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Peripheral nerve injuries are common. Despite numerous advances in microsurgical technique and interfascicular nerve grafting, many treatment principles obtained from World War II experiences as set forth in the cumulative works of Seddon and Woodhall are still applicable today. Current research focusing on pharmacologic agents, immune system modulation, enhancing factors, and entubulation chambers, although promising, have had little clinical application so far, and the results of nerve repair remain modest with only 50% of patients regaining useful function.
In this chapter, the diagnosis and treatment of peripheral nerve injuries are described, with the details of surgical technique and postoperative care included in the discussion of each nerve. For details of embryology, microscopic anatomy, and physiology, the reader is referred to other works. The appropriate reconstructive operations are described in other sections of this book, and cross references are provided.
Each segmental spinal nerve is formed at or near its intervertebral foramen by the union of its dorsal, or sensory, root with its ventral, or motor, root. In most of the thoracic segments, these mixed spinal nerves retain their autonomy and supply one intercostal dermatomal and myotomal segment. In virtually all other segments of the spinal axis, the spinal nerves join with others to form a plexus that innervates a limb or a special body segment that no longer retains the primitive myomeric pattern. A total of 31 mixed spinal nerves leave their respective foramina on each side of the spine to innervate the homolateral trunk and extremities: eight cervical, 12 thoracic, five lumbar, five sacral, and one coccygeal.
A typical mixed spinal nerve has three distinct components: motor, sensory, and sympathetic ( Fig. 62.1 ).
Several rootlets leave the anterolateral sulcus of the spinal cord and unite to form each motor root. The fibers traversing these roots arise from the anterior horn cells and innervate the skeletal muscles.
The sensory fibers arise from pain, thermal, tactile, and stretch receptors. Cell bodies for these fibers are located within the dorsal root ganglia with axons entering the posterolateral sulcus of the cord via several rootlets. The fibers conveying joint or position sensibility and some tactile fibers turn cephalad in the dorsal columns and do not synapse before reaching the gracile and cuneate nuclei at the cervicomedullary junction. Pain and temperature fibers synapse in the substantia gelatinosa and cross to ascend in the dorsal spinothalamic tract. Tactile fibers enter, synapse, and cross to ascend in the ventral spinothalamic tract.
The sympathetic component of all 31 mixed spinal nerves leaves the spinal cord along only 14 motor roots. The cells of origin are in the intermediolateral cell column that extends throughout the thoracic and upper lumbar cord segments. The fibers exit from the cord with the 12 thoracic and first two lumbar motor roots, enter the respective mixed spinal nerve, and promptly emerge from it as white rami. The white rami pass anteriorly to the corresponding sympathetic ganglion. Synapse may occur within the ganglion with which the ramus is associated, and postganglionic fibers pass back to the mixed spinal nerve as a gray ramus. More often, however, the fibers entering the ganglion via the white rami pass for variable distances up or down the paravertebral chain to synapse at higher or lower levels. The postganglionic fibers pass along gray rami to cervical, lower lumbar, or sacrococcygeal mixed spinal nerves having no white rami. Sweat glands, blood vessels, and erector pili are innervated also in a segmental pattern.
Mixed spinal nerves, having left the intervertebral foramina, receive their sympathetic component and promptly branch into anterior and posterior primary rami. The posterior primary rami are directed posteriorly and supply the paraspinal musculature and the skin along the posterior aspect of the trunk, the neck, and the head. The upper three cervical posterior rami are larger than their corresponding anterior rami, supplying relatively large areas of the scalp posteriorly and the musculature around the craniocervical junction. With these exceptions, posterior primary rami are small, and the major part of each spinal nerve continues laterally in an anterior primary ramus to enter a plexus or to become an intercostal nerve.
Anterior primary rami of all the cervical, the first thoracic, and all the lumbosacral nerves join in the formation of plexuses. Alteration of the metameric pattern results from the migration of dermatomes and myotomes into the limb buds. The upper four cervical anterior rami form the cervical plexus, and the lower four cervical and first thoracic anterior rami form the brachial plexus. The first three and a part of the fourth lumbar anterior rami form the lumbar plexus. The sacral anterior rami along with the fifth lumbar and a part of the fourth join to form the lumbosacral plexus. The enlargement and prolongation of the limb bud markedly alter the myotomal pattern, resulting in the union of some myotomes and the division or partial extended migration of others. The fibers of any one mixed spinal nerve may be distributed through several peripheral nerves. By the same token, any one peripheral nerve may contain fibers from several spinal nerves.
The area of skin supplied by the fibers of a single spinal root is called a dermatome. Segmental dermatomal patterns ( Fig. 62.2 ) are well preserved in the thoracic region but not in the limbs. Migration of the limb buds accounts for the displacement of midcervical dermatomes along the lateral aspect of the arm and radial aspect of the forearm and of the lower cervical and upper thoracic dermatomes along the medial aspect of the arm and the ulnar aspect of the forearm. Lumbar and sacral dermatomal alignment along the various aspects of the lower extremity is similarly explained. The line separating the more rostral segmental dermatomes from the more caudal ones is called the axial line and may be followed into the spinal axis.
Each nerve fiber, or axon, is a direct extension of a dorsal root ganglion cell (sensory), an anterior horn cell (motor), or a postganglionic sympathetic nerve cell, and it is either myelinated or unmyelinated. Sensory and motor nerves contain unmyelinated and myelinated fibers in a ratio of 4:1 ( Fig. 62.3 ). In the unmyelinated or sparsely myelinated fibers, several axons are wrapped by a single Schwann cell. In the more heavily myelinated fibers, the Schwann cell by rotation forms a multilaminated structure that encloses a myelin sheath around a single axon. The segment of myelinated nerve fiber enclosed by a single Schwann cell is referred to as an internode and varies in length from 0.1 to 1.8 mm, with the more heavily myelinated fibers having the longer internodes. The point at which one Schwann cell ends and the next begins is relatively sparse in myelin and is called the nodal gap, or node of Ranvier ( Fig. 62.4 ). The axon with its Schwann cell and myelin sheath is surrounded by a veil of delicate fibrous tissue called the endoneurium. Seen longitudinally, the endoneurium forms a tube encircling individually the Schwann cell sheaths that cluster together to form a fascicle (or funicle as termed by Sunderland). Each fascicle or separate group of sheathed axons is surrounded by a denser layer of perineurium. The entire group of fascicles with their surrounding perineurium is encased as a mixed spinal or peripheral nerve in a denser epineurium. The blood supply to the peripheral nerve enters through the mesoneurium, which is loose connective tissue extending from the epineurium to the surrounding tissues. There is an extrinsic (segmental) and an intrinsic (longitudinal) blood supply to each nerve. The intrinsic blood supply that runs longitudinally within the epineurium, perineurium, and endoneurium is fairly extensive and allows surgical mobilization without complete devascularization over variable lengths of nerves.
The internal topography or fascicular arrangement of the radial, median, and ulnar nerves was described by Sunderland in 1945 as a complex network of branching and intermingling fascicles that constantly change throughout the course of the nerve ( Fig. 62.5 ). Studies have shown that although the fascicular arrangement is complex in the proximal aspect of a peripheral nerve, the distal fascicles can be dissected over long distances before merging occurs ( Fig. 62.6 ). This characteristic is important to the surgeon when intraneural dissection is required for accurate neurorrhaphy.
Any part of a neuron detached from its nucleus degenerates and is destroyed by phagocytosis. This process of degeneration distal to a point of injury is called secondary, or Wallerian degeneration ( Fig. 62.7 ). The reaction proximal to the point of detachment is called primary, traumatic, or retrograde degeneration. The time required for degeneration varies between sensory and motor segments and is related to the size and myelinization of the fiber.
During the first 3 days after injury, definite morphologic changes become apparent in the axon. Response to faradic stimulation can be obtained for periods of 18 to 72 hours. After 2 or 3 days, the distal segment becomes fragmented, and with subsequent fluid loss the fragments begin to shrink and to assume a more oval or globular appearance. A concomitant fragmentation and shrinkage of the myelin sheath parallels the axonal degenerative change. By day 7, macrophages have reached the area in greater numbers, and clearing of the axonal debris is virtually complete after 15 to 30 days. Schwann cell division by mitosis is evident by day 7, the cells increasing in number to fill the area previously filled by the axon and myelin sheath.
The primary retrograde degeneration proceeds for at least an internode or more, depending on the degree of proximal insult, and it is histologically identical to Wallerian degeneration. The changes in the parent cell body vary to some degree with the type of cell and the nearness of the injury to the cell body. The more proximal the site of injury, the more pronounced the changes. Chromatolysis with swelling of the cytoplasm and eccentric placement of the nucleus is commonly evident. This reaction within the cell body is evident by day 7, and death or evidence of beginning recovery is apparent after 4 to 6 weeks. With recovery, the edema begins to subside, the nucleus migrates toward the center of the cell, and Nissl substance begins to reaccumulate.
Distal to the point of injury or to the proximal extent of retrograde degeneration there is an endoneurial tube filled with Schwann cells to accept regenerating sprouts from the axonal stump. Axonal sprouting may occur within the first 24 hours after injury. All axonal sprouts initially are unmyelinated whether they arise from a myelinated or an unmyelinated fiber. If the endoneurial tube with its contained Schwann cells has been uninterrupted by the injury, the sprouts may pass readily along their former courses, and after regeneration the surviving cells innervate their previous end organs. If the injury has been severe enough to interrupt the endoneurial tube with its contained Schwann cells, however, sprouts that may number 100 from any one axonal stump may migrate aimlessly throughout the damaged area into the epineurial, perineurial, or adjacent regions to form a stump neuroma or neuroma in continuity. Other migrating axonal sprouts barred from their endoneurial tube by scar tissue might enter empty endoneurial tubes of other injured funiculi or, as shown by Cabaud et al., may regenerate through newly formed endoneurial tubes only to terminate in myotomal or dermatomal areas other than their own. Axons regenerate as if they are influenced by certain neurotrophic substances contained within distal nerve tissue. Experimental work showed that in a primate model and through an inert silicone Y chamber, axons grow toward nerve tissue in preference to muscle or tendon. Some degree of end-organ specificity also exists in the experimental model, and there is a critical gap (2 mm) under which this neurotrophic effect does not exist.
Lesser injuries without disruption of the endoneurial and Schwann cell sheaths are associated with excellent or acceptable anatomic regeneration. Conversely, more extensive injuries with complete disruption of the entire nerve, with wide separation of the ends of the nerve, and with the regenerating fibers obstructed by extensive scar tissue result in little or no return of function.
The classification of nerve injuries proposed by Seddon in 1943 was generally accepted but rarely used. He divided nerve injuries into three groups:
Neurapraxia, designating minor contusion or compression of a peripheral nerve with preservation of the axis-cylinder but with possibly minor edema or breakdown of a localized segment of myelin sheath. Transmission of impulses is physiologically interrupted for a time, but recovery is complete in a few days or weeks.
Axonotmesis, designating more significant injury with breakdown of the axon and distal Wallerian degeneration but with preservation of the Schwann cell and endoneurial tubes. Spontaneous regeneration with good functional recovery can be expected.
Neurotmesis, designating a more severe injury with complete anatomic severance of the nerve or extensive avulsing or crushing injury. The axon and the Schwann cell and endoneurial tubes are completely disrupted. The perineurium and epineurium also are disrupted to varying degrees. Segments of the latter two may bridge the gap if complete severance is not apparent. In this group, significant spontaneous recovery cannot be expected.
A more useful classification was described by Sunderland in 1951. This classification is more readily applicable clinically, with each degree of injury suggesting a greater anatomic disruption with its correspondingly altered prognosis. In this classification, peripheral nerve injuries are arranged in ascending order of severity from the first to the fifth degree. Anatomically, the various degrees represent injury to (1) myelin, (2) axon, (3) the endoneurial tube and its contents, (4) perineurium, and (5) the entire nerve trunk ( Table 62.1 ).
Degree of Injury | Histopathologic Changes | Tinel Sign | ||||||
---|---|---|---|---|---|---|---|---|
Sunderland | Seddon | Myelin | Axon | Endoneurium | Perineurium | Epineurium | Present | Progresses Distally |
I | Neurapraxia | ± | − | − | − | |||
II | Axonotmesis | + | + | − | + | + | ||
III | + | + | + | + | + | |||
IV | + | + | + | + | + | − | ||
V | Neurotmesis | + | + | + | + | + | + | − |
In first-degree injury, conduction along the axon is physiologically interrupted at the site of injury but the axon is not disrupted. No Wallerian degeneration occurs, and recovery is spontaneous and usually complete within a few days or weeks. This injury coincides with the neurapraxia of Seddon. The loss of function varies. Usually, motor function is more profoundly affected than sensory function. Sensory modalities are affected in order of decreasing frequency as follows: proprioception, touch, temperature, and pain. Sympathetic fibers are the most resistant to this type of injury. If sensory modalities are markedly affected, paresthesias may be present for several days. If they are disturbed at all, sympathetic function often returns promptly; the modalities of pain and temperature also are commonly preserved or return promptly. Proprioception and motor function usually are the last to return. Electrical excitability of the nerve distal to the site of injury is preserved. A characteristic of this injury is the simultaneous return of motor function in the proximal and distal musculature; this would never occur in injuries with Wallerian degeneration in which the “motor march” is evident because of progressive regeneration or reinnervation of the more proximal motor units earlier in the course of recovery. Because there is neither axonal damage nor regeneration, no advancing Tinel sign is present. In most instances, the final result is complete restoration of function.
In second-degree injury, disruption of the axon is evident, with Wallerian degeneration distal to the point of injury and degeneration proximal for one or more nodal segments. The integrity of the endoneurial tube (Schwann cell basal lamina) is maintained, providing a perfect anatomic course for regeneration. Any permanent deficit is related to the number of neural somas that die, such death being more common in injuries at the more proximal levels. Clinically, the neurologic deficit is complete with loss of motor, sensory, and sympathetic function. Motor reinnervation is accomplished in a progressive manner from proximal to distal in the order in which nerve branches leave the parent trunk. Commonly, an advancing Tinel sign can be followed along the course of the nerve usually at the rate of 1 inch per month, tracing the progression of regeneration. Usually, good functional return is achieved.
In third-degree injury, the axons and endoneurial tubes are disrupted but the perineurium is preserved. The result is disorganization resulting from disruption of the endoneurial tubes. Scar tissue within the endoneurium can obstruct certain tubes and divert sprouts to paths other than their own. Clinically, the neurologic loss is complete in most instances, and because of the additional time required for the regenerating axon tips to penetrate the fibrous barrier, the duration of loss is more prolonged than in second-degree injury. Returning motor function is evident from proximal to distal but with varying degrees of permanent motor or sensory deficit. As in a second-degree injury, an advancing Tinel sign usually is present; however, complete return of neural function does not occur, distinguishing this from a second-degree injury.
In fourth-degree injury, the axon and endoneurium are disrupted but some of the epineurium and possibly some of the perineurium are preserved, so complete severance of the entire trunk does not occur. Retrograde degeneration is more severe after this degree of injury, and the mortality among neuronal soma is higher, sometimes resulting in a significant reduction in the number of surviving axons. Essentially, nerve continuity is maintained only by scar tissue, preventing proximal axons from entering the distal endoneurial tubes. Axonal sprouts exit through defects in the perineurium and epineurium and wander about in the surrounding tissues. There is no advancing Tinel sign. Prognosis for significant return of useful function is uniformly poor without surgery.
In fifth-degree injury, the nerve is completely transected, resulting in a variable distance between the neural stumps. These injuries occur only in open wounds and usually are identified at the time of early surgical exploration. The likelihood of any significant bridging by axonal sprouts is remote, and the possibility of any significant return of function without appropriate surgery is equally remote.
Sixth-degree (Mackinnon) or mixed injuries occur in which a nerve trunk is partially severed, and the remaining part of the trunk sustains fourth-degree, third-degree, second-degree, or rarely even first-degree injury. A neuroma in continuity is present, and the recovery pattern is mixed depending on the degree of injury to each portion of the nerve. Surgical intervention to correct the fourth-degree and fifth-degree components may sacrifice the function of lesser injured fascicles.
When a peripheral nerve is severed at a given level, all motor function of the nerve distal to that level is abolished. All muscles supplied by branches of the nerve distal to that level are paralyzed and become atonic. Significant changes on electromyography (EMG) are not apparent for 8 to 14 days, at which time transient fibrillation potentials on needle insertion may become apparent. Spontaneous fibrillations may become evident after 2 to 4 weeks, coinciding with the onset of atrophic change within the muscle fibers. Atrophy of muscle bulk progresses rapidly to 50% to 70% at the end of about 2 months. Atrophy continues at a much slower rate, and the connective tissue component of the muscles increases. Striations and motor endplate configurations are retained for longer than 12 months, whereas the empty endoneurial tubes shrink to about one third their normal diameter. Complete disruption and replacement of muscle fibers may not become complete until after 3 years.
Several methods are used to evaluate motor return after peripheral nerve injuries. They involve assessment of muscle strength against gravity and against graded resistance. The use of pinch meters and grip meters and evaluation of endurance, speed of movement, and individual muscle function helps to document the progress of motor return. The British Medical Research Council established the following system for assessing the return of muscle function after peripheral nerve injuries: M0, no contraction has returned; M1, perceptible contraction in proximal muscles has returned; M2, perceptible contraction in proximal and distal muscles has returned; M3, all important muscles act against resistance; M4, all synergistic and independent movements are possible; M5, recovery is complete ( Table 62.2 ).
Motor | Recovery |
---|---|
M0 | No contraction |
M1 | Return of perceptible contraction in proximal muscles |
M2 | Return of perceptible contraction in proximal and distal muscles |
M3 | Return of function in proximal and distal muscles of such a degree that all important muscles are sufficiently powerful to act against resistance |
M4 | Return of function as in stage 3; in addition, all synergistic and independent movements are possible. |
M5 | Complete recovery |
Sensory loss usually follows a definite anatomic pattern, although the factor of overlap from adjacent nerves may confuse inexperienced surgeons. After severance of a peripheral nerve, only a small area of complete sensory loss is found. This area is supplied exclusively by the severed nerve and is called the autonomous zone or isolated zone of supply for that nerve. A larger area of tactile and thermal anesthesia is readily delineated and corresponds more closely to the gross anatomic distribution of the nerve ( Fig. 62.8 ); this larger area is known as the intermediate zone. When a nerve is intact, and the adjacent nerves are blocked or sectioned, an area of sensibility exceeds the gross anatomic distribution of the nerve; this area is known as the maximal zone.
It has long been recognized that the autonomous zone becomes smaller during the first few days or weeks after injury, long before regeneration is possible. Livingston suggested that this is caused by ingrowth of adjacent nerves, but resumption of or increase in function in anastomotic branches from adjacent nerves is a more plausible explanation. This decrease in the area of sensory loss might be interpreted by an inexperienced surgeon as evidence of regeneration or of incomplete injury and might be responsible for needless delay in exploration of the nerve.
In injury to the median and ulnar nerves, one study found that pinprick was the first perception to return, followed by 30 cycles/s vibratory stimulus, and then moving touch. The perception of constant touch and the perception of a 256 cycles/s vibratory stimulus were the last to return ( Table 62.3 ). These investigators inferred that the early return of pain perception resulted from the faster regeneration of the small-diameter pain fibers. The larger-diameter touch fibers regenerated more slowly. The return of moving touch perception, mediated by quickly adapting fibers and Pacinian corpuscles, before the return of constant touch, mediated by slowly adapting fibers and the Merkel discs, was explained by differential maturation of the respective receptors, rather than by the diameter of the fibers alone. The system of evaluating by moving touch, constant touch, vibratory stimulus, pinprick, and the Weber two-point discrimination was proposed as a method for screening patients to determine specific exercises for reeducation of constant-touch perception. The evaluation of sensory return after peripheral nerve injuries is important regardless of the site of the injury. This is especially true in the upper extremity, where sensibility in the hand is extremely important.
I | Myelinated and unmyelinated fibers (restore perception of pain and temperature) |
Pseudomotor function | |
II | Touch perception |
Perception of 30 cycle per second (cps) of vibratory stimulus | |
Perception of moving touch | |
Perception of constant touch | |
Perception of 256 cps vibratory stimulus |
The clinical evaluation of sensory return also is done using other methods, such as pinprick appreciation and von Frey hairs. The British Medical Research Council established the following six-level grading scale for sensory return: S0, absence of sensibility in the autonomous area; S1, recovery of deep cutaneous pain within the autonomous area; S2, return of some superficial cutaneous pain and tactile sensibility within the autonomous area of the nerve; S3, return of superficial cutaneous pain and tactile sensibility throughout the autonomous area with disappearance of overreaction; S3+, some recovery of two-point discrimination within the autonomous area; S4, complete recovery ( Table 62.4 ).
Sensory | Recovery |
---|---|
S0 | Absence of sensibility in autonomous area |
S1 | Recovery of deep cutaneous pain sensibility within autonomous area of the nerve |
S2 | Return of some degree of superficial cutaneous pain and tactile sensibility within autonomous area of the nerve |
S3 | Return of superficial cutaneous pain and tactile sensibility throughout autonomous area, with disappearance of any previous overresponse |
S3+ | Return of sensibility as in stage 3; in addition, there is some recovery of two-point discrimination within autonomous area |
S4 | Complete recovery |
Two-point discrimination has been shown to directly correlate with return of hand function and object identification. The pick-up test (a timed test to measure fine and manual dexterity) and the triketohydrindene hydrate (ninhydrin) printing test also have been shown to be of use.
Complete severance of a peripheral nerve abolishes all reflex activity transmitted by that nerve. This is true in severance of the afferent or the efferent arc. Commonly, however, reflex activity is abolished in partial nerve injuries when neither arc is completely interrupted and is not a reliable guide to the severity of injury.
Interruption of a peripheral nerve is followed by loss of sweating and of pilomotor response and by vasomotor paralysis in the autonomous zone. The area of anhidrosis usually corresponds to, but may be slightly larger than, the sensory deficit. This area may be outlined easily by the starch-iodine test, by the ninhydrin printing test popularized by Aschan and Moberg, or by instruments for determining skin resistance (Richter dermometer). Another objective test described by O’Riain and by Leukens is the wrinkle test. When normal skin is immersed in water for a time, wrinkling occurs. Denervated skin does not wrinkle under these circumstances. As reinnervation occurs, wrinkling of the skin returns. If the injury is incomplete, and especially if it is associated with causalgia, sweating may be excessive and may involve areas beyond the intermediate zone of the nerve. Vasodilation occurs in complete lesions, and the area affected is at first warmer and pinker than the rest of the limb. After 2 to 3 weeks, however, the affected area becomes colder than the adjacent normal areas and the skin may be pale, cyanotic, or mottled in an area often extending beyond the maximal zone of the injured nerve. Trophic changes occur commonly and are most evident in the hands and feet. The skin becomes thin and glistening and, when subjected to trauma that ordinarily does little harm, breaks down to form ulcers that heal slowly. The fingernails become distorted, are often ridged or brittle, and may be lost entirely.
Osteoporosis often follows peripheral nerve injuries. It is more likely to be pronounced in incomplete lesions associated with pain. Incomplete lesions of the median nerve seem to be associated more often with osteoporosis, with changes occurring in the distal phalanges of the thumb and index and long fingers. Partial ankylosis from fibrosis of the periarticular structures also may develop. These changes are similar to atrophy of disuse but are much more severe.
Complex regional pain syndrome (CRPS) represents autonomic and pain transmission dysregulation, resulting in peripheral sensitization with allodynia, dysesthesia, hyperpathia, and a reduced tolerance for pain when using the affected area for basic function. The condition occurs most commonly after a traumatic injury or iatrogenic insult. Classification of CRPS is based on the structures injured. The International Association for the Study of Pain delineated two main categories of the syndrome, replacing traditional terms, and through efforts by their Taxonomy Committee ( iasp-pain.org ), they continue to update descriptions and terms. Although the attempt to simplify CRPS into types I and II is attractive, considerable overlap in pathology exists. CRPS I (formally reflex sympathetic dystrophy , RSD) theoretically represents patients who have had a musculoskeletal injury without a defined neural injury. CRPS II (causalgia) includes patients who fulfill the same criteria but who have evidence of a neural injury. In addition, there have been further efforts to define sympathetic-mediated and nonsympathetic-mediated varieties, with temporal transitions into “warm” and “cold” subtypes.
The most evident presentation in CRPS is avoidance behavior and an altered recovery pattern when the patient tries to use the area of the body that has been injured. CRPS may occur after a fracture, crush injury, routine surgical procedure, or a minor innocuous appearing injury. Chemical or electrical burns, metabolic neuropathies (e.g., diabetes mellitus), or infections, such as postherpetic neuralgia, all can contribute to this polymodal-mediated hyperpathia. A female predisposition has been noted, and upper extremity involvement is most frequently seen. CRPS also has been associated with smoking.
Early hallmark signs include a marked reduction in use or stimuli response of the affected area (e.g., an extremity) with sensitization and at times autonomic dysregulation. The condition may be self-limiting, but if not identified and treated aggressively, it can progress with a reduction in use and permanent impairment. Patients identified early (<6 months) have a better prognostic outcome than those with a delayed diagnosis (>1 year). This must be tempered, however, because a premature diagnosis in an impressionable patient who becomes invested in literature on the topic may actually lead to a self-fulfilling prophecy.
Harden et al. validated the Budapest criteria of CRPS to aid clinicians in identifying the signs and symptoms in four categories ( Table 62.5 ). Although defined as types I and II, CRPS frequently exhibits with both musculoskeletal and neural injuries. Clinicians must be alert to disproportionate postoperative or posttraumatic clinical responses, such as allodynia, dysesthesia, hyperpathia, hyperalgesia, and hypoesthesia. The patient’s exaggerated response to a relatively common injury may tempt the clinician to discount this as a psychologic issue. However, disproportionate symptoms can be caused by an interruption of a nerve pathway, which results in abnormal firing of nociceptive mediators and dysfunction in neuromodulation within internuncial, ascending, and descending pathways in the spinal cord. There are differences in opinion as to whether certain psychologic traits predispose patients to CRPS or whether the psychologic factors are a sequela of the injury. In addition, secondary gain issues also must be considered and dealt with because, whether intentional or not, they inadvertently affect recovery.
1 | Continued pain disproportionate to any inciting event |
2 | At least one symptom in three (clinical diagnostic criteria) or four (research diagnostic criteria) of the following:
|
3 | One sign at time of diagnosis in two or more categories:
|
4 | No other diagnosis better explains the signs and symptoms |
Sympathetically mediated cases may result in homeostatic dysregulation of the autonomic nervous system, which clinically presents as edema, vasomotor effects, sudomotor dysfunction, temperature change, and color change (warm subtype), frequently occurring in the early phase. The affected area may be erythematous, swollen, and warm to touch with hyperhidrosis. Suspected metabolic and inflammatory mediators further enhance the vicious circle with progressive peripheral, and at times, central sensitization. Visual, emotional, and tactile stimuli may trigger impressive and disconcerting pain behavior. Even focal well-defined neural injuries may result in symptoms that are nondermatomal and nonsclerotomal (maladaptive neuroplasticity) in presentation, challenging one to consider the possibility of additional, more central cortical reprogramming, which is certainly concerning. This can progress to later phases with further alienation of the area and loss of volitional motion and trophic changes.
The extremity may appear pale and cool to touch (cold subtype), with altered skin texture and hair distribution, reduced nail growth, abnormal posturing, contracture, and reduction in bone mass. Although described under the former taxonomy of RSD, Bonica’s description of sequential clinical stages still serves as a good reference for surgeons ( Table 62.6 ).
Stage | Onset | Symptoms | Duration |
---|---|---|---|
Stage 1 dysfunction | 1-3 months | Burning pain beyond dermatomes (follows thermatomes) Spasm and tendency for immobilization |
2-8 weeks |
Stage 2 dystrophy | 3-7 months | Vasoconstriction Unilateral cold extremity Hair loss Tendency for weakness, tremor, and spasticity (flexed arm, extended legs) |
2-4 months |
Stage 3 atrophy | >7 months | Smooth glossy edematous skin Pale or cyanotic skin Lymphedema Atrophy of distal muscles Spasm, dystonia, tremor |
>4 months |
Stage 4 | Several months to years | Loss of job and spouse in rare advanced severe cases Unnecessary surgery Orthostatic hypotension Hypertension Heart attack Neurodermatitis Angiectasis Depression, death caused by suicide |
A few months |
Although certain features of CRPS can be quantified, no laboratory or biochemical testing is diagnostic. Patients exhibiting sympathetic dysregulation may have alterations delineated through autonomic testing, quantitative sudomotor axonal reflex testing, thermography, and asymmetric temperature measurements. The clinician’s tactile temperature threshold difference may require upward of 5°F, although actual measurement is much more sensitive. Limb volume comparisons can be performed by submersion testing; however, such testing is frequently not readily available or practical. Reduced bone mass density may be suspected on standard radiographs with reduced bone density and periarticular reabsorption. The most sensitive radiographic study appears to be the triple phase bone scan. Changes seen on MRI have been described with noted muscle edema, interstitial edema, and hyperpermeability; however, it still is not very sensitive or specific.
Although validation studies of treatment modalities for CRPS are still lacking despite the many thousands of patients treated, there is agreement that the best results are obtained with early diagnosis and an active function-oriented program that is multidisciplinary. Validation of a patient’s symptoms is important, as is identification of possible secondary gain. Treatment strategies include pharmacologic, procedural, functional exercises, and psychologic evaluation. The treatment regimen is extremely time consuming and requires much patience and a coordination of efforts. Medication support generally includes antiinflammatory medication, analgesics (oral or topical), tricyclic antidepressants, calcitonin, bisphosphonates, selective serotonin reuptake inhibitors, anticonvulsants, and other antidepressants. The use of ketamine infusions in select patients has been proposed.
Interventional options include selective peripheral neural blocks/ablation techniques, trigger point injections, sympathetic blocks (single or indwelling), dorsal column stimulators, intrathecal infusions, and rarely sympathectomies (chemical or surgical). Descriptions of preventive anesthetic approaches for patients undergoing surgery have been limited. Favorable responses in pediatric patients with high-intensity physical therapy regimens alone have been reported. Therapy should be directed not only to all the joints of the involved extremity but also include more generalized movement patterns. Mirror-assisted movement patterns also may be incorporated. Some concern exists about overzealous therapy aggravating the condition; however, movement is paramount. For patients suspected of having sympathetic-mediated pain, a sympathetic blockade may be helpful for information and treatment. Kleinert et al. and Lankford reported favorable results with sequential stellate ganglion blocks combined with physical therapy in patients with CRPS involving the upper extremity. Pain relief and improved motion have been reported in 80% to 93% of patients with CRPS after sequential sympathetic blocks, although one study reported a 19% temporary response, and the patients required surgical sympathectomy. Poplawski, Wiley, and Murray reported 27 patients treated with intravenous regional blocks of lidocaine and corticosteroid followed by standard physical therapy. They found that the most important factor in predicting a favorable outcome was an interval between onset and treatment of less than 6 months.
Peripheral nerves can be injured by metabolic or collagen diseases; malignancies; endogenous or exogenous toxins; or thermal, chemical, or mechanical trauma. Only injuries caused by mechanical trauma are considered here. Every patient who has injured a limb or limb girdle should be evaluated for possible musculoskeletal, vascular, and peripheral nerve damage ( Table 62.7 ).
Extremity | Bone | Nerve | % |
---|---|---|---|
Upper, 74% | Humerus | Radial | 70 |
Median | 8 | ||
Ulnar | 22 | ||
Radius and/or ulna | Radial | 35 | |
Median | 24 | ||
Ulnar | 41 | ||
Lower, 20% | Femur | Complete sciatic | 60 |
Tibial component | 20 | ||
Peroneal component | 20 | ||
Tibia and/or fibula | Tibial | 7 | |
Peroneal | 70 | ||
Both nerves | 23 |
Gunshot wounds often are complicated by peripheral nerve injury. Spontaneous recovery is expected in over 50%. The expected time to recovery after gunshot wounds is 3 to 9 months, with high-velocity injuries taking longer than low-velocity injuries to heal. Neurapraxia and axonotmesis occur with equal frequency in gunshot wounds.
Bone or joint injury is often associated with peripheral nerve lesions. Primary injury of a peripheral nerve may result from the same trauma that injures a bone or joint; however, sometimes the neural injury is caused by displaced osseous fragments, by stretching, or by manipulation, rather than by the initial injuring force. Secondary injury results from involvement of the nerve by infection, scar, callus, or vascular complications. These complications include hematoma, arteriovenous fistula, ischemia, or aneurysm.
The radial nerve is most commonly injured. Of humeral shaft fractures, 14% are said to be complicated by injury of this nerve. Of radial nerve injuries, 33% are associated with fracture of the middle third of the humerus; 50%, with fracture of the distal third of the humerus; 7%, with supracondylar fracture of the humerus; and 7%, with dislocation of the radial head.
The ulnar nerve is injured in about 30% of patients with combined skeletal and neural injury involving the upper extremity. This injury is most commonly associated with fractures around the medial humeral epicondyle, but often it results from the formation of callus around the elbow.
The median nerve is injured in only about 15% of combined skeletal and neural injuries of the upper extremity. It is injured most commonly in dislocation of the elbow or secondarily in the carpal tunnel after injury of the wrist or distal forearm.
Axillary nerve stretch injuries occur in approximately 5% of shoulder dislocations. The peroneal nerve is injured most commonly at the fibular neck in fracture of the tibia and fibula or dislocation of the knee.
Branches of the lumbosacral plexus are injured in less than 3% of pelvic fractures; this plexus is reportedly injured in 10% to 13% of posterior dislocations of the hip. The tibial nerve may be injured in fractures of the proximal tibia and injuries around the ankle.
Peripheral nerve injuries should be carefully excluded in every patient with an acute extremity injury. Equal diligence should be applied in evaluation after surgery, manipulation, casting, and recovery from skeletal injury to detect secondary neural injury.
Immediately after a severe injury to an extremity, recognition of a peripheral nerve injury is not always easy. Pain is often so severe that patient cooperation is limited at best. The preservation of life and limb is always the first objective. When possible, however, some simple tests should be conducted to detect injuries of major nerves of the extremity. In the upper extremity, loss of pain perception in the tip of the little finger indicates ulnar nerve injury. Loss of pain perception in the tip of the index finger indicates median nerve injury, and inability to extend the thumb in the hitchhiker’s sign usually indicates radial nerve injury, although the extensor tendons may be severed and render this test invalid. Similarly, in the lower extremity, loss of pain perception in the sole of the foot usually indicates sciatic or tibial nerve injury, whereas inability to extend the great toe or the foot indicates peroneal or sciatic nerve injury. As with the radial nerve, injury to the tendons or muscle bellies may render these tests useless. They may be carried out quickly, however, and usually serve as effective screening procedures.
In evaluating peripheral nerve lesions, a precise knowledge of the course of the nerve, of the level of origin of its motor branches, and of the muscles that these branches supply is essential. Knowledge of common anatomic variations in nerve supply is extremely helpful. One must be familiar with the various zones of sensation and with the areas in which sweating may be diminished or absent and in which skin resistance may be increased. Evaluation of motor loss is crucial. This evaluation can be accurate only if one can palpate or see the tendon or muscle belly under consideration. If one relies on analysis of movement alone as an indication of intact nerve supply, errors can be made because of substitution and trick movement. Opposition of the thumb to the little finger can be accomplished by many patients even though the nerve supply to the opponens pollicis is completely severed and the muscle is paralyzed. In addition, the wrist can be partially extended, even when the muscles supplied by the radial nerve are completely paralyzed, by simple flexion of the fingers, and the elbow can be forcefully flexed, even when the musculocutaneous nerve is completely severed and the biceps paralyzed, by substitution of the brachioradialis. Palpation of the opponens pollicis, extensor tendons of the wrist, and biceps tendon or muscle prevents such deceptions. Some muscles cannot be tested by palpation or sight; these include the lumbricals, the short adductor of the thumb, and the interossei except for the first dorsal. There are enough muscles supplied by each nerve that can be so tested as to allow an accurate diagnosis in most instances. The muscles that can be examined accurately and easily are enumerated in the discussion of each nerve. A clinical assessment of the strength of the muscles is helpful. A scale recommended by Highet has been widely accepted. According to that scale, the following designations are assigned: 0 for total paralysis, 1 for muscle flicker, 2 for muscle contraction, 3 for muscle contraction against gravity, 4 for muscle contraction against gravity and resistance, and 5 for normal muscle contraction compared with the opposite side.
Although a well-performed physical examination by an experienced examiner can usually provide sufficient information to accurately diagnose the presence or absence of a major nerve injury, further diagnostic studies are occasionally helpful, particularly in closed injuries in which the physical integrity of the nerve is in question. High-resolution ultrasound and MRI can accurately assess the physical integrity of the nerve immediately after injury and provide valuable information for surgical decision making. Intraneural and perineural injuries also can be identified with both of these techniques.
The best and most accessible correlative electrophysiologic confirmations of a peripheral neural injury are nerve conduction and electromyographic mapping assessments. The surgeon must have specific objectives when ordering these tests to obtain the most useful information for clinical management. The timeline in ordering the studies is also important because the changes after injury and recovery follow a well-described pattern. The presence, location, severity, and possibly the prognosis of the neural insult can be determined from these studies, and information regarding the recovery pattern can be obtained when the study is done sequentially over time. Alternative electrophysiologic uses include dynamic electromyographic assessment when considering optimal muscle transfer strategies, before tenotomy, or botulinum toxin injections in central and peripheral neuropathic conditions. Electrical stimulation can be used for optimal nerve localization when considering blocks or ablation procedures. Generally, both nerve conduction velocity studies and EMG are ordered for routine neural injury assessments because the information gained is complementary. Although full neuropathic changes are not observed in these studies for 2 or 3 weeks after injury, there may be instances in which early baseline studies should be done.
Standard nerve conduction techniques include orthodromic motor and antidromic-orthodromic sensory studies and retrograde studies (e.g., F wave study). F wave studies are especially useful for investigating peripheral nerve injuries that are more proximal and less accessible through other techniques. The suspected location of neural compromise is identified, and a protocol to electrically stimulate proximally, distally, and across the segment is formulated. Depending on whether it is an orthodromic or antidromic study, the evoked potential will be recorded at some defined point proximal and distal to the injury with a surface or needle electrode ( Fig. 62.9 , Segment A ).
After a severe traumatic neural insult and Wallerian degeneration, there is a progressive structural degradation and neurotransmitter compromise expressed by alteration in nerve conduction and evoked motor and sensory configuration. Immediately after injury, conduction proximal and distal to the insult usually elicits a normal response, although stimulation across the injured segment may vary, depending on the presence of axonal or myelin injury. As Wallerian degeneration ensues (within 5 to 10 days), there is a progressive reduction in the amplitude and alteration in the configuration of the evoked potentials ( Fig. 62.9 , Segment B ). If the insult produces only a temporary physiologic block (e.g., neurapraxia), conductivity distal to the lesion remains preserved even after 10 days and a more favorable prognosis can be expected. Evoked sensory amplitude assessments and comparisons also can assist in delineating further pathology.
With a more severe injury, not only is a conduction block across the segment present but a progressive decline in amplitude is noted in evoked potentials when stimulating distal to the injury; sometimes there is complete absence of a response (e.g., axonotmesis). Eventually, electromyographic changes evolve. Over a period of months, repeat studies may be performed to follow neural recovery patterns depending on the case.
Manual muscle testing is routine with any musculoskeletal examination, but it is not sensitive for picking up more subtle neuropathic pathology. Myotomal sampling of the involved extremity with needle pick-up electrodes (e.g., monopolar, concentric, and single fiber) yields information regarding neuropathic injury and pathology. It can distinguish a recent injury from a chronic condition that predated the injury (e.g., workers’ compensation or litigation). The basic monopolar needle electrode samples approximately eight muscle fibers, and by assessing different sites, fair representation of specifically innervated myotomal groups is possible. The muscle initially is observed at rest (insertional activity, approximately 200 ms) and subsequently during volitional muscle recruitment. During the initial postinjury phase, needle sampling should be normal unless there has been a prior injury ( Fig. 62.10 ). Recruitment at this point may vary depending on injury pattern and effort. At 10 to 14 days after neural injury, abnormal spontaneous rest potentials evolve (positive sharp waves) appearing in denervated myotomes where axonal injury has occurred ( Fig. 62.11A ). Between 14 and 18 days, fibrillations appear ( Fig. 62.11B ). Voluntary motor unit potentials, if present, may have attenuated amplitudes reflecting axonal compromise. Abnormal denervation patterns can be correlated with established intraneural topographic reference guides to assist in a clear anatomic mapping of the injury. Abnormal spontaneous rest potentials may last indefinitely until the muscle has become reinnervated or fibrotic.
At approximately 3 months after injury, some peripheral neural sprouting occurs and the motor unit potential amplitude progressively increases; this is preceded at times by polyphasic configuration potentials. Between 2 and 6 months after injury, larger than normal appearing potentials are established and remain so until the reinnervation is completed, at which time the motor unit potential configuration returns to a more normal-appearing pattern. Some surgeons monitor denervated myotomes over months (e.g., 3 months) before exploration, depending on the nature of injury and clinical presentation.
The Tinel sign is elicited by gentle percussion by a finger or percussion hammer along the course of an injured nerve. A transient tingling sensation should be felt by the patient in the distribution of the injured nerve rather than at the area percussed, and the sensation should persist for several seconds after stimulation. It should be tested for in a distal-to-proximal direction. A positive Tinel sign is presumptive evidence that regenerating axonal sprouts that have not obtained complete myelinization are progressing along the endoneurial tube. With progressive regeneration, the positive response fades proximally, presumably because of progressive myelinization along the more proximal part of the regenerated segment. Distal progression of the response along the course of the nerve in question can be measured, and some have used the rate of this progression to establish prognosis or suggest the need for exploration. A distally advancing Tinel sign should occur in Sunderland types 2 and 3 nerve injuries. A Sunderland type 1 injury or neurapraxia should not show an advancing Tinel sign because Wallerian degeneration and axonal regeneration do not occur. A Sunderland type 4 or type 5 injury would not show an advancing Tinel sign unless repaired. The presence of such a sign alone with its progressive distal migration is encouraging. Electrodiagnostic techniques for the evaluation of nerve-evoked potentials and EMG in the office and operating room provide sophisticated means for evaluating the progress of nerve regeneration and for assessing neuromas in continuity. The work of Kline et al. in evaluating whole nerves and the reports of Terzis and of Williams and Terzis in assessing single fasciculi are recommended. A few regenerating sensory fibers can result in a positive Tinel sign; the presence of such a sign cannot be construed as absolute evidence that any motor fibers are regenerating or that significant sensory return is to be expected. Somatosensory evoked studies may be used as an adjunct including intraoperative monitoring for certain procedures (e.g., external fixation for limb lengthening).
Sympathetic fibers within a peripheral nerve are resistant to mechanical trauma. The presence of sweating within the autonomous zone of an injured peripheral nerve reassures the examiner to a degree, suggesting that complete interruption of the nerve has not occurred. Preservation of sweating can be determined simply, as pointed out by Kahn, by observing beads of sweat through the +20 lens of an ophthalmoscope. The time-honored sweat test (iodine starch test) consists of dusting the extremity with quinizarin powder. Sweating is induced by various means. The powder remains dry and light gray throughout the denervated area and assumes a deep purple color throughout the area of normal sweating. The ninhydrin print test as recommended by Aschan and Moberg is another method of assessing sweat patterns in the hand.
The skin resistance test is another method of evaluating autonomic interruption; in it a Richter dermometer is used. The autonomous zone with absence of sweating shows an increased resistance to the passage of electrical current. The adjacent innervated areas have a normal resistance, and further decreased resistance in these areas can be elicited by high external temperatures that do not affect the denervated area. The area outlined by the Richter dermometer roughly approximates the autonomous zone of the nerve in question.
Electrical stimulation through the intact skin has been used in one form or another by many investigators and clinicians for a long time. Faradic stimulation is often of little value because normally innervated muscles may fail to respond to this current. Additionally, if response to faradic stimulation is still present after 3 weeks, the muscles in most instances are capable of voluntary contraction, and no additional information is obtained by the study. Galvanic stimulation is useful in determining chronaxy and the strength-duration curve. These determinations frequently give early evidence of denervation after nerve injury and are useful in following the evolution of reinnervation, which is less readily assessed by other methods.
As in any other injury, initial management of a patient with peripheral nerve damage should begin with careful assessment of the vital functions. When indicated, appropriate actions to prevent cardiopulmonary failure and shock should be taken and systemic antibiotics and tetanus prophylaxis should be provided. When the extent of any injury to the major viscera has been determined, and appropriate resuscitative measures have been started, the injury to the peripheral nerve should be evaluated and the specific nerve deficit should be assessed carefully.
An open wound in which a peripheral nerve has been injured should be cleansed and debrided thoroughly of any foreign material and necrotic tissue, using local, regional, or general anesthesia. If the wound is clean and sharply incised, if the condition of the patient is satisfactory, and if a repair can be done in a quiet and unhurried setting with adequate personnel and equipment, immediate primary repair of the nerve is preferred. If the general medical condition of the patient does not permit adequate repair or if circumstances otherwise cause an undue delay, we prefer to perform the neurorrhaphy during the first 3 to 7 days after injury; in this instance, the wound is sutured, dressed sterilely, and observed for evidence of sepsis.
When open wounds are caused by blasting, abrading, or crushing agents, and when contamination with foreign material is severe, the wound is cleansed and debrided thoroughly, and a sterile dressing is applied. If the ends of the nerve can be identified, they are marked with sutures, such as Prolene or stainless steel, which can be easily identified later. In the absence of a significant nerve gap, loose end-to-end apposition prevents retraction of the nerve segments and makes later repair easier. In the presence of a segmental gap in the nerve, suturing the ends to the soft tissues prevents their retraction. Soft-tissue coverage of the wound consistent with the management of the injured part is carried out, and the nerve is repaired at a later date when the soft tissues have healed and the extent of neuroma formation is evident, usually 3 to 6 weeks after injury.
A closed injury in which a peripheral nerve has been damaged requires careful assessment of residual function and documentation of discrete deficits. After the initial pain has subsided and the wound has healed, early active motion of all joints of the involved extremity should be started. When necessary, gentle passive exercises that avoid disrupting nerves and tendons may be instituted. All joints of the extremity must be kept supple, and soft-tissue contractures must be avoided. Exercises help keep the soft tissues of the extremity in a better physiologic state so that when the nerve has regenerated, rehabilitation is easier. The specific effects of electrical stimulation of muscles are unclear. Regardless of the details of the treatment program, the patient must become actively involved in it to prevent contractures and to strengthen muscles with intact innervation. Similarly, an extremity with a peripheral nerve injury should not be immobilized indefinitely. Dynamic and static splinting to support joints and to prevent contractures should be used intermittently.
When closed fractures are complicated by peripheral nerve deficits, awaiting reinnervation seems reasonable, and early surgical exploration usually is avoided. Early ultrasound imaging of the involved nerve can determine the extent of injury. The progress of return of function in the injured extremity is evaluated with periodic EMG, nerve conduction velocity studies, and frequent clinical evaluation. Conversely, if the nerve deficit follows manipulation or casting of a closed fracture in the absence of a prior nerve deficit, early exploration of the nerve is favored.
Few worthwhile reports have been published on the results of neurorrhaphy and the factors that influence them, first, because few investigators have had access to a large enough group of patients to make evaluations statistically significant and, second, because reports have only rarely been based on sound criteria of regeneration. Valuable reports have been compiled from studies of such injuries incurred in World War II and later conflicts. As a result of these studies, the influence of many factors on regeneration after nerve suture is now better understood.
Rarely should a fracture interfere with nerve repair. In the usual situation, a nerve may be explored if the fracture requires open reduction. In many open injuries the nature of the wound may be such that early repair of the nerve cannot be done satisfactorily. Every effort should be made by repeated debridement of necrotic material to promote rapid healing of any open wounds without sepsis. Nerves may be repaired successfully during a second debridement, followed by closure and healing. Associated vascular injury can adversely affect nerve regeneration because of tissue ischemia.
Several important factors that seem to influence nerve regeneration are (1) the age of the patient, (2) the gap between the nerve ends, (3) the delay between the time of injury and repair, (4) the level of injury, (5) the condition of the nerve ends, and (6) the experience and techniques of the surgeon. The first five of these factors are discussed here.
Age undoubtedly influences the rate and degree of nerve regeneration. All other factors being equal, neurorrhaphies are more successful in children than in adults and are more likely to fail in elderly patients; why this is true has not been completely explained, but it may relate to the potential for central adaptation to the peripheral nerve injury. We do not know precisely what results can be expected in either of the extremes of age because practically all significant studies have dealt with military personnel whose average age was 18 to 30 years. A close correlation has been noted between age and two-point discrimination obtained after median and ulnar nerve repairs (30 mm at 20 to 40 years; 15 mm at 11 to 20 years; 10 mm at <10 years). After digital nerve repair, however, the final two-point discrimination was not as closely related to age. Another study found that a higher percentage of patients younger than 20 years at the time of repair had two-point discrimination of less than 6 mm than did patients older than 20 years.
The nature of the injury is the most important factor in determining the defect remaining between the nerve ends after any neuromas and gliomas are resected. When a sharp instrument, such as a razor or knife, severs a nerve, damage is slight proximally and distally, and although the nerve ends inevitably do retract, the gap can usually be easily overcome. Conversely, when a high-velocity missile severs a nerve, proximal and distal nerve damage is extensive. Ultimately, both ends must be widely resected to expose normal funiculi, producing a larger gap. The gap is increased farther if part of the nerve is carried away by a missile, as in shrapnel injuries. Methods of closing troublesome gaps include (1) nerve mobilization, (2) nerve transposition, (3) joint flexion, (4) nerve grafts, and (5) bone shortening. The greater the defect, the more dissimilar the funicular pattern of the two ends because of the constantly changing arrangement of fibers within the nerve as it progresses distally. This is particularly important in the more proximal portion of peripheral nerves. Agreement is widespread that excessive tension on a neurorrhaphy harms nerve regeneration. Nerve grafting is advised if, after the nerve is mobilized, the gap cannot be closed by flexing the main joint of the limb 90 degrees. The observed upper limit of a gap beyond which results deteriorate is approximately 2.5 cm. The observations of Kirklin, Murphey, and Berkson in 1949 that recovery is slightly better when the gap is relatively small remain valid.
Delay of neurorrhaphy affects motor recovery more profoundly than sensory recovery, most likely because of the survival time of denervated striated muscle. There is significant loss of motor endplates and increased muscle fibrosis by 18 months after denervation; therefore nerve repair needs to be performed early enough to allow reinnervation of muscle before this occurs. Experimental studies have shown better axonal survival with early nerve repair.
As a rule of thumb, Omer suggested that about 1% of recoverable nerve function is lost for each week of delay after 3 weeks postinjury. The influence of delay on sensory return is unclear; in the Veterans Administration study, little influence could be found and useful sensation returned in a few patients when suture was performed 2 years after injury. The critical limit of delay beyond which sensation does not return is unknown.
Our practice is to perform neurorrhaphies in clean, sharp wounds immediately or during the first 3 to 7 days. In the presence of extensive soft-tissue contusion, laceration, crushing, or contamination in which the proximal and distal extent of the nerve injury is impossible to delineate, a delay of 3 to 6 weeks is preferred.
The more proximal the injury, the more incomplete the overall return of motor and sensory function, especially in the more distal structures. Conditions are more favorable for recovery in the more proximal muscles because (1) the neurons that innervate the distal portions of the limb are more severely affected by retrograde changes after proximal injury, (2) a greater proportion of the cross-sectional area of the nerve trunk is occupied by fibers to the proximal muscles, and (3) the potential for disorientation of regrowing axons and for axon loss during regeneration is greater for the distal muscles than for the muscles more proximally situated after a proximal injury. Except for parts of the brachial plexus, useful function at times returns regardless of the level of injury if the critical limit of delay has not passed.
The condition of the nerve ends at the time of neurorrhaphy is important. Meticulous handling of the nerve ends, asepsis, care with nerve mobilization, preservation of neural blood supply, avoidance of tension, and provision of a suitable bed with minimal scar all exert favorable influences on nerve regeneration. Distal stump shrinkage has been found to be maximal at about 4 months, leaving the distal fascicular cross-sectional area diminished to 30% to 40% of normal size. Intraneural plexus formation and fascicular dispersal make accurate fascicular alignment and appropriate axonal regeneration more difficult. A neurorrhaphy with a satisfactory external appearance is no guarantee of optimal internal fascicular alignment. Fascicular malalignment is a common finding. It is generally agreed that the nerve ends should be prepared in such a way that a satisfactory fascicular pattern is apparent in the proximal and distal stumps. No scar, foreign material, or necrotic tissue should be allowed to remain around the ends to interfere with axonal regeneration. Sometimes resection of the nerve ends so that satisfactory fasciculi are exposed leaves a gap that cannot be closed by end-to-end repair. As noted previously, clinical and experimental evidence indicates that excessive tension on the neurorrhaphy at the time of repair and when an acutely flexed limb is mobilized later causes excessive intraneural fibrosis. These findings and the promising results achieved after the interfascicular nerve grafting technique advocated by Millesi and by Millesi, Meissl, and Berger suggest that such a technique is preferable to repair of nerves under too much tension or with limbs in acutely flexed or awkward positions.
In the presence of a traumatic peripheral nerve deficit, exploration of the nerve is indicated as follows:
When a sharp injury has obviously divided a nerve, early exploration is indicated for diagnostic, therapeutic, and prognostic purposes. Neurorrhaphy can be done at the time of exploration or can be delayed.
When abrading, avulsing, or blasting wounds have rendered the condition of the nerve unknown, exploration is required for identification of the nerve injury and for marking the ends of the nerve with sutures for later repair.
When a nerve deficit follows blunt or closed trauma and no clinical or electrical evidence of regeneration has occurred after an appropriate time, exploration of the nerve is indicated. This also is true when a nerve deficit complicates a closed fracture. In this instance, it has been our practice to observe the patient for evidence of nerve regeneration for an appropriate time, depending on the nerve and its level of muscle innervation. Then if regeneration has not occurred, we favor exploration. In situations in which a nerve has been intact before closed reduction and casting of a fracture, but a significant deficit is found immediately after, we explore the nerve as soon as feasible.
When a nerve deficit follows a penetrating wound, such as that caused by a low-velocity gunshot, the part is observed for evidence of nerve regeneration for an appropriate time. If there is no evidence of regeneration, exploration is indicated.
Conversely, delay in exploration of a nerve injury is indicated if progressive regeneration is evidenced by improvement in sensation, motor power, and electrodiagnostic tests and by progression of the Tinel sign.
It has been the time-honored policy to advise primary suture when possible. This recommendation is logical when one considers what happens to the distal end of the nerve, motor endplates, sensory nerve ends, muscles, joints, and other tissues of the denervated extremity. The controversy concerning whether primary or secondary nerve repair is better is unresolved. Primary repair done in the first 6 to 8 hours or delayed primary repair done in the first 7 to 18 days is appropriate when the injury is caused by a sharp object, the wound is clean, and there are no other major complicating injuries. Ideally, such repairs should be performed by an experienced surgeon in an institution where adequate equipment and personnel are available. The development of magnification devices, new instruments, and new techniques and the modification of a variety of small instruments for use in nerve surgery have improved the technique of early repair. Primary repair should shorten the time of denervation of the end organs, and fascicular alignment should be improved because minimal excision of the nerve ends is required. Regarding war wounds, however, primary sutures have compared unfavorably with early secondary suture.
When the diagnosis of division of a peripheral nerve has been made, if conditions are suitable and repair is indicated, one should not delay repair in anticipation of spontaneous regeneration. Only if the patient’s life or limb is seriously endangered should the operation be long postponed. A fracture is not a contraindication for operation. Operation before the fracture becomes united may be advantageous for two reasons: (1) if bone shortening is necessary, resection of an ununited or partially united fracture is a much less formidable procedure than resection of a fully united bone; and (2) restriction of joint motion is minimal if the nerve is repaired soon after the injury; later, motion would be more limited, perhaps so severely as to prevent flexing the joint enough to overcome a gap between the nerve ends.
A nerve stimulator should be available for all peripheral nerve procedures; many satisfactory permanent and disposable ones are available commercially. A stimulator is indispensable in investigating partially severed nerves and neuromas in continuity and in locating and preserving nerve branches given off proximal to or at the lesion that are still functioning but are encased in scar tissue. Intraoperative recording of somatosensory evoked potentials and nerve action potentials is useful in surgical planning and assessing nerve lesions. These techniques require sensitive and sophisticated recording and monitoring equipment and trained technicians. (For details of these monitoring techniques, the reader is referred to the references at the end of this chapter.)
Despite the technical difficulties involved in these methods, we have found intraoperative recording to be helpful when evaluating partial nerve lesions and neuromas in continuity. Instruments for handling and dissecting delicate tissues always are essential. Nerve surgery in the extremities also is made easier by the use of a pneumatic tourniquet, suction apparatus, and bipolar electrocautery. Gelfoam and thrombin are useful for controlling the bleeding from the cut ends of nerves. For suture material, we prefer 8-0, 9-0, and 10-0 monofilament nylon. The tensile strength, easy handling qualities, and minimal tissue reaction of nylon make it the most desirable suture material now available for neurorrhaphy. In our experience, most epineurial repairs are best done with 8-0 or 9-0 nylon. For perineurial or epiperineurial repair, 9-0 or 10-0 monofilament nylon is preferable.
Peripheral nerve operations can be done with the patient under general, regional, or local anesthesia for the upper extremities or general, spinal, or local anesthesia for the lower extremities. Local anesthesia has the advantage of allowing evaluation of the passage of sensory impulses through the injured nerve. If evaluation is to be accurate, however, little if any anesthetic agent should be injected around the nerve, and, consequently, the procedure is painful. There is always the possibility that the agent would infiltrate the tissues around the nerve and interfere with motor response to stimulation. As a rule, we prefer general anesthesia for surgery in the upper extremities and neck and general or spinal anesthesia for surgery in the lower extremities.
Before preparing and draping, the correct side and site are identified and the site is marked with an indelible surgical marking pen. Because the exact length of an incision can rarely be predicted, it is mandatory that the entire extremity and its environs be prepared. For an operation on the upper extremity, the axilla, shoulder, neck, and chest should be included in the field of preparation; for an operation on the lower extremity, the buttock and the area up to the iliac crest posteriorly should be included. In operative procedures involving the distal portions of nerves only, such as below the elbow or knee, a well-padded pneumatic tourniquet placed above the elbow or knee is used, limiting the sterile field. A sterile tourniquet also can be helpful for more proximal lesions.
After preparation of the entire field, the proposed incision is marked on the extremity and is crosshatched with washable ink before any of the landmarks are covered. It is a good policy to mark the incision along the course of the nerve in the entire prepared area. The extremity is encased in a sterile stockinette so that it can be moved freely over the sterile drapes. If it is desirable to watch the movement of the muscles in the hand when the nerve is stimulated, the hand can be left exposed and bare.
In no type of surgery is the incision more important. Every incision should extend well proximal and distal to the lesion and when possible should follow the course of the nerve. An incision should never cross the flexor creases of the skin at a right angle. Short incisions are probably the cause of more futile nerve operations than any other factor except surgeon inexperience. One should never hesitate to extend an incision a great distance—even from the axilla to the wrist to overcome a large defect in the ulnar or median nerve.
It is essential that the injured nerve be exposed first proximal to and then distal to the lesion before approaching the site of injury. Dissection and exposure are made simpler, and there is less chance of damaging the nerve and any branches remaining in the scar. If one is confronted with a neuroma in continuity, the nerve should be stimulated proximal and distal to the lesion and the response recorded. When a nerve is dissected from scar tissue, it should be stimulated repeatedly to locate any branches that still might be functioning. Before the nerve is mobilized completely, sutures are placed in the epineurium proximal to and distal to the lesion for orientation so that if neurorrhaphy is necessary the ends can be joined without rotation. Also, inspection of the external surface of the nerve may allow alignment of the longitudinal epineurial vessels; this, too, can aid in appropriate rotation of the nerve ends.
Handling of the nerve during mobilization is made easier by the use of vessel loops. Any part of the nerve not being operated on at the moment should be covered with moist sponges.
If the nerve has not been completely severed, or if a neuroma in continuity is present, it can be difficult to decide whether neurolysis, partial neurorrhaphy, or complete neurorrhaphy would be best. The surgeon may need to call on all of the experience at his or her command to arrive at the wisest decision. Stimulation proximal to the injury for motor response distal to it is essential. If local anesthesia is used, stimulation distal to the lesion may give an idea of whether a significant number of sensory fibers have escaped injury or have regenerated, but sensory response is far less reliable than motor response. If a pneumatic tourniquet is used, it should be deflated to allow the muscles and nerves to recover from ischemia so that stimulation of the nerve to elicit motor response has more validity. Examination at the site of injury may assist in determining what course to pursue. The neuroma can be injected with saline solution, and if the solution passes up and down the nerve trunk with little difficulty, the neuroma probably should be left alone. This can be misleading, however, and unless both motor and sensory responses to stimulation are good, endoneurial exploration is advisable.
When an endoneurial exploration is undertaken, it should be borne in mind that neurolysis or partial or complete neurorrhaphy may be necessary, and one should preserve intact as much of the epineurium and normal nerve as possible. The epineurium is incised longitudinally proximal to the lesion, beginning not more than 0.5 cm from the level of gross changes in the nerve as determined by palpation. The incision is not extended more proximal to this point unless necessary because the epineurium may become frayed; and if neurorrhaphy becomes necessary, more of the nerve may have to be sacrificed. For the same reason, the distal end of the incision is limited. The flaps of epineurium on each side may be retracted laterally by nylon sutures and are undermined widely. The funiculi are separated if possible with a pointed or diamond-bladed knife, using sharp or blunt dissection as necessary. Spring-loaded microscissors also are helpful in this dissection. The surgeon constantly should be aware of the possibility of plexus formation between fascicles and protect these. Distinguishing between intraneural fibrosis and plexus formation is extremely difficult. If most of the fasciculi are intact and can be separated and traced through the neuroma, nothing further should be done. If stimulation fails to elicit a response, and few if any intact fasciculi can be found, resection of the neuroma and neurorrhaphy are probably indicated. Use of magnifying loupes or the operating microscope is essential when performing intraneural dissection to avoid injury to intact nerve tissue (see Chapter 63 ).
Partial severance of the larger nerves, such as the sciatic nerve and the cords and trunks of the brachial plexus, is common. In such an injury, partial neurorrhaphy is best. It is occasionally necessary and justifiable in smaller nerves but is never quite as satisfactory technically as is complete neurorrhaphy. The decision to perform partial neurorrhaphy is likewise often difficult. The decision should be made only after the most careful investigation of the lesion. If one half of the nerve, especially a large one, is disrupted, partial neurorrhaphy is advisable. If the motor response to stimulation is good, however, it would be unwise in some nerves, such as the peroneal or ulnar, to risk injury of good motor funiculi in an attempt to restore sensation to a small area on the dorsum of the foot or to the little finger. If most of the fascicles in smaller nerves are severed, and if stimulation cannot show important function in the few that remain, complete neurorrhaphy probably is better. Suture of a few fascicles usually is impractical.
When the decision has been made to perform partial neurorrhaphy ( Fig. 62.12 ), the incision is extended longitudinally in the epineurium proximally and distally several centimeters, as necessary. The intact funiculi are dissected out for the same distance. The ends of the injured part of the nerve are resected to normal tissue. At the cut ends, an end-to-end neurorrhaphy is performed. If the epineurium is inadequate for placement of epineurial sutures, epiperineurial or perineurial (fascicular) sutures suffice. The proximal and distal dissection should be extensive enough to prevent kinking of the loop of intact nerve.
When a nerve has been completely severed, and when conditions as already outlined are appropriate, neurorrhaphy after sufficient resection of the proximal and distal ends of the nerve is indicated. Sometimes a considerable gap or defect (actual loss of nerve tissue) remains after excision of any glioma and neuroma, and selecting a method for overcoming the gap is difficult. Extension of the incision proximally and distally can be helpful in permitting adequate dissection for closure of the gap. In general, direct neurorrhaphy may be possible with fairly large gaps in the median and ulnar nerves near the wrist and elbow after mobilization of proximal and distal segments, whereas gaps of 2 to 3 cm in the brachial plexus and radial, sciatic, and peroneal nerves and the median nerve at the midforearm level may require nerve grafting. Regardless of the technique used, there is general agreement that nerve repair under excessive tension is detrimental to satisfactory regeneration. It generally is recommended that if a single 8-0 nylon epineurial suture can maintain approximation of the nerve ends, excessive tension is not present.
There are several methods of closing gaps between nerve ends without appreciable damage to the nerve itself. The methods most often used are mobilization of the nerve ends and positioning of the extremity. Other methods include nerve transplantation, bone resection, bulb suture, nerve grafting, and nerve crossing (pedicle grafting).
Most small gaps can be closed by mobilizing the nerve ends for a few centimeters proximal and distal to the point of injury. Mobilization of both nerve ends to some degree is required in all peripheral neurorrhaphies. The exact amount of mobilization a peripheral nerve can tolerate before its regenerating potential is compromised is unknown; however, extensive dissection of a nerve from its surrounding tissues does disrupt the segmental blood supply, causing subsequent ischemia and increased intraneural scarring. Mobilization has been shown to be more detrimental to the distal nerve segment. Nicholson and Seddon suggested that extensive mobilization adversely affects recovery after median nerve repairs in the forearm. Only 50% of patients had recovery to the M3 level or better if the gap was more than 2.6 cm and required extensive mobilization. Large gaps require extensive dissection of the nerve from its adjacent tissues for a relatively tension-free epineurial repair. Before subjecting a peripheral nerve to extensive dissection, the surgeon should have some idea of the maximal nerve gap over which mobilization may become a futile endeavor. The nerve gap is determined at the time of surgery with the extremity in the anatomic position and after distal and proximal neuroma excision. Guidelines are extremely variable in the literature (2.5 to 9.0 cm, depending on the location; Table 62.8 ).
Nerve | Location | Distance (cm) |
---|---|---|
Upper Extremity | ||
Radial | Midarm | 8 |
Median (not transposed) | Midforearm | 4.5-6.5 |
Ulnar (not transposed) | Midforearm | 3.2-5 |
Posterior interosseous | Forearm | 1 |
Lower Extremity | ||
Sciatic | Midthigh | 6-9 |
Tibial | Knee | 4.5-9 |
Peroneal | Knee | 6.4-8.1 |
When mobilizing a peripheral nerve, care should be taken to avoid excessive stripping of the small vessels to the nerve. Motor and essential sensory branches should be carefully protected. Gaps distal to the motor branches of a peripheral nerve are closed more easily with mobilization. The branch of the radial nerve to the brachioradialis muscle commonly prevents closure of a gap proximal to the point where this branch emerges from the nerve, but if the biceps brachii is functioning, this branch can be sacrificed without much loss of function. Excessive tension must be avoided at all times.
Relaxing nerves by flexing various joints and occasionally by other maneuvers, such as abducting, adducting, rotating, and elevating the extremity, is as important as mobilization in closing large gaps in nerves. Through use of both methods, long gaps can be closed in nearly all of the peripheral nerves, and many unsatisfactory neurorrhaphies result from failure to make the most of their possibilities. When joints that are excessively flexed or awkwardly positioned are mobilized later, tension on the neurorrhaphy may be too great and may cause intraneural fibrosis that compromises axonal regeneration. Consequently, a joint should never be flexed forcibly to obtain end-to-end suture. It is a reasonable policy to flex the knee and elbow no more than 90 degrees. Also, flexion of the wrist more than 40 degrees is probably unwise. After the wound has healed sufficiently, the joint can be extended about 10 degrees per week until motion is regained. Flexing joints is most important in repairing gaps in the long nerves of the extremities. External rotation and abduction are helpful when repairing radial and axillary nerves, as in elevation of the shoulder girdle in brachial plexus injuries. Rarely, extension of a joint can be helpful, as in extension of the hip in sciatic injuries. Strong consideration should be given to nerve grafting in preference to drastic positioning of the extremity to produce a tension-free neurorrhaphy.
The anatomic course of some nerves can be changed to shorten the distance between severed ends. This is true especially of the ulnar nerve at the elbow. The median nerve also can be transposed anterior to the pronator teres if the lesion is distal to its branches to the long flexor muscles of the forearm, and the tibial nerve can be placed superficial to the soleus or gastrocnemius in the leg if the lesion is distal to its branches to the calf muscles. Most surgeons recommend transposition of the proximal end of the radial nerve anterior to the humerus and deep to the biceps to obtain needed length. Considerable length can be gained in most patients by the simpler maneuver of externally rotating the arm, provided that the mobilization has been carried into the axilla and that the branches of the radial nerve to the triceps muscle have been dissected well up the nerve.
In civilian injuries, bone resection almost never should be necessary to accomplish neurorrhaphy. Even in war wounds, it was rarely employed, and when it was used, it was usually because the joints of the extremity had become so stiff from immobilization caused by fracture or injudicious use of casts that limited flexion. Intact long bones and most bones in children rarely should be shortened to aid in nerve repair. Bone resection is of particular value in the upper arm for closing large gaps in the ulnar, radial, or median nerves when the humerus already has been fractured. If early delayed suture is done in such patients before the fracture has healed, shortening the bone if necessary is not difficult. After the fracture has healed, however, osteotomy is more difficult. It rarely is worthwhile to shorten the femur in injuries of the sciatic nerve unless this bone already has been fractured; then shortening of the bone can be helpful. Both bones of the forearm or leg in the absence of a fracture should never be shortened.
Interfascicular nerve grafting as described by Seddon and later by Millesi is indicated when primary nerve repair cannot be done without excessive tension. In general, a nerve gap that is caused simply by elastic retraction usually can be overcome with local nerve mobilization, limited joint positioning, and primary repair. If the defect is caused in part by loss of nerve tissue, however, nerve grafting is our procedure of choice. Autogenous sural nerve is the preferred source of graft. Good results have been reported using an interfascicular nerve autografting technique to close gaps without undue tension in injuries to the digital, medial, ulnar, and radial nerves. In the upper extremity especially, good results were achieved in repairing injuries to these nerves. Of 38 patients with median nerve grafts, 82% achieved useful motor recovery (M3 or better) and all but one regained protective sensibility. Of 39 patients with ulnar nerve grafts, all achieved useful motor recovery (M2+ or better) and 28% regained two-point discrimination. Of 13 patients with radial nerve grafts, 77% achieved an M4 or M5 level of function. Kallio and Vastamäki showed good or excellent results in 47 of 98 patients treated with interfascicular grafting for median nerve injuries.
Nerve-crossing operations in the extremities are rarely wise or possible. When a combined median and ulnar lesion is so great that the gap cannot be closed in either nerve in any other way, the ulnar nerve can be sectioned again in the upper arm, creating a segment long enough to bridge the gap between the two ends of the median nerve. The distal end of the median nerve is sutured to the distal end of the free segment of the ulnar nerve to form a U-shaped neurorrhaphy. The vasa nervorum should be left intact. The ulnar nerve is partially transected proximally to allow for sufficient graft length. At a second operation 6 weeks later, the ulnar nerve is completely transected and sutured into the distal segment of the median nerve. This procedure has been advised in situations such as nerve injury caused by massive ischemic necrosis of the forearm, but in light of current knowledge, other nerve grafting techniques seem more appropriate in these situations.
Selecting a cutaneous nerve for nerve grafting should be done with great care. The sural nerve is the most commonly used, and in most situations it is recommended. From each leg, 40 cm of graft material can be obtained. The lateral antebrachial cutaneous nerve for digital nerve grafts can be used so that another limb would not be involved in the surgical procedure. Anatomic studies have shown no significant difference in fascicular area, area of the entire nerve bundle, and percentage of the nerve bundle occupied by the actual nerve fascicles. The lateral antebrachial cutaneous nerve is found most easily just lateral to the biceps tendon alongside the cephalic vein. Through a longitudinal incision, 20 cm of graft material can be obtained. The medial antebrachial cutaneous nerve, the terminal articular branch of the posterior interosseous nerve, and the dorsal sensory branch of the ulnar nerve also have been used for digital nerve grafting. The medial antebrachial cutaneous nerve is found adjacent to the basilic vein. The posterior interosseous nerve is located at the wrist just ulnar to the extensor pollicis longus tendon lying on the interosseous membrane. The superficial radial nerve is an excellent source of graft material when used in grafting a high radial nerve laceration because the neurologic deficit that otherwise would be created already exists. It is not recommended as a routine source because its sensory contribution to the hand is significant, especially when the median nerve is deficient.
The use of fresh nerve allograft can potentially allow functional recovery equivalent to autograft; however, it requires systemic immunosuppression. Tacrolimus (Prograf) inhibits activation of T-cell proliferation and is administered starting 3 days preoperatively and continued for 18 months postoperatively. Grafts are selected from ABO blood type–compatible individuals (cadaveric or living related donors) and stored at 4°C in University of Wisconsin solution for 7 days before implantation. Rejection and increased vulnerability to opportunistic infection are potential complications. Acellularized nerve allografts are now available with the advantage of decreased host rejection. These grafts maintain the physical structure of the epineurium, perineurium, and endoneurial tubes, which are rapidly revascularized and repopulated with host cells. They are available in diameters of 1 to 5 mm and in lengths up to 5 cm. A multicenter retrospective study involving 56 patients and 71 nerve repairs demonstrated functional recovery in 86% of procedures, with sensory recovery ranging from S3 to S4 and motor recovery from M3 to M5. The majority of grafts were used in common digital and digital nerves (48 of 71); however, they were also used in median (10 of 71), ulnar (6 of 71), and radial nerves (2 of 71). The mean gap length was 23 ± 12 mm (range, 5 to 50 mm).
Evaluation of outcomes showed recovery in 89% of digital nerves, 75% of median nerves, and 67% of ulnar nerves. Although autograft is superior, acellularized nerve allograft has the advantages of shortened surgical time, avoidance of additional surgical site morbidity, and relatively unlimited supply.
Synthetic conduits can be used to bridge neural gaps. Various conduit materials have been investigated including silicone, type I collagen, polyglactin, poly- l -lactic acid (PLLA), polyglycolic acid (PGA), and polyvinyl alcohol (PVA) hydrogel. We have had no experience with the use of synthetic conduits, but their use often is considered when there is the possibility of insufficient autogenous nerve graft. Currently, these are recommended for reconstruction of smaller-diameter sensory nerves with defects less than 3 cm.
Fibrin clot, micropore tape, collagen tubulization techniques, adhesives, and many varieties of sutures and suture techniques have been proposed for neurorrhaphy. Neurorrhaphy by suture with nonreactive and nonabsorbable materials, such as stainless steel and monofilament nylon, has the widest application and acceptance. Magnification, appropriate small instruments, and meticulous technique are essential. Experimental evidence is conflicting concerning the relative merits of epineurial and perineurial (fascicular) neurorrhaphy techniques. Clinical evidence to support the use of one technique over the other is meager and inconclusive. The technique selected by the individual surgeon depends on training and experience. Proponents of repair supplementation with autologous fibrin glue, or other commercially available “nerve glues,” cite less tendency for gapping at the repair site, fewer sutures required for the repair, and a possible barrier to invading scar tissue as advantages. None has been shown to increase the strength of the repair, and only one has been shown not to block axonal regeneration when interposed between nerve ends. Our preference is epiperineurial repair at the periphery of the nerve combined with perineurial (fascicular) neurorrhaphy for large fascicles within the nerve. Sunderland pointed out that funicular (fascicular) repair cannot be done accurately in every instance because (1) funicular patterns at nerve ends match exactly only after clean transection, (2) the numbers of funiculi at nerve ends may not correspond, and (3) any discrepancies in funiculi within the nerve would require excessive intraneural suture material. He suggested that funicular repair might be practical when (1) funicular groups are large enough to take sutures that maintain funicular apposition, (2) nerve ends show a funicular pattern that would predispose to wasteful regeneration of axons if epineurial repair were done, and (3) each funicular group is composed of nerve fibers to a particular branch occupying a constant position at the nerve ends. The last arrangement can be seen in the median and ulnar nerves at and above the wrist and the radial nerve at and just proximal to the elbow. Sunderland recommended suturing groups of funiculi in such situations.
After exposing and dissecting the ends of the nerves, determine that any remaining gap can be closed by end-to-end repair without excessive tension.
Resect the glioma and neuroma with a sharp razor blade or a diamond-bladed knife against a sterile wooden tongue depressor in a nerve miter box or with sharp nerve scissors.
Make serial cuts about 1 mm apart in the end of the nerve until normal-appearing fasciculi are exposed; this is best determined by use of the operating microscope. If doubt remains concerning the amount of any remaining scar in the nerve end, frozen histologic sections of the nerve are helpful. Have permanent histologic sections made for later review to help in determining the prognosis.
If the distal end contains glioma, or if more than one third of the proximal end consists of neuroma, carry out additional trimming as required.
Control excessive bleeding with thrombin or Gelfoam.
If positioning of the extremity is required to relieve tension, use an assistant at this point. Sometimes a traction or sling suture of 7-0 or 8-0 nylon passed through the nerve may be required. Our preference in such a situation is the gentle placement of a straight stainless steel Keith or Bunnell needle transversely through each of the nerve stumps with the nerve ends approximated, transfixing the nerve to the adjacent soft tissues.
Determine appropriate rotational alignment by observing the orientation of surface vessels and the appearance and location of fasciculi within the nerve. Epineurial orientation sutures placed 1 cm from each cut edge also are helpful.
Place a piece of plastic or rubber glove material beneath the nerve for visual contrast and less cumbersome handling of sutures. For this repair, 8-0 or 9-0 monofilament nylon usually is sufficient.
Place the first suture in the posterior or deep surface of the nerve in the epineurium, and leave the suture long to make later rotation of the nerve easier. Place the next three sutures in the remaining three quadrants of the nerve, and leave them long, too.
Determine as accurately as possible that no kinking or deviation of the fasciculi has occurred, and place sufficient interrupted sutures of 8-0 or 9-0 nylon to produce a satisfactory neurorrhaphy ( Fig. 62.13 ).
Rotate the nerve with the quadrant sutures to ensure satisfactory posterior surface repair. A 5-0 stainless steel suture can be placed 1 cm from each end of the repair in the epineurium to act as a radiographic marker to detect a rupture. (We rarely use this.)
Before wound closure, remove the sling suture or steel needles from the nerve ends and place the extremity through a limited range of motion to assess positional tension at the repair site. This helps to determine the extent to which the extremity can be safely mobilized postoperatively.
To perform perineurial (fascicular) neurorrhaphy, the surgeon must be proficient in the use of the operating microscope and must be able to handle the delicate 10-0 suture with ease and speed.
Expose the nerve injury, and resect the ends of the nerve as described for epineurial neurorrhaphy (see Technique 62.1).
Place the nerve ends in proper rotation.
Using magnification, attempt to identify corresponding groups of fasciculi in the proximal and distal nerve stumps. It is helpful at this point to diagram the arrangement of the fascicular groups on sterile paper from glove or suture packages.
Transfix the nerve ends to the soft tissues with stainless steel straight needles.
Incise the epineurium longitudinally proximally and distally to expose the fasciculi; approximate them individually with interrupted 9-0 or 10-0 nylon sutures ( Fig. 62.14 ). Where the nerve is composed of multiple small fasciculi, approximate several fasciculi as a group.
After the fasciculi have been matched and approximated, close the epineurium with interrupted nylon sutures, or if the neurorrhaphy is secure and there is no tension on the repair, omit the epineurial closure to decrease the amount of fibrosis after surgery.
(MILLESI, MODIFIED)
Keep the extremity in the extended position so that the graft is not under tension after surgery.
Expose the nerve as for epineurial neurorrhaphy (see Technique 62.1).
Beginning in normal-appearing tissue, dissect and expose the proximal and distal stumps.
Incise the epineurium on the stumps in areas where the nerve appears normal.
Excise a circumferential cuff of epineurium from each stump.
Use the operating microscope to carry out intraneural dissection in the normal part of the nerve, working toward the neuroma and glioma in the proximal and distal ends. Attempt to identify large fasciculi and groups of smaller fasciculi.
Ensure hemostasis by coagulating the smaller vascular branches with bipolar microcoagulating forceps.
As intraneural fibrosis is encountered, transect each fasciculus or group of fasciculi individually at the level where the fibrosis begins. When this dissection has been completed, the fasciculi and groups should be transected at different levels depending on the extent of scarring. Four to six fasciculi or fascicular groups, all of different lengths, now should be present in each end of the stump.
Deflate the tourniquet and compress the wound with saline-moistened packs.
Draw a sketch of each nerve stump, and attempt to identify the corresponding fasciculi and groups of fasciculi in each. The more proximal the lesion, the less well defined the fascicular groups. Use clinical judgment in matching the fasciculi and the fascicular groups in the ends of the stumps.
By measuring the gaps remaining between the fasciculi and fascicular groups at each end of the nerve, estimate the length of nerve graft needed. Each major fasciculus or group requires a segment of graft; the graft should be 10% to 15% longer than the combined gaps to be filled.
Nerves that can be used as donors are the sural, the saphenous, the lateral cutaneous of the thigh, the lateral and medial cutaneous of the forearm, the posterior cutaneous of the forearm, the superficial branch of the radial, the dorsal branch of the ulnar, and the intercostals (see Source of Nerve for Interfascicular Nerve Grafting). We prefer the sural nerve for most situations. A level for transection should be selected to allow the proximal end of the donor nerve to retract beneath fascia or muscles and avoid as much as possible the formation of a painful neuroma.
If the sural nerve is to be used, expose it through a short transverse incision posterior to the lateral malleolus.
Separate the nerve from the small saphenous vein that lies just anterior and superficial to it.
Determine the course of the nerve in the calf by applying traction to the nerve.
Along the course of the nerve, make additional transverse incisions to allow further dissection. If long segments of nerve are to be harvested, a single longitudinal incision is used ( Fig. 62.15 ). This minimizes the potential harm caused by traction on the donor nerve during a difficult dissection. Although scissors or nerve strippers can be used during this part of the procedure, exercise care to avoid injuring the nerve graft.
Transect the nerve so that its proximal end retracts beneath the fascia in the proximal calf.
Close the incisions in the calf, and keep the graft moist with saline during the rest of the operation.
Dissect any excess fat from the ends of the graft, and section the graft so that shorter grafts of appropriate lengths can be placed between the ends of corresponding fasciculi or fascicular groups.
Using the operating microscope, place each graft between the corresponding fasciculi and secure the epineurium of each end to the perineurium of the fasciculus or fascicular group with a single suture of 10-0 monofilament nylon ( Fig. 62.16 ).
If the extremity has been positioned in extension and if the grafts are placed without tension, the single sutures are sufficient. To reinforce the repair site and minimize the need for sutures, fibrin glue can be used as described by Narakas by mixing equal parts of thrombin and fibrinogen.
Obtain meticulous hemostasis and close the wound. Avoid suction drainage tubes.
The same technique can be used for a nerve lesion in continuity or for repair of an unsuccessful primary neurorrhaphy.
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