Median nerve injuries to the forearm are quite common and can lead to devastating functional sequelae in the hand if not treated promptly and appropriately. Most nerve injuries should be repaired as soon as possible after the injury, and current widely used microsurgical techniques can lead to a desirable outcome for most patients. Despite improvements, there are still many patients with median nerve injuries who do not achieve an ideal prognosis and are left with irreparable complications. This article will discuss the current techniques for managing median nerve injuries with the goal of preventing or mitigating the potential negative sequelae of these injuries.
The median nerve travels medial to the upper arm and crosses into the forearm at both ends of the pronator teres muscle. The median and ulnar nerves may have an anomalous traffic branch (Martin-Gruber traffic branch) in the proximal forearm, a traffic branch from the median nerve to the ulnar nerve, where the ulnar nerve continues down to innervate the small muscles of the hand formerly innervated by the median nerve. Similarly, both may also have branching traffic branches in the palm of the hand (Riche-Cannieu traffic branch). In this case, the ulnar nerve usually sends nerve bundles to associate with the palmar muscles innervated by the median nerve. If these branches are present, repair of the median nerve will achieve better results than expected.
The median nerve is quite deep in the proximal forearm, so its injury at this location is usually a deep penetrating injury with severe soft tissue damage. As it travels down the forearm, its location becomes increasingly superficial, especially in the distal wrist before it goes into the carpal tunnel. Thus, distally, the median nerve is particularly susceptible to injury, even superficial lacerations or hospital-acquired injuries.
Median nerve injuries are common during daily activities, usually in younger patients with lacerations to the wrist (glass or other sharp objects) and in older patients in motor vehicle (especially motorcycle) crashes. In a longitudinal review of nerve injuries in the United States, 2700 median nerve injuries were documented by Lad et al. in 2006. Of these patients, 78% were male, 61% were between the ages of 18 and 44, a total of 71% were enrolled in teaching centers, 94% were seen in metropolitan hospitals, 37% met the index for hospital emergency department visits, and the data for receiving repair treatment within the first week were unclear. Their hospitalization costs were within $28,000. There are no statistics on repair methods and outcomes by injury type.
In a review of experiences with nerve injury treatment from recent Middle East conflicts, Birch et al documented 261 nerve injuries in 100 patients, of which only 29 (11% of all nerve injuries) involved the median nerve. They reported that mortality rates from the recent conflict were reduced compared to previous reports, but patients continued to live with the concomitant of more severe, extreme injuries.
Clinical presentation.
Patients with median nerve injuries have a very typical clinical presentation. It is usually an open wound. Puncture wounds to the adjacent nerve of the hand or blast injuries require a thorough examination. Complete injury to the proximal median nerve usually results in sensory deficits in the thumb, index finger, middle finger, and radial half of the ring finger. Proximal injuries may also result in weakness or motor deficits in the pronator teres, radial carpal flexor, palmaris longus, flexor digitorum longus, flexor digitorum profundus, and/or flexor digitorum profundus of the middle finger. Lacerations of these muscles can also result in poor function, and in those with normal sensation and poor flexion function, it is more often due to direct injury rather than median nerve damage. When the median nerve is damaged, the piriformis muscle strength also becomes weaker.
Isolated injury to the median nerve in the distal forearm results in weaker muscle strength in fewer muscles, involving only the flexor muscles of the forearm, but this injury is rare because lacerations deep enough to damage the median nerve usually also injure the flexor tendons. In cases where the nerve alone is injured from a puncture injury that does not involve the flexor tendon, the predominant symptom is a loss of sensation in the innervated finger. There may also be antagonistic weakness due to paralysis of the intermetacarpal muscles in the area of median nerve innervation.
All patients with nerve injury will have Tinel’s sign at the location of the nerve injury, which is a gentle tap along the nerve to identify the level of injury at which the patient will have an electric shock sensation transmitted distally along the nerve’s course. After the nerve is repaired, this location will act as a regenerating axon conducting stimuli from the distal side along the nerve walk.
Diagnosis.
The diagnosis of median nerve injury can be based on purely clinical grounds. In the face of an open wound with symptoms of median nerve denervation, the diagnosis is usually determined by surgical exploration. In patients with late presentation, it is more difficult to diagnose the location and extent of the injury. Site diagnosis and the extent of injury after the patient presents late is very difficult. Likewise, in those cases of closed median nerve injury and some medically induced injuries, diagnosing the level of injury to the nerve is also very difficult.
A comprehensive overview of the application of electrodiagnostic testing to the assessment of nerve injury is beyond the scope of this article, but there are several key points.
Electrodiagnostic tests are useful for nerve injury, can help diagnose the level of nerve injury, and have the potential to help understand whether the nerve is intact. These tests may also diagnose the presence of abnormal nerve communication. Patients with incomplete nerve tears may have a loss of function (movement or sensation) in a portion of the same innervation that has tested normal and functions well. In incomplete nerve injuries (nerve disuse), compound muscle action potentials (CMAP) and nerve action potentials (NAP) are still preserved distal to the injury. For the preserved CMAP and NAP, stimulation of the proximal nerve also shows partial or complete conduction block. As the nerve recovers, conduction block slowly decreases and does not interfere with normal function despite some continually slowing conduction. In complete nerve injury (axonal disruption), CMAP and NAP show decreases distal to the injury roughly proportional to the degree of axonal loss. Both are completely lost at 11 days post-injury and cannot be improved except by repair.
Although conventional teaching indicates that early electrical stimulation tests (early 3 weeks after injury) are not helpful, there may be some benefit in performing these manipulations in the beginning weeks. In extensive soft tissue injuries where it is difficult to identify the level of nerve damage, early electrodiagnostic testing can be used to determine the level of injury independently and precisely because the axon of the nerve dissection will have a bioelectrical response that lasts for a week but cannot be transmitted through the location of the receptive. In addition, the presence of motor unit action potentials suggests that the neuropathy is incomplete. Generally speaking, most information can be obtained if electrical stimulation testing is performed 3 weeks after median nerve injury.
Neuroimaging techniques are still in their relative infancy, but the increasing interest of radiologists by and improvements in magnetic resonance neurology (MRN) techniques have led to some promising advances. For mild strain injuries, MRN will show enlargement of the injured region of the traveling nerve and surrounding fluid areas. For higher-violence nerve injuries (axonal disruption) there may be continuity neuromas present, or nerve disorders and neuroma formation may be seen in the proximal nerve. These changes are well observed in both T1- and T2-weighted images, and the two may complement each other.
Treatment.
Most median nerve injuries require surgical intervention if only for nerve exploration and nerve release to rule out more severe injury.
Although several diagnostic modalities were discussed earlier, the severity of nerve injury cannot always be confirmed without nerve exploration. Nonetheless, in a closed injury (e.g., stretching) or a small puncture injury that manifests neurological deficits only a few weeks after injury, caution is required to assess cautiously by electrodiagnostic methods or MRN. If there is no evidence of complete nerve disruption, a period of time may be given to attempt recovery. Generally speaking, this period is approximately 6 months, allowing time for regeneration but not so long that loss of motor endplates in innervated muscles at the level of injury becomes a problem. Injuries at the shoulder level from stretching injuries or arthroscopic medically induced injuries are particularly difficult to decide when to treat. The author would like to see a positive Tinel’s sign, which may occur sooner if the nerve has only experienced a traction injury. Combined with signs of clinical functional healing and an electrical response sign of muscle nerve reinnervation within 6 months, this usually predicts a very good prognosis. In the case of open injuries with significant nerve dissection or no signs of nerve recovery within 6 months, the author will usually perform nerve exploration and repair.
Most median forearm nerve injuries are accessed through a longitudinal incision along the course of the nerve. An incision is made from the proximal to the distal end to mark and protect the branch. In the proximal and middle 1/3 of the forearm, the nerve travels beneath the muscle and requires careful approach from proximal to distal until the site of injury. In the distal 1/3 of the forearm, it is easier to expose for release repair. The most difficult location to expose is between the biceps of the pronator teres. In this segment, most of the nerve branches innervating the proximal forearm muscles emanate, including the anterior interosseous nerve. In the pronator teres segment, the branches innervating the lateral forearm muscle group emanate here. If there is an injury in this segment, nerve release must be performed very carefully to prevent damage to any intact motor branches. Regardless of the site of nerve injury for which nerve release is performed, great care must be taken to prevent stripping even the smallest possible intact portion, as this guides the course of the nerve and avoids disorganization of the motor and sensory nerve fiber bundles during nerve regeneration.
If explored early (5-7 days after injury), most sharp injuries can be repaired. Large nerves can be repaired using high-powered magnification (magnification 3.5 or greater), but graft and smaller branch repairs require the use of a microscope. Well done extra-neural membrane repair (concentricity) will provide good results. Performing nerve bundle repair requires intraneural dissection as well as more advanced microsurgical skills. The edges must be trimmed of fibers and nerve fragments to ensure repositioning of the protruding axon, but this will usually be minimal if it is a sharp force injury. The wrist needs to be flexed to 45 degrees, but if moderate flexion of the wrist and flexion of the metacarpophalangeal joint does not allow for nerve repair, some other technique is applied. The median nerve must be aligned to prevent axonal mismatch, and usually the superficial vessels (distal to the nerve) and surrounding tissue can help with alignment. The author typically repairs the nerve with 8-0 nylon sutures, but will use thicker sutures such as 6-0 or 7-0 polypropylene for epineural sutures. Localized injuries may require extra-neural release several centimeters from either end to facilitate repair of the injured site and restore the intact nerve circuit.
For median nerve injuries that cannot be repaired by ligature, there are primarily autologous nerve grafts or bridging using other modalities that can be used for nerve defect repair. Most physicians prefer autologous grafts, and in the case of thick nerves in general with the median nerve, the preference remains from the lateral fibula of the lower leg. Other methods of repairing the defect are the creation of collagen ducts that have allowed the nerve to regenerate.
For substantial high-energy injury to the nerve, nerve grafting may be an option that may enable and can provide functional recovery. There are few reports on this option. There is one report of good recovery of exogenous motor function by transfer from the posterior rotator, radial extensor carpi radialis shortis branch, and sensory recovery by repair of the lateral cutaneous nerve of the forearm, but reports of persistent pain for 4 years after surgery. More clinical studies by experienced surgeons are needed to develop the best treatment modality in this area. Most agree that postoperative care is helpful in the treatment of median nerve injuries. Sensory restoration exercises are recommended to improve the quality of perception, but recent studies have shown little success with these approaches.
Complications.
The main complication of median nerve injury is poor function. Injuries to the nerve that are not repaired can lead to a host of problems, including distressing neuromas and potentially chronic regional pain syndromes. Therefore, median nerve injuries should be repaired. Because of the lack of sensation in the fingers, patients with unrepaired median nerve injuries are likely to experience further injuries such as burns or other injuries. The lack of thumb function as well as poorer sensation results in poorer motor function of the entire hand.
Complications after direct nerve suturing are relatively rare, but can trigger pain and neuroma formation if damaged early after repair.Thomsen et al. studied 163 patients with direct collagen-coated nerve repair and did not find any evidence of neuroma formation or clinical signs of neuroma (pain at the repair site or Tinel’s sign). In nerve grafts, failure of the regenerating axon to enter the nerve graft can lead to neuromatosis formation. Meek et al. reported 41 peripheral nerve grafts, all of which received either a peroneal nerve graft or a medial forearm skin graft (mainly referring to nerve defects). Although this study had a variety of results, they noted that the most common complication was the formation of a neuroma located at the graft site. This occurred in 7 of their 41 patients (17%).
In conclusion, failure of the first nerve repair or failure of the nerve graft requires re-exploration as well as re-repair. Functional loss of median nerve injury and potential pain due to repair failure are unacceptable outcomes.