Minimally Invasive Surgery for Chronic Pain Management: An Evidence-Based Approach 3030501876, 9783030501877

Table of contents :
Foreword I
Foreword II
Preface
Acknowledgments
Contents
Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury
1 Introduction
2 Diagnosis of Neurogenic Temporal Headaches
2.1 Identification and Technique
3 Diagnosis of Neurogenic Occipital Headaches
3.1 Identification and Technique
4 Diagnosis of Pectoralis Minor Syndrome
4.1 Identification and Technique
5 Diagnosis of Neurogenic Groin and Genital Pain
5.1 Identification and Technique
6 Diagnosis of Neurogenic Wrist Pain
6.1 Identification and Technique
Further Reading
Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation
1 Introduction
2 Neuroma Pain Characteristics
3 Etiology
4 Diagnosis
5 Surgical Technique: General Considerations
6 Surgical Technique: The Distal Target Exists and Nerve Can Be Reconstructed to Repair the “Nerve Biofeedback Loop”
7 Surgical Technique: Creation of a “Distal Target” to Close the “Nerve Biofeedback Loop” in the Absence of Anatomical Distal Target
8 Surgical Technique: General Wound Repair and Dressing Options
9 Postoperative Care
Further Reading
Diagnosis and Treatment of Neurovascular Temporal Headaches
1 Introduction
2 Neurovascular-Temporal Pain Syndrome Characteristics
3 Etiology (Differential Diagnosis)
4 Diagnostic
5 Surgical Technique
6 Postoperative Protocol
Further Reading
Diagnosis and Treatment of Occipital Neuralgia
1 Introduction
2 Occipital Pain Syndrome Characteristics
3 Etiology
4 Diagnostic
5 Surgical Technique
6 Postoperative Protocol
Further Reading
Diagnosis and Treatment of Pectoralis Minor Syndrome (Neurogenic Thoracic Outlet)
1 Introduction
2 Pectoralis Minor Syndrome Characteristics
3 Etiology
4 Diagnostic
5 Surgical Technique
6 Postoperative Protocol
Further Reading
Diagnosis and Treatment of Groin and Genital Pain
1 Introduction
2 Neurogenic Groin Pain Characteristics
3 Etiology
4 Diagnosis
5 Surgical Technique: General Considerations
6 Surgical Procedure
7 Postoperative Care
Further Reading
Diagnosis and Treatment of Central Neurogenic Wrist Pain
1 Introduction
2 Central Neurogenic Wrist Pain Characteristics
3 Etiology
4 Diagnosis
5 Surgical Technique
6 Postoperative Care
Further Reading
Nutritional Recommendations to Address Pain: Focus on Ketogenic/Low-Carbohydrate Diet
1 General Nutritional Guidelines to Provide to the Patients
2 MCT Oil and Intermittent Fasting
Further Reading

Citation preview

Minimally Invasive Surgery for Chronic Pain Management An Evidence-Based Approach Giorgio Pietramaggiori Saja Scherer Editors

123

Minimally Invasive Surgery for Chronic Pain Management

Giorgio Pietramaggiori  •  Saja Scherer Editors

Minimally Invasive Surgery for Chronic Pain Management An Evidence-Based Approach

Editors Giorgio Pietramaggiori Plastic and Reconstructive Surgery Global Medical Institute Lausanne, Switzerland

Saja Scherer Plastic and Reconstructive Surgery Global Medical Institute Lausanne, Switzerland

ISBN 978-3-030-50187-7    ISBN 978-3-030-50188-4 (eBook) https://doi.org/10.1007/978-3-030-50188-4 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Foreword I

As an academic plastic surgery program director, I felt the responsibility to develop a formal training in peripheral nerve surgery to improve the quality of life of the increasing number of patients suffering from chronic pain. Peripheral nerve surgery is one of the most rapidly evolving branches of plastic surgery. Migraine surgery, targeted muscle reinnervation and the robotic prosthetics are just a few examples of this ever-expanding specialty within plastic surgery. Outcomes from these surgeries are positive with over 70% improvement in pain across the literature, largely overcoming results from other approaches. This book is one of the first practical guides to lead the surgeons through the techniques of peripheral nerve decompressions, selective neurectomies (in case of damaged nerves) and nerve repair, with a very clear, step-by-step approach. The techniques described are minimally invasive which makes them less likely to create complications and more acceptable by patients and other doctors. Dr. Pietramaggiori and Dr. Scherer have been in the forefront of this specialty, thriving to push its boundaries since several years, dedicating their efforts towards the management of refractory chronic pain with important publications and presentations in international conferences and excellent clinical results. For this reason, I will recommend it to all plastic surgeons in activity, from young residents to key opinion leaders of our specialty, to encourage going through new frontiers and exploring new approaches for “ancient” diseases, so far considered with no solutions. Franco Bassetto, MD Director Plastic and Reconstructive Surgery Department of Neuroscience University of Padua, Italy

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Foreword II

Chronic pain debilitates millions of patients throughout the world with the vast majority only having palliative options for treatment. Many end up on chronic opioids with the attendant consequences of dependency, loss of function in society and far too often, death by overdose. As we learn more about pain syndromes, it appears that pain for many of our patients is related to either peripheral nerve compression or neuroma formation following injury. Despite great medical advances and new pharmaceutical agents to support these individuals, there remains a great need for innovation in this area. This is particularly true in the area of minimally invasive surgical procedures. Giorgio Pietramaggiori MD, PhD and Saja Scherer MD, have assembled global experts to address these important clinical problems. I have known both of them for 15 years when they started out in my laboratory at Brigham and Women’s Hospital and Harvard Medical School in Boston. One of the things they discovered was how the peripheral nervous system can be modulated by the application of micro mechanical forces. After leaving the lab, they went on to complete their plastic surgical training doing specialized work in peripheral nerve surgery. They now are in practice in Lausanne, Switzerland, where they have become internationally recognized for treating peripheral nerve disorders. In their book, they have a comprehensive review of the basic anatomy where most common peripheral nerve disorders occur. They discuss in detail specific anatomical areas such as the head and neck, thoracic outlet, upper extremity, groin and pelvis. The chapters are clinically focused and evidence-based. This book will be very helpful to surgeons who treat these patients as well as trainees, medical students and patients that suffer from pain due to peripheral nerve injuries and compressions. Dennis P. Orgill, MD, PhD Division of Plastic Surgery, Medical Director, Wound Care Center Brigham and Women’s Hospital Professor of Surgery, Harvard Medical School Boston, USA

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Preface

Patients suffering from chronic pain due to nerve compression and injury deserve precise diagnosis and treatment. These pain syndromes may not respond to conservative approaches leading to drug overuse and dependence. Chronic neurogenic pain is also related to extended inability to function at work, in society and with family, affecting all spheres of health and well-being. Patients and their physicians often feel frustrated by the lack of improvement, leading to ill relationships. Because of this stagnant situation, depression and isolation often complete the clinical scenario. A multidisciplinary approach is in most cases warranted to optimize diagnosis, treatment and post-operative care of patients. Learning from our mentors, we developed our three golden rules when facing neurogenic pain: 1. Wait at least 6-12 months from onset of symptoms before peripheral nerve surgery is considered in most cases (sometimes the situation evolves without surgery for the better). 2. Selective nerve blocks need to confirm the target nerve (there must be an anatomical and physiological correspondence from the suspected target nerve and the symptoms). The block should be performed by the surgeon to guide him/her to a better evaluation of results and planification of surgery. A really positive block achieves a “wow” effect, often shedding tears from the eyes of the patients and their families and correlating with satisfactory surgical outcome. 3. Nerves are not divided unless already terminally damaged (if there is no evidence of injury to a nerve, the nerve should be spared and put in the best conditions to regenerate and function, by decompression, neurolysis and liberation from scar tissue). We decided to write this book to protect, transmit and stimulate further developments of peripheral nerve surgery, a relatively young subspecialty of plastic surgery with immense potential to help people. We asked the world’s experts that we were so fortunate to have with us in this project to be concise, precise and practical. A special mention has to go to Dr. Dellon, Mackinnon and Guyuron, the pioneers of peripheral nerve surgery and migraine surgery. Dr. Robert Hagan and Dr. Ziv Peled, dear friends and peripheral nerve surgeons, trained us in the beginning of our ix

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exploration showing us the amazing (and yet not fully understood) potentials of peripheral nerve surgery. Their commitment to improve people’s life inspired us to undertake the same mission. We hope that this book will be useful for other doctors to develop or start peripheral nerve surgery to help patients across the world, hoping that no more people will be left behind thinking that their pain does not exist. Lausanne, Switzerland 

G. Pietramaggiori, MD, PhD S. Scherer, MD

Acknowledgments

To our Parents, Brothers and Sisters and Mentors who let us free to decide who we wanted to become, To our Children, Santo, Gia and Gaya who remind us every day who we are and where we came from, To our Patients, in particular the ones that we could not help yet, who give us a reason to continue our research, pushing the frontiers of where we will be a little further every day.

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Contents

 Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury ������������������������������������������������������������������������������������������������������������  1 Giorgio Pietramaggiori, Laurent Thierrin, and Saja Scherer  Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation ������������������������������������������������������������������������������������������������������ 15 Sean Figy, Steven Schulz, and Ian Valerio  Diagnosis and Treatment of Neurovascular Temporal Headaches������������������ 27 Giorgio Pietramaggiori and Saja Scherer  Diagnosis and Treatment of Occipital Neuralgia���������������������������������������������� 35 Giorgio Pietramaggiori and Saja Scherer  Diagnosis and Treatment of Pectoralis Minor Syndrome (Neurogenic Thoracic Outlet) ���������������������������������������������������������������������������� 47 Giorgio Pietramaggiori and Saja Scherer  Diagnosis and Treatment of Groin and Genital Pain���������������������������������������� 53 Sanchit Sachdeva and Shai M. Rozen Diagnosis and Treatment of Central Neurogenic Wrist Pain�������������������������� 63 Steven Rueda and Sonu A. Jain  Nutritional Recommendations to Address Pain: Focus on Ketogenic/Low-Carbohydrate Diet �������������������������������������������������������������� 69 Susan A. Masino and David N. Ruskin

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Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury Giorgio Pietramaggiori, Laurent Thierrin, and Saja Scherer

1

Introduction

The symptoms of neuropathy include continuous or paroxysmal dysesthesia (abnormal or unpleasant sensation), hyperesthesia (excessive sensitivity of the skin), cold intolerance, and allodynia (pain from stimuli that normally are not painful). Often patients have trouble sleeping and develop anxiety and depression with long term persisting neuropathic pain. Neuropathic pain is suspected when symptoms arise from a known anatomic compression point or scar tissue (Fig. 1) along the somatic territory of a nerve. In the point of compression or injury, a Tinel sign will be classically positive, manifesting as tingling (or “pins and needles”) in the distribution of the nerve by lightly tapping over it. To confirm the hypothesis that a dysfunctional nerve is the cause of pain, a targeted nerve block with a small volume (1–5 cc) of local anesthesia (typically lidocaine with epinephrine) should be performed under ultrasound guidance proximal to the site of suspected compression or injury. The anesthesia should alleviate almost immediately at least 50% of the pain (possibly close to 100%), while resting and moving, in order to be considered positive. Immediately after the nerve block, patients are asked to touch the sensitive area and make movements that were not possible or limited by pain. Only the patient is considered accountable for estimating the relative reduction of pain and we recommend asking some questions while still under the effects of the nerve block, such as:

G. Pietramaggiori (*) · S. Scherer Plastic and Reconstructive Surgery, Global Medical Institute, Lausanne, Switzerland e-mail: [email protected]; [email protected] L. Thierrin Anesthesia, Clinique de La Source Lausanne, Lausanne, Switzerland e-mail: [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_1

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Temporal pain: auriculo-temporal nerve and superficial temporal vessels Occipital pain: Greater and lesser occipital nerves and occipital artery Greater occipital nerve

ATN

Lesser occipital nerve Brachial plexus Pectoralis Minor Syndrome: brachial plexus and axillary vessels

Wrist pain: posterior interosseus nerve and anterior interosseus nerve Posterior interosseus nerve Anterior interosseus nerve

Iliohypogastric nerve Ilioinguinal nerve

Groin and genital pain: ilio-inguinal, ilio-hypogastric nerves and genitofemoral nerve

Genitofemoral nerve Genitofemoral nerve

Fig. 1  Main nerve targets for pain management

1. If surgery could achieve half of this improvement, would you be satisfied? 2. Would you be able to go back to work/perform better in your daily activities? 3. Would you be ready to risk a worsening of the pain to achieve this state? Knowing that anesthetic blocks often achieve more dramatic results (but only temporary) and that pain rarely worsen after nerve preserving surgery, strongly positive blocks (achieving nearly 100% pain relief) often correlate with satisfactory outcome. In our practice, we repeat nerve blocks at least twice before considering a patient eligible for surgery. We systematically use in our practice a high-frequency ultrasound probe for nerve blocks. We highly recommend to implement ultrasound in the peripheral

Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury

3

nerve surgery  practice for quicker and more reliable diagnosis. Ultrasoundguided nerve blocks can be adopted fairly quickly by surgeons as they already master surgical anatomy. When this is not possible, patients can be referred to a pain specialist for a specific nerve block. Novel technologies allow for relatively affordable, small probes that can be connected to a tablet or smartphone (for example, Philips Lumify, Philips Andover, MA, USA). We recommend using non-echogenic blunt needles (for example, Stimuplex, B.  Braun, Bethlehem, PA, USA) for peripheral blocks for better visualization and to limit the risk of iatrogenic nerve injury. Small volumes of local anesthetic (1–5  cc maximum) are delivered to target possibly only one nerve at the time. Cortisone can be added to the mixture to obtain extended relief in some cases (some days to some weeks). Nerve decompression is the gold standard procedure in the presence of a compression neuropathy and the absence of an objective nerve injury. In the case of a posttraumatic or surgical nerve injury, nerve reconstruction with allograft or autograft should be considered as first option. If distal nerve ends cannot be found or the nerve lesion is too extensive, a selective neurectomy can be performed and treated as described in chapter “Diagnosis and Treatment of painful neuromas: Targeted Muscle Reinnervation”. The risk of this approach is the reformation of a more proximal iatrogenic neuroma on the same branch. As a consequence, the procedure of selective neurectomy must be reserved to specific cases where a neuroma has already developed, and a reconstruction of the nerve is not possible or indicated. Patients need to be well informed of possible surgical options that will be chosen depending on intraoperative findings, as well as the possibility that surgery may not significantly change or even worsen neuropathic pain. We discuss in this opening chapter some of the anatomic and technical details to perform the nerve blocks that are used to diagnose the neuropathies whose surgical treatment is detailed in the following chapters. A blind subcutaneous infiltration of local anesthesia is often enough for confirming a neuroma or neuropathy of a superficial sensitive nerve branch. For deeper, more proximal nerves, passing through complex anatomical layers, an ultrasound-guided block is preferred representing a certainly more precise and safer approach. This chapter provides some useful tips and tricks for peripheral nerve surgeons already using or willing to implement ultrasound-guided nerve blocks in their practice.

2

Diagnosis of Neurogenic Temporal Headaches

Neurogenic temporal headaches can be caused by irritation or compression of the auriculotemporal nerve (ATN) and superficial temporal artery. The ATN is a terminal temporal sensitive end of the mandibular branch of the trigeminal nerve (V3). It is found in the preauricular region and it divides—approximately at the level of the insertion of the helix—in two main branches, temporal

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Fig. 2  In the temporal region, the auriculo­ temporal nerve and superficial temporal artery and veins cross several times

Auricolo temporal nerve

STA STV

Lymphatic vessels

(anterior) and parietal (posterior), along with the superficial temporal artery (STA), temporal veins (STV), lymphatic vessels, and sympathetic plexus (Fig. 2). The ATN cannot be visualized with standard ultrasound probes, while the superficial temporal artery can be palpated and identified with ultrasound or Doppler (Fig. 3). The most reliable way to consider a patient eligible for surgery in case of suspected neurogenic  primary temporal pain is to perform the auriculotemporal local anesthesia block during a pain crisis. While this is often not practical (patients need to be able to come in the office in pain), a positive result to local anesthesia (marked by sudden and significant reduction of pain during a crisis) is a highly positive prognostic factor for the response to surgical decompression.

2.1

Identification and Technique

The STA can be easily identified with ultrasound color Doppler or simple Doppler. In the preauricular region, with the patient in a sitting position, the probe is positioned longitudinal or perpendicular to the axis of the ear (Fig. 3a), and the superficial temporal artery is identified in close proximity and superficial to the mandibular condyle (Fig. 3b).

Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury

a

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b Auriculo-temporal Superficialis nerve fascia

c

Superficial temporal artery

Mandible condyle

Fig. 3 (a) Position of the ultrasound probe to identify the temporal neurovascular bundle. (b) The superficial temporal artery can be identified in the proximity of the mandibular condyle. (c) Identification of the superficial temporal artery with color Doppler is enough to perform the temporal neurovascular block. (⊗) Target infiltration point

The superficial temporal artery and concomitant veins are identified by color Doppler under the superficialis fascia (Fig. 3c). Local anesthesia (0.5-1 cc) is infiltrated around these structures (⊗).

3

Diagnosis of Neurogenic Occipital Headaches

Compression of the greater and lesser occipital nerves is the main cause of occipital neuralgia. Patients suffering from occipital neuralgia often have a constant low-­ level pain that exacerbates during the crisis. The greater and lesser occipital nerves originate from the cervical roots C2–C3. The greater occipital nerve (GON) passes around the obliquus capitis muscle and then pierces the semispinalis muscle, passing under the trapezius muscle (TM) to pierce the tendinous insertion of the TM toward the subcutaneous tissue of the scalp. The lesser occipital nerve (LON) travels along the posterior edge or within the sternocleidomastoid muscle (SCM) and pierces similary to the GON through the tendinous insertions of the SCM and TM at the level of the nuchal line. At this level, common branches between the GON and LON are often found and the greater occipital nerve regularly crosses over the occipital artery (Fig.  4). The occipital nerves cannot be identified with standard

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ultrasound techniques at the nuchal line, while the occipital artery represents a consistent anatomic landmark. The infiltration of the occipital neurovascular bundle can include cortisone to extend the benefit of the block for about one to two weeks. We choose to block both nerves at the nuchal line as our prefered surgical approach addresses both the GON and the LON through the same incision at this level.

3.1

Identification and Technique

With the patient in a sitting position or laying on the opposite side, the head in slight flexion, the probe is positioned cephalad to the area between the lateral insertion of the trapezius and the medial insertion of the sternocleidomastoid muscle (Fig. 5a). The main structure to be identified is the occipital artery that can be appreciated under the common insertion of the occipital muscles (Fig.  5b). Color Doppler (Fig. 5c) allows for the targeted infiltration of 2.5-cc mix of local anesthesia and cortisone around the artery (⊗) between the deep and superficial aponeurosis where the nerve branches usually are found. This nerve block should anesthetize the ipsilateral half of the back of the head. The pain relief should be immediate and often involves remission of pain in the back or through the eyes and in the temporal area.

Greater occipital nerve Transverse Section Nuchal line Occipital Nerves

Lymph nodes

Occipital Artery

Triangle boundaries Tendinous Nuchal insertion line trapezius Trapezius Splenius capitis

Nuchal line Lesser occipital nerve

Tendinous insertion SCM

Sternocleidomastoid muscle Splenius capitis muscle Trapezius muscle Third occipital nerve

Fig. 4  In the occipital area, between the tendinous insertions of the trapezius and sternocleidomastoid muscles the greater and lesser occipital nerves cross and emerge to reach the subcutaneous tissue. These nerves intersect the occipital artery and lymphatic vessels

Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury

a

b

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Superficialis fascia Superficialis aponevrotic plane Deep aponevrotic plane Occipital artery Occipital nerve Bone

c

Fig. 5 (a) Position of the ultrasound probe to identify the occipital neurovascular bundle. (b) The main anatomical landmark is the occipital artery that can be identified under the superficial aponeurotic plane. (c) Identification of the superficial occipital artery with color Doppler is enough to perform the occipital neve block. (⊗) Target infiltration points

4

Diagnosis of Pectoralis Minor Syndrome

Pectoralis minor syndrome is due to the compression of the brachial plexus under the insertion of the pectoralis minor muscle. The brachial plexus and axillary artery and vein can be well identified under the clavicle below the insertion of the pectoralis minor muscle on the coracoid (Fig. 6). In order to diagnose a pectoralis minor syndrome (compression of the brachial plexus by the proximal tendon of the muscle) and distinguish it from a more proximal compression at the scalene triangle or costoclavicular space, the muscle itself should be infiltrated to reduce its tone. The infiltration of the pectoralis minor muscle should improve rapidly the ability of the patient to move the ipsilateral upper limb without being limited by pain.

4.1

Identification and Technique

The coracoid bone is palpated. With the patient in supine position, arm in 90° abduction, the probe is positioned longitudinal to the muscle body (Fig. 7a). The brachial plexus and axillary vessels are identified (Fig. 7b), and the probe is moved distally until these structures are not in the field. The pectoralis major is identified above the

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Clavicle Coracoid Subclavian artery

Subclavian vein

Brachial plexus

Pectoralis minor muscle

Fig. 6  The pectoralis minor muscle compresses at the level of its proximal insertion on the coracoid process the brachial plexus and the axillary artery and vein

pectoralis minor. Up to 10 cc of local anesthesia can be used to infiltrate the body of the pectoralis minor muscle (⊗) (Fig. 7c). The best technique involves three injections (from lateral to medial) at a distance of approximately 2 cm to infiltrate evenly all three heads of the muscle. Physical examination within 10 min from injection should demonstrate significant decrease of pain and paresthesia at rest and with provocative maneuvers. Extended therapeutic effect can be achieved with botulinum toxin infiltrations.

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Diagnosis of Neurogenic Groin and Genital Pain

The ilioinguinal and iliohypogastric nerves (originating from L1) cannot be easily visualized with conventional ultrasound probes and run deep in the abdominal muscle wall under the oblique muscles (Fig. 8).

Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury

a

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b Pectoralis major Pectoralis minor Subclavian vein Subclavian artery Brachial plexus Pleural space

c

Fig. 7 (a) Position of the ultrasound probe to identify the pectoralis minor muscle. (b) Under the proximal part of the pectoralis minor muscle the brachial plexus and axillary artery and vein are found. (c) Infiltration of the pectoralis minor muscle should be performed within the muscle fibers more distal to the passage of the brachial plexus and blood vessels. (⊗) Target infiltration point

5.1

Identification and Technique

The probe is positioned at the level of the umbilicus with the patient in a supine position (Fig. 9a). Three planes of muscles can be identified from external to internal: the external oblique, the internal oblique, and the transverse abdominal muscle (Fig. 9b). At the level of the umbilicus horizontal line, the ilioinguinal and iliohypogastric nerve are found usually between the internal oblique and transverse abdominal muscle close to each other (Fig. 9b, c). More distally, between the anterior iliac spine and the umbilicus, the iliohypogastric nerve travels cranial to the ilioinguinal nerve under the external oblique muscle and usually within the internal oblique. At this level, the injection of 5–10 cc of local anesthetic can be directed more caudally to block the ilioinguinal nerve or more cranial to block the iliohypogastric nerve. The diagnostic block should significantly and rapidly reduce the pain at rest and during provocative movements. A blind subcutaneous anesthesia block can be performed as an alternative approach, proximal to a painful scar, but results are less specific and only useful

10 Fig. 8  At the level of the umbilicus the iliohypogastric and ilioinguinal nerves can be identified between the transverse muscle of the abdomen and the internal oblique muscle

G. Pietramaggiori et al.

Transverse abdominis muscle Iliohypogastric nerve Ilioinguinal nerve

Internal oblique muscle

External oblique muscle

ASIS Inguinal ligament External inguinal ring Genitofemoral nerve

Femoral vessels

Genitofemoral nerve

Pubic tubercle

when surgical revision of the scar tissue alone is planned. While revision surgery in scar tissue is more difficult and has less predictable results, this more distal approach avoids a second scar and prevents the risks of partial motoric denervation of the abdominal wall muscles. Another nerve that can be involved in neurogenic pain in the groin and genital area is the genitofemoral nerve. This nerve runs along the spermatic cord in males or round ligament in females outside the external inguinal ring. An ultrasound-­ guided peripheral nerve block should be performed at the external inguinal ring when the ilioinguinal and iliohypogastric block do not achieve complete pain remission in the genital area (not shown).

Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury

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b

External oblique muscle Internal oblique muscle Transverse muscle Iliohypogastric & ilioinguinal nerve Intra-abdominal space

c

Fig. 9 (a) Position of the ultrasound probe to perform the iliohypogastric and ilioinguinal nerve block. (b) Nerves usually run at this level between the transverse muscle and the internal oblique. (c) The infiltration dissects a space where the ilioinguinal and iliohypogastric nerves are found. (⊗) Target infiltration level

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Diagnosis of Neurogenic Wrist Pain

Neurogenic wrist pain, without wrist instability, can be addressed by a technique, described by Dellon, called “partial joint denervation.” Several sensitive nerves innervate the wrist joint. Previous surgical techniques to relieve chronic pain in this joint aimed to address all or several of these nerves through rather complex surgeries. The posterior interosseous nerve (PIN) and anterior interosseous nerve

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Interosseus membrane

Distal

Proximal

Anterior interosseus nerve

Posterior interosseus nerve

Fig. 10  In the distal third of the forearm, the posterior interosseous nerve (PIN) and anterior interosseous nerve (AIN) are found above and below the interosseous membrane

(AIN) provide the main sensitive innervation of the central dorsal and volar capsule of the wrist, respectively (Fig.  10). Selective PIN and AIN denervation, referred as partial wrist denervation, may suffice to achieve pain control in wrist joint.

6.1

Identification and Technique

In the distal third of the forearm, about 2 cm from the radioulnar joint, the probe is placed perpendicular to the axis of the limb (Fig. 11a). The posterior interosseous nerve (PIN) and anterior interosseous nerve (AIN) cannot be seen with standard ultrasound probes, but are found just above and below the interosseous membrane (Fig. 11b). The interosseous membrane is visualized and 2.5 cc of local anesthetic are injected above and below (⊗) it (Fig. 11c). Patients report an almost immediate reduction in pain in the wrist at rest and during movements when the block is positive.

Surgical Anatomy and Diagnosis of Peripheral Nerve Compression and Injury

a

b

Proximal

Posterior interosseus nerve

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Anterior interosseus nerve

Distal Ulna Interosseus Pronator Radius membrane quadratus

c

Fig. 11 (a) Position of the ultrasound probe to identify the posterior interosseous nerve (PIN) and anterior interosseous nerve (AIN) along the dorsal distal third of the forearm. (b) The posterior interosseous nerve (PIN) and anterior interosseous nerve (AIN) are found above and below the interosseous membrane. (c) The interosseous membrane is visualized and infiltration is performed above and below it. (⊗) Target infiltration level

Further Reading 1. Albrecht E, Cadas H, Moret V. Manuel pratique d’anesthésie locorégionale échoguidée. Paris: Elsevier Masson; 2014. 2. Baerentzen F, Maschmann C, Jensen K, Belhage B, Hensler M, Borglum J, et al. Ultrasound-­ guided nerve block for inguinal hernia repair: a randomized, controlled, double-blind study. Reg Anesth Pain Med. 2012;37:502–7.

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3. Moore DC. Regional block: a handbook for use in the clinical practice of medicine and surgery. Springfield: Charles C Thomas; 1979. 4. Sanders RJ, Annest SJ. Pectoralis minor syndrome, subclavicular brachial plexus compression. Diagnostics (Basel). 2017;7(3):46. 5. Shim Jh KOSY, bang MR, et al. Ultrasound-guided greater occipital nerve block for patients with occipital headache and short term follow up. Korean J Anesthesiol. 2011;61:50–4.

Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation Sean Figy, Steven Schulz, and Ian Valerio

1

Introduction

Neuromas result from various mechanisms of nerve injury. Common causes of nerve injury that result in neuromas include traumatic, blunt, avulsion, stretch, and iatrogenic injuries as well as amputations. Neuromas can occur in transected nerves and form over the terminal ends of the nerve bundles (Fig. 1a). They can also form as neuromas in continuity, with abnormal scar formation to a partially injured nerve with some distal axons remaining intact (Fig. 1b). To understand the disordered healing of nerves that leads to neuroma formation, it is important to recognize the underlying mechanism of injury and how it affects the different respective components of a nerve. In 1951, Sunderland described a classification of peripheral nerve injury by stratifying the injury by the anatomic components of the nerve itself. Specifically, for type I nerve injuries, the main structural integrity of the nerve remains intact; however, the conduction capability is “stunned” or abnormal. Type I injuries typically resolve spontaneously with time. In type II nerve injuries, damage occurs within the actual axons (axonotmesis). The endoneurial, perineurial, and epineurial structures remain intact, but the nerve axon degenerates via Wallerian degeneration. Type II nerve injuries typically possess intact distal S. Figy Division of Plastic Surgery, Department of Surgery, The University of Nebraska Medical Center, Omaha, NE, USA e-mail: [email protected] S. Schulz Department of Plastic Surgery, The Ohio State Wexner Medical Center, Columbus, OH, USA e-mail: [email protected] I. Valerio (*) Division of Plastic and Reconstructive Surgery, Department of General Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_2

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Intact nerve

b Intact nerve

Injured segment

Injured segment

Neuroma In Continuity

End Neuroma

Injured segment

Fig. 1 (a) Neuroma occurring at a transected end of a nerve with disorganized regenerating nerve fibers growing over the terminal end of the nerve bundles. (b) Neuroma in continuity where some distal fibers remain intact

targets, which allow the regenerating axon to find its distal target once again as it grows down its endoneurial sheaths. Type III, IV, and V injuries all include the axonal injury as evidenced by type II injuries, yet these progressive nerve injuries each add an additional layer of anatomical tissue structure involvement. Type III injuries include endoneurial injury, whereas perineurial injury is found in type IV injuries and type V injuries exhibit epineurial injury (neurotmesis). Type IV injuries commonly give rise to neuromas-in-continuity, while type V injuries will commonly develop either neuromas-in-continuity or neuromas if not treated appropriately. In 1988, Mackinnon expanded types of nerve injuries to include a more complicated, but clinically relevant peripheral nerve injury, which is the type VI injury. Type VI nerve injuries consist of a combination of the above five types of nerve injury. The physiologic response to nerve injury involves the proximal nerve attempting to regenerate to a distal target. This process can become disorganized leading to the formation of neuromas. Symptomatic neuromas-in-continuity and neuromas contribute to various degrees of pain for patients, having a substantial impact on society. Acute and subacute pain symptoms can evolve into chronic pain and long-term morbidities and disability for patients. This leads to frequent and prolonged narcotic prescriptions, inability to work, or inability to wear a prosthetic further limiting a patient’s function and overall quality of life, as well as added costs and loss of production in society. When neuromas-in-continuity and neuromas are treated appropriately, patients may be able to avoid the pitfalls of polypharmacy, experience decreased opioid utilization and associated dependence, and avoid cognitive impairment and weight gain associated with many of these multimodal pain therapies.

Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation

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Neuroma Pain Characteristics

• Dysesthesia, hyperesthesia, paresthesia, and cold intolerance over the injured nerve and in the distal anatomical territories of competence. • Positive Tinel sign at the location of the neuroma. • Loss of function due to pain elicited by motion and contact over the affected part of the body.

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Etiology

• Traumatic or iatrogenic nerve injury (from cut, crush, excessive stretch on peripheral nerve sensitive fibers).

4

Diagnosis

• History of trauma or surgery, whether it be accidental or iatrogenic (amputation/ surgical). • Physical examination: patients describe sharp pain (readily reproducible with palpation) and Tinel sign over the neuroma site. • Distal dysesthesia, hyperesthesia, paresthesia, and cold intolerance. • Diagnostic block with local anesthetic under ultrasound guidance proximal to the suspected area of damage will temporarily aid in lessening, or even completely resolving, the painful symptoms. • MRI may not necessarily directly identify the neuroma in many cases but may be useful to evaluate for other organic causes of pain, such as myositis, abscess, and osteomyelitis.

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Surgical Technique: General Considerations

• Incision planning for neuromas must take several things into account. Previous incisions and the locations of the intended targets is paramount. Often, when approaching neuromas, incisions must be made more proximal than the location of the neuromas themselves. As the amputation incisions typically run transversely across an extremity, the incision for a delayed neuroma case is most often longitudinal over the areas of neurovascular bundles. • Dissection should be done in the usual standard fashion by accessing the neuroma through traditional avascular myofascial planes. However, care should be taken to not inadvertently cause additional injury to neuro-vascular structures. Once the neuroma is identified, a complete neurolysis should be performed to dissect and release it from the surrounding tissues and scar. Dissection should be

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•

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extended proximally and distally to have adequate exposure of the complete neuroma and the nerve to be reconstructed as well as to permit one to resect back to healthy proximal nerve for setting up to perform optimal nerve reconstruction procedures. Any nerve repair or reconstruction that does not adequately debride devitalized or scarred nerve will surely end with a poor outcome and less than ideal ability for the nerve to undergo optimal regeneration. Indeed, the preparation of the nerve may be the most critical component in peripheral nerve reconstruction and/ or repair. The quality of the residual nerve should never be compromised for the sake of length and leaving proximal nerve scar or injury behind. Local anesthesia is infiltrated (e.g., authors prefer a standard 0.25% Marcaine plain mixed with 1% lidocaine containing 1:100,000 epinephrine) proximal to the injured end prior to transecting the nerve. Under high-power optical aids such as loupes or a surgical microscope, a fresh no. 10 blade scalpel or similar nerve transection device should be used to resect the neuroma completely, ensuring the injured nerve is transected back to healthy, uninjured nerve tissue level. A gentle sawing motion using the length of the scalpel blade will permit a clean cut with minimal crush injury to the underlying nerve (Fig. 2a). On direct high-powered loupe or microscopic observation, there should be “endoneurial bleeding” within each of the fascicle units (Fig. 2b). The sacrificed nerve pedicle length is necessary to ensure healthy nerve for reconstruction. In rare cases where the nerve pedicle cannot reach the nerve targets, nerve allografts or autografts can be used to lengthen the nerve pedicle. For those with more advanced pathological support capabilities, extemporaneous pathological evaluation of nerve biopsies can also be utilized. Fascicular density has been proposed as a potential marker for nerve health. Residual scar clearance and connective tissue to fascicle ratio under H&E or toluene blue staining have

a

b

Fig. 2 (a) The proximal/uninjured end of the nerve is transected with a scalpel blade by a gentle sawing motion. (b) Homogeneous endoneural bleeding is observed at high-power magnification, confirming a healthy blood supply to the nerve end prior reconstruction

Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation

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also proven useful to some peripheral nerve surgeons to guide injured nerve resection and preparation. Additionally, tissue stains for specific nerve structural components can be utilized. Acetylcholine staining will preferentially identify motor nerves and axonoplasmic pattern staining of carbonic anhydrase will identify sensory nerves. The utility of pathology services for evaluation of nerves prior to repair or reconstruction can be limited by the time it takes for nerve processing, which can exceed 3 h in some cases. It is the authors’ preference to use direct visualization of fascicles and “endoneurial bleeding” as our institution’s standard in debriding nerve injuries back to healthy levels for improving regeneration potential.

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 urgical Technique: The Distal Target Exists and Nerve S Can Be Reconstructed to Repair the “Nerve Biofeedback Loop”

• When faced with a nerve injury resulting in neuroma, the first option should be a direct repair of the nerve or immediate reconstruction to maintain its original functions when possible. Nerves prefer to have a distal target to communicate, and thus, nerve repair should focus on reestablishing as near as normal “biofeedback loop” to the original nerve function (e.g., sensory nerves to sensory, motor nerves to motor, or mixed motor sensory to mixed motor sensory in topographical alignment). • Direct repair or coaptation: Direct micro-suture of the prepared proximal and distal nerve ends without undo tension remains the ideal situation when possible. External neurolysis and dissection of the nerve from the surrounding tissues and scar may aid to liberate the nerve, facilitating a tension-free direct repair in certain instances, but the surgeon should be aware of the perineural and epineural blood supplies as further dissection and release can injure these vessels and compromise the overall outcome if too extensive in nature. • Epineural sutures using a nylon 8–0 or 9–0 under high-powered loupe or microscopic observation at the coaptation site should align the cut ends of the prepared nerve in a way that matches the intrinsic topography of the nerve when possible (Fig. 3a). • Care should be taken not to capture or entrap any of the nerve fascicles within the micro-sutures and ensure no fascicles escape or protrude from the epineurial repair site itself and no bunching is observed at the repaired ends (Fig. 3b). • Connector-assisted repair (CAR repair): Nerve connectors are open tubes that capture and contain the neural elements close to each other (Fig.  3c). These adjunctive tools can be used in a variety of ways. They can be used to merely add an additional layer outside of a direct neural repair (Fig. 3d). In this setting, the nerve is passed through the connector completely and is delivered to the other side. A direct neural repair is made as explained above, the nerve connector is then passed over the coaptation site so that the nerve repair lays in the center of

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a

c

b

d

f e

g

Nerve wrap

h

Nerve Graft

Nerve wrap

Nerve graft

Fig. 3 (a) Direct repair technique: epineural suture. Repair is performed by single epineural stitches using a nylon 8–0 or 9–0 under high-powered loupe or microscopic observation. Careful attention to fascicular topography may ensure better outcomes. (b) No bunching should be noticed after the repair. (c) Conduit/connector assisted repair (CAR)-clinical example. A conduit made of autologous, allogeneic, or synthetic materials can be used to protect the coaptation site. (d) CAR visual rendering-nerve connector placed over a coaptation site. (e) Nerve connector used to bridge a small gap. (f) Nerve graft repair with nerve wrap. When gaps are between 10 and 70 mm, a nerve allograft or autograft may be used to bridge the gap and reconstruct the nerve. After the proximal and distal nerve ends have been sutured to the grafts, a wrap made of autologous, allogeneic, or synthetic material can be used to protect the reconstruction site. The wrap in this case is secured in place with microclips, which in no circumstances should impose any pressure on the nerve. (g) The nerve conduit/wrap is used to protect only the repair sites. (h) The nerve conduit/wrap may be used to protect the repair sites and the graft in case a particularly intense scarring is expected (secondary operations and or sites with only scarce soft tissue coverage)

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the connector tube. A suture is then placed from the epineurium to the connector on either side of the repair to secure the connector in place. This technique has been described as a connector-assisted repair (CAR repair, Fig. 3d). When gaps are less than 10 mm, a connector can be used to bridge the residual nerve gap. The proximal nerve end is delivered into the connector tube and secured in place with an epineurial stitch to the connector, typically in two to three locations around the nerve. The distal nerve end is then delivered into the connector and similar securing stitches are placed distally (Fig. 3e). This technique will direct axonal growth within the connector to its distal target. Superficial veins of the foot or wrist or even veins in the surgical field can be utilized as conduits in an autograft fashion. • Nerve wraps: After a direct neural repair/coaptation is completed, a nerve wrap can be used to encase the coaptation site itself. The nerve wrap should be able to completely envelope the repair site and can be secured in placed with either epineural sutures or microclips that create a gentle, none constricting cerclage around the nerve repair coaptation site. Care should be taken not to capture the nerve or its associated components within the micro-sutures or microclips. Nerve wraps can be made of autologous (including veins, free muscle grafts, and/or surrounding vascularized tissue flaps), allogeneic, xenograft, or synthetic materials. • Nerve grafts: When the nerve gap is between 10 and 70 mm, a nerve allograft or autograft can be used to span the nerve gap. Donor nerves can vary depending on surgical site and indication. Nerve gaps longer than 70 mm will typically require autografts as serial allografts require multiple coaptations which may reduce nerve regeneration outcome. It should be noted that when the caliber of the nerve to be repaired is larger than the graft, multiple cable grafts will be required to reconstruct the nerve gap. These should be sutured to the nerve with effort given to mimicking the intrinsic topography of the nerve relative to fascicular bundles. In patients who are prone to neuroma formation, caution should be taken as autografts pose a risk for donor site neuroma formation. Moreover, donor site morbidity should not be discounted as harvest of autografts will result in donor site insensibility. • Nerve wraps or conduits can be used to protect the coaptation sites between the original nerve ends and the graft. Nerve wraps can be used to cover the coaptation sites or the entire graft and the coaptation sites (Fig. 3f–h).

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 urgical Technique: Creation of a “Distal Target” S to Close the “Nerve Biofeedback Loop” in the Absence of Anatomical Distal Target

• In cases where one cannot repair the injured nerve to restore its “original or normal” nerve continuity and its anatomical distal target, one may have to choose a nerve reconstruction technique used to establish a “new distal target.”

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c

b

Nerve Nerve graft wrap

Repair site

Fig. 4  Nerve transposition techniques. (a) Nerve implantation. When there is enough intact nerve end after resection of the injured part and enough soft tissue coverage, the nerve stump is buried deep into muscle tissue. (b) Nerve destination relocation: when the nerve stump is too short or too little mobile, a graft can be used to transpose it into the muscle and a nerve wrap/conduct can be used to protect the repair site. (c) Clinical example of destination relocation

• Nerve implantation: Burying the nerve within a local muscle or within bone has been described as a way to prevent the development of secondary symptomatic neuromas. Simple micro-sutures as well as MiTek anchor fixation have been described to maintain the nerve end in their new location. When transposing the transected nerve end, the nerve stump should be buried deep within the extremity such that there is adequate soft tissue overlying it to protect it from compressive forces (Fig. 4a). Similarly with bone fixation, the nerve stump should be implanted in such a way that the bone does not impinge the nerve stump during movement. • Centro-central neurorrhaphy: When two terminal branches can be identified, the distal stumps can be sutured end to end. Alternatively, intrafascicular dissection is performed under surgical microscope followed by direct coaptation of two terminal fascicles. The coaptation can be protected by a connector, wrap, or fibrin glue or buried as deep as possible in local muscle tissue. • Nerve destination relocation: Another recent neuroma treatment strategy involves using an allograft to redirect and relocate the regenerating nerve after neuroma excision to a new distal target site. This technique has been termed “nerve allograft to nowhere” or “graft to nowhere.” In this technique, the neuroma is completely resected as described previously, and the healthy prepared stump is coapted to an allograft of varying lengths (Fig. 4b). The nerve to nerve allograft coaptation site may or may not be wrapped with a connector or nerve wrap, and the distal open end of the nerve allograft is then buried usually more proximally within a deep aspect of a surrounding muscle bed (Fig. 4c). The premise of this technique is that the nerve regeneration stagnates or is impeded from completely regenerating down the endotubules within the allograft thus causing the regenerating axons to dissipate over the length of the allograft. • Regenerative peripheral nerve interfaces (RPNIs): Originally designed to create motor signals for prosthetics, RPNIs were incidentally noted to also have a beneficial effect on neuroma pain. A small muscle graft is secured around the prepared end of a nerve with micro-sutures and/or fibrin glue (Fig.  5a). The

Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation Fig. 5 Regenerative peripheral nerve interfaces (RPNI). (a) A free, devascularized muscle graft is secured by fibrin glue or micro-sutures around the nerve end, and implanted into deep muscle tissues. As the free muscle graft revascularizes into the new location, it is innervated by the donor nerve. (b) Clinical example of RPNI

a

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Distal nerve end stumps

Free muscle tissue

b

reimplanted muscle graft is devascularized and de-innervated and thus must revascularize from surrounding tissues to survive. Once this muscle graft is revascularized, the nerve stump can begin to regenerate and thus reinnervate the motor end plates and nerve targets within the free muscle graft tissue. This approach is proposed to reduce symptomatic neuroma formation and allow for nerve regeneration into a new muscle graft (Fig. 5b). • Targeted muscle reinnervation (TMR): Initially devised to provide myoelectric control for prosthetics, TMR has also been found to yield significant improvement in neuroma as well as phantom limb and residual limb pain. The proximal prepared nerve stumps after neuroma resection are directly transferred to motor nerves located within the surrounding muscles (Fig. 6a).

24 Fig. 6 (a) Targeted muscle reinnervation (TMR) or targeted nerve implantation (TNI). The sensitive nerve stump (yellow) is sutured to a motor nerve branch (light blue) of the surrounding muscle tissue. The major difference between TMR and TNI is the size of the motor unit targeted by the transfer. TMR recruits a larger motor unit such that cutaneous signals could potentially be elicited. (b) Clinical example of TMR

S. Figy et al.

a

Free nerve end Suture Motor nerve (transected) Muscle

b

Selected motor nerve branches to surrounding muscle fibers are transected, creating freshly deinnervated motor nerves and “opening” motor end plates to new nerve input (Fig. 6b). A nerve stimulator can be used to identify distal motor nerves that control distinct muscle fibers. The identified motor nerve fiber is then transected and directly neurotized to the proximal sensitive nerve stump to form “intuitive signal generators,” which will reinnervate muscle units. • When TMR is used for bioprosthetics, the reinnervated muscle units become “intuitive signal generators” and can be mapped. Sensors and pattern recognition control software and hardware within a bioprosthetic can interpret these signals to provide intuitive control and even sensation to the device. • Targeted nerve implantation (TNI): TNI is also based on direct coaptation of the distal end of the formerly injured sensitive nerve by transferring and implanting the nerve to nearby motor branches within a muscle. The goal in TNI, however, is not for myoelectric control and therefore the described technique allows for more distal targets with limited concern for overlapping myosomes while achieving similar results to TMR in neuroma pain control. • Targeted muscle reinnervation with vascularized RPNI (TMR with vRPNI): This technique combines components of the TMR, RPNI, and TNI. For TMR with vRPNI, distal motor nerve branches serve as the targets for proximal nerves. Following direct neurotization, the freshly denervated muscle which will eventually become reinnervated through the sacrificed motor branch is imbricated over the coaptation to provide additional available motor end plates accepting and capturing regenerating axons.

Diagnosis and Treatment of Painful Neuromas: Targeted Muscle Reinnervation

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• For TMR, TNI, and TMR with vRPNI, if a desired target is too far for a nerve pedicle to reach without tension, a nerve allo- or autograft can be used to create a bridge from the pedicle to the target. However, this scenario is a rare occurrence in our hands. • Nerve caps: Other techniques that have been used to address end stump neuromas include nerve caps and other nerve ablation devices. Nerve caps have been described with synthetic, xenograft, and vein or muscle auto−/allograft implants. Nerve caps should be placed on the prepared nerve and secured in place with epineural sutures. The cap should be fit to a size that does not constrict the nerve as it enters the cap. There have been some promising results with caps; however, additional long-term studies of their effectiveness with objective nerve pain assessments are currently lacking. • Nerve ablation can be done both with chemical and radiofrequency methods. This is typically done with ultrasound guidance. The ablation should be done at a level above the neuroma so the signal is blocked proximal to the painful stimulus. Chemical and radiofrequency neurolysis are generally less effective than surgery and may require multiple procedures to be effective.

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 urgical Technique: General Wound Repair S and Dressing Options

• The incisions are closed in multiple layers with Scarpa’s fascial layer closure with 2–0 PDS (Johnson & Johnson) or Maxon (Medtronic) interrupted sutures. The skin layer is repaired with intradermal 3–0 or 4–0 non-braided resorbable suture (i.e., Monocryl®, Johnson & Johnson) and/or 3–0 or 4–0 nylon or polypropylene nonresorbable sutures (Ethilon® or Prolene®, Johnson & Johnson). In most cases, no surgical drain is needed. • Dressing is by semipermeable polyurethane dressing (Tegaderm™ post-op, 3M), other island dressing, Steri-Strips (Johnson & Johnson), or incisional wound V.A.C. therapy (Prevena™, Acelity) depending on the situation and surgeon’s preference.

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Postoperative Care

• Depending on the history and type of medications taken by the patient before surgery, postoperative pain can be in most cases managed with analgesics and nonsteroidal anti-inflammatory medications. Patients who did not discontinue the use of medications such as opioids, neuroleptics, and antidepressants need to decrease progressively the doses. Antibiotics are prescribed when indicated. • Patients may shower 48 h post surgery and need to limit the range of motion of joints across the operation site for 2–3 weeks not to compromise the reconstruction. Patients typically can resume prosthetic wear at approximately 6–8 weeks postoperatively and should avoid strenuous physical and/or sport activities for approximately 3 months after surgery.

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• While some patients will report immediate improvement of pain after surgery, a substantial portion may see a temporary worsening in pain symptoms. Despite this temporary uptick in pain symptoms, the majority of these patients report a steady progression in pain amelioration over the following 2- to 6-month postoperative period with significant pain score improvement compared to preoperative baseline scores. Overall success rates have been around 70% in long-term follow-­up. Recidives (reformation of neuromas more proximal on the same nerve) are possible and may require additional surgeries.

Further Reading 1. Arnold D, Wilkens S, Coert J, Chen N, Ducic I, Eberlin K. Diagnostic criteria for symptomatic neuroma. Ann Plast Surg. 2019;82(4):420–7. 2. Dumanian G, Potter BK, Mioton L, Ko JH, Cheesborough J, Souza J, Ertl WJ, Tintle S, Nanos GP, Valerio IL, Kuiken TA, Apkarian AV, Porter K, Jordan SW. Targeted muscle reinnervation treats neuroma and phantom limb pain in major limb amputees: a randomized clinical trial. Ann Surg. 2019;270(2):238–46. 3. Eberlin KR, Ducic I. Surgical algorithm for neuroma management: a changing treatment paradigm. Plast Reconstr Surg Glob Open. 2018;6(10):e1952. 4. Herndon JH, Eaton RG, Littler JW. Management of painful neuromas in the hand. J Bone Joint Surg. 1976;58A:36. 5. Sunderland S.  Nerve injuries and their repair: a critical appraisal. New  York: Churchill Livingstone; 1991.

Diagnosis and Treatment of Neurovascular Temporal Headaches Giorgio Pietramaggiori and Saja Scherer

1

Introduction

Pain syndromes located in the temporal area are common and have a wide range of expressions from normal occasional headaches to invalidating daily pain. The origin of pain is often miscellaneous and demands for a multidisciplinary approach to treat and exclude other causes of temporal headaches such as tension headache, cervicogenic headache, temporomandibular joint disorders, dental malocclusion, ENT inflammatory and infectious pathologies, meningitis, traumatic brain injuries, giant cell arteritis, vasculitis, etc. Migraine patients can suffer from a predominant temporal trigger site (pain predominantly expressed in the temples, monolateral or bilateral), while other diagnosis such as cluster headaches may coexist with neurovascular temporal headaches. Patients that have been diagnosed with migraine or cluster headaches may present with chronic, refractory temporal pulsating unilateral or bilateral headaches along the course of the auriculotemporal neurovascular bundle. For these patients, minimally invasive temporal decompression surgery has been effective to control pain intensity, duration, and frequency. Temporal headaches with a peripheral neurovascular trigger have been described by Guyuron to be related to the pain transmission via the auriculotemporal nerve and superficial temporal artery, the zygomaticotemporal nerve, and rarely the zygomaticofacial nerve, all terminal branches of the trigeminal nerve. Guyuron has also described nummular temporal headaches, characterized by painful zones along the frontal or parietal branch of the superficial temporal artery. Medical treatment and conservative approaches are the first-line treatment for persisting temporal headaches in migraine and cluster headache patients. In case of

G. Pietramaggiori (*) · S. Scherer Plastic and Reconstructive Surgery, Global Medical Institute, Lausanne, Switzerland e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_3

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suspicion of giant cell or another temporal arteritis, a diagnostic biopsy of the superficial temporal artery is indicated and mandatory. Botulinum toxin injections in the temporal area as described in the FDA protocol and by Guyuron for migraine headaches can reduce frequency and intensity of headache crises, but long-term injections of botulinum toxin in the temporal muscle may result in aesthetically unpleasant temporal hollowing. Botulinum toxin injections are particularly effective in patients suffering from neuralgia of the zygomaticotemporal nerve and much less or ineffective for headaches along the auriculotemporal neurovascular bundle. It is still unknown whether pain originates mainly from the somatic sensitive nerve fibers, blood and lymphatic vessels, or perivascular autonomic plexus. We describe here a nerve-preserving technique to achieve temporal headache pain control by decompression of the auriculotemporal nerve and superficial temporal artery. Patients eligible for this procedure suffer from primarily temporal headaches defined as typically pulsatile pain arising along the auriculotemporal neurovascular bundle. Patients commonly try to mitigate pain temporarily by direct pressure on the superficial temporal artery, icing or other cooling agents. The auriculotemporal neurovascular bundle contains, in addition to sensitive nerve fibers and blood vessels, sympathetic fibers and lymphatic vessels (Chap. 1, Fig. 2). These structures are in close relationship and cross their path several times. It is possible that the contact points between these structures trigger pain as a consequence of mechanical irritation or dysregulation of the autonomous nervous system. Surgery is indicated if the point of maximum pain along the auriculotemporal neurovascular bundle has been consistent in location throughout the crises for at least one year and therefore can be easily identified by the patient with a fingertip. Surgical indication is based on frequency of crises, drug response, anamnesis, and a positive arterial Doppler at the site of maximum pain. One to two positive (complete remission of pain) local anesthesia blocks during crises confirm the diagnosis and increase significantly patients’ awareness of the possible positive outcome of surgery.

2

Neurovascular-Temporal Pain Syndrome Characteristics

• Acute, intense, exploding, pulsatile pain in the temporal region along the course of the superficial temporal artery (most frequently frontal branch). • Pain in the region of the auriculotemporal nerve (ATN, temporo-frontal area, ear) with possible irradiations to the mandible, maxilla, and forehead. • Pain is unilateral or bilateral. • Patient can identify the point of maximum pain, which corresponds to a positive Doppler signal. • Usually early morning pain, awakens the patient. • Commonly, pain augments with physical activity. • Possible aura with autonomic symptoms such as nausea, vomiting, and visual disturbances.

Diagnosis and Treatment of Neurovascular Temporal Headaches

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Etiology (Differential Diagnosis)

These diagnoses can coexist (typically migraines and cluster headaches) with auriculotemporal neurovascular bundle neuralgia and/or should be investigated before surgery: • • • • • • • • • • •

4

Migraines Cluster headaches Tension headaches Cervicogenic headaches Pathologies of the temporomandibular joint Dental malocclusion ENT inflammatory and infectious pathologies Meningitis and other intra-cerebral pathologies Posttraumatic brain injuries Giant cell arteritis Vasculitis

Diagnostic

• Neurovascular auriculotemporal pain syndrome characteristics. • Pain responds partially to direct compression or cold packing on the maximum tender point. • Pain commonly responds to precocious (at the onset of symptoms) intake (oral/ sublingual, intranasal, or subcutaneous injections) of extracranial vasoconstricting agents (e.g., triptans, ergotamines). • Positive response to diagnostic block (almost complete reduction of pain): infiltration of 1cc of local anesthetics with vasoconstrictive agents (e.g., lidocaine with 1:100.000 epinephrine). The selective neurovascular auriculotemporal bundle block during a crisis is the most accurate diagnostic test.

5

Surgical Technique

• Identify the superficial temporal artery by palpation (Fig. 1a) in the preauricular area. • Confirm exact location by Doppler ultrasound (Fig. 1b) and/or ultrasound color Doppler of proximal and/or distal frontal branch. • Mark a 1–1.5 cm incision site anterior to the ear, approximately 1 cm anterior to the root of the helix (Fig. 1c). • Infiltration of the area with 2.5 cc of 1% lidocaine with 1:100,000 epinephrine. • Ten minutes after infiltration, using high-power magnification loops, an incision is made through the superficial fascia (Fig. 2a).

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G. Pietramaggiori and S. Scherer

b

c

Fig. 1  (a, b) Identify the superficial temporal artery by palpation and confirm exact location by Doppler ultrasound. (c) Mark a 1 cm incision line anterior to the ear, approximately 1 cm anterior to the root of the helix

a

b

Fig. 2 (a) Ten minutes after subcutaneous infiltration of the area with 2.5 cc of lidocaine 1% with 1:100000 epinephrine an incision is made through the superficial fascia. (b) The first structures coming into sight under the superficial fascia are usually the superficial temporal veins. Dissection is carried out to liberate the vein(s) from surrounding structures

• The first structures coming into sight under the superficial fascia are usually the superficial temporal veins. Dissection is carried out to liberate the vein(s) from surrounding structures (Fig. 2b). • The main trunk of the auriculotemporal nerve is exposed and decompressed from the preauricular ligaments (Fig. 3a). • The artery is found anterior and slightly deeper than the main nerve trunk. The common trunk and the bifurcation into parietal and frontal branches are easily identified (Fig.  3b). The artery is decompressed and denuded from any ­surrounding adventitial fibro-connective tissue (arteriolysis). The tridimensional curly shape and pulsations of the artery can be appreciated at this stage.

Diagnosis and Treatment of Neurovascular Temporal Headaches

a

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b

Fig. 3 (a) The auriculotemporal nerve (ATN) is exposed anteriorly to the vein and decompressed from the preauricular ligaments. (b) The superficial temporal artery (STA) is found anterior and slightly deeper than the main nerve trunk. After liberating the artery from the fibro-connective perivascular adventitia the tridimensional curly shape and pulsations of the artery can be appreciated

a

b

Fig. 4  All nerve branches are separated from the artery paying attention not to cause any injury. (a) Branches of the ATN having tight adhesions in the proximal part of the STA. (b) Several branches are also found along the artery and become evident as the arteriolysis is performed

• All nerve branches are separated from the artery (Fig. 4a, b) paying attention not to cause any nerve injury. A contact point, possibly compressing/irritating the nerve, is usually found as the artery is followed proximally (Fig. 4a) and should be released. One or more nerve fibers follow the artery along its course and should be carefully dissected (Fig. 4b). • The artery, the vein, and the nerve are isolated, liberating each visible compression point along their course (Fig. 5).

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Fig. 5  The artery (red loop), the vein (blue loop), and the nerve (white loop) are isolated, liberating each visible compression/ contact point along their course

• When a conflict between the artery and the nerve is not otherwise addressable (e.g., an arterial branch making a loop around the nerve), a biopsy of the artery can be taken and sent to pathology, paying attention not to injure the nerve fibers. When sudden visual symptoms during crisis (e.g., visual loss), deformation of the artery, and focal persistent pain along the course of the vessel are present, arteritis should be excluded, and a biopsy must be taken and sent to pathology. Results from pathological analysis in our patients show an aspecific, non-obliterating lesion called endothelial hyperplasia or endofibrosis. Since no difference in pain relief was observed when the biopsy was performed compared to neurolysis and arteriolysis alone, we recommend starting with the less invasive, artery sparing approach. • Skin is repaired with intradermal 5-0 non-braided resorbable suture (Fig. 6a, b). • Dressing is by Opsite® (Smith and Nephew) spray (Fig.  6c) and Steri-Strips (Johnson & Johnson, Fig. 6d).

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Postoperative Protocol

• Steri-Strips are removed 2–5 days post-surgery. • Patients can go back to work and normal life the same day or the day after surgery. • Sport and physical efforts are allowed from day 7. • Pain relief is permanent in 80% of the patients and expected to manifest within the first few days for most patients and progressively over 3 months for the rest.

Diagnosis and Treatment of Neurovascular Temporal Headaches

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Fig. 6 (a, b) Skin is repaired with intradermal 5/0 non-braided resorbable suture. (c, d) Dressing is by opsite® (Smith & Nephew) spray and steri-strips (Johnson & Johnson)

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Further Reading 1. Gulekon N, Anil A, Poyraz A, Peker T, Turgut HB, Karakose M. Variations in the anatomy of the auriculotemporal nerve. Clin Anat. 2005;18:15. 2. Guyuron B. Migraine Surgery. New York: Thieme Publishing Group; 2018. 3. Janis JE, Hatef DA, Ducic I, Ahmad J, Wong C, Hoxworth RE, Osborn T.  Anatomy of the auriculotemporal nerve: variations in its relationship to the superficial temporal artery and implications for the treatment of migraine headaches. Plast Reconstr Surg. 2010;125:1422. 4. Speciali JG, Goncalves DA. Auriculotemporal neuralgia. Curr Pain Headache Rep. 2005;9:277. 5. Totonchi A, Pashmini N, Guyuron B. The zygomaticotemporal branch of the trigeminal nerve: An anatomical study. Plast Reconstr Surg. 2005;115:273.

Diagnosis and Treatment of Occipital Neuralgia Giorgio Pietramaggiori and Saja Scherer

1

Introduction

Occipital neuralgia (ON) is one of the most frequent disabling headache syndromes. Based on the significant long-term relief after decompression surgery in over 85% of the patients treated in our institution as well as similar results reported in literature, we strongly believe that nerve compression is one of the main causes of ON according to the international classification of headache disorders. The incidence of disabling ON is rather rare in the general population (3.2:100,000), while it is frequently seen in posttraumatic whiplash injuries presenting as occipital pain syndromes or as a coexisting condition in migraine and cluster headache patients. Usually patients with ON coexisting with migraine and/or cluster headaches suffer from constant occipital baseline pain between crises of higher-­ intensity pain, but occasionally intervals between crises can be pain free. We hypothesize that central processes during migraine crises may decrease the firing threshold of sensitive peripheral nerves passing through compressive anatomical structures during migraine crisis. This may explain the reason why pain is not constant and  significant reduction of intensity and frequency of migraine crises are reported after occipital decompression surgery. The main nerves responsible for ON are the greater occipital nerve (GON), and/ or the lesser occipital nerve (LON). The role of the third occipital nerve (TON) alone or in combination with the GON and LON has not been demonstrated yet as contributing factor to ON. The GON raises mainly  from the C2 root, travels upwards, passing tightly around the obliquus capitis inferior muscle, and then piercing more cranially the

G. Pietramaggiori (*) · S. Scherer Plastic and Reconstructive Surgery, Global Medical Institute, Lausanne, Switzerland e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_4

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semispinalis capitis muscle about 3.5  cm inferior to the nuchal line and 1.5  cm lateral to the midline. The GON emerges from the lateral edge of the trapezius with a superolateral trajectory. At the nuchal line, the occipital artery and lymphatic system (Chap. 1,  Fig. 4) cross the GON.  This neurovascular crossing point is mechanically compressed between the occipital bone and the common tendinous insertion of the trapezius and sternocleidomastoid (SCM) muscles. After the passage through the nuchal line, the GON terminates in the subcutaneous scalp tissue to innervate the occipital scalp. The LON originates mainly from the C3 nerve root and then pierces the fascia of the lateral sternocleidomastoid (SCM) muscle to then travel along its medial border. Equally to the GON, the LON travels cranially, 6–7 cm from the midline, and it is compressed by the common tendinous insertion of the trapezius and SCM at the a

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Fig. 1 (a–c) The patient is asked to place one finger on the point corresponding to the origin of pain. This point is marked; most of the times it corresponds to the passage of nerves, arterial and lymphatic vessels under the tendinous insertion of the trapezius and sternocleidomastoid (SCM) muscles. (d–f) A 3.5 cm incision line is drawn across the point of maximum pain, over the passage of the greater occipital nerve (GON), lesser occipital nerve (LON), and occipital artery (not shown). The edges of the trapezius muscle and sternocleidomastoid are indicated by the dotted lines

Diagnosis and Treatment of Occipital Neuralgia

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nuchal line. The LON then reaches the subcutaneous tissue to innervate the occipitotemporal scalp. Different surgical techniques have been described to address ON.  Nerve-­ conserving decompression is chosen by most authors to address GON neuralgia, while the surgical approach for LON neuralgia ranges from nerve-conserving decompression techniques to resection of the LON with nonsignificant neuroma formation. For patients that do not respond to more peripheral approaches, the standard midline approach (as described by Guyuron) is preferred to ensure extensive proximal decompression of the GON to the obliquus capitis inferior muscle. This approach offers only limited access to the crossing point between GON-LON, occipital artery, and lymphatic vessels in our experience. We observed that most patients suffering from ON can point with one fingertip to the pit between the trapezius and the SCM to indicate the point of maximum and/ or origin of pain. We define this zone the occipital triangle (Chap. 1, Fig. 4), where the GON-LON neurovascular bundle is maximally compressed. The triangle is comprised between the nuchal line superiorly, the proximal lateral border of the trapezius muscle medially, and the proximal medial border of the SCM muscle laterally. A selective and superficial nerve block is performed in the center of the occipital triangle. When the block is positive, patients can be treated with a minimally invasive, nerve-preserving surgical technique via an oblique 3.5-cm incision across the occipital triangle allowing for best visualization and safe decompression of the GON-LON neurovascular bundle at the nuchal line. Through this access, more proximal potential compression points of the GON, such as the passage through the semispinalis capitis muscle, can be reached and addressed. This minimally invasive decompression technique for ON can be performed in an ambulatory setting under local or general anesthesia with fast recovery.

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Occipital Pain Syndrome Characteristics

• Intense pain originating from the occipital area (Chap. 1, Fig. 4). • Pain is unilateral or bilateral. • Pain irradiating in the occipital-temporal regions in the territory of the greater and lesser occipital nerves. • Patient can identify the point of maximum pain, which is between the tendinous insertion of the trapezius and sternocleidomastoid muscles in the occiput (Fig. 1a–c). • Patients commonly suffer from daily baseline pain (rarely are pain-free). • Occipital pain is exacerbated by physical activities and is associated with muscle tenderness in the back and neck. • Intense crises can cause pain behind the eyes. • Patients tend to take anti-inflammatory medications and myo-relaxants almost every day. Drugs can decrease pain, but rarely can achieve full pain remission.

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• Occipital pain can be accompanied by hypoesthesia, hyperesthesia, or allodynia in the occipital scalp. • Visual aura, nausea, vomiting, and visual disturbances are particularly common during ON crises.

3

Etiology

• Idiopathic. • Posttraumatic (e.g., whiplash injury), work-related, iatrogenic. • Multifactorial, unknown.

4

Diagnostic

• Pain as described above. • Point of maximum pain corresponding to occipital nerve trajectory at its main compression points. • Pain only partially responds to common analgesics, anti-inflammatories, or antimigraine drugs. • Headaches improve after infiltration in the point of maximum pain (Fig. 1a–c) of local anesthetics. • Cortisone infiltration in the same point can induce significant pain improvement for one to two weeks in most of the cases.

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Surgical Technique

• Identify point of origin/maximum pain – occipital triangle between the insertions of the trapezius and sternocleidomastoid muscle (Chap. 1, Fig. 4, Fig. 1a–c) by palpation. • Draw an incision line of 3.5–4.5 cm across the point of maximal pain, along the bisector between the lateral edge of the trapezius muscle and the nuchal line (Fig. 1d–f). • Prepare the area to be treated with skin disinfection and injection of lidocaine with 1:100,000 epinephrine along the incision line (Fig.  2). In some cases (patients not agreeing on local anesthesia, posttraumatic or special patients’ conditions), the procedure can be performed under general anesthesia. • Patient is lying comfortably in lateral decubitus. • Ten minutes after local anesthesia infiltration, under high-power magnification, incise the skin and subcutaneous tissue with a no. 15 blade. Pass through the superficialis fascia. A Weitlaner self-retractor can be inserted (Fig. 3a). • The fibrous-tendinous insertions of the trapezius and sternocleidomastoid muscle on the nuchal line are exposed (Fig. 3b). • Carefully dissect using scissors the proximal and distal superficial fibrous tissues compressing the occipital neurovascular bundle between the trapezius and the

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Fig. 2  Prepare the area to be treated with skin disinfection and injection of lidocaine with 1:100,000 epinephrine along the incision line

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Fig. 3  (a) Incise the skin and subcutaneous tissue with a no. 15 blade. Pass though the superficialis fascia. A Weitlaner self-retractor can be inserted at this point. (b) The fibrous-tendinous insertions of the trapezius and sternocleidomastoid muscle on the nuchal line are exposed. (c, d) Carefully dissect using scissors the proximal and distal superficial fibrous-tendinous tissue between the trapezius and the SCM muscle insertion. The fibers of this tissue are very tight and hard, attention should be paid not to injure any neurovascular branches emerging from the deeper tissues

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sternocleidomastoid muscle insertion (Fig. 3c, d). Attention should be paid not to injure any neurovascular branches emerging from the deeper tissues. • The nuchal line corresponding to the common tendinous insertion of the occipital muscles (Fig. 4a, dotted blue line) needs to be released in order to decompress the LON-GON neurovascular bundle. • The fibrous-tendinous tissue compressing the neurovascular bundle may be several millimeters thick in the proximal area and needs to be released completely with scissors, paying attention not to lesion any nerve or vascular branches (Fig. 4b). • After the release of the nuchal line, an enlarged occipital lymph node can be present at the crossing point of some branches of the lesser (LON) and greater (GON) occipital nerves. Branches of the occipital artery can also be found in this area deeper than the nerves (Fig. 5a).

b

a Fig. 4  (a) The nuchal line corresponding to the muscular insertion of the occipital muscles (dotted blue line) needs to be released in order to decompress the occipital neurovascular bundle. The dotted white lines indicate the lateral edge of the trapezius muscle and the medial edge of the sternocleidomastoid muscle (SCM). The arrow indicated the point where some fibers of the greater occipital nerve (GON) emerge from the depth. (b) The nuchal fibrous tendinous tissue (between the two dotted white lines) compressing the neurovascular bundle may be several millimeters thick in the proximal area and needs to be released completely with scissors or blade paying attention not to lesion any nerve or vascular branches compressed just underneath it

Diagnosis and Treatment of Occipital Neuralgia

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b

Fig. 5  (a) After the release of the nuchal line, an enlarged occipital lymph node can be present at the crossing point of some branches of the lesser (LON) and greater (GON) occipital nerves. Branches of the occipital artery can also be found in this area usually deeper than the nerves. (b) At higher magnification some nerve fibers adherent to the lymph node can be appreciated. In case the lymph node compresses the neurovascular bundle, it can be excised and sent for pathological analyses, paying attention not to injure any vascular or nerve branches often present on or around it. Results from a few pathological analyses of occipital lymph nodes did not show any peculiar abnormalities in our patient population besides signes of chronic inflammation

• At higher magnification, some nerve fibers adherent to the lymph node can be appreciated (Fig. 5b). In case the lymph node compresses the neurovascular bundle, it can be excised and sent for pathological analyses, paying attention not to injure any vascular or nerve branches often present on it or in its immediate vicinity. Results from a few pathological analyses of occipital lymph nodes did not show any peculiar abnormalities (other than signs of chronic inflammation) in our patient population. • After the release of the nuchal line and excision of the lymph nodes, the greater occipital nerve (GON), lesser occipital nerve (LON), and communicating branches (CB) become apparent. Deeper to the nerves, branches of the occipital artery start to become visible (Fig.  6). Some tendinous tissue is still in place under the nerves and vessels and need to be released to complete the decompression. • The GON is decompressed in the proximal and medial direction. The tendinous edge of the trapezius muscle fascia is released. Arterial branches crossing the trajectory and compressing the nerve are also released (Fig. 7a).

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Fig. 6  After the release of the nuchal line and excision of the lymph nodes, the greater occipital nerve (GON), lesser occipital nerve (LON), and communicating branches (CB) become apparent. Deeper to the nerves, branches of the occipital artery start to appear. Some tendinous tissue is still in place under the nerves and vessels and need to be removed to complete the release

Occipital Artery

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Fig. 7  (a). The GON is decompressed in the proximal and medial direction. The tendinous edge of the trapezius fascia (pulled by pincets) is released along the course of the nerve. (b) In order to avoid injuries to the nerve in the sub-trapezius plane, a light retractor may be used. All proximal tight structures around the nerve should be released to complete the decompression

• In order to avoid injuries to the nerve in the sub-trapezius plane, a light retractor may be used (Fig. 7b). From this access, the nerve is followed proximally and all compression points released till no tight structure is felt around it. • Once the nuchal line is completely released over the passage of the occipital nerves, the branches of the occipital artery become more visible (Fig.  8).

Diagnosis and Treatment of Occipital Neuralgia Fig. 8  Once the nuchal line is completely released over the passage of the occipital nerves, the branches of the occipital artery become more visible. Sometimes another layer is found between the main nerve branches and the main arterial branches, possibly the superficial fascia of the occipitofrontal muscle or a deeper layer of the nuchal line

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Sometimes another structure is found pulling from underneath on nerve and arterial branches, possibly the superficial fascia of the occipitofrontal muscle or a deeper layer of the nuchal line tendon. This structure should be released to complete the decompression. The trajectory of the occipital artery is widely variable. Oftentimes, branches are found piercing through the GON and passing above and below the nerve branches. We recommend liberating all points of contact between the artery and the nerve branches. When not otherwise possible, some branches can be ligated/coagulated and sent to pathology. Most of the times, in our patients’ population these arteries show an aspecific non-obliterating morphologic change called intimal hyperplasia or endofibrosis, whose origin remains uncertain. After careful hemostasis, subcutaneous tissue and skin are repaired in two layers with intradermal 4/0, resorbable, non-braided suture (Monocryl®, Johnson & Johnson, Fig. 9a) and the area is infiltrated with local anesthesia (mix of lidocaine with 1:100,000 epinephrine and Chirocaine 0.5%). The final wound is between 3.5 and 4.5 cm; no drains are needed. If bilateral, one side can be done after the other or two operations can be planned.

Postoperative Protocol

• Wound dressing is with spray-on film (Opsite®, Smith & Nephew) dressing and dry compresses (Fig. 9b). • Compresses are removed 48  h after surgery, shower earliest 48  h after the procedure. • Light work is allowed 5–7 days after surgery. • Light physical activity is allowed 10–15 days postsurgery. Unlimited physical activity can be permitted after 1 month to 3 months depending on the postoperative individual recovery and type of activity.

44 Fig. 9 (a) After careful hemostasis, skin is repaired with intradermal 4/0, resorbable, non-braided suture (Monocryl®, Johnson & Johnson) and the area is infiltrated with local anesthesia (mix of lidocaine with 1:100,000 epinephrine and chirocaine 0.5%). (b) The final wound is between 3.5 and 4.5 cm, no drains are needed. Wound dressing is with spray-on film dressing and dry compresses

G. Pietramaggiori and S. Scherer

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• Early pain relief from surgery can be expected with a progressive improvement and stabilization of symptoms during a period of 1–3 months. • Complete sensitive recovery of the scalp is commonly reported after 15 days to 3 months. • Complications are rare and include transient hypo- and hyperesthesia of the scalp as well as prolonged hypersensitivity of the scars.

Further Reading 1. Blake P, Nir RR, Perry CJ, Burstein R. Tracking patients with chronic occipital headache after occipital nerve decompression surgery: A case series. Cephalalgia. 2018;14:333102418801585. 2. Lineberry K, Lee M, Monson A, Guyuron B. Intraoperative corticosteroid injections in migraine surgery: efficacy in preventing refractory symptoms. Plast Reconstr Surg. 2015;135(2):393e–6e. https://doi.org/10.1097/PRS.0000000000000862. 3. Janis JE, Hatef DA, Reece EM, McCluskey PD, Schaub TA, Guyuron B. Neurovascular compression of the greater occipital nerve: implications for migraine headaches. Plast Reconstr Surg. 2010;126(6):1996–2001. https://doi.org/10.1097/PRS.0b013e3181ef8c6b.

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4. Peled ZM, Pietramaggiori G, Scherer S. Anatomic and compression topography of the lesser occipital nerve. Plast Reconstr Surg Glob Open. 2016;4(3):e639. https://doi.org/10.1097/ GOX.0000000000000654. 5. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, third edition (beta version). Cephalalgia. 2013;33(9):629–808.

Diagnosis and Treatment of Pectoralis Minor Syndrome (Neurogenic Thoracic Outlet) Giorgio Pietramaggiori and Saja Scherer

1

Introduction

The scalene triangle, the costoclavicular space, and the pectoralis minor are the main compression points of the brachial plexus. When the main compression point is diagnosed to be under the pectoralis minor muscle, treatment is by surgical release of the insertion of this muscle on the coracoid with a minimally invasive procedure (Chap. 1, Fig. 6). This procedure does not treat every case of nTOS, but for a selected cluster of patients, it is very effective.

2

Pectoralis Minor Syndrome Characteristics

• Dull, intense pain exacerbated by upper limb movements, from the axilla and anterior chest wall below the clavicle. • Pain in the distribution of the median, radial, and ulnar nerves (all three regions at the same time possible or one or two prevalently). Pain in the upper limb often irradiates to the neck, occipital, facial, and shoulder regions. • Main tender point below the coracoid at the passage of the brachial plexus under the insertion of the pectoralis minor muscle. • Possible paresthesia of all five fingers (worse in the fourth and fifth finger).

G. Pietramaggiori (*) · S. Scherer Plastic and Reconstructive Surgery, Global Medical Institute, Lausanne, Switzerland e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_5

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Etiology

• Posttraumatic (mainly traction injuries, motor vehicle accident, fall). • Sport (involving repetitive throwing or lifting). • Idiopathic, multifactorial, unknown.

4

Diagnostic

• Pain as described above. • Tinel sign positive below the coracoid and/or other trigger/compression points along the course of the three nerves of the arm (possible double, triple, or multiple crush syndrome). • Provocative maneuvers: neck rotation, head tilt, upper limb tension test, and elevated arm stress test. • Numbness along the arm and hand, particularly the fingers. • Electromyography for nTOS is often negative, and measurement of medial antebrachial sensory cutaneous nerve is more often positive in patients with nTOS. • Radiologic studies: MRI and conventional RX. They may show anomalies such as a cervical rib or anomalous first rib (rare). They are used rather as an exclusion criteria of other possible origins. • Pain improves with infiltration of local anesthetics in the pectoralis minor (muscle block) performed under ultrasound guidance. Lidocaine infiltration would act in about 60 sec. to a few minutes and last about 30 min. • Pain improves a few days after botulinum toxin infiltration of the pectoralis minor performed under ultrasound guidance.

5

Surgical Technique

• General anesthesia. • The arm and shoulder are completely disinfected, and draping is made so that the upper limb can be freely moved during the operation (Fig. 1a). • A 4-cm longitudinal incision is made parallel to the deltopectoral groove centered 1 cm distal to the coracoid (Fig. 1b). • Careful dissection is carried through the subcutaneous tissues to avoid damage to any supraclavicular sensitive nerve branches. The cephalic vein (CV) is exposed and protected (Fig. 2a).

Diagnosis and Treatment of Pectoralis Minor Syndrome (Neurogenic Thoracic Outlet)

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Fig. 1 (a) The arm and shoulder are completely desinfected and draping is made so that the position of the upper limb can be changed during the operation. (b) A 4 cm longitudinal incision is made parallel to the deltopectoral groove centered 1 cm distal to the coracoid

a Pectoralis Minor

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• The pectoralis major muscle is gently pushed caudally and the deltoid with the cephalic vein is pushed laterally and cranially (Fig. 2b). • Between the pectoralis major muscle and the deltoid, the tendinous insertion of the pectoralis minor muscle on the coracoid comes into view (Fig. 2c) and it is fully exposed through careful dissection (Fig. 3a). • The tendon is released with bipolar coagulation under direct view by pulling it upward and releasing it fiber by fiber (Fig. 3b). Attention should be made not to release some fibers of the tendon of the coracobrachialis muscle (the fibers are not generally in contact with the tendon of the pectoralis minor muscle, have a different orientation, and move with the movements of the arms).

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Fig. 2 (a) Careful dissection is carried through the subcutaneous tissues to avoid damage to any supraclavicular sensitive nerve branch. The cephalic vein is exposed and protected. (b) The pectoralis major muscle is gently pushed caudally and the deltoid with the cephalic vein is pushed laterally. (c) Between the pectoralis major muscle and the deltoid, the tendinous insertion of the pectoralis minor muscle on the coracoid comes into view

• The release is completed when the fat pad wrapping the brachial plexus is apparent (Fig. 4a). Gentle palpation allows for identification of the subclavian artery and main trunks of the brachial plexus. • After infiltration with a mixture of local anesthesia (e.g., 0.5% chirocaine and 1% lidocaine), the wound is repaired with 4/0 non-braided, resorbable suture (Fig. 4b). • The wound is dressed with Steri-Strips (Johnson & Johnson) and dry dressing.

Diagnosis and Treatment of Pectoralis Minor Syndrome (Neurogenic Thoracic Outlet)

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Fig. 3 (a) The tendinous insertion of the pectoralis minor is fully exposed through careful dissection. (b) The tendon is released with bipolar coagulation under direct view by pulling it upward and releasing it fiber by fiber

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Fig. 4 (a) The release is completed when the fat pad wrapping the brachial plexus is fully exposed. (b) After infiltration with a mixture of local anesthesia (i.e., 0.5% chirocaine and 1% lidocaine), the wound is repaired with 4/0 resorbable, non-braided suture

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Postoperative Protocol

• Dressing can be removed 2-5  days post operation. Shower is allowed earliest 48 h after surgery. • Passive and active (with limited range, less than 90°) mobilization is immediate and active beyond 90° after 7  days 1  ×  day. Free full range of motion of the shoulder at 4 weeks. • Work is allowed after 7 days, and light physical activities after 10–15 days. • At 3  months, repetitive sport activities (such as throwing and lifting) can be started but with progressive intensity.

Further Reading 1. Ammi M, Péret M, Henni S, Daligault M, Abraham P, Papon X, Enon B, Picquet J. Frequency of the pectoralis minor compression syndrome in patients treated for thoracicoutlet syndrome. Ann Vasc Surg. 2018;47:253–9. https://doi.org/10.1016/j.avsg.2017.09.002. Epub 2017 Sep 22 2. Ferrante MA, Ferrante ND. The thoracic outlet syndromes: Part 1. Overview of the thoracic outlet syndromes and review of true neurogenic thoracic outlet syndrome. Muscle Nerve. 2017;55(6):782–93. https://doi.org/10.1002/mus.25536. Epub 2017 Mar 21 3. Hagan RR, Ricci JA, Eberlin KR. Novel surgical approach for decompression of the scalene triangle in neurogenic thoracic outlet syndrome. J Reconstr Microsurg. 2018;34(5):315–20. https://doi.org/10.1055/s-0037-1621728. Epub 2018 Feb 2 4. Sanders RJ, Annest SJ.  Thoracic outlet and pectoralis minor syndromes. Semin Vasc Surg. 2014;27(2):86–117. https://doi.org/10.1053/j.semvascsurg.2015.02.001. Epub 2015 Feb 18 5. Sanders RJ, Annest SJ. Pectoralis minor syndrome: subclavicular brachial plexus compression. Diagnostics (Basel). 2017;7(3):pii: E46. https://doi.org/10.3390/diagnostics7030046.

Diagnosis and Treatment of Groin and Genital Pain Sanchit Sachdeva and Shai M. Rozen

1

Introduction

Neurogenic groin/testicular/labial pain syndrome, which may include the groin as well as the testicle or labia majora, is also commonly referred to as ilioinguinal, iliohypogastric, and genitofemoral neuralgia. This syndrome usually arises from peripheral nerve lesions, specifically the ilioinguinal nerve, genitofemoral nerve, and sometimes the iliohypogastric nerve (Chap. 1, Fig. 8). These nerves originate in the lumbar plexus (L1–L4) and typically have multiple branches and overlapping territories. The pathophysiology of chronic groin neurogenic pain is quite complex and not very well understood. It most commonly presents as a result of surgery in the inguinal region. With the ubiquitous nature of these surgeries (approximately 500,000 inguinal hernia repairs and 600,000 hysterectomies performed annually in the United States), groin neurogenic pain is unfortunately a common complication, affecting numerous patients in the United States and worldwide. Specifically, the nerves may either be entrapped or inadvertently ligated during these procedures, which manifest itself in the classical sensory deficits as well as distinct electric pain of groin neuralgia. This said, it has been our experience that many patients develop pain, several years after surgeries, especially when a surgical mesh was used. This is likely due to subsequent progressive scarring and contraction over the years, in which the nerve becomes entrapped and pain initiated. Additionally, it is important to note that a S. Sachdeva (*) UT Southwestern Medical School, UT Southwestern Medical Center, Dallas, TX, USA e-mail: [email protected] S. M. Rozen Department of Plastic and Reconstructive Surgery, UT Southwestern Medical Center, Dallas, TX, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_6

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small set of groin neurogenic pain cases have been cited to have other, often idiopathic, etiologies. Consequently, this subgroup of patients poses a unique challenge to physicians in terms of diagnosis and treatment.

2

Neurogenic Groin Pain Characteristics

• Hypoesthesia, allodynia, and hyperalgesia along the distributions of ilioinguinal, iliohypogastric, and genitofemoral nerves often irradiating toward the lumbar plexus. • Patients often distinctly describe their pain as having stabbing, tingling, burning, and electrical qualities. • In addition to physical manifestations, patients often cite emotional repercussions of their chronic neurogenic groin pain, leading to a remarkable decrease in overall quality of life. • Often, neurogenic groin pain causes patients to have reduced mobility, ability to perform routine tasks, and motivation to enjoy life. • Many patients cite inabilities to fall asleep or even stay asleep. • Patients may develop a dependence on pain medications including opioids, neuroleptics, and antidepressants, all used in the treatment of neurogenic pain. This makes neurogenic groin pain a life-debilitating condition.

3

Etiology

• Direct injury or scar entrapment of ilioinguinal, iliohypogastric, and genitofemoral nerves. • Most commonly associated with inguinal hernia repair (with and without mesh). • Other invasive surgical procedures in the inguinal region including but not limited to appendectomy, hysterectomy, and vasectomy have been known to cause groin and testicular or labial neurogenic pain as well. • Idiopathic.

4

Diagnosis

• Obtain a detailed and complete history from the patient. This includes measures related but not limited to onset, severity, duration, quality, and radiation of the pain as well as any past surgical history and pathology in the area. • The physician must perform a detailed physical exam while looking for classic symptoms of neurogenic pain such as hypoesthesia, allodynia, and burning or electric pain sensations. • Distinguish between postoperative pain and neurogenic pain. It is generally recognized that a period between 6 months and 1 year after onset of symptoms be

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given to allow any inflammatory response to diminish before further surgical intervention. • Administration of selective Ilioinguinal nerve, iliohypogastric nerve, and genitofemoral nerve blocks. Positive relief of pain after these blocks is often used as a diagnostic tool for groin neuralgia. Sequential blocks can help more specifically identify the injured nerves, often reducing the need to perform unnecessary surgery on other nerves within the inguinal region.

5

Surgical Technique: General Considerations

• Surgical treatment on groin neuropathic pain involves either neurolysis or neurectomy of the affected nerves. • Neurectomies proximal to the scarred area are more often performed since in most cases, the nerves are damaged rather than simply compressed. • Surgical approach is often proximal to the inguinal zone: finding and liberating the nerves caught in scar tissue may not be beneficial because the pain producing neuroma within the injured nerve will persist.

6

Surgical Procedure

• The lower part of the abdomen is prepped including the umbilicus superiorly, anterior superior iliac spine (ASIS) laterally, and the pubic tubercle and the proximal anterior portion of the tight inferiorly (Fig. 1). • The incision is drawn usually two fingerbreadths cranial and parallel to a line drawn between the pubic tubercle and ASIS. The incision can be extended toward the pubic tubercle depending on the painful zone, location, and results of the diagnostic tests (Fig. 1). • Infiltration of 5 cc lidocaine with 1:100,000 epinephrine along the incision line. • Once the skin and Scarpa’s fascia are incised, the external oblique muscle fascia is encountered. It is then incised along its fibers to expose the internal oblique muscle (Fig. 2a, b). • The ilioinguinal and iliohypogastric nerves are identified on the surface or within the fibers of the internal oblique muscle (Fig. 3a). If scarring extends more laterally, dissection should be carried out proximal and lateral to find the intact nerve within normal muscle tissue. Nerve ends entrapped in scar tissue may have a much less predictable location often on the deep aspect of the transverse muscle or on the iliacus muscle (Fig. 3b, c). • The proximal nerve ends are followed to the point where they start to be embedded in scar tissue. A transition area of partially injured nerve proximal to the scar tissue may be visible under high-power magnification loops or microscope (Fig. 4a). • Nerves are showered with local anesthesia (e.g., 0.25% Marcaine and lidocaine with epinephrine) proximal to the injured end (Fig. 4b).

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Anterior superior iliac spine Incision site Inguinal ligament Pubic tubercle

Fig. 1  After the patient is approriately draped the anterior superior iliac spine and pubic tubercle are palpated and marked and a line is drawn in between. The incision site is marked at 2 fingerbreadths superior to this line which represents inguinal ligament

• The nerves are cauterized with a bipolar cautery, proximal to the supposed area of injury (Fig. 5a). • A portion of the nerve with the supposed proximal area of injury is resected back until homogeneous intrafascicular bleeding is observed in the proximal end (Fig. 5b). The excised part can be sent to pathology to confirm the intrafascicular scarring and non-injured proximal end. • The proximal, non-injured end of the nerve is implanted deep into proximal muscle tissue (Fig. 5c). • The exact same procedure is performed on the iliohypogastric nerve when indicated. Most commonly the iliohypogastric nerve runs 2–3 cm cranial and parallel to the ilioinguinal nerve. • A similar procedure is utilized for the cauterization and neurectomy of the genitofemoral nerve, but care must be taken to identify and preserve the vas deferens and spermatic cord medially in men patients. The senior author tends to do this through a proximal extension of the original incision, but some authors advocate

Diagnosis and Treatment of Groin and Genital Pain Fig. 2 (a) Once the skin and Scarpa’s fascia are incised, the external oblique muscle fascia is encountered. It is then incised along its fibers to expose the internal oblique muscle. Most of the times the iliohypogastric and ilioinguinal nerves are identified on the surface or within the fibers of the internal oblique muscle at this level. (b) Schematic representation of Figure 2a

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b

Cranial

External oblique fascia Internal oblique muscle Lateral

Medial

Caudal

a small and separate medial incision in correspondence of the external inguinal ring. • Once the genital branches of the genitofemoral nerve are identified (Fig.  6a), they are carefully dissected off the spermatic cord/round ligament as proximal as possible. The intact nerve end is showered with local anesthesia (e.g., 0.25% Marcaine and Lidocaine with epinephrine). • Under traction, the nerve is cauterized (Fig. 6a) and resected proximally until homogeneous intrafascicular bleeding is observed in the proximal end (Fig. 6b). • The nerve is then allowed to retract back into the preperitoneal area (or pushed back into it) through the external inguinal ring (Fig. 6c).

58 Fig. 3 (a) Within the fibers of the Internal oblique muscle, a few centimeters above the inguinal ligament, the terminal, sensitive branches of the ilioinguinal and iliohypogastric nerves are identified (ilioinguinal nerve shown, retracted by elastic). These two nerves have a parallel trajectory, the iliohypogastric running approximately 2 cm superior to the ilioinguinal. (b) Extensive scarring may perturbate normal anatomy: injured nerves after inguinal hernia repair are often entangled in scar tissue which can extend within the fascicles of the nerves. Dissection within the area of the mesh/scar tissue to identify the nerves is difficult and frustrating; thus, it is recommendable to extend the incision proximal and lateral to find the intact nerve ends within normal muscle tissue. (c) Schematic representation of Fig. 4b

S. Sachdeva and S. M. Rozen

aExternal Oblique Muscle Aponevtosis (Fetracted)

lioinguinal nerve Cranial Lateral

Internal Oblique Muscle

Medial

Inguinal Ligament

Caudal External Oblique Muscle Aponevtosis

Iliohypogastric Nerve

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Scare Tissue and Surgical Mesh Cranial Lateral

Medial Ilioinguinal nerve Caudal

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c

Iliohypogastric nerve

Scar

Lateral

Medial

Ilioinguinal nerve Genitofemoral nerve

Inguinal ligament

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59 Cranial

b

IIiohypogastric nerve

Injured nerve ends Scar IIiohypogastric nerve IIioinguinal nerve

Proximal injured nerve segment

Lateral

Scar

Medial

Lateral

Medial

IIiolnguinal nerve

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Fig. 4 (a) The intact nerve ends are followed to the point where they start to be embedded in scar tissue. A transition area of partially injured nerve proximal to the scar tissue may be visible under high-power magnification loops or microscope. (b) Nerves are showered with local anesthesia (e.g., 0.25% Marcaine and lidocaine with epinephrine) proximal to the injured end

a

Cranial

Lateral

b

Cranial

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Caudal Cranial

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Fig. 5 (a) The nerves are cauterized with a bipolar cautery, proximal to the estimated area of injury. (b) A portion of the nerve proximal to the area of injury is resected posteriorly until homogeneous intrafascicular bleeding is observed in the proximal end. (c) The proximal, non-injured end of the nerve is implanted deep into proximal muscle tissue

60 Fig. 6 (a) A similar procedure is utilized for the cauterization and neurectomy of the genitofemoral nerve, but care must be taken to identify the vas deferens and spermatic cord medially. The senior author tends to do this through the original incision but some authors advocate a small and separate medial incision. (b) Once the genital femoral branches are identified, they are carefully dissected off the cord as proximal as possible. The nerve is showered with 0.25% Marcaine and and lidocaine with epinephrine, and under traction, the nerve is cauterized and cut. (c) The nerve is then allowed to retract back into the preperitoneal area through the external inguinal ring

S. Sachdeva and S. M. Rozen Cranial

a

Inguinal ring

Lateral

Medial Spermatic cord

Caudal Cranial

b

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Proximal injured nerve segment Scar tissue

c

Caudal Cranial

Medial

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• After careful hemostasis, the entire area is infiltrated with local anesthesia (e.g., 0.25% Marcaine) for postoperation analgesia. • Continuous, 2/0 braided suture is utilized for fascia repair (Vicryl® Johnson & Johnson). • Skin is repaired with intradermal 4/0, resorbable, non-braided suture (Monocryl® Johnson & Johnson). • The wound is dressed with a semipermeable wound dressing (e.g., Tegaderm Post-­Op® 3M).

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Postoperative Care

• Some degree of postoperative pain is expected so patients are discharged with pain medications, nonsteroidal anti-inflammatory medications, and perioperative antibiotics when indicated. • Shower not earlier than 48 h post surgery. • Limited lifting to no more than 5 kg in the first 2 weeks. • Patients are allowed to resume normal activities 48h post surgery but are instructed to avoid strenuous physical and sport activities for 3 months. • Patient reports of pain resolution are varied. Most patients will report alleviation of pain within 3 months, but some will have varying degrees of pain up to 6 months. • Overall successes have been around 80% in long-term follow-up. For patients with persistent pain, a retroperitoneal approach may be considered for neurectomies.

Further Reading 1. Cesmebasi A, Yadav A, Gielecki J, Tubbs RS, Loukas M. Genitofemoral neuralgia: a review. Clin Anat. 2015;28(1):128–35. 2. Kerstman E, Ahn S, Battu S, Tariq S, Grabois M.  Neuropathic pain. Handb Clin Neurol. 2013;110:175–87. 3. Kingsnorth A, LeBlanc K. Hernias: inguinal and incisional. Lancet. 2003;362:1561–71. 4. Nagarkar P, Ramanadham S, Chamseddin K, Chhabra A, Rozen SM.  Neurectomy for the treatment of chronic postoperative pain after surgery of the trunk. Plast Reconstr Surg. 2017;139(1):204–11. 5. Watson JC, Dyck PJ. Peripheral neuropathy: a practical approach to diagnosis and symptom management. Mayo Clin Proc. 2015;90:940–51.

Diagnosis and Treatment of Central Neurogenic Wrist Pain Steven Rueda and Sonu A. Jain

1

Introduction

Innervation of the wrist joint is provided by a significant number of different nerves in the upper extremity. Amongst the nerves reported to have a role in innervation of the wrist joint in the present literature are the ones listed in Table 1. The original technique described by Wilhelm et al. required five incisions and extensive dissection to address all the ten nerves displayed in Table 1. This technique of total wrist denervation had good outcomes, with early reports of good to excellent pain relief rates between 69 and 84%. Subsequent publications from Dellon reported on results of partial wrist denervation, where the anterior interosseous nerve (AIN) and/or the posterior interosseous nerve (PIN) were solely targeted (Chap. 1, Fig. 10) to address central wrist pain. AIN and PIN are the main nerves responsible for the sensation of the volar and dorsal capsule of the wrist joint. Remarkably, pain control rates sometimes exceeded that accomplished by total wrist denervation with up to 90% of patients showing improvement with a much less invasive approach. This approach is not indicated in the presence of carpal instability and when mainly radial side (mainly due to

S. Rueda Department of Orthopaedic Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA Hand and Upper Extremity Center, The Ohio State University Wexner Medical Center, Columbus, OH, USA S. A. Jain (*) Hand and Upper Extremity Center, The Ohio State University Wexner Medical Center, Columbus, OH, USA Division of Hand Surgery, Department of Plastic and Reconstructive Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_7

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Table 1  Nerves of the wrist joint

Anterior interosseous nerve Posterior interosseous nerve Palmar cutaneous branch of median nerve Superficial radial sensory branches Dorsal ulnar sensory branches Median nerve volar branches Medial antebrachial cutaneous nerve Lateral antebrachial cutaneous nerve Posterior cutaneous nerve Ulnar nerve motor branches

carpometacarpal instability) or ulnar side (mainly attributable triangular fibrocartilage complex issues) joint pain is the main cause of wrist pain. In our experience, partial joint central denervation of the wrist is a very useful surgical technique with plenty of literature to support its use.

2 • • • •

3

Central Neurogenic Wrist Pain Characteristics Uncontrolled chronic, mainly central wrist joint pain. Patients have trouble sleeping due to pain during the night. Pain is at rest and during movement, not necessarily relieved by resting. Patients must have failed a prior trial of conservative treatment with splinting, steroid injection, and oral pain medication to be considered eligible for this procedure.

Etiology

• Most commonly originates from arthritis (age-related or posttraumatic). • Pain following wrist sprain or distal radius fractures (possible traction injury or neuroma of the nerves). • Pain following surgery (possible compression or injury directly to the nerves), typically fixation of distal radius fractures. • Carpal instability as partial origin of pain should be excluded: partial wrist denervation is a procedure primarily offered to patients suffering from uncontrolled joint pain in the absence of carpal instability.

4

Diagnosis

• Pain without radiologic proof of bone malalignment, ligament injury, non-healed fractures, infections. • Exclusion of carpal instability. • Selective nerve blocks with or without ultrasound guidance are indicated to assess the response of the patient’s symptoms before undergoing surgery. Sequential blocks (e.g., first the PIN and then the AIN) may lead to a more selective (only PIN or AIN) and less invasive surgery.

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• Some ideal candidates for these procedures are as follows: –– Patients who cannot afford long postoperative recovery. –– Patients who cannot be immobilized for prolonged periods. –– Patients who oppose to any internal hardware or prosthetics. –– Patients who are not ready to decide about definitive salvage.

5

Surgical Technique

• Regional or local anesthesia, patient supine, hand positioned on a hand table. • Tourniquet inflated at 250 mmHg, when regional anesthesia is used, otherwise no tourniquet. • A single, longitudinal, 3-4-cm midline dorsal incision line is drawn 2 cm from the distal radioulnar joint proximally (Fig. 1a). • Infiltration of 5 cc lidocaine with 1:100,000 epinephrine along the incision line. • Subcutaneous blunt dissection is done with Littler/Stevens scissors preserving any superficial nerves and veins until the deep fascia is identified (Fig. 1b). • The extensor retinaculum is exposed (Fig. 2a). • Bipolar cautery is used to coagulate any perforating vessels. • A step-cut incision is designed on the retinaculum to facilitate later repair (Fig. 2b). a

b

Fig. 1 (a) A single, longitudinal, 3–4 cm midline dorsal incision line is drawn 2 cm from the radiocarpal joint. (b) Subcutaneous blunt dissection is done with Littler scissors preserving any superficial nerves and veins until the deep fascia is identified

a

b

Fig. 2 (a) The extensor retinaculum is exposed. (b) A step-cut incision is designed on the retinaculum to facilitate later repair (image from cadaver dissection)

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• The tendons of the fourth compartment are visualized after elevation of the retinaculum (Fig. 3a). • The tendons of the fourth compartment are retracted with the help of a self-­ retainer to expose the (PIN) and interosseous membrane (Fig. 3b). • The PIN is showered with a solution of local anesthesia (e.g., 0.25% bupivacaine and 1% lidocaine with epinephrine) (Fig. 4a). a

b

Fig. 3 (a) The tendons of the fourth compartment are identified and visualized after elevation of the retinaculum (image from cadaver dissection). (b) The tendons are retracted with the help of a self-retainer to expose the posterior interosseous nerve (retracted by a red loop)

a

b

c

Fig. 4 (a) The exposed posterior interosseous nerve is showered with a solution of local anesthesia. (b) A segment of PIN is resected by micro-scissors and bipolar cauterization. (c) The proximal end of the nerve is buried deep into muscle tissue

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• A segment of PIN is removed via bipolar cauterization (Fig. 4b) and the proximal end of the nerve is buried deep into muscle tissue (Fig. 4c). • A 25-gauge needle is then used to identify the proximal most aspect of the distal radioulnar joint. A mini-C-arm can be used to confirm adequate localization of the needle placement. • A window of interosseous membrane is excised extending to a point 2 cm proximal to the distal radioulnar joint. This marks the most proximal possible point of fullthickness interosseous membrane resection to ensure resection of AIN sensory branches and prevent iatrogenic injury to the motor branches to pronator quadratus. • When the full-thickness membrane is resected between the distal radioulnar joint and the point 2 cm proximal to it, the sensory branches of the AIN are visualized just deep to the resected interosseous membrane (Fig. 5). • A segment of AIN is resected by micro-scissors and bipolar cauterization paying attention not to lesion any motor branches to the pronator quadratus. • The proximal end of the nerve is buried deep into proximal muscle tissue. • The extensor retinaculum is approximated in a lengthened position by 4–0 or 5–0 braided absorbable sutures (Fig. 6, Vicryl® Johnson & Johnson). Fig. 5  After opening a window in the interosseous membrane the anterior interosseous nerve is exposed (AIN, *). Sensory branches only are present in its most distal part (pointed by the pincets, image from cadaver dissection)

Fig. 6  Final repair of the extensor retinaculum (image from cadaver dissection)

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• Skin is repaired with intradermal 4/0, resorbable, non-braided suture (Monocryl® Johnson & Johnson). • The wound is dressed with a semipermeable wound dressing (i.e., Tegaderm Post-­Op® 3M).

6

Postoperative Care

• Postoperative pain is limited and can be kept under control with a few days of oral pain and nonsteroidal anti-inflammatory medications. • No postoperative immobilization is required, but some limited movement will allow for better wound healing and decrease the chances of neuroma formation. • Free mobilization is allowed after 10 days. • Wrist pain relief is usually immediate and durable.

Further Reading 1. Dellon AL. Partial dorsal wrist denervation: resection of the distal posterior interosseous nerve. J Hand Surg Am. 1985 Jul;10(4):527–33. 2. Dellon AL.  Partial joint denervation I: wrist, shoulder, and elbow. Plast Reconstr Surg. 2009;123(1):197–207. 3. Ishida O, Tsai TM, Atasoy E. Long term results of denervation of the wrist joint for chronic wrist pain. J Hand Surg Br. 1993;18(1):76–80. 4. Weinstein LP, Berger RA. Analgesic benefit, functional outcome, and patient satisfaction after partial wrist denervation. J Hand Surg Am. 2002;27(5):833–9. 5. Wilhelm A. Articular denervation and its anatomical foundation: A new therapeutic principle in hand surgery. On the treatment of the later stages of lunatomalacia and navicular pseudarthrosis (in German). Hefte Unfallheikd. 1966;86:1–109.

Nutritional Recommendations to Address Pain: Focus on Ketogenic/ Low-Carbohydrate Diet Susan A. Masino and David N. Ruskin

1

 eneral Nutritional Guidelines to Provide G to the Patients

Diets very low in carbohydrates, high in healthy fat, and moderate in protein content are termed “ketogenic” and represent an established metabolic therapy developed over 100 years ago for refractory epilepsy. The limited availability of carbohydrates and sugars forces metabolism to shift from being primarily glucose-dependent to primarily ketone body-dependent, mimicking the metabolic state of fasting. Ketone bodies (β-hydroxybutyrate, acetoacetate, and acetone) derive from breakdown of fatty acids in the liver and can be used in place of glucose as a cellular energy source extrahepatically including in nervous tissue and brain. The ketogenic diet is well established as a treatment for weight loss in obese patients prior to surgery. The role of ketogenic/low-carbohydrate diets on pain and inflammation is emerging in literature, with an increasing amount of evidence supporting the benefits in conditions such as chronic migraine, neuropathic pain, inflammatory bowel syndrome, Parkinson’s disease, and rheumatoid arthritis. Such outcomes align with basic laboratory research showing reduced nociception and inflammation. We suggest implementing ketogenic/low-carbohydrate diets in the perioperative period, particularly in situations when pain exists presurgery and/or is expected for a significant time postsurgery. Table 1 outlines foods to eat freely, eat moderately, and avoid to promote ketogenesis. A useful, simple worksheet developed by the Charlie Foundation (www.charliefoundation.org) and endorsed by the Epilepsy S. A. Masino (*) Psychology Department and Neuroscience Program, Trinity College, Hartford, CT, USA Life Sciences Center, Trinity College, Hartford, CT, USA e-mail: [email protected] D. N. Ruskin Psychology Department and Neuroscience Program, Trinity College, Hartford, CT, USA e-mail: [email protected] © Springer Nature Switzerland AG 2020 G. Pietramaggiori, S. Scherer (eds.), Minimally Invasive Surgery for Chronic Pain Management, https://doi.org/10.1007/978-3-030-50188-4_8

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Table 1  Recommended foods and foods to avoid. Where possible, wild caught fish and grass-fed animal products are preferred Eat freely Meat/poultry Eggs Fish

Eat moderately Legumes Non-green vegetables Low-sugar fruits (e.g., berries)

Cream Cheeses Nuts Greens Non-starchy vegetables Avocados Butter, oils (olive, avocado, MCT, coconut)

Avoid Bread/pasta/rice Processed/fried foods Dried fruits Sugary fruits (e.g., watermelon) Potatoes, including French fries Muffins/pastries/cookies Cake/pie/donuts Soda pop (incl. diet)/fruit juice Sugar/honey/syrup Margarine, vegetable oil

Foundation ­(www.epilepsy.com) is titled “Does What I Eat Affect My Epilepsy” and contains some basic explanation and guidance to the beginners through food choices for promoting ketogenesis. Coffee and tea can be consumed freely. No sugar is admitted, instead stevia and erythrol are used as sweeteners. General anesthesia needed for major surgeries is compatible with continuing ketogenic diet treatment, with little to no interference of ketosis with anesthesia. Patients with diabetes require very careful monitoring and should be stabilized on a low-­carbohydrate diet prior to surgery. In any patient following a ketogenic diet, ketosis is maintained during anesthesia and surgery by avoiding dextrose/glucose-based i.v. solutions and other carbohydrate-containing products. We recommend continuing non-glucose/dextrose-based intravenous solutions such as lactated Ringers postsurgery if needed. Ideally, the patient will adhere to a nutritional modification for at least 4 weeks pre- and postsurgery. As research progresses and we understand more deeply the impact of nutrition on health, a low-carbohydrate diet before and after surgery can help alleviate postoperative pain. Effective and nonaddictive treatments with few side effects as an adjunct to treat chronic/refractory pain are needed desperately. The ketogenic/low-carbohydrate nutritional approach can be implemented immediately, and an increasing amount of evidence is supporting its benefits.

2

MCT Oil and Intermittent Fasting

MCT (medium-chain triglycerides) oil is a safe and effective way to increase ketones in the blood and experience mild ketosis without adhering to a strict ketogenic diet. Doses up to 15 g twice a day (one tablespoon) are considered adequate

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to achieve this goal. Patients should start with smaller doses and increase to a full tablespoon as tolerated. In addition to promoting ketosis, MCT oil acts as a ideal energy substrate for the nervous sistem (instead of glucose), decreases hunger and promotes weight (fat) loss. Side effects include gastrointestinal discomfort at higher doses. The combination of MCT oil with several hours of fasting (for example, 16–18 h of fasting and 6–8 h with food) promotes ketosis regardless of the diet a patient is following during the eating window and represents a simpler way to benefit from ketogenesis.

Further Reading 1. Di Lorenzo C, Coppola G, Sirianni G, et al. Migraine improvement during short lasting ketogenesis: a proof-of-concept study. Eur J Neurol. 2015;22:170–7. 2. Freeman JM, Vining EP, Pillas DJ, et al. The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998;102:1358–63. 3. de los Santos-Arteaga M, Sierra-Domínguez SA, Fontanella GH, et al. Analgesia induced by dietary restriction is mediated by the κ-opioid system. J. Neurosci. 2003;23:11120–6. 4. Masino SA, Ruskin DN. Ketogenic diets and pain. J Child Neurol. 2013;28:993–1001. 5. Melchior RW, Dreher M, Ramsey E, et al. Cardiopulmonary bypass considerations for pediatric patients on the ketogenic diet. Perfusion. 2015;30:423–6.