difficulty with mask ventilation, difficulty with tracheal intubation or both."

For the ease of discussion, this can be further divided into: 1. Difficult bag-mask ventilation (BMV) 2. Difficult laryngoscopy/intubation

3. Difficult cricothyroidotomy

A. Difficult BMV "The inability of a trained anaesthetist to maintain 02 saturation > 90% using a face mask for ventilation and 100% inspired 02, provided that the pre-induction 02 saturation level was > 90%."

1. Mask ventilation is considered a 'basic' skill for airway management during delivery of anaesthesia and resuscitation

2. Main objective of BMV are maintenance of airway patency and oxygenation 3. It is considered difficult when either 1 of the below occurs: (a) unavoidable leak surrounding face mask (b) excessive resistance during ventilation

(c) > 4 L/min gas flow needed during mask ventilation (d) requiring 2-handed mask ventilation (e) need to change operator for BMV

(f) any of these clinical signs; absent chest rise, absent/inadequate breath sounds, cyanosis, desaturation and clinical signs of hypoxaemia (pg. 97)

4. Factors contributing to this clinical situation: (mnemonic OBESSIE) (a) Obese (BMI > 26 kg/m2) (b) Beard

(c) Elderly {> 55 years old) (d) Snorer (e) Stiff ventilation (asthmatics, COAD, ARDS, pregnant)

(f) Improper Sealing with a mask Uaw malignancy, facial deformity) (g) Edentulous (due to depressed cheek) 5. Potential airway obstruction can be contributed by macroglossia, blood, oral secretions, vomitus, food particles or dentures B. Difficult laryngoscopy

"Even after repeated attempts (usually > 2 times with the same blade/ a change of blade), it is not possible to insert the laryngoscope in a such a way that any portion

of the vocal cords can be visualized." C. Difficult intubation

1. "Tracheal intubation fails although it was possible to visualize portions of the vocal cords by laryngoscopy by which the difficulties could be due to

pathological changes of the larynx or trachea." 2. Incidence is approximately 1-3%, but may be higher in ICU patients

3. LEMON law is an assessment tool that is used to identify the risk factors

for difficult intubation: (a) Look externally: facial injury, long upper incisors, prominent teeth, short thick neck, beard, receding mandible, macroglossia (b) Evaluate the 3-3-2 rule (Figure 3.32):

i. Mouth opening (inter-incisor gap) s 3 fb (predicts the ease of ETT and laryngoscope insertion) ii. Hyoid-mental distance s 3 fb (predicts the ability to lift the tongue

into mandible during laryngoscopy) iii. Thyroid cartilage to the floor of the mandible s 2 fb (If larynx is high,

the airway will be tucked under the base of the tongue making it hard to visualize)

Figure 3.32: Evaluation of 3-3-2 rule

(c) Mallampati � 3 (d) Obstruction: Pathologies involving the upper airway (peritonsillar abscess,

retropharyngeal abscess, epiglottitis) or congenital anomalies of upper airway

(e) Neck mobility: It can be restricted due to prior surgery with scar, post­

irradiation scar, rheumatoid arthritis, unstable cervical spine (reduces the ability to align the anatomic axes), poor cervical range of movement and TMJ dysfunction

D. Failed intubation

1. "Placement of the ETT has failed completely." 2. Causes are: (Mnemonic INTUBATION)

Infection (laryngeal) Neck mobility abnormality

Teeth abnormality (loose, prominent)

Upper airway abnormality (stricture, swelling)

Bull's neck appearance (heavy thick neck caused by hypertrophied muscles)

Ankylosing spondylitis Trauma/ tumor

Inexperienced medical officer Oedema of the upper airway

Narrowing of the upper airway E. Difficult cricothyrotomy

1. After identifying a difficult airway, the neck should always be inspected for the ease of anticipated cricothyrotomy if intubation were to fail 2. Mnemonic SHORT

Surgery (previous)

Haematoma or any swelling around neck

Obesity Radiation (previous) Tumor * Refer Appendix 8, 9, 10, 11 for the algorithm in managing difficult airway in different situations based on the consensus given by the Difficult Airway

Society, 2004

Awake fibreoptic intubation (AFOI)

1. This is the gold standard of intubation if there's a potential or known

difficult airway during preoperative assessment of a patient and should be

performed by those who are familiar with fiberoptic intubation or bronchoscopy

2. The patient will be awake and spontaneously breathing throughout the

procedure 3. Sometimes the patient might benefit from some amount of sedation (pg.

153), analgesia (pg. 155) or amnestic (pg. 153) drugs to tolerate and cooperate with the procedure

4. This technique is done before inducing GA, it utilizes the fiberoptic scope (60 cm length) which has been preloaded with an armored ETT (Figure

3.33A) and is advanced through an anaesthetized airway (Figure 3.338)

via mouth or nose (if there is mouth restriction) 5. Perform oropharyngeal suctioning fiberoptically glycopyrrolate (pg. 159) for better visualization

and

administer

6. Additional LA can be given fiberoptically (through the working port) via "spray-as-u-go" technique as it passes through the airway structure

7. Once vocal cords are visualized, the fiberoptic scope is advanced further into the trachea, ask the patient to inhale deeply, ETT is railroaded (Figure 3.33C) and fiberoptic scope is removed while maintaining the position of ETT

8. Once ETT placement is confirmed (pg. 120), ETT is anchored (Figure

3.33D) and patient will be given anaesthesia for the planned procedure (A full overview of AFOI is beyond the scope of this handbook)

A - ETT prel o a,d ed t. o t. h e fi be r, o pfic S CO [Pe

C - ETT raill roat d e d a n d fibe ropt i ic s c,o, p e re m ove d

B - Fi b ero p tic sco pe a d va n ce d t h rough ttl e a n ae s thetize d a i rway

D - ETT anchored! afte r c,o : ftlrm at i o in

Figure 3.33: Steps of awake fiberoptic intubation (AFOI)

9. Indications of AFOI are:

(a) previous history or anticipated (by airway assessment and clinical examination) difficult airway (b) suspected or known cervical spinal cord injury

Cricothyrotomy

1. A procedure where an opening is made at the cricothyroid membrane to secure an airway for the means of oxygenation (either through BVM or jet ventilation),

aka cricothyroidotomy

2. It can be done either via needle (needle cricothyrotomy) or scalpel (open/surgical cricothyrotomy)

3. Advantages: simple, fast, minimal bleeding and minimal training required

4. Indications: (a) failed intubation after � 3 attempts (b) failed to maintain oxygenation of SpO2 > 90% at 100% 02 with BVM ventilation

(c) failed to maintain ventilation with BVM ventilation causing cyanosis, absent breath sounds and haemodynamic instability 5. Contraindications: bleeding diasthesis, laryngeal or tracheal injury, neck 6.

oedema/swelling and cervical injury

Complications: oesophageal subcutaneous emphysema 7. Steps (Figure 3.34):

puncture,

bleeding,

pneumothorax

and

(a) position the patient with neck hyperextended to optimize and expose the

laryngeal prominence (b) locate the cricothyroid membrane with your dominant hand (from the laryngeal prominence, slide the finger down until a dip or depression is appreciated which is the membrane) (c) stabilize the trachea with your non-dominant hand using the thumb and middle finger

(d) needle/cannula (12-14 G) is connected with water filled syringe

(e) insert and direct the needle/can nula caudally through the cricothyroid membrane

(f) aspirate the syringe upon advancing the needle/can nula (g) presence of air bubble confirms the placement of needle/can nula in the trachea (h) slide the cannula towards the trachea and remove the needle

(i) connect the can nula to the ventilation system and start to oxygenate * Refer pg. 64 for risk factors of difficult cricothyrotomy

A : Locate t h e ,c ri cot h yrn id m e m blian e

B : I n sert a n d d i r ect th e n ee d le/ cann u l a , c a u da l ly t h rough the crirnthyroi d m em brane ( as pi ra te whi[e adva n c i ng )

C : S lide the cann u l'.a towards the trachea a n d ll"emove the m eed. le

D : Con n ect the can n u[ a to t ih e ve n til ati on system an d sta rt to o xygena te

Fig u re 3 . 34: Ste ps of c :ricothyrotomy Cl.I

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� ,S! �

AIRWAY EQUIPMENTS ious patient (obtunded 1ue. thus preventing the sing airflOIN obstruction

Table 3.5: Basic equipments for venti lation Equipment

1 . Facem as k

nnel and anatomical ly

Explanation

Function: Supply oi and anaesthetic vapors directly Parts: (Figure 3 . 35 and 3. 36) 1. Made of rubt>er or plastic 2 . Tra nsparent material (al lows detection 1 3. Consists ot

it's face with the ftange ,hould end at the angle

(a) (b) Figure 3.35: Adult facemask

( c) (d)

Body Ortfice or mount {connected to a piece) Rim edge (inflatable cushioned r I nflation valve (rim size adjustab

Which size to choose? Inflatable rim should form a good seal aro when the mask ls ntte t h e ETT, e nsuri ng the ti p ends before Murph y's at lhe proxim� J e nd of" ETT openin g so that it wil l � b eyo n d the I E TT ig ht throughout th e l ength of the cTT u nti J the o periy sha ped! to faci litate ETT insertio n

Figure 3.57 : G u m el astic boug ie

jutting o ut b eyo n d EIT

Insertion : (Figure 3 _51 1 _ The Coude tip part the trachea .and El place wh ile perfom 2_ Proper placement i (a) 'trachea l clicks' rings (b) 'hold-up' or sligl (c) coughing (if pat

Problem:

1 . Soft tissue damagE

2. Rupture of the bror Functions: Used when

there is ,d despite good visualiza Fig ure 3.58: Insertion of g um elastic boug ie

E q11.1i pm e nt y tube of diffe rent size/type Jlt ai1Way)

Exp l a n ati o n

(:b ) Styl ,et

P arts : M alleab le, coated wire W h ic h1 s�z.e to c h oose? 1 . S ma l l stylet for Err �.o 11

2. Adu lt stylet for ETT �-5 IY

1en ( 50-70cm: Figure 3 . 60A and B) ) 2 insuffi a1ion {Fig ure 3.60C ) ,oluble gel ·e-eM isting tu be via adaptor and the internal lumen u ntil

I F igui re 3 .:59 A : S ty let

timize the view of the laf'/1\X (it displaces age of the new tube and ensures that the

A, p p,l ic tu l o n :: 1 . I ns, e rl a 1 1 1Jbri ca.ted stylel in 1 eye ( Fig u re 3.59 B) 2 . B en d 1he re m3in i li9 stylet ; not slip down and protrude 3 . The sty !et should be s.bai proxi mal cul whe:re it iis p1 P ro b l e m : Soft tiss LJ1 e inj u ry due to s,tyre t

1e new tube is railroaded over the catheter

ter du ring e,c-change

Fi g u re J. . 5'9 H: t..u bricated styl et i n s erted in ETT

1rynx ,agrus during laryngosco py nitubated with plai n ETT, ora l a nd

Equipment

(c) Airway exchan ge catheters (Cook -... airway exch anger}

1 . Long catheter with an internal lun 2. Ada ptor: perm its ventilation and < Figure 3.60A :Airway excha nge catheters

trween the ainaesthelic bre�rlh ing co ot e n ts a n d

n g along the 1 u be for verification

Function : 1 . To exchange ETT o r tracheostom 2. Fo r protected e:xtubalion {in d iffi �

Parts :

tooth in the ph aryn x )

on fro m g a st r ic

Expla n ation

Figure 3.60 8: Internal lumen for 0 2 i nsufflation

.s the v o cal cords during in se rtion ) atio n of ti 'he vocal co rd s d uri n g

Figure 3.60 C : Adaptor

Appllc atlon:

1 . Catheter is lubricated with water i 2. Catheter is passed through the p, 3. 0 2 insufflation can be performed the new tube is placed 4. Laryngoscope can be used to op1 soft tissues that might .resist pass; catheter is in-situ) 5. Pre-existing tube is removed and tl as a guide P roblem : 1 . Soft tissue injury 2. Accidenta l dislodgement of cattle

E q u:i: p m e nt i bevel or a side hor e r(an Je com es occluded) • ; p aediatric, aka plai n . E TT) e.al wall and the ETT, th us ntents/oral secre1ions a nd

(d ) Mag1i l l f,o rcep

Exp' l a n ati o n

F u1 11 c t iio n : 1 _ Aids the inse rti o n of n asa li ETT into ffle l;i 2 . Aids the inse rtion of N GT into 1h e oesopt 3 .. To inse rt th roat pack in cases which are i1 oto rh i rm logy s u rgery 4. To re m ove fo reign bodies. (e.g_ extra c�d

F ig u re 3.61 : Magm fo -rccep •( a n gled t 3 . Eindo tra.c hea' I tu be ( E T T )

)

F u nc t io n : 1 . Prov-ides a pa ssa,g e for gases ·to flow bE sys.tem to the· patient's. lungs

2, Allows provisio n of P PV

3 . Fo r l u n g p rotect ion from con tam i nati1 na sophary:n gea l mailte r (bl:ood)

F ig u re 3.62.A: E ndotra che a l l tube

P art s : 1 . Plastic , con cave t� be (Fig ure 3T62A) 2. Pre sen ce· or a radio-opaqu e li ne exlendi1 on th e CX R: 3 . A bold b l ack i l i n e above die cuff (shook! pa! 4 . Left fa cing b evel (a llow.1 better visuafizi intu bation )

Equi:pm e nt

E x p la n ati o n

5 . M u rp hy's eye ( Figure 3.62B): ai hole above the alte rnative rnu:te of ve nti'!ation should U, e bevel i 6 . ETis can be eilfuer 1 cu'lfud (i"n adu ft), or un cu ffed {i 11 7 . C uff p ro\lid es an aiflig ht se. a l b etw een th e trachi prote eti ng1 the lu ngs from aspi'l'ation of g ast ric co en ab li n g effl cien�. venUlation 8 . Pilot ba l loon 1is pl'aced p roxima l ly for cuff in bUor

s

Figure 3. 62B ; M u rphy's eye

Wl h ic: h sE ze to c h oose? 1 . ETT is sized by its internal diameter ( I D ) in m m 2 . Roug h g uide fo.r; (a} E TT s iize = Age + 4 4 ( ETT in chi '1'dren = diameter of th e liHle fin ger (b} Length (cm) of 3!11 dmring th e ETT at the l i1 p :

poste rior . a s pect of Ta n d th e d ur3tion l'I

3 x ETT size , o r Agg: + 1 2 2 { e ) Cuff pressu re: 20-25 mmHg

Equ 1 i'p m e nt

Exp'l a n ati o n

ETT an d laryn gos, co pe sizes fTabl'.e 3_6A.):

Ta ble 3 .6A: ETT a nd la iryn goscope size

:ieyon d the

Age

ETT s i :e z

Pre rn m ie

2_5

S m th

3 . 5-4

Neo n ate

3-3. 5

1 -2 yr

4-5

8- 1 2 yr

6-6 . 6

4-6 yr

Adu l l {fema 1 Adu It (m ale } A 1>·1:,,l i cat i on (pg. 56 ):

B la de s ize

ID

0-1 1 -2

5 ..5_5

2

7J0-8 .0

4-5

7 $-8 . 5

2-3

4-5

Prob le 1n s : 1 . The sl� 11 da rd ElT sh3pe wi l l exert som e pr,e s,s ure OIi') the th e laryn x (deg re e of danr n g e depends ,o n lie size of ET of intu b;:11ion ) 2 . Additives to p lastic (in I E TT) may provo'ke �issue imtatim 3 .. H igh pre•ssme cuffs can ca11.Jse cuff-related iaj mies

Equi'pm e nt

Ex pi 1matfon

4 . Spe cia Uy desi gined tra chea l! tube s (a) Armou red lubes (rernforce d} ( ib ) Pr, e form ed tubes (RAE - Ri n g , Ada ir, E lwy ni ) (c ) Microla�e.al tubes (MLT) (d ) Laser Cubes (Mallinck1odr ILaser- F I ex ™ ) (e ) Dou ble lu men tube (Robe rts haw tube, B ron c hocath) (f) Single lum en bl'fonchia! b l:ock er ( Un ivanl , .A rndt , Cohen, tube ) (91 ) il'ach eosiomy lu1>es

Full oveNiew of th ese sp,e cially desig ned tracil eal tubes are I scope of this hand book

OXYGEN THERAPY Physiology (02 cascade)

1. The air (atmosphere) has 02 concentration of 21% and a total pressure of 760

mmHg 2. Partial pressure of 02 (PO2) is the product of fraction of inspired 02 (FiO2) and the barometric pressure (PB)

PO� = FIO,x PB = 21 % X 760

= 1 59

3. 02 is inspired (PO2 of 159 mmHg) into the respiratory tract through ventilation

where it is warmed and humidified (nose, pharynx, larynx, trachea, bronchus, bronchioles, alveolus - PO2 of 149 mmHg) 4. Subsequently, gas exchange occurs where the 02 from alveolus (PAO2 of 100

mmHg) moves down to end capillary (PaO2 of 32-40 mmHg) through diffusion across the alveolar membrane

5. Simultaneously, dissolved CO2 from the pulmonary artery will take part in this

gas exchange process across the alveolar membrane into the alveolus for

elimination 6. The O2-rich blood will move into pulmonary vein, left side of the cardiac and

pumped into the systemic arterial blood 7. Majority of the 02 is transported via combination with Hb (fully saturated 1.0 g Hb carries 1.34 ml of 02) and very minimally transported in the dissolved form (3.0 ml 02 dissolved in every 1.0L of plasma)

8. 02 in arterial blood will be delivered to the tissue capillaries and finally to the cells for metabolism to take place (mitochondria - PO2 of 4-22 mmHg) and

produce energy 9. This stepwise decrease in the 02 concentration and pressure gradient (PO2) is known as 02 cascade (Figure 3.63)

10. Any pathologies that occurs in any step of the 02 cascade may alter the 02 delivery to the tissues Pathophysiology 1. Hypoxaemia means a low arterial oxygen tension (PaO2) below the

normal expected value (85-100 mmHg) while hypoxia means low 02

content at the tissue level

2. Tissue hypoxia is estimated to occur when the mitochondrial PO2 is approximately less than 7.0 mmHg 3. Hypoxia occurs when there is an imbalance of 02 demand and supply in the body;

(a) increased 02 demand or consumption: fever, sepsis, surgery, pain, trauma, burns, shivering, myocardial ischemia/infarction, seizures (b) decreased 02 supply or delivery: insufficient ambient pO2 (high altitude), impaired gas exchange in the lungs (ventilation, diffusion,

perfusion), impaired myocardial function (producing low cardiac output state), Hb defects (quantitative: anaemia and qualitative: carbon monoxide poisoning/methaemoglobinaemia), impaired cellular utilization (cyanide poisoning)

(c) Tissue hypoxia can also be further classified as (Table 3.7)

150

- >-

1 )9 mm H g

1 14 9 mm H g I

I

::C'

E E

100

-

...

, a.

I I

I I

I

i oo mm H g

.

I I I

95 mm H g

I

so

>-

I I

4,o mm H g

'

I l I

I I I

I I

0

I

Atmos p1, ere Hl um idifi e d air ( dry air)

Al veolus

Figure 3.63: Oxygen Cascade

Art erial b lood

1

4-22 m m Hg I

E n d tiss u e , c aplll ary M itoc h ond ria blood

S ite

Source: Modified diagram from 'The Physiology Viva: Questions & Answers' by Kerry Brandis, used by kind permission.

02 therapy

1. 02 therapy merely means the administration of 02 concentration greater than the ambient air (21%) in order to prevent or treat the symptoms of hypoxia by increasing the PAO2 2. Hypoxia is not only relieved by 02 therapy, there are other systemic

pathologies (Table 3.7) that contributes to an inadequate tissue

oxygenation 3. 02 should be considered as a drug (British National Formulary, 2010),

therefore it should be prescribed according to the clinical condition and

proper monitoring is vital to ensure adequate oxygenation and to avoid wastage 4. However, excessive and inappropriate 02 therapy (100% 02 > 12 hours

or < 100% 02 for longer duration) may lead to toxicity which manifests as pulmonary epithelial damage (broncho-pulmonary dysplasia), retinal damage and convulsions (especially in neonates)

02 therapy classification

1. Normobaric 02 therapy: Supplemental 02 at or just above atmospheric pressure required to saturate the Hb in the bloodstream 2. Hyperbaric 02 therapy: Supplemental 02 that has to be delivered by

dissolving it in plasma at pressure greater than the atmospheric pressure. Usually used in life threatening carbon monoxide poisoning in the attempt of displacing the carbon monoxide from haemoglobin (A full overview of

hyperbaric 02 therapy is beyond the scope of this handbook) 02 supply

1. 02 are supplied by various sources depending on the location. Some of the

available sources are: (a) Cylinders: should only be used if there is no piped 02 available, pipeline failure (backup source)

(b) 02 pipeline: these are 02 source delivered through the wall outlets available in various areas in the hospital

(c) 02 concentrator: would only be considered for domestic use, military purposes or where bulk supply is not available due to geographical constraints

Indication 1. Pulmonary conditions (a) acute hypoxaemia pneumothorax

(b) chronic

hypoxaemia:

pneumonia, COAD,

asthma,

chronic

pulmonary

embolus,

disease,

pulmonary

lung

hypertension secondary to respiratory disease, obliterative bronchiolitis,

severe bronchiectasis, pulmonary fibrosis, interstitial lung disease and OSA

2. Non-pulmonary conditions

(a) heart: Ml, heart failure, APO, congenital heart disease with pulmonary hypertension

(b) haematological: Anaemia, carbon monoxide poisoning and sickle cell crisis (c) CNS: brain injury, pneumocephalus (d) shock (cardiogenic, septicaemic, anaphylactic) (e) metabolic acidosis (f) neuromuscular disease (myasthenia gravis, Guillain-Barre syndrome,

porphyria, botulism, diaphragmatic palsy, polio) (g) chest wall disease (kyphoscoliosis, ankylosing spondylitis, morbid obesity BMI � 40)

(h) post-operative state (respiratory centre depression secondary to opioids, anaesthetics and sedatives) (i) palliative care for symptom relief

Table 3.7: Classifications of hypoxia

Ty pes of

Pathology

Hypoxic hypoxia

lo

Hypoxia

i nspired PO 2

Hypoventilation

Exam ples

• • • •

• Impa ired alveolarcapilla ry diffusion Ventilation/ Perfusion m ismatch

• • • • • •

Anaem ic hypoxi a

Inadequate Hb quantity

C i rc u latory

lo cardiac output

H i stotoxic hypoxi a

Comprom ised oxidative phosphorylation

(stagnant hypoxia)

I nadequate H b qual ity

• • • • •

.

High altitude Hypoxic mixtu re of gas (very rare ) I m paired respiratory center (opioids, general anaesthesia . sedatives , encephalopathy, head injury) Neuromuscular disease ( yasthenia G ravis, Guillai n-Barre syndrome, spinal cord injury, motor neurone disease, myopathy, dystrophy, polio , neurom uscular blocking agent usage) Chest all abnom1alities (kyphoscoliosis, a nkytosing spondylitis , morbid obesity B M I � 40, pleural fibrosis) Asbestosis , sarcoidosis Diffuse interstitial fibrosis AR DS . toxic/inflammatory pneu monitis Obstructive disease: COAD , asth ma Restri ctive disease: interstitial pulmonary fibrosis , pneumothorax , ARDS, pleura empyema Vascular disease: pulmonary oedema , pulmonary embolism Ana emia Carbon monoxide poisoning Sickle cell crisis Thalassemia Shock {cardiogenic, septicaemic, anaphylacti c) Cyanide poisoning

Management:

1. Acute respiratory failure: the inability of the respiratory system to achieve adequate gas exchange either via insufficient oxygenation (hypoxaemic) or insufficient C02 elimination (hypercapnic) 2. Presentation of acute respiratory failure

(a) Compensatory manifestation: Tachypnoea (> 35 breaths/min), usage of accessory muscles, nasal flaring, intercostal retraction (b) Sympathetic hypertensive

manifestation:

Palpitation,

sweating,

tachycardia,

(c) Hypoxia manifestation: Restlessness, altered consciousness, headache, confusion, cyanosis, bradycardia, hypoventilation, hypercapnia

3. Rule of thumb (a) Type I respiratory failure i. PaO2 s 60 mmHg, arterial 02 saturation (SaO2) s 90% with

normal pCO2 when breathing room air ii. Use high concentration of 02 via non-rebreathe mask with reservoir bag (± ventilator intervention)

iii. Target range of SpO2 94-98% (b) Type II respiratory failure i. pO2 s 60 mmHg and pCO2 � 55mmHg

ii. Those with previous normal lungs may need 02 and ventilator

intervention iii. Those with likely or known underlying lung disease (hypercapnic respiratory failure) will need titrated and controlled 02 therapy using the Venturi mask starting with 28% (try to avoid mechanical ventilation as far as possible due to the fact that weaning from the

4. Goals

ventilator will be difficult) iv. Target range of SpO2 for hypercapnic respiratory failure is 88-92%

(a) Relieve hypoxaemia (maintain pO2 > 60 mmHg which provides SpO2 of > 90% based on the 02 dissociation curve) by using appropriate 02

delivery device (pg. 100) (b) Reduce the work of breathing

(c) Reduce the work of myocardium to meet the 02 demand

5. Monitoring

(a) Methods used are:

i. Pulse oximetry: preferable method as it is simple and noninvasive ii. Other vital sign parameter: blood pressure, heart rate, respiratory rate and level of consciousness

iii. ABG analysis: an invasive method but gives a precise result

(b) Bear in mind, SpO2 can appear normal in those with certain conditions such as anaemia (reduced 02 content) and normal pO2 but abnormal blood pH and pCO2

(c) Prescribed 02, delivery device and desired target SpO2 or pO2 range should be recorded and clearly written on the vital signs observation chart (d) Frequency of measurements or monitoring will be tailored according to case-by-case basis

(e) 02 therapy should be adjusted as necessary according to the desired target SpO2 or pO2 range (improvement of signs and symptoms of hypoxaemia should also be noted) (f) Any sudden deterioration of SpO2 and other vital sign parameters may

need a re-evaluation of the patient and warrants another ABG 6. Weaning 02 therapy (a) 02 therapy should be given continuously once initiated and should not be stopped abruptly (b) Abrupt discontinuation can deplete the small reservoir of alveolar 02 resulting in fall of pO2

(c) Weaning off from 02 therapy can be considered when the patient's underlying pathology, vital signs and clinical condition has stabilized and improved (d) Weaning is gradually attempted by decreasing its concentration (using

Venturi mask, simple face mask or nasal cannulae) for a fixed period (for e.g. 30 minutes), re-evaluating the SpO2, vital and clinical parameters periodically

(e) Patients with chronic respiratory disease may fail to be weaned off from 02

therapy, instead they may require low concentrations 02 therapy for prolonged period of time (this is when long term domiciliary 02 need to be

considered upon discharge)

Ta ble 3,.8 : Clas s ificau o,n of 0 2 DeUv, e ry Devices

ment ese1Vo i r bag, (m ust fit ,) us .l ng1

02 flow rate ,o f

D eg1r,e e•s of depen dency/ C laiss ifi eatiion

l:.xamp les

Low d e pendency

1 _ Used w hen su pI torrect hy po,x ia 2_ P auents are spo

re s pira. t ory Cli stre ss Ill

col! retention

1 _ Vari ab le 1p e,rt:o rmance de-v ices

Nasal rannulaeJ prong/ iea-llh eter

( F i 0 2 d e l i v, e ir e �C/J

C" ::r CD '< C') "O !l) 0 3 CD CD ::J �CD 0 C/J C/J ::J C/J ::J "O "O 0 0 ::J C/J C/J -• C/JI < CD °S!. ::J !l) ;:I! !l) CD .., 0

ro - ·

ro .., CD

"O CD !l) CD c.. C" 0 C: C/J CD C/J 0 CD "O ::r CD c.. ::::::!. ::J CD

-

"O -· c.. c: @ !l)

::J CD C/J � C/J -· � !l)

:E C/J !l)

::r ,.... ::r ;:;: u;· o5 · 3 '
potent than morphine

1 . 1 /1 0 analgesia potency of morphine 2. Metabolite; norpethidine (produce neu roexcitatory effects: ag itation , tremors, twitches. hallucination, multifocal myoclonus and seizures) 3. N a1oxone does not reverse and may in crease the problems related to norpethidine toxicity

�,.

1 . 1 /1 analg es i a potency of morphi n e 2 . Atypical centrally acting analgesi c because of its combined effects as an opioid agonist and a serotonin and nor.ad renaline reuptake in hibitor

.. MAC ( 0/4

l n dU di on and mainhmam:e or anaesfflesia

2.0

De1sH ura.ne

Mainte mm c.e or anaesthesia

6.0

l s o fih.1mm e

Mainte nan ce of anaest;h esia

1 . 1 5,

N it ro u s Ox ide

Adj un ct i nha lational l n halationa 1 a na l gesia in la bo r ( 50 : 50 mix:rure )

(N:P ] ,

(refer bel ow fo r advers, e , e ffects)

t

U ses

Sev, o fl u rane

Caution in renal insufficien cy and elderly

a

3·6

Vol atJI e na m e

1 04

(< poten1

Refer pg1. 1 47

A•d ve rse effects o·f N::P ad ministratio n; •· E ,cpans,io n of air-fi 'lfed s ;pa ces� pneumothorax. b o • • PONV - C hronic exposure : Vitam tn IB 1 2 deficie ncy, infertil

Effects -O pioid

+

Table f

S pec ial poi nts

....

Analgesic type

Fentanyl

1 . Rena.I insufficiency 2. Gastri.c u lce r/erosion J_ Concu rrent anticoag ulant therapy 4. Reactive airway d isease

+ Rena l/ hepatic impairment

juvant

Ana lg esia (throug h inhibition of prostagla.nd ins) Anti-inflammatory Anti-em etics

C aution in: 1 . asthma 2. stoma.eh (gastric) u lcer or bleed ing 3. kidney impairment 4. previous problems with anti­ inflammatories 5. platelet dysfunction

M orphine

Peth idine

(m eperidine)

Dose/ route of adm i n istration

OnHt D u [ (m i n) (h

IV 1 .0- 1 .5 µg/kg (50 1,191kg for cardiac an aesthesia) lntrathecal: 1 0-2 5 1-'9 E pid ural: 1 .0 1,191kg Pateh: 25, 50. 7 5 , 1 00 1,19

1 2-24

IV 1 .0-1 .5 mg/kg tds I M 0.8-1 . 0 mg/kg tds

1 -2 1 0- 1 5

IVI IM/SC 0 . 1 -0.2 mg/kg lnlrathecal: 1 O D µg Epid ural: 2.5 -5.0 mg or 50 µglkg

1 -2

1 .5 1 5-60

...

1 . Absorption of d rug wi l l be alte red in those with altered gastric emptying 2. Rectal admin istration produces delayed and variable uptake 1 . A g lucocorticoid 2. Less m ine ra locorticoid property hence less wate r retention

Tromadol

POIIV 1 .0-2 .0 mg/kg tds

60

2

1

Analgesic type

� M B) Ag e nt/ M u scle Relaxant ·atio n 1 m oilf � twitc h ·i g h t i min

S i de Effe-cts

Spe c ia I po ] 111 ts

Myalg ia, h istamine release, transient i n crease in I C P/ I OP, j K• level (fata l i n rena l fa ilure , bu ms , crush in juries, u pper motor neurones} ,. trigge r *ma l ignant hyperlh ermia , bradyca rd ia, *suxamethoniu m apn o ea

1 _ Fast onse 8 mglkg ), .. pse udocholineste ra se d efiden cy

15, m i n ia ble)

B ronchos pa sm seco n dary to h istamin e release

1 _ N o n orga n de pendent metabolism

Hyp-0ten sion a nd bradycard ia

2_ Less hista mine re lease ( bron c ho-s pasm u nco m m m1 )

15, m i n ia ble)

larg,e doses ca use m ild vag olyti c effect (ta chyca rd ia}

Can be us, e d in mod ified IRSI (pg . H 7)

i5 m i n ia ble)

NSAIDS 1 . D ic lofenac (Voltaren)

2_

Mefanamic Acid (Ponstan)

3. Ibu profen (Brufen)

Selective COX -2 inh ibitor 1 _ Parecoxib (Dynastat)

Dose/ route of adm i n istration

O nset (min)

D u ration (hours)

PO 25-75 mg bd/tds

-

-

PO 250-500 mg tds

-

-

PO 400 mg tds/qid

-

-

-

-

-

-

-

-

-

-

IV 40- 80 mg/day

2. Etoricox ib (Arcoxia)

PO 60- 1 20 mg/day

Acetaminophen (paracetamo I)

Adu lt: Oral, rectal , I V dose 1 _0 g 6 hou rly or 5-1 5 mg/ kg {max 4 .0 g/day) Paeds: supp 30 -40 mg/kg

3. Celecoxib (Celebrax)

Dexamethasone {corticosteroid)

PO 200-400 mg O D

I IV 4 _0-8 _0 mg tds

Non

Ad

i c Ag,e nt tion of fl f h rs ) -8

-8

-2

Ta ble• 5 . 5 : N e u rom u scula r B l ocki ng ( I

S pe c i1 a l po i nts ·t _ 2_ 3_ 4_

Do not use in IVRA (pg_ 1 4 1 ) More ca rd iotoxic (exce pt in levo-bu pivaca i ne ) 0 _75% is contraind icated i n obstetri c patients 0 _ 5% (hyperba ric solutio n: a dd ition of g l ucose 8 % ) is u sed in spina l a naesthesia providing im mediate o nset 5_ Addition of ad ren alin e le ng1hens the du ration of action

D ru g type/nam e

1 . Depo l a risi ng age nt ( a ) S uxam eth o n i u m/ S ued n y lch o1 l i n e

·t _ N ot intended fo r sp ina l anaesthes ia 2_ Less card iotoxic com pa red lo bu piva ca i ne 3_ Less motor blo ckad e ( be neficial in obstetric a na lgesia, chro nic pain manageme n t and general post-op e pid ural i nfusion }

1 _ Ca n be u sed to obtun d sym path etic reflex d u ri ng la ryngoscopy, a naesthesia of the a i rway via nebu l izer, a co ntent in E M LA cream , l:VRA. and ve ntri cu lar dysa rryth m ias 2_ Ad dition of ad re n alin e le ng1hens the du ration of action 3_ If given via ETT - n eeds twice the dose 4 _ Antiarrhythm i c ag ent {ventri cu lar)

1 _ To pical anaesthesia for m i nor procedu res ( IV ca rmu latio n in p aed iatri cs) 2_ U se as min i mal amou nt as. possible on inta ct sk i n 3 _ May ca use ery1h ema, itch i n g , bla nch i ng

.2 . N on -depo la.rizii ng age111 t (a ) Trac ri u m

Intubati n g d ose

M a i nte n a nce

O n set

I V 1 _0-2 J D mg/

-

30 -6 0 sees

4-i

0_ 1 mglkg

3- 5

20-'.'. (va r

min

3 -5

20-2 (var

1 -2

20-2

kg

d ose

I M 3.0 mg/kg ( mm:: 1 50 m g )

IV 0 -4-0_ 5 mg/ kg

( b ) C is -auac ri u m

I V 0 _ 1 5-0 -4 m glk: g

(c) Rocurorni ium

IV 0 _6-0_ 9 mg/ kg

O J)2 m g/kg

0_ 1 mg/kg

min

min

D 111 1

(retu 25% Ill e

(var

, l in e rg 'ics

lia ble 5 . 6 : L oca. l A n aestheti 1

Spec ia l poi 111ts

pl'70 1ong t h e d uration of a dion of suxamethoniu rn m,a l for all non-depolarizi ng iN M B ag ent active in profou n d bloclk :me reve rsal for ro cu roniu m (a m i noste ro id group} :tive i n variab le depth of b lock (i n clud ing profou nd C be used i n "CICV" situation (if rocu ro n i u m is used} �rses opioi d ind uced sid e effects ( re sp i ratory ession , p ruritus ) e qu antity can be given without s ign ifica nt toxicity :J ra pid ,i njection of flu m aze nil w h ich can lead thdmwal sym ptoms s u ch as agitation (trem or, tatio ns , a nxiety) a nd em otio n a l !ability ( confusion , 1oria, de pression ) �dation m ay occur (ne,e d repeated dosing )

he effects of n eosti igm ine) S pec i al po i n ts

1cture wh ich crosses the blood brain ba rrier a n d may trnl anti ch olin ergic syndrome (confusion , a mnesia ,, r stru ctu re , therefore it doesn 't cros s fil e blood bra i n

raid of any central effects

Ty1 p,e

B u piva ea i ne (a m ide) (0 . 2 5'% , 0 . 5'%,, 0. 75% )

D ose (iro u te ) Infi ltratio n/ e pid ural : 2 . 0 rn glk g/4 h r lntrath ecal : 8- 1 2 mg (block u p to H 0)

lntrathecal : 1 4 -20 mg (block up to T4 }

Ro p,ivaca i ne (a m ide) (0 .2 % , 0 . 5 % , U. 75% , 1 % )

In� 1.tr atio n/ epid ural : 3 . 04. 0 mg/kg

Li g 110C!1 i 11 e (a m ide) (0 .2 % , 0 . 5 % , 1 % , 2%, 4% , 5 % )

IV,. i nfi ltration , ep i du ra l : 3 . 11-4 . 5 mg/kg

E M LA. ( Eutect i ic m ixtu re o f f o c a l a na est hes i a : l i g n oc a i n e 2.5 % a111d p ri loc a i 111e 2 .5%)

O n set ( m i n ) 5- H J (depe nds mi route , concentration , v,o I u me a nd d ose )

1 0L1 5 (depe nds on route , con cenlration , vo I u me a nd d ose ) 1 -2

Topica l ( in AFO I or with ad re n a l i ne ): 7_0 mgtkg

< 5 kg : 1 -0 g > 5 kg : 2_0 g > 1 0 kg : H I g > 20 kg : 20 g Adu lt 2 . 5- W .O g

1 - Crea m a pplied on p Ian n ed site a nd cover with an oodus ive d ressing 2. _ 1 ho ur late r cream is wi pe off and proced u re , can beg i n

LA sys.tem ic toxicrty ( LAST ): Refe r Ap pend i:x 1 2 and i1 3

D u ral act i m 4

4

Tab le 5 . 7 : Reve rsa l Age n t a nd Antich o Type

S pecia l p o i nts

Low doses gives th e 13,-effe cts and hig h doses g ives a-effects

·ug )

As p reviously mentioned above

u ra l )

\)

I

Increases the BP by i ncrecasing 1he heart rate an d cardia c contra ctio n *Tachyphylaxis In creas es the BP by vasoconstri ction (have s i m ulta n eous bradyca rd ia Ch ose n for obstetric RA d ue to th e better feta! acid-hase profi le compared to usin g e phedrine (in l arge doses ) Resembl es ad re na l i n e but m ore prolo nged effect and l ess effe ct on 1h e hea rt

Nl e- ostig m i n e

S uga mm ade x

Nla l oxo ne F l u m �ze n i'I

n ose/ mu te

IV (U:1 5-0.07 mg/kg

Routine reve rsal : IV 2 .0 mglkg (in TO F 2) IV 4 .0 rng lkg (in PTC 2 ) Immed i ate/ res cue revers al : IV 16 mg/kg

-

0. 002 mg/kg/dose or O .. 1 0 .2 mg ( every 2 m inutes )

0.2 mg then O . 1 mg every 1 m inute (mmc 1 mg )

Effe cts

B ra dycardia I n cre ase bron chia l secretio ns lea ding to bron ch oscon sb-icfion I ncre ase salivation M iosis

1 . Can 2. RevE 3. l n em

No data to sugg est risk for ad verse effects on a ny targ e,t organ

1 . S pee 2. Effec blod 3. Can

Opioid antagonist On set within 2 min utes La sts '"' 45 m inutes

1 . RevE de pn 2. Larg1

B enzod i azepi ne antagon ist Almost i m mediate onset

1 . Avoi ( to wi1 pal pi eu ph 2. Res-E

Ant i cho l i n e rg i cs (adj u n ct to ne u rn :m uscula. r b lockade reve rsa l a nd cou nte r t Type

Dose/ ro ute

G I ye opyrro f ote

!IV S J::1- 1 0

Atro p i ne·

IV 0.0 1 -0 .0 2 mg/kg

µ.g/k.g

E fects f

Ta chycard i ai Bron eh ad ilatio n Red uoe sa livation (anti- sialagog ue ) and bronch ial secretions Less ta chyca rd i a Bette r anti-sialagogue y D e cr, e a:se GI T motilit

H as a te rtiary stn present with cen a gitation ) H a s a qu ate mal)I barrie r hence de,

;th es i ai

ine, h en ce th e sym path om i m etic

m1imeti c d rugs , it can cau se erratic Jertherm i a

rnfll etase enzyme or anticlotting agents, it increases the ene biosynlhesis or antidotting ag ents, it increases the ;,late let-activatin g factor or antidotting agents, it increases the n derstood ,o r an1idotting agents, it increase s the 1ypoglycae m ia

steron e path way inte rferen ce

Ta ble 5.8 : Ba sic Res u sc itatio n D rugs Dmg ty pe

Mec h a n is m of acti o n

D ose/ roUJfe

U sage

Ad re n i}l inel E p,i nep h ri n e

Sympathomimeti cs (a and �-ag on ist)

IV 0_ 1 mg bolus IV 1 _Q mg bolu s IV o_m -l:L1 µ glkg/m i n i n fusio n (via IETT need twice l:V dose} Nebu lizer 0 _4 ml/kg (max: 5 m l )

Ana phyla:xis Ca rd ia c a rrest lo,w C O states ( as inotropic d1 B ro nchospasm Crou p

Atro p i ne•

Anti eh olin ergic agent

As previously rnn entionedl IV, I M , ETT

B radycard ias

E p, li ed ri n e

1 _ In direct action : release of Noradrenaline 2_ Direct action :. a and �-ag o11 ist

IV 3_0-i6_0 mg bolu s or 11 07 mg/kg bolus

Hypotension (in sp in al/ ep,idi

IV 25- 1 00 mcg bolus

Hypotension (in obstetric RJ

P he nylep lil ri ne

Sympathomimeti cs (a1 -agon i st)

Ta b l e 5. 9 � H erba l a n d Dietary S u p p l em ents Affectii n g A111a e� N a me of h erlbi d i et sup p lem e nt

E phed rn ( M a H u a 1 11 � )

-5, hen ce it may in crea se til e n idazol am .. Lig nocaine and

Ga rl ic

Jents' effiects d ue to the clotting agents, it increases ,t he s (> 400 mg/day)

G iin ge r

G i n k g o h i lo ha

s or d ietary supp lements G in sen g

G, l!uc osa m i ne Hl e rib a l d i u retics (gre e n tea, s aw pa l m etto)

C om m o n uses

Pos s i b f,e effects o n a n �esth es i a

Ap petite suppressant Ashtma and bron ch itis CNS sti m ula nt (street na m e : �Clou d 9" an d " Herbal Ecstasy" )

Predomin ant com pou nd is e ph,e dr p ro pe rty ! n the presen ce of other sym pathc hypertension, arrhythm ias and h y1

Anti-emeti c

!Inh ibits, prosta gland i n an d le L1kotri, lln the presence of an1iooa gulants risk of bleed i ng

Loweri ng of choleste rol , trig lyce ride and B P Anli-inffa m m ato ry Anti-emeti c

Potent i nh i bitor of 11 rom boxane s 1 11 n t h e presence of anticoagu lants risk ·o f bleed i ng

Pe rip h e ra l vascula r d isease (i m proves blood circ ulation) D ementia Lowers blood! glu cos,e

Anti-oxidant property a n d in h ib its I I n the presen ce of anticoa gulants ris k of bleed i ng

0:steoa rthritis

Aids g lycosa m inoglycan synthes is May interact with insu lin ca using r

l mmu nom od ulation I ncreases ph ys i ca l sta m i n a a nd me nta l co noontratio n

Pharm aco lkin etic profile is pardy u ! n the presence of anticoa gulants risk of bleed i n g

N atu ra l we ight loss re medy En larged prostate a nd u rinary infla mmation

Postu lated ren in-an giotensin-a ldo! Leads to ele c ,t rolyte i m balance

� "-> n m ► -cc Cr n g «:i (') CD ..,

@

a. "C

(/) o ::::J m C1> 2a. co ::::, CD

co

q Q) :::::!: o

a. 0 ::::, ::::, ::::, )> )> a. �- o, � ::::, (J) 01 Q) (/) ,.... 3 - CD Q) Q) (/) ::::, � ,.... a. ::::, .i::,. =r-

---i "1J -, Q) ::I: 0 ::::, ,....

�a. c.... r

�- · o3
c5" o -o Q)ea .., '-=:: Q)

� ::::, CO CD O> (I) •0,• ,.... =r" I\.> CD

...... ,.... o· ..,,

0

•

Q) ::::, Q)

CD (/)

-,

::::, a. C (') ,.... -· 0

,_ ::::, =r- o co _ (/) -· w 0 ::::, 0

Q)

«:I CD - · Cl> !:!?. ,.... (/) =r• CD O Cl> -, «:i w

-·

::0 m "T1 m ::0 m

Z (')

m en )> z C "T1 C

::0

-I ::c

St. J oh n 's w o rt

Anti-depressant ( m i ld-m ad erate ) Anxiolysis

� z

Viita.m i n E

Anti-ageing Prevent stroke

m ::0 ::0 m

c, en

Potent i nd ucer of he patic cytoch rome P4 metabolis m of drugs s u ch as a lfe ntan il, r I N SAIDs Potentiate or p ro longs the anae s'tihetic ai sed ative properties lin the presence of anticoagu lants or anti, ri sk of bleed i rig Affect thyroid g land fu ncticm I ncreases the• B P in hyperten sive patient

* The Ame riran Soc iety of An esth esiolog ists su gg ested 'tihat patients discontin ue the use of herbal medication 2-3 weeks prior to su rg,e ry

756-763.

3. Miller RD, Eriksson LI, Fleisher LA et al. Miller's Anesthesia (7th edition). Churchill Livingstone: Philadelphia; 2010. 4. Yentis S, Hirsch N, Smith G. Anaesthesia and intensive care A-Z (4th

edition). Churchill Livingstone: Edinburgh; 2009. 5. Becker DE, Rosenberg M. Nitrous Oxide and inhalation anesthetics. Anesth Prog 2008; 55: 124-131.

6. Sasada M, Smith S. Drugs in anaesthesia and intensive care (3 rd edition). Oxfor d University Press: New York; 2003. 7. Allman KG, Wilson I. Oxford handbook of anaesthesia. (2nd edition). Oxford University Press: New York; 2006.

8. Papaioannou V, Dragoumanis C, Theodorou V et al. The propofol infusion 'syndrome' in Intensive Care Unit: from pathophysiology to prophylaxis and treatment. Acta Anaesth. Belg 2008; 59: 79-86.

9. Fudicker A, Bein B. Propofol infusion syndrome: Update of clinical manifestation and pathophysiology. Minerva anestesiol 2009; 75: 339-344.

10. Spinal anaesthesia. Available at: http://www.nysora.com. Accessed on 20/5/14.

11. Suxamethonium chloride Injection BP: Product information. Available at: https://gp2u.com.au. Accessed on 26/5/14. 12. Soliday FK, Conley YP, Henker R. Pseudocholinesterase deficiency: A

comprehensive review of genetic, acquired, and drug influences. AANA Journal 2010; 78(4): 313-320.

13. James MFM, Hift RJ. Porphyrias. British Journal of Anaesthesia 2000;

85(1): 143-153. 14. Rang PH, Dale MM, Ritter JM et al. Rang and Dale's pharmacology (7th edition). Churchill Livingstone: Philadelphia; 2012.

15. Peck TE, Hill S, Williams MA. Pharmacology for anaesthesia and intensive care (3rd edition). Cambridge University Press; 2008.

16. Bansal T, Hooda S. Ropivacaine - A novel and promising local anaesthetic drug. Asian Journal of Pharmaceutical and Clinical Research. 2012; 5(1): 13-15.

17. Sugamaddex. Available at: http://www.ema.europa.eu. Accessed on 30/5/14.

18. Endotracheal drug delivery. Available at: http://calsprogram.org. Accessed on 14/8/14.

19. Hodges PJ and Kam PCA. The peri-operative implications of herbal medicine. Anaesthesia 2002; 57: 889-899. 20. Wong A and Townly SA. Herbal medicines and anaesthesia. Continuing anaesthesia, critical care & pain 2011 ; 11: 14-17.

6 PERIOPERATIVE MONITORING 1. Anaesthesia can be provided by a qualified specialist anaesthetist or a trainee/medical officer under a specialist supervision

2. It has always been quoted that "an alert anaesthetist is the best monitor, and the best monitoring equipment will do no good without one". The core principals of monitoring in anaesthesia are: (a) the anaesthetist must be present throughout the conduct of anaesthesia

(b) equipment and alarm limits must be checked before use (c) monitoring devices must be connected before induction and kept until recovery (in recovery bay or PACU) (d) if an essential monitoring device is not used, reason must be stated (e) record of the monitoring must be documented in the anaesthetic chart/ record/ form (Appendix 2)

(f) the same principles apply for monitored anaesthesia care (commonly

practised outside OT environment), regional and local anaesthesia 4. In an effort to ensure that patient's safety is not compromised intraoperatively,

American Society of Anesthesiologists (ASA) has developed and implemented standards for intraoperative monitoring in 1986 which was then further revised

in 1998 (Table 6.1). 5. These standard of care have been universally adopted by almost all anaesthetic providers.

6. Practicing standard and optimum monitoring enables the anaesthetist to anticipate and recognize any physiological changes with regards to their clinical condition and plan appropriate response or management hence minimizes the anaesthesia-related mortality or morbidity perioperatively. In Malaysia, based on certain centres, the essential standard perioperative monitoring are; (a) Non-invasive blood pressure (NIBP) (b) ECG (c) Pulse oximetry

Essential additional intraoperative monitoring are; (a) Capnography (C02 monitor)

(b) Airway gases and anaesthetic agent analyzer

(c) Respiratory dynamic monitoring: airway pressure, pressurevolume (compliance), flow-volume, respiratory rate, tidal volume, l:E ratio, PEEP (d) Temperature probe (e) Circuit disconnection alarm (a) Arterial line (invasive BP) (b) Central venous line (CVP monitoring) (c) Neuromuscular monitoring (d) Urine output monitoring (e) Cerebral oximetry

(f) BIS monitor and entropy (depth of anaesthesia) (g) lntracranial pressure (h) Pulmonary artery pressure and cardiac output monitoring (i) Transoesophageal echocardiography

7. In this chapter we will deal briefly with common available monitoring modalities. Most importantly is to monitor the cardiorespiratory system followed by other systems depending on the situation and requirements

8. The extent of monitoring depends largely on the age, general fitness of the patient, nature of surgery and planned anaesthetic technique. Monitoring information comes hand in hand with clinical information which allows early recognition and appropriate management of critical incidents Table 6.1: ASA standards for basic anaesthetic monitoring

Sta n da rd 1

Standa rd 2 i. OxygenaUon ii. V:entilaUon

m. C ii rc u la.tion

Qualifi ed amiestlhesia personnel shall be presen in the room tJh roughou th e conduc 0, 1 a l general anaesthetics., regional .anaes heti cs and mo nitored anaesthes ia ca re

Du ring all an aes th etics, me patiien t's oxygenation , venfla Uo n , cir,culation , a nd temperature shall be contin ually" evaluate d Oxygen (0 2 ) analyzer for ·nspired gases

2 . Pu lse oximetry

Ausoulta i on of breath sounds

2 . Ca pnog ra phy (d u ling mechanical v ,e ntilatio n)

3. Obse rvation of the pa ient's c l inical sig n s (during regional ana esthes ia) 1 . HR and BP re cord ed , e very 5 mi nute s

2 . Co nti nuo us ECG display

Those rece ivi ng GA shall have, ·n add ition o, the above at leas one of the follow ing: Pa lp• a tion of pulse

iv. -Y:em peratu re

rn raa rteria l press ure tracin g 2 . Auscultation of heart sounds 3 . Pu lse pie hysmog raphy/ ,oxim etry Ultraso und peripheral pulse monitonng

Monito r tem _ erature when clin ically s ig ni Icant ch an ge s i n body temperat ire are i ntended , a nticipated , or susp ected

Table 6.1: ASA standards for basic anaesthetic monitoring (excerpted from

Standards of the American Society of Anesthesiologists: Standards for Basic

Anesthetic Monitoring /2011 of the American Society of Anesthesiologists. A copy of the full text can be obtained from ASA, 1061 American Lane, Schaumburg, Illinois 60173)

*"Continuous" defined as prolonged without interruption at any time; #"continually" defined as repeated regularly and frequently in steady rapid succession

ESSENTIAL STANDARD PERIOPERATIVE MONITORING

I. Non Invasive Blood Pressure Monitoring 1. Blood pressure (BP) is the pressure exerted by circulating blood on the arterial wall 2. Two forms of measurement:

(a) Manual (auscultatory - Figure 6.01)

(b) Automated (oscillometry - Figure 6.02) 3. The frequency of measurement is tailored individually and recorded

perioperatively 4. Blood pressure cuff size should be appropriate where the width should be

approximately 40% of the arm circumference 5. Clinical points: (a) A bigger cuff size would give falsely lower values and vice versa

(b) Arrhythmias, external movements, shivering and excessive movements interferes with the blood pressure measurement

F i g u re 6 . 0 1 : M a n u all BP'

! Fig u re 6.D2 : A 1 dom ate d B P

6 . Arterial BP can be measured almost anywhere from the brachia! to the radial artery in the upper limbs or tibial and peroneal artery in the lower limbs 7. Generally as we go towards the peripheries, the systolic will increase and diastolic will decrease. However the mean arterial pressure (MAP) will remain constant

·--------------------------� =

MAP Di,a sto lic B P + 1 13 pu ls , e press u r,e, (P u l se p ressu re = Systolic B P - D�asto U c BP' ),

·--------------- -----------� II. Electrocardiograph (ECG)

1. Records the electrical activity of the heart continuously

2. Provides information on the heart rate, rhythm, state of the conduction systems and any ischaemia or infarction of the myocardium 3. According to AAGBI (Association of Anaesthetist of Great Britain and Ireland) guidelines, ECG monitoring is essential in any anaesthetised patient whether under general or regional anaesthesia 4. With regards to 12-lead ECG, it is evident that 90% of detectable ventricular ischaemic changes occurs in lead VS, therefore a modified VS system can be used during intraoperative 3 bipolar lead ECG monitoring,

which is called CMS (central manubrial) 5. CMS configuration involves placing the right arm lead (active or red) over

manubrium sterni, left arm lead (yellow) at VS position (6th intercostal space at the anterior axillary line) and inactive lead (green or black) at left

shoulder (Figure 6.03) 6. Lead 1 1 is best for detecting arrhythmias

Ill. Pulse Oximetry

Figure 6.03: CMS configuration

1. It complements the clinical observation (colour of the mucous membrane) of the patient and monitors the arterial 02 saturation which is expressed as percentage of the 02 capacity in the haemoglobin (Hb) and routinely used to detect hypoxia (pg. 92)

2. Different saturations will provide varying pulse tone, hence once the low limit has reached, an alarm will be audible to the anaesthetist

3. Principle: (a) lights of two wavelengths (red light: 660 nm and infrared light: 940 nm)

are emitted and transmitted across a pulsing vascular bed (e.g. fingers, ear lobe, toes) via a peripheral probe and reabsorbed at the other end by a photo detector (Figure 6.04)

(b) the re-absorbance due to the pulsating arterial wave are computed and

the background reabsorption from tissues and venous blood are excluded

(c) this differential computation will calculate an 02 saturation value over 520 seconds based on the derivation from experimental normogram and displays a waveform (Figure 6.05)

(d) normal value ranges between 97-100% but this can be lower in long­ term smokers, chronic lung disease and cardiac anomalies (80-95%)

(e) value < 90% is considered as hypoxia. Measurements are accurate from 70-100%, but < 70% the accuracy falls rapidly and became unreliable

4. Advantages: (a) portable and easy

(b) non-invasive and fast measurement (c) relatively cheap (d) continuous oxygenation monitoring 5. Limitations:

(a) do not reflect 02 delivery (need to know the Hb and cardiac output for the calculation)

(b) inaccurate measurement in movements, vasoconstricted skin, rapid atrial fibrillation, low saturation 02 (< 70%), nail polish, shivering, electrical interference (cauterization) and during hypotensive episodes (< 80 mmHg) (c) dyshaemoglobinaemias:

Presence

carboxyhaemoglobin can either overestimate (in both) respectively

Figure 6 . 04: Pulse ox i metry prob e

of

spuriously

methaemoglobin underestimate

or

and

Figure 6.0 5 : Pulse ox im etry m eas urement

ESSENTIAL ADDITIONAL INTRAOPERATIVE MONITORING

I. Capnography

1. This is a numeric measurement and real time waveform display (capnogram) of the expired CO2 during ventilation 2. It is measured by the capnograph whereby it monitors the sample of expired CO2 from the breathing circuit attached to the ETT and it is mandatory during GA

3. Value that is measured during GA is the end tidal CO2 (ETCO2) which is the maximum PCO2 measured at the end of exhalation. Normal range is 30-45 mmHg

4. The ETCO2 is slightly lower than the PaCO2 levels, making it a close substitute

for the anaesthetist to monitor the CO2, hence adequacy of ventilation 5. Capnograph detects the CO2 using infrared absorption method

6. Uses: (a) quantitative assessment of perioperative ventilation (b) confirm the correct placement of the ETT or LMA (c) identifying breathing attempts while patient is on NMB agents (able to detect spontaneous breathing)

(d) monitoring during weaning from mechanical ventilation (observing the trends to predict readiness of extubation) (e) different waveforms signifies various

pathology

(bronchospasm,

pulmonary embolism: Table 6.3) (f) predicting survival during CPR (ETCO2 < 10 mmHg after 20 minutes of resuscitation provides a reliable indicator that further resuscitation will not be successful)

7. Normal capnogram consist of 4 phases (Figure 6.06 and Table 6.2)

Figure 6.06: Normal capnogram

Table 6.2: Normal capnogram explanation

Phase E·v ent ln s piratory baseline ,( A-B, } I II

Exptratory upstro:k e ( B�C)

Ill

Alveolar/Expiratory plateau

0

Ins piration downstrnke· (D�I= )

(C-D )

a IP Table 6.3: Different types of capnogram

Rem.arks

Corresponds toi inspiration (devoid of CO2 ) Exp, i ration begins (CO 2 expired and

rises)

Expiration endii ng (CO2 rich ), Value at the end of this phase is knovvn as the ETCO 2 (point D),

Inspiration begins and beginni ng of the next cycle Angle bet'INeen phase I I and I l l (normally 1 00 °' )

Angle between phase I l l and 0 is (1 ( noirma lly 90 )

Graph

-

.

,

-

--

.

I

'

'

"

I •.•

I

.lj j i � �,

.r

a .a. a

�Cl "°

35

-· I o

Clinical condition

Remar1cs

1 . Bronchospasm or auway obstruction

Increased a ang Prolonged phase I I and steeper phase I l l

1.

emp ed spontaneous bl'ea ing during partial muscle B paralysis ( aring o 2. Surgical movements on the chest and abdomen

Cleft at the phase I l l ( a a curare cle )

1 . Oesophageal in balion

ashout o residual gastric CO and eventually be zero

1 . Spontaneous bl'ea ing

Phase Ill no we defined

1 . Hyperven ilalion/ high • ute ntilation 2. Hypothermia

Sustained

1 . Hypoventila ·on1 l�N n • ute enblation 2. Hypertherma 3. Sedation (respira ory depressant drugs) 1.

gnan hyperthennia 2. Parti a· y obstruction 3. High metabolism 4. Absofption of e ogenous CO (laparoscopy)

ETCO,

ETCO

high

GmduaDy increasing ETCO,

Gra p h

:_hn nn

CUn i, c al co, n dition

Remari ks

1 . Soda lime exti au stil on causing col rebreathin g

I n creased 13 angle Sudd.e n and 9 raaua1 ra i$e of bas,e line and th e ETCO2

1 . Pulmonary embol ism 2. Cardi opulmonary arr1est 3. Severe hypote:ns!. o n 4. Card i opulmonaJIY bypass.

1 . Cardi ogen ic osci nations ( occurs en the respiratory frequency of mechan ical ventilation is tow)

Gradually d ecreas!ngi ETCO l

Classic ri pp1 I e 1effed duri ng the end of ,explrath:m secondary to the to and fro movement (due to hea rtbeat) of expi red , g ases at the sensor

II. Airway gases and anaesthetic agent analyser 1. During GA, it is considered the minimum standard to monitor 02, CO2 and vapour agents (anaesthetic gases) in the form of fraction inspired and end tidal concentration (Figure 6.07) continuously 2. Currently it is common practice to use low flow anaesthesia and usually a higher

FiO2 (fraction of inspired oxygen) is administered in order to minimise the risk of hypoxia

3. CO2 monitoring are also essential as hypercarbia will lead to vasodilatation, increased ICP, acidosis and hypocarbia will lead to vasoconstriction

4. Concentration of anaesthetic gases (pg. 154) are monitored with a "minimum alveolar concentration (MAC: pg. 148)" indicator using infrared method and this is necessary to control the depth of anaesthesia intraoperatively

Figure 6.07: Airway gases and anaesthetic agent monitoring (yellow outline is magnified beside this figure)

Ill. Respiratory dynamics : airway pressure, tidal volume, compliance 1. Respiratory rate in a spontaneously breathing patient can be done simply by

manual calculation or estimation 2. Respiratory dynamics monitoring such as peak pressure, mean airway

pressure, tidal volume and pressure-volume loop (compliance) values (Figure 6.08) are provided by modern computed ventilators (during GA) 3. It is important to monitor these values as they provide clues to important events such as pneumothorax, obstruction, bronchospasm, leaking, acute pulmonary oedema etc.

Figure 6.08: Respiratory dynamic monitoring (yellow outline is magnified beside this figure)

IV. Temperature 1. GA causes dose-dependent drop in core body temperature and to a lesser degree may also impair the body thermoregulation postneuraxial anaesthesia (pg. 125) 2. Perioperative hypothermia can occur as early as before the induction of GA due

to the cool ambient OT temperature. This is further compounded immediately

after the induction of GA

3. It is pertinent to monitor the temperature in all patients whose receiving GA of

more than 30 minutes and those having major operations under neuraxial

anaesthesia

4. The pattern or stages of hypothermia post-induction of GA are as below: (a) First stage (Redistribution) : Occurs within the first hour and immediately after induction of GA where there is core-toperiphery body heat redistribution due to mixture of warmer core blood with the less warm peripheral blood. The decrease of body core temperature is

approximately 1.0 to 1.5 ° C (b) Second stage (Linear) : Occurs within the next two to three hours of

GA. It is a slower process where the body heat loss exceeds the body

heat production

(c) Third stage (Plateau) : Occurs within the next three to four hour of GA. Core temperature starts to plateau indicating that the heat loss equals to the heat production

5. Hypothermia acts as a general suppressant of body activity leading to complications such as vasoconstriction, arrhythmias and shivering

6. Hyperthermia causes increased 02 consumption and derangement of enzymatic and body reaction (caused by overheating, malignant hyperthermia, sepsis) 7. Skin Temperature is measured using various thermometer devices and skin

probes. It can be affected by vasoconstriction and cooling effect of the environment

8. Core temperature is the temperature of blood perfusing the abdomen, central nervous system and the thorax. Normal core temperature ranges from 36.3-37.0

oC which is 2-4 oC cooler than the peripheries (arms and legs) 9. This narrow range of core temperature is to ensure an optimal environment for key enzymatic reaction to occur

10. lnadvertant perioperative hypothermia is defined as s 36.0 °C

11. Sites that can be used to monitor core temperature: (a) nasopharynx: can be affected by air (b) oesophagus: can be affected in open heart surgery when the surrounding tissues are cooled. Lower oesophagus is better (c) rectal: can be affected by cool blood from the lower limbs, heat­

producing rectal coloniser and insulating effects of faeces. Generally, it is 0.5-1.0 oC higher than other parts of body

(d) tympanic membrane: Good estimate of core temperature and temperature of the brain by using infrared method. Ear canal should be cleared from wax before measurement (e) blood temperature: can be obtained by thermistor available at tip of Schwanz-Ganz catheter. This is the most accurate core temperature

12. Active warming is a process of transferring heat to the patient. Devices at Figure 6.09, 6.10, 6.11 are commonly used to prevent perioperative hypothermia

Figure 6.09: Forced-a ir Fig ure ti . 1 0 : Circ: ulatin g wanner wate r mattress

Figure 6. 1 1 : Blood/ Fl uid warmer

OPTIONAL MONITORING

I. Invasive arterial blood pressure or intra-arterial pressure

1. It measures the pressure or amount of force by the circulating blood over an

artery and it is regarded as the most accurate and reliable blood pressure

measurement technique 2. Provides a constant real-time or continuous beat-to-beat measurement of the

systolic, diastolic and mean arterial blood pressure 3. Consist of a percutaneously cannulated artery which is later connected to a

continuous column of fluid, pressurized flush bag and a pressure transducer

where the blood pressure is read (Figure 6.12) 4. Advantages over NIBP:

(a) more accurate (especially in very low blood pressure range or during arrhythmias) (b) more suitable for close, continuous and prolonged monitoring like in the intensive care units

(c) allow blood sampling

(d) less traumatic (if repeated blood pressure readings needed) (e) allow analysis of the arterial waveform and can be part of more advanced monitoring (e.g. cardiac output monitoring)

5. Disadvantages:

(a) invasive procedure with risks of thrombosis, ischaemia and infection (b) skill needed to insert the catheter (c) patient will be less mobile

--

--- - - _ _ ...

Figure 6.12: Invasive arterial BP monitoring

II. Central Venous Pressure (CVP)

1. A catheter with multiple lumen (3, 4 or 5) inserted under aseptic technique via

landmark method or ultrasound guidance into a central vein (internal jugular vein, subclavian vein) which will give a pressure value known as central venous pressure (CVP): Figure 6.13 and 6.14

l f i gure 6 . 1 3 : Central veno us cannul l at i, o n u nder u l tras, o un d g u i dance

Fig ure 6. 1 4 : C entra l ven ous cat hete -r

( trip ! e I unum} i n situ

2. It gives a clue of the pressure in the thoracic vena cava which reflects the preload of the heart

3. CVP is measured at the level of 2nd intercostal space at the sternal angle where

the tip of the measuring catheter should be placed just at the opening of the right atrium 4. Normal CVP range is 7-12 mmHg which may vary between individuals and from time to time in the same individual

5. CVP trend of the measurement is more useful than a single value, even though studies has shown that CVP does not correlate well with intravascular fluid volume, it still remains an important tool used by clinicians

6. A failing right heart will cause the pressure to rise as the impaired forward flow

causes a rise in the backpressure to the central venous system 7. It is affected by intravascular volume of the patient, cardiac performance,

position of patient and any factors affecting the intrathoracic pressure such as

mechanical ventilation, pneumothorax etc. (Table 6.4) 8. Other uses of central venous catheter:

(a) Administrations of drugs (inotropic agents), as this route ensures steady and smooth delivery of the potent drug to the circulation (b) Administration of hyperosmolar fluid (hypertonic saline) (c) Administration of total parenteral nutrition (d) Blood sampling

Table 6.4: Factors affecting CVP Fa ctor. s i n c; r e asing the CVP' (impaired rig ht ventricle co ntra cti I ity)

1 . Hyp ervolaemia .2. Hea rt fail u re or ri ght heart fa ilure (i nfa rct, pericard1tis) 3. S evere mitral stenosis 4. Tricu spid regi U rgitation 5. H ig h p u lmonary vas cula r resi sta n ce (p u l mo n ary embol ism. pul monary hyperten si on ) 6. fn cr,e a se intra thoracic pressure (cardiac tam ponade• ten si on pne umoth o:r ax, mechan ica l ventil aUo n )

Faet:ors de creasi ng th e CVP (inadequate ve nous retu rn ) 1 . Hypovolemi a (haemorrhage) 2. S h ock (extreme vasodi l ation ) 3. Third sp ace loss

Ill. Neuromuscular monitoring 1. Used in patients receiving muscle relaxants or neuromuscular blocking agents during GA 2. It is a peripheral nerve stimulator (TOF-Watch®: Figure 6.15) which will guide

the anaesthetist to assess the degree or intensity of neuromuscular blockade based on the response of muscle to a supramaximal peripheral nerve

stimulation

3. Usage of this device will reduce the incidence of residual neuromuscular blockade postoperatively

4. There is also a neuromuscular transmission module available which is incorporated with the anaesthetic machine. This has the same principle as the peripheral nerve stimulator (Datex-Ohmeda M-NMT®: Figure 6.16)

5. Signs and symptoms of residual nerve blockade: (a) generalized fatigue (b) diplopia and visual disturbances (c) decreased hand grip strength

(d) 'Tongue depressor test' negative

(e) impaired ventilation (C02 retention on ABG)

F i g u re 1 6 .1 5, : Peniph , e ra l liilerve st , i mu lato r

F i g u re 6.1 6,: Ne Uiromuscu la r transnil is s i o n mo dule

6. There are 5 patterns of peripheral nerve stimulation: (a) Single twitch stimulation: used during induction of GA, to assess the baseline response to neuromuscular blocking agent (a control twitch height will be recorded prior to induction of GA)

(b) Train of four (TOF) stimulation: most commonly used during GA and in ICU. It allows assessment of the degree of neuromuscular blockade

based on the presence of number of twitches. Forexample, absence of

4th response (T4) or twitch (T4) represents 75-80% ACh receptor blockade. Whereas absence of T3, T2, T1 reflects 85%, 85-90% and 90-98% ACh receptor blockade respectively

(c) Tetanic stimulation: rarely used except during PTC stimulation (d) Post-tetanic count (PTC) stimulation: used to assess the intensity of neuromuscular blockade when there is no response to single twitch or TOF

(e) Double burst stimulation: usually used when there is suspicion of

residual neuromuscular blockade postoperatively. It allows manual or

tactile detection of twitch response in subtle degrees of neuromuscular blockade

7. Sites of nerve stimulation:

(a) ulnar nerve: to assess adductor pollicis muscle response

(b) posterior tibial nerve: to assess flexor hallucis brevis muscle

(c) facial nerve (temporal branch): to assess orbicularis occuli muscle

IV. Urine output 1. Urine output reflects the integrity of kidney function although not

absolutely 2. Prudent to maintain urine output of 0.5 to 1.0 ml/kg/hr in adults, 1.0 ml/kg/hr in children and 2.0 ml/kg/hr in infants

3. For precise monitoring of urine output, the urethra needs to be catheterised and urine collected in the urine collection device (Figure 6.17)

V. Cerebral oximetry

Figure 6.17: Urine collection device

1. Non-invasive monitoring device which provides continuous realtime monitoring of the cerebral oxygenation and indirectly perfusion which is commonly used in surgeries at risk of cerebral ischemia (cardiothoracic, major vascular,

neurosurgery) and ICU

2. Involves application of a pair of adhesive pads (Figure 6.18) over bilateral part of the forehead (bilateral frontal lobe area)

3. It has similar principle like the pulse oximetry by which the cerebral oxygenation is determined by the amount of light being absorbed by the oxyHb in the regional blood

4. In this device, the pads will emit and capture the reflected to and fro near-

infrared light that passes through the cranium and underlying frontal cerebral cortex tissue

Figure 6. 1 8: Bilateral adhesive pads on the forehead

Figure 6.19: Cerebral oximetry monitor

5. Eventually it measures the regional cerebral tissue oxygen saturation (rSO2) and the normal range is 60-80% (Figure 6.19) 6. An initial baseline value must be recorded prior to induction of GA and values of 20-25% below baseline is considered as hypoperfusion 7. Values must be correlated with the patient's clinical condition and factors which can alter the reading are hypotension, reduced cardiac output, hypo or hypercapnia, acidosis, reduced FiO2, anaemia and pre-existing cerebral infarct

VI. Bispectral index (BIS ™ )

1. BIS system is an complex technology and an adjunct to supplement the anaesthetist in optimising the delivery of anaesthetic agents in ensuring adequate depth of anaesthesia, hence reduces the incidence of awareness during GA 2. A sensor electrode is placed on the patient's forehead (similar to entropy: Figure 6.20) to obtain an EEG, these EEG data are analysed and processed using an

algorithm which will finally be translated into a single number (Table 6.5) representing the clinical state of the brain

Table 6.5 : BIS reading

BIS Read iing

C l i n ical State

0

U n respon si; ve

1 -40

Deep hypnotic state

4 1 -J 60

Moderate hypnot i c state

6 1 -90

Light hy pnoti c state

9 1 - 1 00

Awake,

3. Values during GA is 40-60 which indicates a low probability of awareness with recall

4. Potential artifacts can be due to: (a) poor skin contact with the sensor electrode (high impedance) (b) muscle activity or rigidity

(c) sustained eye movements

(d) improper sensor electrode placement (e) unusual or excessive electrical interference (electrocautery, ECG, pacemaker spikes, EMG activity)

VII. Entropy module 1. A module that is incorporated in the anaesthetic machine (Ohmeda®) and

designed to monitor the depth of anaesthesia 2. Similar to BIS, it also incorporates the placement of sensor electrode on the patient's forehead (Figure 6.20)

Fig u re 8 . 20: Senso r e l ectrode on the patien t 's fo rehead

Figure 8.:21 : E ntropy m od u le

3. It uses an algorithm to process the EEG and frontal electromyography (FEMG)

signals by measuring the irregularities in the spontaneous brain and facial muscle activity which will eventually produce two values

4. Two mentioned values are (Figure 6.21 ): (a) Response entropy (RE): sensitive to facial muscle activity (2 sec

reaction time) and a rapid parameter based on EEG and FEMG signals.

It indicates signal of early awakening and patient is responding to external stimuli

(b) State entropy (SE): a stable parameter based on EEG signal and used to assess the hypnotic effect of anaesthetic agents (pg. 108) on the

brain 5. RE and SE values approximately 40 indicates a low probability of awareness with recall and other clinical ranges are as described in Table 6.6 Table 6.6: Clinically relevant RE and SE values

RE

Va l u e

Cli n ica l state

0

No, brain .a ctivity

An aesthesia

40 -60

Fully awake

1 00

SE

N o brain activity

0

Anaesthesia

40 -60

Fully awake

91

VIII. lntracerebral Pressure (ICP) monitoring 1. Commonly instituted in critical care unit 2. Patients with high risk of raised ICP such as traumatic brain injury, intracranial tumor, cerebral oedema, hydrocephalus will need this monitoring

3. Persistent high ICP (Table 6.7) will lead to reduced cerebral perfusion pressure (CPP) which causes cerebral ischaemia or mechanical compression causing brainstem herniation which will eventually lead to death (mortality rate of 20%)

�------------------�

r - - - - - - - - - - - - - - - - - - �

I C PP = m e a n ,a rte r1 l a l b 1 ood 1

p res s u re (MAP ), •· mea n lntracr, a nl, a l pressure ( M l· C ) I

Table 6.7: Causes of increased ICP

I ncrea se d b ra in vol u me,

I n creased b : l ood vol ume•

I n crease ci cereb ros pi na I fl u i d ,(C S F)

Space occu p,y ' n g lesio n {haematomas ,. abscess , a n eu rys m ) C erebra oedema ( h ea d i nj u ry. m etabol i c e nce p h a l o path i e s . ca rd io p u I m o n a r y arrest) Ven ou s outflow obstru cti on

Hype rc apn i a ca u s ing va s od i lati on , o f cere b ra l ve s s e l s h e n c e i n c r e a se d i n bl,o o d now

Hyperaemia

Obs ru ction of CS F fl ow

I ncrn ased prod u ction of CSF Decreased absorpti on of CSF

4 . Main aim of ICP monitoring is to ensure optimal CPP (80-100 mmHg) for

cerebral blood flow and avoid secondary injury of the brain (delayed from the

time of injury and non-mechanical in nature: cerebral ischaemia, progressive increased ICP)

5. Early recognition (decreased consciousness, altered pupil reflex, impaired motor function) is important to determine appropriate intervention (medical or surgical)

6. Various kinds of monitoring devices can be inserted to monitor the ICP 7. Continuous ICP monitoring (Figure 6.22) is pivotal to evaluate the response to therapy and evolution of the injured brain 8. ICP range; (a) 3-15 mmHg: normal in adults (supine) (b) > 15 mmHg: abnormal

(c) > 20 mmHg: pathological (severe increase)

9. Placement of monitoring device will be done by the neurosurgeons types of the device are as below; (a) intraventricular catheter (ventriculostomy): "gold standard" (Figure 6.23) (b) subarachnoid bolt or screw (c) subdural or epidural catheter or sensor

(d) fiberoptic transducer-tipped catheter (intraparenchymal) i

Ventr icul\ar

S u barac hTio d

Fig u re 8.22 : ICP m o n ito r i ng

Figu re 6.23 : lntrave ntri cu lar catheter (vent ri c ulostomy)

IX. Pulmonary artery pressure and cardiac output monitoring 1. Pulmonary artery pressure (PAP: Figure 6.24) monitoring is done by floating the pulmonary artery catheter (Figure 6.25) via the internal jugular vein to the pulmonary artery in selected critical cases

Figu re 6.2 4: Pulm onary artery pressure, card iac o u l i;>u l an d card i ac index me asurement (yellow outlin e )

Fig u re 6 . 25 : Pul monary arte ry cathete r

2. Insertion of pulmonary artery catheter enables measurement of PAP (normal

mean is < 20 mmHg). Value of > 25 mmHg indicates pulmonary hypertension 3. Other uses are; (a) measuring pulmonary capillary wedge pressure (PCWP reflects left atrial and ventricular pressure with its normal range of 4-12mmHg)

(b) measuring cardiac output (using thermodilution principle) and derivation of cardiac indices (cardiac index: Figure 6.24, stroke volume, systemic vascular resistance, pulmonary vascular resistance)

(c) assessing volume status (d) sampling of mixed venous blood to calculate shunt fraction

4. Refer Table 6.8 and 6.9 on factors that can affect the reading of PAP and PCWP Table 6.8: Factors affecting PAP I n c rea se i n PAP

·1 . Left ve ntricu l l a r fai I u r,e 2 . Pulmonary vascular disease (pul monary embolism , pulmonary oed ema , pu l monary embo ism) Table 6.9: Factors affecting PCWP

De, c reased P:AP

1. .2. 3. 4.

Volume depletion Drugs (sildenafi l . epoprosteno, I ) Asp, i ration Pu monary stenosis

Increase in PCWP

1. 2. 3. 4. 5.

Left ventricular failure Cardiac tamponade Pulmonary oedema Hypervolaemia Mitral stenosis or regurgitation

Dacr,e as a i n 'PCWP 1 . Hypovo�aem ia

.2. Afterlo, a d reducUon {v,asodilators)

5. Pulmonary artery catheter insertion and floatation is not favoured nowadays due to studies proving the risk of complications outweighs the benefits in outcome

and availability of other less invasive cardiac output monitoring techniques

6. Complications include infection, rupture of pulmonary artery, thrombosis,

bleeding, catheter knotting and arrythmias 7. Less invasive cardiac output monitoring device available are pulseinduced

contour cardiac output monitoring (PiCCO ™ ), lithium dilution cardiac output monitoring (LiDCO ™ ), Flo Trac/ Vigileo ™ (uncalibrated pulse contour analysis­ based haemodynamic monitor) and USCOM (ultrasonic cardiac output monitor)

X. Transoesophageal echocardiography (TOE) 1. Basic principles of ultrasound can be referred to pg. 293, the only difference is the probe transducer location 2. In this context, probe will be advanced orally into the oesophagus via blind insertion or guided by laryngoscope without any resistance

3. Advantages of TEE: reproducible, rapid detection of any new cardiac pathology and rapid assessment of ventricles/valves 4. Indications as recommended by ASA:

(a) Cardiac and thoracic procedures: open valvular heart surgery (to assess the result of valve repair/replacement), thoracic aortic surgery and to detect new pathology in coronary artery bypass graft for further anaesthetic and surgical plan

(b) Non-cardiac surgery: in surgeries or patient anticipated to develop cardiorespiratory and neurology compromise. In unexplained intractable haemodynamic instability post-surgical intervention, TEE can be considered if expertise and the equipment itself are available

5. Complications are uncommon and ranges between 0.2-5.6% - Dental injury

- Accidental ETT extubation

- Laryngeal palsy - Accidental endobronchial intubation and hypoxaemia - Bronchospasm (especially paediatrics)

- Oesophageal ulceration/injury/bleeding - Oesophageal perforation - Osophageal hematoma - Dysphagia - Arrhythmia

- Distraction from anaesthetic care - Death

6. Contraindications: (a) Absolute

- Previous oesophagectomy - Previous bariatric surgery - Suspected/known cervical injury

(b) Relative

- Oesophageal stricture/diverticulum/varices - Tracheoesophageal fistula - Hiatus hernia

- Large descending thoracic aortic aneurysm - Unilateral vocal cord paralysis - Post-radiation therapy

* A full overview on each monitoring device is beyond the scope of this handbook REFERENCES AND FURTHER READING 1. College of Anaesthesiologists, Academy of Medicine of Malaysia:

Recommendations for patient safety and minimal monitoring standards during anaesthesia and recovery (4th edition) 2013. Available at: www.acadmed.org.my. Accessed on 7/9/14.

2. American Society of Anesthesiologists. Standards of the American Society of Anesthesiologists: Standards for Basic Anesthetic Monitoring. Available at: http://www.asahq.org/Standards/02.html. Accessed on 2/6/14.

3. Update in anaesthesia. Pressure and blood pressure measurement. Available at: www.worldanaesthesia.org. Accessed on 5/6/14.

4. Dash PK. Electrocardiogram monitoring. Indian J. Anaesth 2002; 46(4): 251-260.

5. Kamat V. Pulse Oximetry. Indian J. Anaesth 2002; 46(4): 261-268. 6. DeMeulenaere S. Pulse oximetry: Uses and limitations. The Journal for Nurse Practitioners 2007; 3(5): 312-317.

7. Kodali BS. Capnography outside the operating rooms. Anesthesiology

2013; 118(1 ): 192-201. 8. Rudra A, Chatterji AK, Rudra J. Non-invasive monitoring during anaesthesia. Indian J. Anaesth 2002; 46(4): 246-250.

9. Babita Ghai, Jeetinder Kaur Makkar, Jyotsna Wig. Neuromuscular

Monitoring: A Review J Anaesth Clin Pharmacol 2006; 22(4): 347-356. 10. Sessler DI. Temperature monitoring and perioperative thermoregulation. Anesthesiology 2008; 109(2): 318-338. 11. Arbour R. lntracranial hypertension: Monitoring and nursing assessment. Crit Care Nurse 2004; 24: 19-32

12. National Institute for Health and Clinical Excellence. Diagnostics

Assessment Programme. Depth of anaesthesia monitors Bispectral Index (BIS), E-Entropy and Narcotrend-Compact www.nice.org.uk/dg6. Accessed on 4/7/14.

M.

Available

at:

13. Bruhn J, Myles PS, Sneyd R et al. Depth of anaesthesia monitoring: what's available, what's validated and what's next? Br J Anaesth 2006;

97(1): 85-94. 14. Fischer GW and Silvay G. Cerebral oximetry in cardiac and major vascular

surgery. Intensive Care and Cardiovascular Anesthesia 201 O; 2: 249-256. 15. Bruns AR, Norwood BR, Bosworth GA et al. The cerebral oximeter: What

is the efficacy? AANA Journal 2009; 77(2): 137-144. 16. Shah MR, Hasselblad V, Stevenson et al. Impact of the pulmonary artery catheter in critically ill patients: Meta-analysis of randomized clinical trials. JAMA 2005; 294 (13): 1664-1670. 17. Schwann NM, Hillel, Hoeft A et al. Lack of effectiveness of the pulmonary artery catheter in cardiac surgery. Anest Analg 2011; 113(5): 994-1002. 18. Cote

G,

Denault

A.

Transesophageal

echocardiography-related

complications. Can J Anaesth 2008; 55: 622-647. 19. Mathur SK, Singh P. Transoesophageal echocardiography related

complications. Indian J Anaesth 2009; 53: 567-574. 20. Practice guidelines for perioperative transesophageal echocardiography:

An updated report by the American Society of Anesthesiologists and the

Society

of

Cardiovascular

Anesthesiologists

Task

Force

Transesophageal Echocardiography. Anesthesiology 2010; 112: 1-13.

on

7 P E RI P E RATIVE F LU I D AN D E LECTROLYTES Fluid balance is usually considered as that balance between the body and its environment. It is for a fact that when a disease or impairment strikes, the balance of the whole internal body will be disturbed. It is vital that the understanding of this basic physiology concept that can determine the morbidity and mortality. NORMAL PHYSIOLOGY OF BODY FLUID COMPARTMENT 1. Water encompasses 60% of the body weight of an average adult. The total body water is divided into the (Figure 7.01):

(a) extracellular fluid spaces (ECF = ½ or 40% of body weight) (b) intracellular fluid spaces (ICF = ½ or 20% of body weight) 2. Both components (ECF and ICF) are separated by the cell membrane and sodium pump; this pump actively ensures sodium remains largely in the ECF

3. The cell contains large anions (protein, glycogen) which subsequently draws in K+ to maintain electrical neutrality (Gibbs-Donnan equilibrium)

4. These mechanisms ensures that Na+ and its balancing counterpart anions (Ci­ anci HCO3-) are the basis of ECF osmolality while the K+ has the corresponding function in the ICF

5. The ECF can be further divided into:

(a) lntravascular space (within the circulation) - ¼

(b) Interstitial (extravascular fluid surrounding the cells) fluid spaces- ¾ 6. The intravascular space has its own:

(a) Intracellular component of red (haematocrit: 40-45%) and white cells (b) Extracellular component in the form of plasma (55-60% of total blood volume)

Intracellular space (ICF ) ½ or 40% bod y we ight Na•: 8mm ol/L K.. : 51mmol/l �C .._... LI. u LIJ

Figure 7.01: Body fluid compartment

Electrolytes 1. Substance by which the components will dissociate in solution into positively (cation) and negatively (anion) charged ions. These are: (a) sodium chloride in solution (saline) which will dissociate into Na+ and Cl-

(b) other electrolytes: Ca2+ , Mg2+ , K+ and P0422. Glucose is not an electrolyte as it does not dissociate in solution

3. Total number of positive charges balances the number of negative charges to achieve electrical neutrality at all times

Effects of surgery on body fluid compartment 1. Major surgery or trauma will primarily cause cellular damage which resulted in the failure of the Na+/ K + pump

2. Therefore Na+ and H20 will leak into the cells rendering them swollen and dysfunctional

3. Further injury will disrupt the osmotic/ oncotic balance between the interstitial and intravascular space, resulting in the transfer of fluid into a functionless volume called the "3rd (third) space"

4. 3rd space is a potential space whereby it does not take part in the

dynamic fluid exchanges at a micro-circulatory level 5. 3rd space loss is an acute sequestration or redistribution of isotonic fluids

from ECF to the non-functional interstitial compartment. Frequently seen in burns, ascites, prolonged exposed bowels intraoperatively and clinically

will present similar to hypovolaemic patients Effects of anaesthesia on body fluid compartment 1. Fluid deficit or reduced intravascular volume prior to administration of anaesthesia most likely secondary to prolonged fasting, usage of diuretics and purgatives (bowel preparation) in surgical patients 2. Neuraxial blockade may result in sympathetic block which results in

vasodilation. Presence of fluid deficit prior to neuraxial technique will cause further marked hypotension

3. Anaesthetic agents used for GA will cause a combination of sympathetic suppression resulting in vasodilation, myocardial depression and histamine release which may significantly reducevenous return, hence

resulting in hypotension which can be further compounded if there is a

presence of fluid deficit 4. PPV initiated immediately after an anaesthetic induction may further reduce the venous return

5. Based on the effects of anaesthetic techniques and agents, there is no question that preoperative assessment and correction of fluid deficits prior to induction of anaesthesia is pivotal and spares the anaesthetist from dealing with the deleterious effects on the haemodynamic status Crystalloids vs Colloids • Solution: Fluid consisting of a solvent, e.g. water, in which a soluble

substance or solute, e.g. sugar or salt, is dissolved • Crystalloid: Fluid consisting of all clear glucose and/or salt containing fluids for intravenous use (e.g. 0.9% saline, lactated Ringer's solution, 5% dextrose, etc.)

• Colloid: Fluid consisting of microscopic particles (e.g. starch or protein) suspended in a crystalloid and used for intravascular volume expansion (e.g. 6% hydroxyethyl starch, 4% succinylated gelatin, 20% albumin, etc.) • Balanced crystalloid: Crystalloid containing electrolytes in a concentration as close to plasma as possible (e.g. Hartmann's solution, Sterofundin, etc.)

I. Crystalloids (Table 7 .1 and 7 .2)

1. These are solution of small water soluble molecules which diffuses easily through semi-permeable membranes 2. It has a high volume of distribution within the ECF (volume expanding effect is only 20-30 minutes), hence increases the interstitial volume and leaving

approximately 10-25% of crystalloid solution in the intravascular space

3. Properties of these solutions are largely determined by their tonicity and their sodium content (affecting their distribution within body compartments)

4. The main component of crystalloids is water, with additional electrolytes and/ or

dextrose 5. They are the primary fluid type for resuscitation, maintenance or replenishing body fluids, correct electrolyte imbalance as they can be provided easily and at

low cost 6. Examples are 0.9% saline, Hartmann's solution, D5W and Sterofundin (a) 0.9% saline: isotonic and widely used in neurosurgical and renally impaired patients due to its osmolality but it has a potential of

developing hyperchloremic metabolic acidosis in large volumes

administration

(b) Hartmann's solution: isotonic and more physiological due to the amount of electrolytes which are similar to serum levels. Used most

often in trauma and surgical patients. However, it is unsuitable in end stage liver diseases (as the lactate is mainly metabolized in liver to glucose, CO2 and H2O). Mixing with PRBCs will lead to clotting due to the presence of calcium in the solution)

(c) Dextrose 5% in water (DSW): isotonic and considered as a crystalloid. Serves as a glucose source to provide calorie and rapidly metabolized

to free water once administered. Free water distributes to both ICF and

ECF. Since the goal of resuscitation is to replenish intravascular volume, D5W is not typically used within this phase of treatment (d) Sterofundin: Replaces ECF losses in the case of isotonic dehydration

where acidosis is present or imminent. Contraindicated in hypervolaemia, severe congestive cardiac failure, renal failure with oliguria/anuria, severe general oedema, hyperkalemia, hypercalcaemia and metabolic alkalosis 7. General advantages: low cost, increase the urinary flow and replaces interstitial

fluid volume

8. General disadvantages: transient haemodynamic improvements (due to the

distribution into ECF), peripheral and pulmonary oedema (due to 3:1 ratio) and dilutional coagulopathy

II. Colloids (Table 7.2 and 7 .3)

1. Homogeneous non-crystalline substances also in a water base and known as

plasma expanders 2. Colloid particles have larger molecular weight than those in crystalloid solutions,

so they tend to provide less free water and stays primarily in the intravascular space as it does not readily cross semi -permeable membranes

3. Presence of proteins or starches will increase the oncotic pressure in the intravascular space and may even draw fluid from interstitial compartment into the intravascular space, hence increases the plasma volume

4. Blood is the only colloid that has the advantage of expanding the intravascular volume and increasing the 02-carrying capacity

5. The synthetic starches adds to intravascular volume, but do not need blood

typing and antigen matching as with blood products (a) Gelofusine: it is a 4% succinylated gelatine (derived from horses) solution in saline that carries a risk of anaphylaxis (b) Hydroxyethyl starch: structurally similar to glycogen which consist of

chains of amylopectin (glucose) molecules etherified and substituted with hydroxyethyl groups. They are effective volume expanders with

longer duration of action than the other synthetic colloids. However, they

carry a risk of renal impairment and coagulopathy (c) Albumin: Derived from human sources, hence it still carries a very low

risk of viral transmission. Can be used to improve the "3rd space loss" (acute peritonitis, burns), hypovolaemic shock, haemorrhage and trauma

6. Examples of colloids are hydroxyethyl starch (venofundin, tetraspan), starches

(dextran), gelatins (Gelofusine), whole blood and packed red blood cells (PRBCs) and albumin (proteins) 7. General advantages: reduced total infused volume (due to 1 :1 ratio), stays longer intravascularly (effect lasts 24-48 hrs), maintains the oncotic pressure, reduce peripheral/cerebral oedema, reduce inflammatory response

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-

.

.

4 . 5-7 .0

5 .0-7.0

308,

27'6

"

P l a sm a - tyte 1 4 8

-

-

'< ::::, · - 3 -

Ste rofu n d i n ® 1 I S 0 ( m m,o l l l )

D extr,o se, 5% ( :m mo lJl )

'i . 2 5 24

=r

CD -,_ CD C/) O 0) "C = 0)

-

277 (50 g/L )

24

5 .0

.

98 -

27

-

-

3. 5-5 .5

5 . 1 -5 , 9

4-8

278

304

29 5

CD 0)

00 G) CD ::::, CD

w-

a. -­ C/) O>

a. < 0)

::::, � C/l CD C/)

or

::::,

C')

-c 0 CD

0) C/) C" CD - C') CD 0 0) C/) = �

� CO C')

C')

-- O 0)

co CD £ 0) � -· 0 ::::, C/)

0 "C 0) :T '
2000

B l ood pressu re Systo l ic D iasto l i c

U nchanged Unchanged

Norm a l Raised

Reduced Reduced

Very low Very low ( u n record a b l e )

P u lse (beats/ min)

S lig h t tachyca rdia

1 00 - 1 20

1 20 (th ready)

> 1 20 (very thread )

C a p i l l a ry refi l l ti m e

Normal

S low {> 2s)

Slow (> 2s)

U ndete cta ble

R e s p i ratory rate

Normal

Normal

Tachypnoea {> 20/m in)

Tachypnoea {> 20/m i n )

U ri n a ry fl ow rate ( m l/hr)

> 30

2 0-30

1 0-20

0- 1 0

Extre m ities

Colour normal

Pale

Pale

Pale and cold

c o m p lexion

Normal

Pale

Pale

Ashen

M e ntal state

Alert

Anxious or aggressive

Anxious or aggressive, or drowsy

Drowsy, confused or u n conscious

Source: Baskett PJF. Management of hypovolaemic shock. BMJ 1990: 300; 14531457 (reproduced with the kind permission of BMJ Publishing Group Ltd.)

6. Below is a formula for allowable blood loss which is approximately 35-40% of the EBV r - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - , I I

, 1

A l l owa b l e blood l os s ( m l )

= lHb start Hb lowest auowable}

EBV

, 1

�-------------------------------------� H b start

Therefore, the example of how to calculate the allowable blood loss of a 70 kg man with a baseline Hb of 12 g/dL: Allowable blood loss

1 2-7 X (70 X 70) 12 0 .4 X 4900 204 1 ntl

* Lowest allowable Hb depends on the patient's co-morbid status (those with poor CVS and respiratory reserve may need higher Hb of 8.0 g/dL to maintain adequate

tissue perfusion and oxygenation)

7. Normovolaemia is maintained by initially replacing the blood loss up to the allowable blood loss volume with either crystalloid at 3: 1 ratio or colloid at 1: 1 ratio (start once the blood loss reaches 15-30% of the EBV) 8. Once the allowable blood loss volume (30-40% of the EBV) is exceeded, blood (PRBCs: packed red blood cells) transfusion should be considered (based on presence of active bleeding, anticipated blood loss, cardiopulmonary reserve, 02 consumption)

9. Whole blood is considered when there's presence of acute and massive blood loss requiring O2-carrying capacity of the RBCs along with volume expansion by the plasma. It is usually supplied as a mixture of approximately 400-500 ml of blood and 60 ml of anticoagulant per unit. The drawback is when the whole blood is > 24 hours old, it tends to lose their platelets and clotting factors function

10. To maximize the benefits of transfusion, it is best to transfuse blood when surgical bleeding is controlled by surgeons 11. Besides taking into account the estimated blood loss and allowable blood loss, other factors that may determine the threshold for blood transfusion are pre­ existing clinical condition (IHD, COAD, anaemia), speed of blood loss from surgical site and type of procedure (minor vs major) 12. Summary of blood compatibility can be referred to Table 8.3

13. Other measures to minimize coagulopathy and intraoperative blood transfusion are; (a) consider IV tranexamic acid in surgery anticipated to have likelihood of increased bleeding (acts as an anti-fibrinolysis and encourages clot stability) (b) adequate depth of anaesthesia and analgesia (to minimize myocardial and brain 02 demand) (c) early recognition of specific bleeding site (surgically or via interventional radiology) (d) maintain normothermia (hypothermia leads to coagulopathy) (e) early activation of Massive Transfusion protocol {MTP: pg. 227, Appendix 14 and 15) which involves blood product transfusion (FFP i.e. fresh frozen plasma, platelets and cryoprecipitate: Table 8.4) if bleeding is still ongoing despite surgical haemostasis (clinical suspicion of DIVC i.e. disseminated intravascular coagulation) and coagulopathic

(f) correct any acidosis, hyperkalaemia and hypocalcaemia (g) serial measurement of Hb and coagulation profile will guide on the blood component transfusion therapy (h) intraoperative blood salvage should be considered if expertise and equipment are available. This is when the patient's own blood is collected, washed, concentrated and re-transfused back intraoperatively (commonly practiced in cardiac, trauma and vascular surgery) Table 8.3: Summary of blood compatibility

C a n receive

Patient blood type

C ryopre c i pitate

Whole blood

RBCs

FFP

Platelets

0

0

0

A , B , 0 or

A, B , O or AB A, B , 0 or AB

A

A

A or O

A or AB

A or AB

B

B

B or O

B or AB

A or AB preferred

AB

AB

AB

AS preferred

AB

Rh +

A, 6 , O or AB

Negative or positive is acceptable R h·

Rh• or Rh·

Rh· preferred

Rh• or Rh·

Rh·

Rh·

AB

Table 8.4: Blood component therapy

B or AB preferred

B or AB

Pro d u ct

I n d icatio ns

Packed re d blood c e l l s ( P RBCs) 1 . Whole blood minus pl asma & platelets ( == 250 ml) 2 . Leucocyte depleted 3 . I rrad iated (min im izes microbia l conta minatio n ) 4 . CMV negative

1 . Active bleeding : (a ) H b < 7 .0 g/d l ( b) Hb 7 .0- 1 0 g/d l (symptomatic anaemia , blood loss)

Pl atelets :::: 40-60 m l 1 single donor platelet (apheresis) :::: volume 200 ml 2 . Leucocyte depleted 3 . I rradiated (minim izes microbial conta minatio n ) 4 . CMV negative 5 . Contains few RBC , hence ABO compatibil ity not requ ired

1 . Bleed i ng due to throm bocytopenia 2. Prophylaxis: bone marrow failure ( < '1 0x 1 0 g/l or < 20x 1 0g/l ) 3. Surgery or invasive procedure ( < 50x 'I Og/l or < 1 00x 1 0g/1 ) 4 . High risk su rgery: ocul ar, neu rosu rgery 5 . Platelet dysfunction

P ro d u ct

I n d i cati o n s

F res h F roze n P l a s m a (FFP) :::: 250 -300 m l 1 . Cagulopathy 1 . Conta ins no R BC , cross-match ing is not 2. Factor d eficiency requ i red 3 . DIVC 2. Conta ins a l l 4 . Thro m botic thrombo cytopenic coagul ation factors purpura 3 . Should be administered as ABOcompatible pl asma C ry o p re c i p itate :::: 1 0-40 ml 1 . Contains no RSC 2 . P l asma compati bility preferred but not requ i red 3 . High l evels of fibrinogen , Fa ctor V I I I , von Willebrand factor, Factor X I I I

Massive Transfusion

1 . Factor V I I I , X I I I deficiency 2 . F i brinogen deficiency (fibrinogen < 1 g/1 ) 3 . DIVC 4 . B l eed ing secondary to uraemia

S pe c i a l poi nts Storage : 4 ° C (shelf life : 42 days) Dedicated blood fridges Tran sfusion : Use wit hin < 30 min at room temperature Blood admin istration set Over 1 -2 hrs (< 4 hrs ) Storage: 1 . Room temperature 2. 5 d ays Tran sfusion : 1 . Requ ires agitation 2 . B l ood administration set 3 . :::: 1 0 m kg over 30 min 4 . U se w ithin 4 hrs

S p e c i a l poi nts Storage: < -25 ° C Transfusion : 1 . Thawed immed iately prior to use (20-30 min utes ) 2. Blood administration set 3. 1 0-20 m l g over 3 0 mini hr 4 . Use within 2 hrs Storage: 1 . < -25° C Transfusion: 1 . Thawed immediately prior to use ( 1 5 m in ) 2 . Blood administration set 3. 5 ml s g over 30 mins 4 . use within 2 h rs

1. Definition of massive transfusion:

(a) > 4 units within 1 hour or (b) blood volume loss or transfusion of half EBV within 4 hrs or (c) blood volume loss or transfusion of one EBV over 24 hrs or (d) > 10 units RBCs in 24 hrs or (e) blood volume loss or transfusion at a rate of > 150 ml/min

2. Perform conventional measures to prevent and correct coagulopathy:

(a) adequate venous access (b) adequate volume replacement and blood product (c) measures to prevent and reverse hypothermia (d) measures to prevent and reverse acidosis (e) consider early "damage control surgery" and followed by surgical definitive haemostasis procedures (if needed) to arrest active bleeding

3. Potential patients who are identified as those suffering uncontrolled haemorrhage and coagulopathy unresponsive to conventional measures warrants a Massive Transfusion Protocol {MTP: Appendix 14 and 15) to be activated according to the local institution's criteria

4. MTP is a comprehensive institutional plan or algorithm to deliver a reasonable target ratio of red blood cell: fresh frozen plasma: platelet (RBC: FFP:PL T} in patients who is anticipated to have massive blood loss in order to facilitate communication between doctors in minimizing the delay in ordering and administering blood products

5. The transfusion laboratory and on call haematologist should be alerted and frequent blood tests should be collected for: (a) full blood count (b) coagulation testing and fibrinogen level (c) ABG and electrolytes

6. Once bleeding arrested and haemodynamically improved, deactivation of MTP should be done and communicated to the relevant staff Postoperative Management

1. Under this subheading, discussion is focussed on blood component

2. 3. 4. 5.

transfusion in patients monitored in ICU/HOU postoperatively where the anaesthetist is directly involved in their continuation of care Transfusion trigger is the Hb level at which the risk of reduced 02 carrying capacity is more than the risk of transfusion, hence this justifies blood transfusion There is no specific end points of what level of haemoglobin should be the threshold or trigger for transfusion Transfusion is considered according to individual basis (presence of haemodynamic instability, cardiorespiratory disease, rate of ongoing blood loss, risk of further blood loss, evidence of end organ compromise) Below are the general rules of blood transfusion as mentioned by the National Blood Centre, Ministry of Health Malaysia: (a) Patients who are haemodynamically stable and normovolaemia will not require transfusion if the Hb is > 9.0 g/dl (b) Patients with low cardiorespiratory reserve or high metabolic activity (sepsis) may need transfusion to ensure a Hb level of � 10 g/dl (c) Transfusion is inevitable in Hb < 6.0 g/dl (especially in acute anaemia) (d) All symptomatic anaemia should be transfused regardless of the Hb level

6. Indications for platelet, cryoprecipitate and FFP transfusion can be referred to Table 8.4 REFERENCES AND FURTHER READINGS

1. National Blood Centre, Ministry of Health Malaysia. Guidelines for the rational use of blood and blood products. 2010. Available at: http:// hsajb.moh.gov.my. Accessed on 20/4/14. 2. Available at Baskett PJF. Management of hypovolaemic shock. BMJ 1990: 300; 1453-1457. 3. Murphy MF, Wallington TB et al. British committee for standards in haematology, blood transfusion taskforce. Guidelines for the clinical use of red cell transfusions. British Journal of Haematology 2001; 113: 24-31. 4. Stainsby D, Maclennan S, Thomas D et al. Guidelines on the management of massive blood loss. British Journal of Haematology 2006: 135; 634-641. 5. Smith EC, Bauer AM, Pivalizza EG et al. Massive transfusion protocol (MTP) for hemorrhagic shock: ASA committee on blood management. 2011. Available at: http://www.asahq.org. Accessed on 18/2/14. 6. National Blood Authority (NBA) (2011). Patient blood management guidelines: Module 1 - Critical Bleeding Massive Transfusion. NBA,

Canberra, Australia. 7. Shah BH, Dente CJ, Harris RS et al. Transfusion management of trauma patients. Anesth Analg 2009; 108: 1760-1768.

9 POST-ANAESTHESIA CARE RECOVERY AREA/ BAY/ POST-ANAESTHESIA CARE UNIT (PACU)

1. After a patient receives any form of anaesthesia for any surgical procedures, i.e. general anaesthesia (GA), regional anaesthesia (RA), plexus block, local anaesthesia or sedation, he/she must be monitored in a designated area for a certain period of time before being discharged to the ward or home. This is typically referred to recovery area/ bay or post­ anaesthesia care unit (PACU) 2. The degree of monitoring and length of stay differs between patients, mainly determined by the type of surgery, anaesthesia, patient's co­ morbids and perioperative events

Facilities and set up

1. The area is part of operating theatre (OT) complex and should be centrally located with easy access to all OT's 2. Should be connected to outside access for transfer of patient to the ward 3. It should be an "open-plan" for easy monitoring or unobstructed view of all patients by the staff nurse (may have curtains for patient privacy) with an easy access during emergencies (resuscitation trolley, portable X-Ray) 4. Ratio of bed space: OT is at least 2: 1 5. There should be spaces dedicated for: (a) drugs and fluids storage (b) esuscitation trolley (drugs, airway devices, bag and mask for manual ventilation, defibrillator machine) (c) trolley for syringes, needles and blood bottles (d) counter for clerical works (e) telephone/intercom for communication to the OT and wards (f) sink for hand washing

6. Each bay space should be equipped with:

(a) 02 pipeline outlet, 02 flowmeter, 02 delivery device (pg. 100) (b) medical air and vacuum outlets (c) vital signs display monitors (pulse oximeter, blood pressure)

(d) (e) (f) (g) (h)

stethoscope medical suction device and catheter patient warming device (forced-air warmer/ radiant warmer) at least two power outlets and emergency power supply adequate lighting and adjustable emergency lighting

7. Some bay space may have:

(a) equipment for anaesthetizing the patient (anaesthetic machine)

Monitoring

1. Basic monitoring for patient must include non-invasive blood pressure, pulse oximetry and ECG (especially for high risk patient) 2. Thermometer, peripheral nerve stimulator and capnograph (those who are still intubated) should be immediately available if needed 3. The vital signs of the patients should be properly recorded and documented in a dedicated space in the anaesthetic chart/ record/form (Appendix 2) 4. Frequency of monitoring varies from every 5 to 10 minutes depending on the type of procedures and anaesthesia that the patient receives. Critically ill patient who is unable to be sent immediately to the ICU will need continuous and more detailed monitoring 5. Information that needs to be documented: level of consciousness or mental state (b) blood pressure (c) heart rate and rhythm (d) respiratory frequency (e) SpO 2 and 02 administration (a)

pain intensity (g) intravenous infusions (h) drugs administered (i) other parameters (tailored to individual clinical condition) e.g. temperature, urinary output, central venous pressure, ETCO 2 , surgical drainage, Hb level (f)

Staff

1. Staff working in the recovery area should be able to observe the patients on a one to one basis until they are able to control their own airway, haemodynamically stable and pain is well controlled 2. Ideally all staff should have "Basic Life Support" knowledge 3. An agreed protocol or checklist on post-anaesthesia care may be outlined and provided for all the staff to refer and comply

Discharge 1. In 1970, Aldrete had proposed a scoring system to evaluate patient's readiness for discharge from PACU and had revised the scoring system in 1995 {Table 9.1). Usage of this scoring system is encouraged 2. Assessment scores will be measured and documented upon admission, 30 minutes and one hour after arrival in PACU. Thereafter, assessment score will be done hourly and upon discharge 3. A score of 10 out of a possible 12 will be deemed safe to be discharged or transferred to the general ward 4. Other clinical criteria that should be taken into consideration on top of the existing scoring system are: (a) surgical site/ dressing not soaked and no persistent bleeding (b) pain score less than 4 (c) temperature � 36 ° C (d) controlled nausea and vomiting

5. Ideally the anaesthetist in charge of the case should see and authorize the discharge if the criteria are met. However, it can be delegated to the trained recovery staff provided that they follow the protocols and guidelines strictly 6. Any problems or discharge criteria not achieved should always be informed to the anaesthetist 7. The patient may be discharged with 02 supplement, ongoing blood transfusion or fluids from PACU 8. Unstable patient or patient with severe complication may require admission to the HOU or ICU for close monitoring Table 9.1: Modified Aldrete Scoring System

Activity: a b l e to move vo l u ntari ly o r on c om ma n d 4 extremities 2 extremities 0 extremities

2 1 0

Resp i ration Able to deep breathe and cough freely Oyspnea , shal low or l imited breathing Apneic

2 1 0

C i rc u lation BP ± 20 mmHg of prea naesthetic l evel BP ± 20-50 mmHg of preanaeslhesia level B P ± 50 mmHg of preanaesthesia level

2 1 0

C i rc u l ation H R ± 20 bpm of preanaesthetic level HR ± 20-35 bpm of preanaesthesia level H R ± 35-40 bpm of preanaesthesia level

2 1 0

Consciousness Fu l ly awake Arousable on ca lling Not respond ing

0 saturation �bl e to ma intain 02 saturation > 92% on room air Needs 02 inhalation to maintain 02 satu ration > 90% 0 , saturation 90% even with 0, supplementation

2 1 0 2 1 0

Source: Reproduced from Aldrete JA. The post anaesthesia recovery score revisited (letter). J Clin Anesth 1995; 7: 89 -91 (reproduced with the kind permission from Elsevier Science)

9. The anaesthetist in charge of the case should hand/pass over the case to the respective PACU staff who is trained in basic resuscitation (doctor or staff nurse) before leaving the patient in recovery are/bay or PACU. Next handover will be between the PACU staff to the ward/ ICU/ CCU staff r - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - ,

I n fo rmati o n to be h a n d e d/passed ov e r i n c l udes:

1 . Patient's identification , diagnosis and significant past medical illness 2. Procedures done, d u ration of anaesthesia , a ny special monitoring utilized 3. Anaesthesia : type , airway device used ( ETT or L IA} , any events or complications perioperatively, amount of opioids given (if used}, fluids balance (inpuVoutput}, patient's vita l s status and postoperative plan ( e .g . a nalgesia/ oxygen su pply/ blood transfusion) for the patient 4. Transfer of care - ward , ICU , or home (for daycare)

COMMON COMPLICATIONS

1. There are a few common complications that can occur in a patient while in recovery room/PACU

2. These includes pain, postoperative nausea and vomiting (most common), respiratory, cardiac and neurological complications • Pain : Please refer Chapter 10 (pg. 255)

• Postoperative nausea and vomiting (PONV)

(a) PONV is an unpleasant experience that a patient can have after anaesthesia. They may only have retching, nausea with or without vomiting. It can occur during the first 24-48 hours post anaesthesia (b) Incidence: About 30% suffered vomiting, 50% developed nausea and up to 80% has PONV in high-risk patients post surgery (c) It can lead to: i. increased intra-abdominal pressure and risks disruption of abdominal or inguinal suture lines ii. gastric aspiration in those with impaired airway protective relexes iii. increased sympathetic response (hypertension, tachycardia) iv. delayed discharge from the PACU v. unplanned admission for daycare surgery vi. reduced satisfaction to the patient as well as family members

(d) There are well established and potential risk factors (Table 9.2)

Table 9.2: Risk factors for PONV (all are potential risks except for paediatric strabismus which is an established risk factor)

Pati ent re l ated

Female gender ( 3 x more common)

H istory of motion sickness/PONY or both Non-smoker

C hi ldren of

3 years old ( does not appl ied to adult)

Low ASA status ( I and I I ) H i story o f migraine

An aesth e s i a related

Preoperative anxiety

U se of volatile/inha lationa l agents U se of N 2O

U se of intra and postoperative opioids

Longer du ration of GA (in surgery > 30 minutes) U se of GA VS RA

U se of neostigm ine S u rgical re lated

Facemask ventilation

Paed iatric strabismus surgery

Open G I T surgery

Laparoscopic surgery rvliddle ear surgery

Opthalmic surgery B reast surgery

Gynaecolog ical surgery

4. There are few scoring systems that has been developed in order to predict the incidence of PONV and was mentioned by SAMBA (Society for Ambulatory Anesthesia)

5. Apfel score is a simplified method of scoring for adult in which the risk factors are female, non-smoker, history of PONV and postoperative opioids (each risk factor is given 1 point). Summation of the risk factors will determine the risk of developing potential PONV, namely sum of points of 0, 1, 2, 3, 4 will produce the risk of 10%, 20%, 40%, 60% and 80% respectively Approach to management:

1. Assess baseline risk - based on the risk factors 2. Decrease the baseline risk

(a) Avoid volatile/inhalational anaesthetics and N2O, opt for RA (if feasible)

(b) Limit opioids usage - use multimodal analgesia (pg. 261) (c) Avoid high dose neostigmine

(cl) Adequate hydration 3. Prophylaxis (based on the scoring)

(a) Score 0-1: Considered low risk (factors). Wait and see. Use rescue treatment if needed (b) Score 2-3: Considered moderate risk. 1-2 antiemetic agents needed (c) Score 3-4: Considered high risk. 3-4 antiemetics agents, consider TIVA and multimodal analgesia approach

4. Interventions (a) Pharmacological (aims to target specific receptors: dopaminergic, cholinergic, serotonergic)

i. 5-HT3 antagonist: IV ondansetron 4 mg, IV g ranisetron 0.35-1.5 mg ii. Corticosteroid: IV dexamethasone 8 mg (adults) and 1 - 1.5 mg/kg (children) iii. Butyrophe nones: IV droperidol 0.625 mg - 1.25 mg, IV/ IM haloperidol 0.5 mg - 4 mg iv. Anticholinergic: transdermal patch scopolamine 1.5 mg v. Dopamine antagonist (phenothiazines) : IV metochlorpramide 2550 mg vi. Opioid antagonist: alvimopan 4 mg vii. NK1 receptor antagonist: aprep itant 40-80 mg viii. Others: IV propofol 10-20 mg (for refractory nausea) , gabapentin 600-800 mg

(b) Non- pharmacological

i. Acupuncture ii. Regional anaesthesia

2. Rescue treatment

(a) Some patient still developed PONV despite prophylaxis being given, therefore rescue therapy is needed (b) Choice of drug: 5-HT3 antagonist (if not given as prophylaxis) or if the

last dose was more than 6 hours (c) Alternatives include dexamethasone, droperidol or promethazine (for patients not suitable to receive 5-HT3 antagonist) (d) Those with severe PONV will be treated with multimodal therapy involving several types of anti-emetics targeting different receptors • Respi ratory com p l ications I . Apnoea and Hypove nti lati on

1. Apnoea: Defined as cessation of breath i ng 2. Hypoventilation : Redu ced frequency of breathing 3. Cli n i cal features : noisy breathing, absent sound of breath i ng, paradoxical movement of chest and abdominal wall, reduced level of consciousness, hypercarbic signs (warm, flushed, boundi ng peripheral pulse, hypertensive) 4. Causes can be divided into 3 categories:

(a) Factors affecting the airway

i. Tongue (falli ng back against posterior pharyngeal wall) ii. Laryngospasm secondary to blood or secretions on the pharynx tracking i nferiorly to the larynx iii. Laryngeal oedema (especially i n paediatrics after using cuff ETT) iv. Bronchospasm (secondary to histamine releasing drug: morph i ne) v. Foreign body (forgotten throat pack) vi. External compression of the neck (haematoma/haemorrhage post­ thyroidectomy , tumou r)

(b) Factors affecting the ventilatory drive

i. Respiratory depressant drug (residual volatile agents, opioids, benzodiazepi nes) ii. Intra/postoperative cerebrovascular accident or raised ICP iii. HyRothermia

(c) Peripheral factors

i. Respiratory muscle weakness (residual paralysis, inadequate reversal dosing, pre-existing neuromuscular disease i.e. myasthenia

g ravis, re na l/hepatic fa i l u re , hypokalaem ia, hypermagnesaemia) i i . Pain ( i n u pper a bdominal and thoracic surgery causing d i a p h ragmatic splinti n g ) i i i. Obesity (associated with OSA) iv. Pneu mo/haemothorax 5. Management: (a) possible ca uses should be excl uded for eas ier and d i rect treatment to the problem (b) manage accord i ng to the poss i ble ca uses (c) general measures : i. Ai rway, breath i n g , ci rcu lation checl< i i . Place patient i n lateral to improve patency of airway and heaa down tilt position to faci litate passage for blood or vom itus out from the oral cavity (perform suctioning) iii. 02 therapy via face mask and apply basic airway manoeuvres (pg . 49) iv. Provide mask ventilation by BVM (pg . 5 1 and 1 1 9) tem porarily v. Attach mon itori ng and CALL FO R H ELP early if i n crisis situation (e.g . laryngospas m , a pnoea or obstructive causes) vi. Take ABG and other blood sam ple deemed n ecessary for the patient for d i ag nostic and th era peutic pu rpose vi i . Defi n itive secu re of the a i rway with ETT if u nable to wake the patient up, a nticipati ng prolonged episodes of a pnoea/hypoventi lation and signs of hypoxemia such as desatu ration ( i neffective ventilation) and severe hyperca rbia II. Desaturation

1 . Occu rs when the patient has deterioration of Sp0 2 below his basel i ne val u e . This ca n be secondary to hypoxaemia 2. Refer Chapter 3 for the ca uses of hypoxae mia (pg . 96) and their management (pg . 9 7) • Cardiovascular com plications

I. Hypotension

1. Defined as reduction i n blood pressure � 20% from the baseline preoperative reading or SBP < 80 m mHg and DBP < 50 mmHg 2. Maybe associated with either bradycardia or tachyca rdia and eventually develop multi organ system failu re if remained i n prolonged hypote nsion 3. Risk factors: inadequate flu id re placement from ongoing losses i ntraope ratively (preoperative bowel prepa ration , GIT losses) or significant bleeding, pre-existing heart failu re , usage of neuraxial anaesthesia 4. Causes include hypovolaem ia (reduce i n preload), vasodilation (reduce in SVR) and im pai red contractility

(a) Hypovolae mia

i. M ost com mon cause for hypotension in PACU i i . Causes: 3rd space loss, burns, ongoing surgical bleeding, polyuria, inadequate fluids intraope ratively iii. All of the above can be managed with fluid resuscitation and boluses exce pt ongoing su rgical bleeding which have to be fu rther evaluated and informed to the surgical colleagu es iv. Inspect the surgi cal wou nd site and possible sites of bleeding according to type of surgical procedures: soaked dressing, urinary catheter, palpate for tensed abdomen and swollen limbs v. Arte rial blood gas can be taken to evaluate the acid base status and Hb level vi. Surgical i ntervention and blood transfusion maybe needed

(b) Vasodilation

i. Causes: neuraxial anaesthesia, anaphylaxis, transfusion reactions, sepsis, residual anaesthetic agents, rewarming ii. Consider other signs and sym ptoms suggestive of the causes above ; feve r, low conscious level, duration of any neu raxial anaesthesia, recent administration of blood or certain drugs iii. reatment include fluid boluses and vasopressor (phenylephrine, ephedri ne, noradrenaline) iv. Prevention of hypotension secondary to neuraxial anaesthesia is to load the patient adequately with fluids prior to the procedure

(c) Im paired venous return

i. Causes: excessive PEEP, pneumothorax, cardiac tam ponade and massive pulmonary embolism ii. Treat promptly and accordingly (immediate 100% 02 , reduce the PEEP, thoracocentesis, pericardiocentesis, th rombolysis)

(d) Im paired contractility

i. Causes: congestive cardiac failure, cardiac tam ponade, pre-existing cardiac disease, arrhythmia (heart block), myocardial ischemia or infarction , drugs (f3-blockers, GA agents), sepsis, hypothyroidism i i. Early recogn ition and suspicion is the key. Request for CXR, 12-lead ECG, send for blood samples (cardiac enzymes, electrolytes, thyroid function test) urgently iii. Treatment depends on the cause: i notropic support, pericardiocentesis, pacing, thyroxine

II. Hypertension

1. Defined as increased of 20% SBP or DBP or MAP above baseline. Frequently seen with tachycardia 2. It can lead to serious end organ damage such as cerebrovascular accident, renal failure and cardiac failure 3. Causes: often due to pai n , anxiety, uncontrolled pre-existing hypertensive disease, hypercapnia, hypoxaemia or excessive intravascular fluid volume, bladder distension , increased intracran ial pressure and hypotherm ia 4. Prevention : Anti hypertensives should generally be conti nued perioperatively except for ACE inh ibitors and diuretics as it may cause labile BP i ntraoperatively 5. Ap proach to management: (a) opti mum treatment of essential hypertension preoperatively (in elective surgery) (b) conti nue oral anti hypertensive medications on the day of surgery (c) identify the baseli ne BP preoperatively for reference poi nt (d) exclude causes (as above)

(e) i n itiate treatment: Depe n d i n g on the cause (opioid a n algesics , sedatives , IV short acti ng anti hypertensive age nts l i ke esmolol , vasod ilators l i ke nitrog lyceri n e , a nticholin esterase if su spect res idual paralys i s , opioid a ntagonist if suspect over sedatio n , w i t h h o l d fl u i d t h e ra p y , u r i n a ry d ra i n a g e , n e u ro s u rg i ca l i nterve ntion , warm i n g thera py) (f) avoid abru pt B P red u ction (more than 20%) for those with no i m med iate ris k (hypertensive u rgencies) (g) resu m e oral anti hypertens ive (if not contra i nd icated ) as soon as poss ible postoperatively to red uce occu rrence of rebou nd hypertension Ill. Dysrhyth mias 1 . Causes: Electrolyte ab normal ity, hypoxaem i a , hypercarbia , acidosis, a l ka losi s , i ncreased sym patheti c discharge and pre-existi ng cardiac disease 2. The m ost com m o n d ys rhyth m i as a re s i n u s tach yca rd i a , s i n u s bradyca rd i a , prematu re ve ntricular beats , ventricu lar tachyca rdia and suprave ntricular tachya rryt h m ias (a) S i n us bradyca rd ia i. Heart rate < 60 bpm i n an a d u lt i i . Causes: hypoxe m i a , hypotherm i a , h i g h levels of spinal a naesthesia , vaga l sti m u lation i i i. Id entify causes and treat accord i n g ly (e .g . with active warm i n g fon hypotherm i a , 02 su pplement and fl u ids) iv. Atropine is the d rug of choice for treatment of bradycard ia g iven in small a l i q u ots v. Heart rate of < 60 bpm may be normal for some patient (those on �­ blocker, ath letes ) (b) S i n us tachycard i a : i. Heart rate > 1 00 b p m ii . Causes: pai n , hypoxe m i a , hypovolae m i a , i ncreased tem peratu re a n d a nxiety i i i. B-blockers (propranolol, esmolol) may be g iven after treati ng possi ble ca u ses such as pa i n and hypovolae m i a

(c) Premature ventricular beats

i. These are a normal electrophysiological pheno menon wh ich may present with palpitation, however they usually do not req u i re further intervention i i. Patients with pre-exi sti ng ischaemic heart disease or Wolff Pa rkinson Wh ite syndrome, presence of prematu re ventricular beats may trigger the onset of a re-entrant tachydysrhyth mia (ventri cular tachycardi a , atrioventri cula r re-entrant tachycardi a) iii. Causes: anxiety , myoca rdial ischae m i a , hypokalaem i a , hypomagnesae mia , sym pathomimetic agents, �-agonist

• Neurological complications

I. Postoperative shivering

1. Thermoregulatory center is i n the hypothala mus . Anaesthesia may i m pai the body thermoregulation (pg. 179) and causes hypotherm i a if it is not actively prevented 2. Sh ivering is a known com plication of hypotherm ia and it occurs as a form of defense mechanism by wh ich it i ncreases metabolic heat production by 6x above the basal level 3. It is a common com pli cation with reported i ncidence va ries from 5-60% after GA and about 30% after RA 4. Besides be i ng uncomfortable for patients , it can also cause few u ndesi red sequ alae such as: (a) increase in patient's oxygen consum ption u p to double or tri ple ti mes along with CO2 production, increase catechola m i nes production and lactic acids (metabolic acidosis) (b) worsen i ng of wound pa i n (c) increase i n intracra n i al pressu re (catastrophe for the susce ptible neurosu rgery patients) and intraocular pressure (d) ca rdiovascular com plications (arrhyth m ias, hypertension) (e) disruption of wound suture , drains, ECG and pulse oxi metry monitoring

5. Although postoperative shiveri ng mainly related to thermoregulatory reason , it can also be secondary to i nflam matory reactions and release of cytoki nes

6 . Risk factors:

(a) you nger age (b) long duration of surgery (c) high concentration of volatile agents (d) endoprosthetic surgery (e) core hypothermia

7. Prevention :

(a) preoperative warming and intraoperative active warming are advocated to mai ntain patient's core tem perature (b) warm i ng methods in clude usi ng forced-air warmer (most effective perioperative active warm i ng), single layer of i nsulation such as standard cotton thermal blanket or plastic wrap (passive warm i ng), usi ng warm intravenous/i rrigation fluids, adjustment of operating theatre h u m idity and tem peratu re

8. Few drugs has been studied and used as pharmacological treatment for post­ anaesthesia shivering, they are: (a) peth idi ne (opioid) : high efficacy; average dose of 25-50 mg bolu s; minimum 0.35 mg/kg. It can be given via many routes i .e. IV , IM , epidu ral, intra-thecal (b) clonidine (a2-agonist) : average dose of IV 75-150 µg bolus (c) ondansetron (5-HT3-antagonist) : IV 8.0 mg given at i nduction (d) others: IV Tramadol 35-50 mg, IV physostigm i ne 0.04 mg/kg

II. Postoperative deli rium

1. Postoperative cogn itive changes or di sturbance can be divided i nto two (2 ):

(a) Postoperative deli rium : acute and transient cogn itive change or mental dysfu nction (b) Postoperative cognitive dysfunction : long term effect of postoperative cognitive change or mental dysfunction (for the p u rpose of this han dbook and relevan ce to the com plication in recovery room , only postoperative deli rium will be described)

2. In cidence of 15% among elderlies undergoi ng elective su rgery but can be higher post-cardiac and h i p su rgery

3. It is an acute transient organic bra i n syndrome developed with in two (2) days postoperatively and characterized according to DSM-IV crite ria for delirium ;

(a) d isturbance of consciousness (altered awa reness of the envi ronment) with ina bility to focus, sustain or shift attention (b) change in cognition including disorientation or development of perceptual disturbances (h alluci nations) th at are not better explained by preexisti ng , esta blished or evolving dementia (c) develops over short period of time (within 2 days postoperatively) and fluctuates d u ring the day (d) identifia ble general medical cond ition (post GA, opioids , anti­ cholinerg ics)

4. Few hypothesis were postulated to explain the mecha n ism by wh ich postoperative delirium occu rs ;

(a) Reduced level of multiple brain neurotransm itters seconda ry to decreased brain oxidative metabolism (b) Increased serum cortisol level seconda!}' to post-su rge!}' and anaesthesia-induced stress to the body (c) Reduced level of acetylcholine (ACh) in conjunction of anti- cholinergic use

5. Clinically can present with ;

(a) Hyperactive : ag itation (usually worsen at nig ht time), irritability, restlessness, uncooperative (b) Hypoactive : somnolence , slowness, sedated (c) Mixed of both

6. Morbidities associated with this cond ition are fractures and head inju ry if patients fall from bed, dehyd ration and haemato ma if they pull out IV catheters/ drains/ tubes 7 . Risk factors:

(a) Age > 65 yea rs old (especially those who practices polypharmacy) (b) Pre-existing dementia , cerebrovascular accid ent, depression, Parkinson's, liver disease, renal failure, congestive hea rt failu re (c) Previous h istory of delirium , tobacco use

(d) Preoperative use of narcotics, benzodiazepi nes, alcohol (e) Severe illness (pneumonia, urinary tract infection, intra- abdominal infection , infected wound) (f) Types of surgery (cardiac, orthopaedics, cataract due to the visual i mpairment and anticholinerg ic use, prolonged surgeries) (g) Metabolic impairment (dehydration , hyper/hypoglycaemia, hyponatraemia, u raemic, acid base disorder) (h) U ncontrolled postoperative pain

8. Perioperative triggers:

(a) Acute pai n (b) Use of physical restraints (c) Malnutrition (d) Addition of three or more medications in 24-48 h (e) Use of a urinary bladder catheter/ full bladder (f) Anaemia (g) Electrolyte and fluid abnormalities (h) Massive surgical blood loss and intraoperative transfusion

9 . Management (Table 9 .3):

Table 9.3: Management of postoperative delirium

No n -pharmaco l o g i c a l i nte rventi o n ( i n ward)

1 . Physical: hydration , 02 therapy, nutrition 2 . Cog n itive: verbal orientation of time and place by medical staff. repetition of re -orientation 3 . Environment: h earing aids. eyeglasses, presence of fa mily member, adequate dayti me and night light 4 . Ed ucation : pertinent for medical staff involving in postoperative care 5. Avoida nce of known modifi able risk factors

P h armacolo g i ca l i n te rve ntion ( i n recovery room )

1 . Address perioperative trigg ers 2. Haloperidol 2 . 5 - 5 .0 mg for refractory hyperactive type (maximum 1 0 mg/day) 3. I V Lorazepam 1 . 0 - 2 . 0 mg (every 4 hours)

REFERENCES AND FURTHER READINGS 1. College of Anaesthesiolog ists, Academy of Medici ne of Malaysia: Recommendations for patient safety and mi n imal mon itoring standards

2. 3. 4.

5. 6. 7. 8. 9.

10. 11.

during anaesthesia and recovery (4th edition); 2013. Available at: www.acadmed.org . my. Accessed on 7/9/14 . Association of Anaesthetists of Great Britain and Ireland: Immediate post­ anaesthesia recovery 2013. Available at: http://www.aagbi .org . Accessed on 20/7/14 . Australian and New Zealand College ofAnaesthetists: Recom mendations foli the post-anaesthesia recovery room. Available at: http://www. anzca.edu.au . Accessed on 20/7/14 . Aldrete JA. The post-anesthesia recovery score revisited. J Clin Anesth 1995; 7: 89 -91. Gan TJ, Diemunsch P, Habib AS, et al. Consencus guideli nes for the management of postoperative nausea and vom iti ng. Anesth Analg 2014 ; 118(1 ): 85-113. Gan T J, Meyer TA, Apfel CC, et al. Society for ambulatory anesthesia guideli nes for the management of postoperative nausea and vom iti ng. Anesthesia and Analgesia 2007 ; 105(6): 1615-1628. ASA refresher course 2009 : Management of postanesthesia care unit. Available at: http://education.asahg.org . Accessed on 20/6/14 . Ruskin KJ, Rosenbau m SH. Anesthesia emergencies (1 st edition). New York: Oxford U n iversity Press; 2011. Pradip KB, Lata B, Rajnish KJ and Ramesh CA. Post anaesthesia shivering (PAS): A review. Indian J. Anaesth 2003; 47(2): 88-93. Rudra A, Chatterjee S, Kirtania J et al. Postoperative deliriu m . Indian J Cri Care Med 2006 ; 10(4): 235-240 . Deiner S and Silverstein JH . Postoperative deliriu m and cognitive dysfu nction. British Journal of Anaesthesia 2009 ; 103(suppl 1 ): i41- i46 .

10 ACUTE PAIN MANAGEMENT Everybody has expe rience pain at one time or another. Pain is one of t h e method of how t h e body com municates or warn the bra in t h at something may be 'off' or wrong (i.e . injury or a disease ) . Presence of body injury causes t h e ne rve endings to transmit pain signals/ messages along the nerves into t h e spinal cord and eventually to t h e brain. Pain is best to be prevented t h an to be treated. Managing pain is very important and it is t he 5th vital sign. Postoperative pain is crucial to be managed adequat ely as pain can p h ysiologically induce th e release of stress h ormones (cortisol and cat ec h olamines), h ypercoagulability and inflammatory mediators (cytokines, bradykinins). Alleviating postoperative pain can lessen t he mentioned effect, promote faster recovery and reduces t he chance of t he pain becoming c h ronic. Pain relief concept works by blocking t hese pain signals or reducing t heir effect on t he brain. For most people, pain with an immediate clear cause and relief is called acute pain (< 12 weeks). Pain becomes c h ronic (> 12 weeks) when it continues after th e injury h as h ealed. The cause of c h ronic pain can be com plicated and becomes a disease by itself. It is h arder to manage as it needs a h olistic approac h .

Severe pain t hat is not relieved can have long term effects: physical, emotional, psyc hosocial and spiritual on t he person involved and th eir family and carers. In t his h andbook we focus more on . What are the main causes of acute pain? Acute pain w h ic h needs treat ment: 1. 2. 3. 4.

pain after surgery pain from injuries or burns pain from disease (arthritis, stones, angina, h eadaches, cancer) labour pain

Who is involved?

1. In the hospital, a range of health care personnel will help the patient to control his/ her pain 2. These includes doctors (e.g. anaesthetists, surgeons), nurses and physiotherapists 3. Many hospitals now have Acute Pain Services (often called APS) which can either be doctor-led or nurse-led team (in most of cases) under the supervision of a doctor to help treat the pain

Assessing pain

1. Pain is a subjective feeling, everyone feels pain differently. The amount or type of pain felt may not be the same as others feel, even if they have had the same operation/ procedure or type of injury 2. Pain can also be altered by things such as physical and emotional factors, culture and beliefs, previous pain and mood 3. Self report of pain is the best assessment or the 'gold standard' in . However, if patients are unable to explain their pain, there are few pain assessment tools that can be used to quantify this 4. Questions that one should ask patients regarding their pain should include:

(a) Where is your pain? Patients should mention or point to any area on the body where there is pain

(b) What does the pain feels like? Patients are encouraged to use their own words to describe. The nature of the pain may give clues to the doctor on what might be the cause. E.g. pain from damage to a nerve may be a burning sensation (c) How much does it hurt? Patients will be asked to describe or rate their pain using one of the methods described below. Reporting pain as a specific term/ number will facilitate the doctors and nurses to quantify the effectiveness of treatment and whether any changes should be made Pain assessment

These are few pain assessment tools to evaluate pain:

1. 2. 3. 4. 5.

simple descriptive scale numeric rating scale visual analogue scale (VAS) Wong-Baker FACES® Pain Rating Scale FLACC scale

I. Simple descriptive scale

1. Patient may also be asked to choose words to rate their pain. Examples of these words are: (a) (b) (c) (d)

No pain Mild pain Moderate pain Severe pain

II. Numeric rating scale

1. A number scale between O to 10 can be used to score pain (suggested age group is between 8 years up to adult) 2. No pain is scored as O and the worst pain they could ever imagine is 1 O 3. Patient will tell the nurse or doctor what their pain is on that scale between 0 to 1 0 4. There is no right or wrong answer as pain description is subjective between patients

1 11t 111111 ■■ 11 ■ 1111111 t t t t t t None

M Iid

Moderate

Severe

Figure 10.01: Numeric rating scale Ill. Visual analogue score (VAS)

1. VAS is a 10 cm line on a piece of paper or ruler with zero (0) marked at one end (no pain) and 10 at the other end (worst pain the patient have ever

felt) 2. Patient will be asked to make a mark on that line to show where the pain is Worst pain I maginable

No pain

Figure 10.02: Visual analogue score IV. Wong-Baker FACES® Pain Rating Scale 1. Younger children can't measure pain using numbers. One way to do this is for them to point to a face that shows how sore they are or how much pain they have at that moment (suggested age group is between 4 to 12 years old) 2. There will be 6 faces that represents an increasing intensity in pain (from left to right) Wong -Baker FAC ES Pain Rating Scale

@ 0

No Hurt

®®® 2

Hurts

Little Bit

4

Hurts

Little More

6

Hurts

Even More

®@ 8

10

Hurts

H urts

Whole Lot

Worst

Figure 10.03: Wong-Baker FACES® Pain Rating Scale

Source: Hockenberry MJ, Wilson D: Wong's essentials of pediatric nursing, ed. 8, St. Louis, 2009, Mosby. Used with permission. Copyright Mosby. To find out more on the Wong-Baker FACES® Pain Rating Scale, visit http://wongbakerfaces.org V. FLACC scale

1. Scoring pain can be more difficult in babies and other patients who can't communicate well (cognitive disability). In these patients we can assess pain by looking at how they behave

2. For example, we look at crying, face expressions, and changes in breathing and heart rate 3. This scale is suggested for age of 2 months old up to adolescent 4. Each category is scored on the 0-2 scale which results in a total score of 010 Table 1 0.01: FLACC (Eace, .Legs, Activity, Cry, Consolability) scale and revised­ FLACC (for children with cognitive disability shown in italic) Scoring

C.itegory

Face

Legs

Activity

Cry

Consolabillty

0

No particular expression or smile

1

Occasional grimace/ Frequent to constant frown , clenched frown: withdrawn or jaw, quivering chin disinterested

Appears sad or womed

Normal position or relaxed

occasional tremors

Lying quleUy, nonnal position . moves easily

Squinning , shifting back and forth , tense

No cry (awake or asleep) Content, relaxed

2

Uneasy, resUess tense

Mildly agitated (e.g. head back and fonh, aggression); shallow, spllntmg respirations, intermittent sighs oans or Whimpers, occasional complaint

Occas,onal verbal outbursts or grunt

Reassured by occasional touching , hugging, or being talked to, distractable

Distress-looking face: expression of fright or panic Kicking, or legs drawn up

Marked increase In spastlcitr, constant tremors or jer11'Lt... ..., , __ _

r,,,,;t,tt"O!i'"°!l f'ilti'tl o_,r;;i;vl t,,m -, flj; - I dmpabrilh!'a.w:1"11dH11rts: :n:l.fmt:l"lft1N1�11IU�OfG'� � i l>'od,aO, «L!l! gwm md, o >ti, •m'Dr lnil,,Hr1m t11 ;,iillll5Ml1al'RD1n:I.

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Recovery or H D U / ICU

o, ns ;m,ay rnanagernern

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Flbmogen < 1.0 �

Tranexamic acid

1 adult therapeut1c dcse

FFP 15 ml.J1tg'

� 3-4 'if

loadiig dose 1 g over 10 mil. lhen nusion of 1 g cwer 8 hrs

-----...

o1 � tr�Pan � to ozhfse on number of unt, :11ed ID o,ot.O:le lhh dMie N!IG ..R DIC RBC

!la:)

--,.. ..,. _

FF!> BP PT rl'llla

• Allllid hypo1hermia. institute active warming • Avoid excesSNe crystalloid • Toler.t.e pennissi"" lwc,tension (BP 81}-100 mrnHg systolic) urd active bleemig ccntrolled • Do not use haemcglobil alone as a iransfusicn trigger

• Warfarin: • add 'dlamin K. prothrombinexlfff' • aiste:ric haemorrhage: • early DIC often presert; ca,sidet c:ryoprecipita:e • Head injury: • aim for plate'.el OO 100 X 1 IJIJ\. • penmsiYe hypojensioo CCIXlaildica:ed

The rou!ine use of rFVlla in trawna patients is noi recommended ciJe to iis lack of effect on moriality (Grade B) and varial>le effect on mcrt>idiiy (Grade C). lnsmJticns may choose ID delielcp a process for 1he use of rFVlla whefe there is.: • IECCnirolled haemcnhage in sa!vage,able pafenl .am! • failed su-gical or radiological meascres lo OCllud llieeding, • adequate blood oornponeni n,pt,cem� illlll · pH > 7.2 ten-perah.we > 340C. Discuss dose with haematologist/tnslusion specialisl ta r.ot llefflsim tt1r usc t1 1ttls � an 1ne muu tie plll'l af �

___

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,...

APTT IIITP FBC

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This work is based on/includes The National Blood Aulhofily's Patient Blood Management Guideline: Module 1 - Critical Bleeding Massive Transfusion which is licensed under the Creative Commoos Atbibution­ NonCommercial-ShareAHke 3.0 Australia licence (reproduced by kind permission)

-

Appendix 1 5: Massive tranfusion protocol (MTP) template

�....:-="",,.!k�:.===���.!.i�

��r!:="fu�...

...

Senior dinician ci-mines that paianl meets crilaria far UTP adivation

Baselne: Ful blood count. coaguliltian screen (PT. INR. APTT, fainogen ). biochemislry, �l blood gases

MONITOR (,wry 30-QI mins):

Notify ..._,_.,.. labomary (....,, contact no. ) to: 'Activate MTP'

L�oratory staff • No:ly haematologistftranslusDO speciaflSI • Prepare and issue blood canpcnenis as tequested • An:icipar,e repeal tes1� and blood ccmponen requnarnents • Mininise tes, tl.marnund 5mes • Consider s1afl resoun:es Haem.itologistltransfusion specialist • Liaise resparly with labcralcry and clincal team • Assisi in in'.e,p,etall 35� pH > 7.2 base excess < -{I lactate < 4 mmol/L Ca 2• > 1 . 1 mmolll platelets > 50 x t 0 9/L PT/APTT < 1 . 5 x nonnal INR s 1 . 5 fibrinogen > 1 .0 g/l

NO

Notify transfusion l aboratory to: ·cease MTP'

Ira:, This work is based on/includes The National Blood Authority's Patient Blood Management Guidelne: Module 1 - Critical Bleeding Massive Transfusion which is licensed under the Creative Commons Attribution-NonConmercial-ShareANke 3.0 Australa lcence (reproduced by kind permission)

-

A pp e n d i x 1 6 : S ev-e n St,eps of Ha n d w as h i n g

1 . R Ui b pa l m to pal m.

2. R u b pa l m over- the bac k

3. R ub p;atm d to pa ! m wH'h flnger:s l rnte r1ace .

4. Fing:er:s Inter oc ked to the opposi ng pa l m and rub back of fin: g rs of b oth han ds ,

th u m b c lasped into op pos ing piil m Qf both hMds.

of both 'ha nds w ith fi nge rs i nterlaced.

6 . Aotatio na I rub bing ( ba,c kwa rd and forwa rd) of the ,c laspool flrtgeNI ,0 11 th-. oppos ing pai lm of b oth h n ds .

7 . R ub both wrests i n rotat 01r I ma MM r. Rin se a nd dry both ha nets th orou;g hly.