Nerve Decompression Surgery

Allen L. Van Beek, Jason D. Fowler, and Holly S. Ryan

Many complications of upper extremity nerve decompressions initially present to the office as a patient inquiry about persistent or worsening paresthesias despite surgical decompression. In the early postoperative period, and with the absence of obvious infection, the most common provider response is undoubtedly that it should continue to improve with time. Unfortunately, there are complications that must be recognized for which interventions other than tincture of time are indicated to achieve the most optimal, long-term patient outcomes.

There are many journal reviews related to the incidence, complications, and subsequent management of nerve compression syndromes; however, the actual incidence of complications is not as clear.1–5 Overall, reported incidence of nerve compression syndromes can be quite high. Carpal tunnel, for example, is reported to have a lifetime prevalence of 3 to 6%, making it the most common upper limb neuropathy and accounting for more than $500 million dollars of health care–related costs in the United States.^1,6,7 Complications after carpal tunnel release are reported as 1 to 25%, with reoperation rates as high as 12%.⁸ Reported complications with cubital tunnel are similar, with reported complication rates of 3 to 20%.^2,9 Additional nerve compression syndromes such as pronator syndrome, anterior interosseous nerve syndrome, posterior interosseous nerve syndrome, and Wartenburg’s syndrome (superficial radial neuritis) have much less published data for analysis of complication rates and subsequent reoperation rates. Overall the incidence of both nerve decompressions and complications is difficult to define, with wide reported ranges. This results in a potentially large number of compilations that must be accurately diagnosed and treated accordingly.

Carpal tunnel release is worth noting specifically given its high reported incidence. With such a common presentation, it is no surprise that it is one of the most common outpatient, elective surgical procedures, with more than 500,000 surgeries performed in the United States each year.¹⁰ The procedure is often considered easy to perform; therefore many different surgical specialties perform it. The various methods for carpal tunnel release have been well described in the published literature, and complications associated specifically with median nerve decompression do not seem to be related to specific surgical approaches in most cases.¹¹ However, complications of carpal tunnel release are reported to be as high as 25%.⁸ It is these complications that leave both the patient and surgeon with significant frustration.

When things don’t go well after nerve decompression, a wrong diagnosis, an inappropriate operation, patient compliance, and unexpected events all become part of one’s thought process. This chapter focuses specifically on complications and deviations from the expected recovery course after upper extremity nerve decompression.

Avoiding Unfavorable Results and Complications in Nerve Decompression Surgery

Preoperative Planning and Assessment

Thorough and accurate preoperative assessment of any neuropathy is essential in determining the presence of nerve compression, the potential surgical indication, and the appropriate procedure. It is important not only to examine the entire length of nerves on patients with neuropathy but also to document clinical examination findings at the time of evaluation (Fig. 67.1). Later comparison and evaluation may be required in the event of either a complication or a slower than expected recovery. The most common compression neuropathy symptoms are numbness, tingling, dropping objects, positional triggering of symptoms, and waking at night with numbness. Findings on examination are Tinel’s sign, neuropathic pain, decreased sensibility, muscle wasting, positive provocative tests with pressure, or fulcrum stress.3,12 Ancillary testing such as nerve conduction, neurophysiological, and imaging studies and ultrasound can be useful when the diagnosis is complex or indeterminant. There is little consensus on the “gold standard” for upper extremity compression neuropathy, and many patients receive operations based on their history and clinical assessment. It is accepted that electrophysiology can provide additional support for a diagnosis, and in some insurance plans it is required before surgery is approved. Electrophysiological studies are especially helpful if complications arise after surgery.¹³ How ever, electrophysiology should also be considered when evaluating atypical presentations, “difficult patients,” and circumstances in which workers compensation or litigation are factors. Ultimately, when the patient is not progressing, the surgeon needs to delineate whether persistent or recurrent compression or other possible surgical complications, such as nerve laceration, injury to surrounding structures, or inaccurate original diagnosis, may have occurred. When the patient is unhappy and the outcome not as expected, the surgeon will be pleased to have accurately documented findings before surgery and had patient discussion regarding surgery and its potential complications.

Summary Box

Complications of Nerve Decompression Surgery

• Injury to the palmar cutaneous branch of the median nerve

• Injury to the recurrent motor branch of the median nerve

• Injury to the medial antebrachial cutaneous nerve

• Median nerve laceration

• Ulnar nerve kinking

• Ulnar motor branch injury during median nerve decompression

• Incomplete median nerve release

• Synchronous pronator or anterior interosseous nerve syndrome (AINS)

• Posterior interosseous nerve compression

• Unexpected and unsuspected diagnoses

When physical examination and electrophysiological studies remain unclear regarding the site of compression or specific diagnosis, imaging should be considered. Narrowing, swelling, radiological signs of inflammation, and even nerve transection documented by imaging provide valuable information to the surgeon concerning preoperative diagnosis and postoperative complications. The advent of high-resolution ultrasound and magnetic resonance imaging (MRI) allow for more specific and reliable anatomical evaluation of nerves. Recent advances in ultrasound have added another evaluation tool for carpal tunnel syndrome (CTS) by evaluating the cross-sectional area of the median nerve through the carpal tunnel. Ultrasound imaging may provide additional benefit by identifying structural anomalies within the tunnel.¹⁴ Also described are using ultrasound-guided carpal tunnel releases and ulnar nerve releases as a potential method to reduce intraoperative nerve injury when using short-scar techniques.^15–17 Additionally, some authors report that cubital tunnel syndrome can present with normal electromyography (EMG) and that ultrasound or MRI can aid in diagnosis if the clinical examination is not convincing.¹⁸ Overall, imaging is not necessary or the standard of care in the treatment of upper extremity nerve compression syndromes, but it can be a valuable tool in the presence of a broad differential diagnosis.

Fig. 67.1 It is essential the entire peripheral nerve be examined, starting at the spinal cord and continuing the examination distally for both motor and sensibility functions.

Persistent Nerve Compression

The rate of incomplete release is approximated at 9 to 23% for carpal tunnel,19–21 namely related to incomplete release of the distal flexor retinaculum. Incomplete cubital tunnel release resulting in revision has been reported, but there is limited data describing the incidence.²² Incomplete release for other upper extremity compression neuropathies is not well described. In our experience, accurate diagnosis and careful thorough decompression has not resulted in persistence or early recurrence.

After release of a compressed nerve, if symptoms recur in the early postoperative period, persist, or become worse, incomplete nerve release and persistent compression should be strongly considered. Care should be taken to fully evaluate the patient for other causes of continued nerve symptoms despite release. If the likely cause of symptoms remains persistent compression rather than other sources, open decompression should be performed, and adjunctive procedures will probably be necessary. When reexploring a nerve that has had an injury, previous surgery adjacent to the nerve, or previous decompression, the surgeon must identify the nerve distal and proximal to the zone of previous surgery before exploring the area of concern. The surgeon should follow the nerve into the zone of injury from proximal and distal healthy nerve to assess, release, and resolve the nerve problem as appropriate. Directly approaching the nerve in the zone of previous surgery is likely to produce an injury to the nerve because of adjacent and adherent scar formation further complicating patient outcome and treatment. Once completely released, adjuvant procedures such as local vascularized pedicle fat flaps, venous tube wraps, collagen, or acellular dermal matrix wraps or transposition to a new position would be recommended.

Recurrent Nerve Compression

The term recurrent compression syndrome is usually reserved for individuals who have had nerve decompression surgery with symptomatic relief or significant improvement lasting for a period of months or years. In our experience, late recurrence is very rare and is most commonly observed in males with heavy repetitive work activities. After the symptom-free interval, progressive nerve compression clinical symptoms and worsening electrophysiological tests begin to occur. Patients presenting with these symptoms should have a thorough repeat evaluation from nerve root to end organs. The question then becomes whether this is a recurrence or an entirely new site of pathology. Clinical examination coupled with electrophysiology studies will help to further elucidate recurrent compression. Generally, when an entirely symptom-free period or dramatic improvement has occurred and the patient develops recurrent symptoms, it is appropriate to consider this as a recurrent compression.

If recurrence is documented and the symptom-free interval is over a period of years, repeat nerve decompression is recommended. As with persistent compression, care should be taken to avoid injuring the nerve by careful proximal and distal exposure before exploring the area of concern. Usually only a decompression would be necessary; however, adjuvant procedures can be used depending on the specific findings and surgeon judgment at the time of exploration and release (such as a vascularized pedicle fat flap).

Synchronous Pathology

The potential of antecedent synchronous pathology must be considered when evaluating a patient who is not improving. Although not a direct complication of surgical release, ideally the original evaluation would have discovered the synchronous pathology and considered additional treatment in conjunction with the original decompression surgery. When this is not the case, both the patient and physician can become frustrated with less-than-ideal outcomes after nerve decompression. Significant synchronous pathology that was undetected during preoperative assessment often leads to persistent symptoms after decompression.

Pathology more proximal in the nerve distribution caused by compression, spinal foramen narrowing, thoracic outlet syndrome, demyelinating diseases, and syringomyelia are all reported as sites of synchronous nerve compression or pathology.^23,24 As with other persistent nerve compression symptoms, imaging, nerve conduction velocity, EMG, and careful clinical examination can accurately determine nerve status. When evaluating a patient for perceived synchronous pathology as the cause for failure to improve, the surgeon should compare the new postoperative findings to those noted preoperatively. If synchronous pathology is a proximal or distal peripheral nerve compression, release at that compression site may improve symptoms if the nerve has not become irreversibly damaged.

Preoperative undetected neuropathic disease like diabetes, demyelinating disease, and infectious disease are potential synchronous pathologies that may complicate or limit recovery. As with additional sites of compression, detection of neuropathy before operative release is ideal, because this can direct patient expectations after nerve release. If preoperative nerve conduction studies are available, the surgeon will be able to assess more accurately the severity, site, and management of the neuropathy. Fibrillation potentials, positive sharp waves, and conduction times that are very slow all point to pathology that may not completely recover after nerve decompression.

Direct Nerve Injury

When not recognized or not reported during an operation, occult direct nerve injury can be an initially frustrating and later a feared complication in follow-up visits. Direct nerve injury can be a result of patient positioning, thermal injury, crush injury, traction injury, injecting with large-caliber needles, direct suture of nerve, or cutting the nerve. Careful and attentive positioning will help to prevent temporary compression-related neuropathies secondary to prolonged, focal pressure or nerve stretch. Thermal injury can be minimized with the use of bipolar cautery. Care should be taken to retract and handle nerves with care to avoid traction or crush injury, and “Rope” retractors should not be used around the nerve. Adequate exposure and the use of operative loupes are indicated to ensure adequate identification and visualization of the nerve being decompressed, especially when the surgical site is fibrotic. When closing incisions, the surgeon must be careful to prevent injury to the nerve with a suture needle (Fig. 67.2) or strangulation of the nerve by including all or a portion of the nerve in the wound closure.

The incidence of direct nerve injury is low for carpal tunnel release and is usually attributed to anatomical variations of the thenar motor branch of the median nerve.^4,25 Similarly, iatrogenic injury to the ulnar nerve during cubital tunnel release has a low incidence, probably because fewer classes of surgeons release this nerve. In my experience, excessively short scars provide poor visualization unless an endoscope is used. In addition, the scissor “sliding” technique required with very short scar approaches puts the nerve being decompressed, as well as proximal nerve branches, at risk for laceration. Use of ultrasound guidance may improve safety. Many types of injury that do not involve direct nerve injury will improve with time. If the nerve does not improve and the Tinel’s sign does not progress distally, electrophysiology and careful clinical assessment should be able to isolate the site of nerve injury. When irreversible nerve injury is suspected, such as severe thermal injuries, crush injuries, or partial or complete nerve laceration, exploration and repair is indicated. If nerve transection or neuroma is discovered, the decision for neurolysis, resection of neuroma with direct repair, or resection of neuroma with nerve graft all require significant surgical judgment, intraoperative electrophysiogical capability, and microsurgical skills. The intervention choice should be performed according to the surgeon’s discretion based on preoperative assessment reinforced with intraoperative findings.

Managing Unfavorable Results and Complications in Nerve Decompression Surgery

Complications Associated with Nerve Decompression

Injury to the Palmar Cutaneous Branch of the Median Nerve

The palmar cutaneous branch of the median nerve (PCBMN) originates from the median nerve 5 to 10 cm above the wrist crease and courses on the radial side of the palmaris longus tendon and third metacarpal shaft. An incision that is too radial to those landmarks risks injury to the PCBMN. The resulting hypothenar dysesthesia, combined with a hypersensitive neuroma, lead to a less-than-ideal outcome (Fig. 67.3).

Injury to the Recurrent Motor Branch of the Median Nerve

The recurrent motor branch of the median nerve (RBMN) is usually located distal to the transverse carpal ligament but may also be through the ligament. Always transecting the ligament adjacent to the hook of the hamate will prevent injury to the RBMN when it is anomalous in location (Fig. 67.4). Injury to the RBMN will lead to thenar muscle atrophy, loss of opposition, and weakness during key pinch functional activities.

Fig. 67.2 It is essential to use small-caliber needles when injecting medications around peripheral nerves. The yellow triangle accurately represents the size of a 27-gauge needle. It is superimposed over a digital nerve fascicle. The 27-gauge sharp needle could easily transect an entire fascicle. An even larger needle could transect a small branch nerve or digital nerve. When injecting around nerves, small-caliber and tapered needles are ideal. Ultrasound-guided injections are also important for avoiding nerve injury during medication injection and when performing axillary nerve blocks for surgical anesthesia.

Injury to the Medial Antebrachial Cutaneous Nerve

The most commonly reported complication of cubital tunnel release is medial antebrachial cutaneous nerve (MABC) injury, kinking, and fibrosis. The incidence is reported to be between 5 and 15%.26 Should a patient present with injury to the MABC after cubital tunnel release, secondary exploration can be difficult because of dense perineural fibrosis surrounding the nerve. Injury to the MABC might also be associated with ulnar kinking because of inadequate release of the aponeurosis of the flexor carpi ulnaris or failure to remove the medial intermuscular septum (Fig. 67.5). MABC and kinking seem to be closely associated when secondary surgery is necessary. In these cases, surgical exploration should proceed with careful exposure of the nerve proximal and distal to the injury site to prevent inadvertent injury to the nerve.