Hand Injuries, Part 2:
Hand Injuries, Part 2:
Each year, more than 16 million Americans sustain hand injuries that require emergency care.1 These injuries may involve the nerves, vessels, tendons and ligaments, bones, joints, nail beds, and skin (Figure 1).
Left untreated—or treated improperly—hand injuries may lead to infection and even permanent disability. Consequently, prompt recognition and effective management are crucial (Figure 2).
In the February 2005 issue of CONSULTANT, beginning on page 242, we detailed the general neurologic, vascular, and musculoskeletal evaluation of patients with hand injuries. We also described how to cleanse, anesthetize, and close wounds to minimize the risk of infection.2
Here we turn our attention to the specifics of diagnosing and managing injuries to the nerves, vasculature, tendons, and ligaments of the hand. In an article beginning on page 393 of this issue, we will complete our discussion of hand trauma; our focus will be on management of fractures, dislocations, nail bed injuries, and bite wounds.
There are 3 distinct categories of nerve injury—neurapraxia, axonotmesis, and neurotmesis. Each is associated with sensory and/or motor nerve deficit; clinical differentiation is based on whether and how quickly nerve function returns.
Neurapraxia results from blunt trauma to a nerve; a transient loss of function occurs, although the integrity of the nerve remains intact. The neurologic deficit usually resolves within 1 to 3 weeks, depending on the severity of the contusion.
Axonotmesis represents axon disruption within a preserved endoneural tube. Wallerian degeneration and subsequent gradual axon regeneration ensue at a rate of 1 to 3 mm per day. The patient eventually recovers full nerve function.
Neurotmesis occurs when all the nerve structures have been damaged. Unless surgical reanastomosis is timely, the loss of function is permanent.
Radial nerve injury. Damage may occur as the radial nerve passes over the dorsum of the wrist. However, injury most frequently occurs proximally and may manifest as an apparent "wrist drop" in which the patient cannot dorsiflex the wrist or demonstrates weakness in wrist dorsiflexion. This finding may also accompany fractures and acute or chronic compression injuries. Regardless of the cause, sensory deficits, paresthesias, and motor dysfunction may be seen in the radial nerve distribution.
Median nerve injury. Lying between the flexor carpi radialis and palmaris longus tendons on the volar surface of the wrist, the median nerve supplies sensation to the radial aspect of the palm and to the palmar surfaces of the thumb, index and long fingers, and radial half of the ring finger. Deficits in median nerve sensory function must be specifically sought, since there is almost complete overlapping from the other nerve distributions. However, sensation to the tips of the thumb and index finger is provided only by the median nerve. Therefore, examine these regions when testing sensory function of the median nerve.
Several possible traumatic causes for acute symptoms of median nerve damage exist; these include wrist fractures, crush injuries, hemorrhage within the flexor retinaculum, burn injuries, and vigorous hand exercises. More often, repetitive motions with the fingers held in flexion and the wrist held in extension—such as typing, driving, and piano playing—lead to chronic symptoms, including numbness, tingling, and burning pain in the tips of the index and middle fingers and of the thumb (carpal tunnel syndrome).
Neurologic examination typically reveals isolated thenar atrophy and the Tinel sign and/or Phalen maneuver. The Tinel sign refers to paresthesias produced along the median nerve distribution in response to percussion of the median nerve at the center of the volar aspect of the wrist. The Phalen maneuver pertains to paresthesias generated when the patient holds his or her hand in full flexion for 60 seconds.
Ulnar nerve injury. The ulnar nerve lies radial to the flexor carpi ulnaris as it passes along the volar surface of the wrist. Because of its proximity to the ulnar artery, injury to one frequently means injury to both.
Injury to the ulnar nerve produces loss of sensation of the volar and dorsal surfaces of the little finger and of at least the ulnar half of the ring finger. The associated motor loss varies little from patient to patient, because there is an overlap of only 10% or less with the median nerve distribution. However, the interossei muscles are usually weakened or paralyzed, rendering patients unable to spread their fingers.
Loss of lumbrical function in the ring and little fingers may lead to the classic clawhand deformity in response to ulnar nerve injury. Another indicator of damage to the ulnar nerve is the Froment paper sign—the inability to maintain strong adduction of the distal phalanx of the thumb against the index finger when holding a piece of paper between the two. (A patient with a positive Froment paper sign will also try to compensate by flexing the thumb against the index finger.)
Treatment. Refer to a hand surgeon any patient with suspected blunt trauma to a nerve, even if evidence of compartment syndrome is lacking. If neurologic symptoms do not appear to improve over time, the hand surgeon may elect to explore the injured hand to identify and repair a surgically correctable lesion if present.
In open wounds with obvious direct nerve injury, prompt nerve repair by a hand surgeon is the ideal, although it may be successfully delayed for several weeks. When indicated, standard wound care (including immediate irrigation and suturing) is necessary to prevent infection.