CHAPTER 230 Pathophysiology of Surgical Nerve Disorders
Causes of Surgical Nerve Injuries
The different causes of PNS injury can generally be divided into three major categories based on the degree of biomechanical force exerted per surface area of the injured nerve and the complexity of the injury. Nerve injuries caused by transection, contusion, stretch, traction, and avulsion are generally sustained when medium- to high-energy force is applied directly or indirectly to nerves, whereas injuries such as compressive neuropathy tend to occur when nerves are subjected to chronic or repetitive low-energy force (Fig. 230-1, 1 and 2 and Table 230-1). Nerve injuries from injection and from radiation and thermal energy involve a rather heterogeneous combination of different injuring factors and can be grouped together as a complex group of nerve injuries (Fig. 230-1, 3).
Medium- to High-Energy Nerve Injuries
Transection
Soft tissue lacerations with objects such as knives, glass, propeller and fan blades, chain saws, auto metal, and surgical instruments may transect nerves in about 30% of cases.1 In the remaining 70% of these injuries, 20% leave the nerve in partial and 50% in complete (lesion in continuity) continuity.1,2 The extent of functional loss is determined by variable degrees of neurotmesis, axonotmesis, and neurapraxia sustained by the nerve,3 even when the nerve or a portion of it remains in continuity (Fig. 230-2B). The extent of functional loss varies from mild and incomplete to severe and total. If a nerve is partially transected, the injury to the fibers cut is, by definition, neurotmetic or Sunderland grade V. In contrast, the fibers not directly transected can have a variable degree of injury and be Sunderland grade II, III, or IV (see Table 230-1 for grading systems for nerve injuries).4 In humans, the partially transected portion of a nerve seldom regenerates spontaneously, but when it does, it is not sufficient to restore function and therefore needs microsurgical repair.5 Functional recovery in some of these patients can be attributed to reversal of neurapraxia or to regeneration in the bruised and stretched portion of the nerve rather than in the transected portion.
The physical appearance of a sharply transected nerve differs from that of a nerve that has sustained blunt transection changes over time. After sharp transection, the epineurium is cut cleanly, and there is minimal contusive change or hemorrhage in either stump. With time, the stumps of the cleanly cut nerve retract and become enveloped in scar. The amount of proximal neuroma and distal nerve stump scarring is much less than that formed in a more contusive or blunt transection. Blunt transection is associated with a ragged tear of the epineurium acutely and an irregular, longitudinal extent of damage to a segment of the nerve. Bruising and hemorrhage can extend for several centimeters up or down either stump. Retraction and proliferative scarring around the stumps are often more severe than that are seen with sharp transection.6
Stretch, Traction, and Contusion with or without Lesion in Continuity
Medium- to high-energy force applied to nerves can result in a combination of different types of serious nerve injury ranging from significant stretch and traction injuries to differing degrees of contusion.7 The perineurium of intact nerves is rich in elastin and collagen, which provide tensile strength.8 However, even 8% stretch leads to a disturbance in intraneural circulation and blood-nerve barrier function,9 whereas stretch beyond 10% to 20%, especially if applied acutely, results in structural failure.10 Such force can therefore occasionally distract a nerve and pull it apart totally or, more commonly, leave it in continuity but with considerable internal damage (Fig. 230-2C). If distracted by substantial force, the nerve becomes frayed, and both stumps are damaged over many centimeters. The retraction and scarring about both stumps are severe. If the nerve is left in continuity, as is more likely, the degree of intraneural damage is variable and may, on occasion, be manifested as a spectrum of nerve fiber changes, including neurapraxia, axonotmesis, and neurotmesis. A stretch mechanism is also responsible for segments of damage to nerves displaced by high-velocity missiles, especially with gunshot wounds.6,8
Traction force applied to nerves is commonly sufficient to tear apart the intraneural connective tissue structure, as well as disconnect axons.11 Such lesions are Sunderland grade IV and are neurotmetic despite physical continuity of the nerve.12 Less frequently, such force results in a more axonotmetic or Sunderland grade II or III lesion, and these lesions may have the potential for effective regeneration because of less disruption of connective tissue.4
Most nerve injuries leave the nerve in continuity, which can make determination of the degree of injury and prognostication of functional recovery quite difficult (Fig. 230-2C). Contusive lesions tend to leave the nerves in continuity. These lesions in continuity can be either focal or diffuse and may even be multifocal with intervening areas of seemingly intact nerve. In the diffuse subtype, which represents the majority of cases, the entire cross section of the nerve has a similar extent of internal damage.13 Clinical and electrophysiologic examination provides guidance about the extent of injury to the nerve fibers such that sparing of one or more fascicles may produce a partial neurological deficit with preserved but diminished nerve action potentials (NAPs) across the injury site.14,15
With the typical lesion in continuity, the nerve is acutely swollen, with extravasation of serum or blood; axons and their myelin coverings disintegrate, and there is disruption of the connective tissue elements16,17 (Fig. 230-3A). Wallerian degeneration occurs, and axonal and myelin debris is phagocytosed from both the injury site and more distal part of the nerve.18 The Schwann cells (SCs), basal lamina, and distal connective tissue elements survive and are well positioned and conducive for axonal outgrowth.19 Unfortunately, the endoneurial and perineurial elements at the injury site proliferate rapidly and lay down poorly structured collagen that interferes with organized and properly directed axonal regeneration.20 Because there is some retrograde damage proximal to the injury site with most nerve injuries, clusters of regenerating axons must first traverse this area of loss.21 These regenerating axons next encounter poorly restructured collagen at the injury site,22 which leads to further disorganization in their orientation and delay in the process of axonal regeneration (i.e., staggered axonal regeneration).23 Axons branch many times as they traverse the site of injury. Such axonal branching in humans may occur several hundred times.24 Other axons may be deflected into peripheral connective tissue layers at the injury site as well as distally. As a result, axons reaching the distal stump are thin, poorly myelinated, and therefore less likely to reach previous distal end-organs than with a more axonotmetic injury. Many serious lesions in continuity are therefore not capable of regeneration of sufficient quality to lead to recovery of useful distal function.2 Some of the complex interrelated factors that ultimately determine the success of axonal regeneration after nerve injury are outlined in Figure 230-3. In clinical practice, because it is difficult to discern the extent of internal damage after this type of injury, most lesions in continuity are monitored clinically and reevaluated at intervals for several months before surgical exploration25 (Table 230-2).
| PARTIAL INJURIES (INCOMPLETE LOSS WITH SIGNIFICANT DISTAL SPARING) |
|
Most patients improve with conservative treatment. Follow with serial clinical examination supplemented with electrophysiologic assessment
|
EMG, electromyographic; NAPs, nerve action potentials.
Avulsion
Brachial plexus injury is a common disorder that is usually caused by a stretch mechanism. Stretch or traction injuries to the plexus most frequently result from extremes of movement at the shoulder joint, with or without actual dislocation or fracture of the humerus or the clavicle. With blunt or traction force, fracture of the scapula, ribs, cervical spine, or any combination of such fractures can also occur.26,27 A clavicular fracture seen with brachial plexus injury does not indicate that the injury was caused by the fracture but rather attests to the extensive force applied to the shoulder joint. On rare occasion, however, compressive upper trunk plexopathy may result in delayed fashion from bony callus generated from clavicular malunion28 (Fig. 230-4). Either upper or lower elements of the plexus may suffer the predominant injury, or with severe traction force, all elements may be involved in addition to the phrenic nerve and even subclavian vessels. All grades of damage are possible. Spinal nerves and roots can be avulsed from the spinal cord or more laterally from truncal or more distal outflow. The stretched elements may be left in continuity and have a mixture of neurapraxia and axonotmesis. A combination of neurapraxia, axonotmesis, and neurotmesis may coexist, but unfortunately, these mixed grades of injuries are more commonly severe in degree with significant neurotmetic components.
years after the injury he started to notice paresthesia in his shoulder girdle emanating from the supraclavicular area and over the course of time became aware of progressive weakness in shoulder abduction. Physical examination confirmed a severe suprascapular neuropathy and mild weakness in deltoid function. Electromyography demonstrated evidence of denervation that was severe in the supraspinatus and infraspinatus and sparse, although active in the deltoid. A and B, Radiographic and clinical appearance of the nonunited midclavicular fracture with substantial callus formation. The patient underwent exploration and external neurolysis of the upper part of the trunk along with the suprascapular and posterior division branches from the trunk that were being impinged by the callus. The callus was resected widely and the fracture repaired by an orthopedic surgery colleague with a plate and lag screw. The patient eventually achieved excellent bony union of the site and progressive improvement in shoulder girdle muscle strength and function. This case illustrates delayed complication from a nonunited fracture with callus causing adjacent nerve compression.Some anatomic features of the brachial plexus may predispose it to traction or even rupture. After the roots penetrate dura, they become spinal nerves. The spinal nerves run in the gutters of the foramina in the vertebrae for which they are named. At this intraforaminal level, the nerves are relatively tethered by mesoneural-like connections to the gutters.29 The spinal nerves then angle inferiorly and appear between the scalenus anticus and scalenus medius muscles and thus gain entrance to the posterior triangle of the neck. Spinal nerves are often injured in a characteristic fashion just as they run off the lip of the gutter of the transverse process. Force here may distract a spinal nerve from the trunk and produce a rupture (Fig. 230-5). Alternatively, such force may produce severe intraneural damage. These result in lengthy lesions in continuity that not only involve the spinal nerves and trunks but may also extend into the divisions and rarely, even into the more distal infraclavicular elements. A common finding with severe stretch injury is to see cords pulled away from more proximal elements of the plexus, such as roots and trunks. Unfortunately, in these circumstances, intraneural damage to these proximal elements often extends close to, if not all the way to the spinal theca or cord.24
A key clinical feature of stretch injuries is that although some may improve, many do not and require operative reconstruction (see Fig. 230-3A). However, these type of injuries pose an especially difficult challenge because there may be no satisfactory operative solution for some of the most severe stretch injuries. If the major injury is neurotmetic, it can involve such a long segment of the nerve that the only operative method for replacing the resulting extensive neuroma is the use of lengthy grafts. The results of repair with such lengthy grafts are often poor, and they are especially prone to fail at the proximal levels, where many stretch injuries begin.
Low-Energy Compressive/Ischemic Nerve Injuries
Peripheral nerves, like other neural tissues, are critically dependent on blood flow. Because it is rarely possible to compress a nerve segment without simultaneously affecting its blood supply, the relative roles of ischemia and physical deformation in compression lesions remain unsettled.30 More recent evidence suggests that although ischemia may be primarily responsible for a mild type of rapidly reversible nerve lesion, direct mechanical distortion is the major factor underlying more severe, long-lasting forms of pressure palsy such as Saturday night palsy or tourniquet paralysis.31–33 Ischemia can produce a wide range of nerve fiber lesions and, if severe and prolonged, results in extensive axonal loss and wallerian degeneration.34 Studies on limb ischemia suggest that there is a critical period of approximately 8 hours after which irreversible nerve injury ensues.35
Compressive Neuropathies
The sequential pathology of nerve fiber injury is rather stereotyped and occurs regardless of the compressive agent except in minor forms of compression.36 Compression of nerve fibers appears to produce changes in myelinated nerve fibers that are unique to this mechanism.37,38 Such changes include alterations in paranodal myelination, axonal thinning, and segmental demyelination.39–42 Axonal injury and therefore wallerian degeneration result from more severe degrees of compression.
The degree of recovery after compression or ischemic injury may be accurately predicted in some clinical situations. The characteristic Saturday night palsy results from compression of the radial nerve against the humerus. Total radial nerve palsy often results, but motor and sensory function is restored in the majority of patients without any need for surgical intervention. Most palsies associated with unconsciousness secondary to anesthesia and poor positioning or pressure during surgery, as well as those related to improper application of plaster casts, carry a good prognosis for spontaneous recovery.43 There are, however, important exceptions. Sometimes the compressive or crushing injury has been severe or prolonged enough to cause damage that is irreversible unless operative repair is undertaken. The brachial plexus and the ulnar, sciatic, and peroneal nerves are most commonly affected by these more severe compressive causes.44 Restoration of function after acute compression and ischemic injury may be uncertain in some circumstances. It may be difficult, for example, to predict the degree of recovery that follows evacuation of hematomas or relief of pseudoaneurysmal compression of such structures as the brachial plexus and the femoral or sciatic nerves.45 There are also circumstances in which two levels of compression may exist.46 A patient with cervical spondylolysis or relatively mild disk disease affecting a root or spinal nerve may be more likely to become symptomatic with an otherwise mild degree of compression of the median nerve at the wrist or ulnar nerve at the elbow. In these circumstances, multiple factors affect the outcome of peripheral nerve surgery, including the identity and level of the nerve involved, the age of the patient, the extent of precompression injury to the nerve, and the timing of corrective surgery.
Compartment Syndromes
Severe crushing injury, skeletal fracture with vascular compromise, and anticoagulant administration resulting in hemorrhage can lead to increased pressure within a fascial compartment. As a consequence, severe compression and ischemic damage to peripheral nerves and other soft tissues can result. A closed compartment syndrome with impending ischemic paralysis requires immediate decompression with properly placed and usually extensive longitudinal fasciotomies.47 Delay in treatment results in ischemic infarction of muscle, nerve, and other tissues, which leads to contractures and other crippling deformities.
Volkmann’s contracture is a serious example of ischemic compression caused by the development of compartment syndrome. There is injury to the brachial artery along with diffuse segmental damage to the median nerve and volar forearm muscles. The large median and sometimes radial nerve fibers serving motor and proprioceptive function are more severely involved than the smaller pain fibers. Electromyography may aid in diagnosis by showing temporary but repetitive and spontaneous motor discharges from muscles most distal to the injury site.48 Swelling of the forearm resulting in a painful paresthetic hand must alert the physician to an impending compartment syndrome long before more obvious signs of vascular compromise are apparent.
