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This article outlines the vascular anatomy of the carpus, describing the extraosseous and intraosseus vascular systems and emphasizing the carpal bones at risk for osteonecrosis. Separate discussions of etiology, diagnosis, and treatment of osteonecrosis of the commonly involved carpal bones are included.

With the aging population and improved methods of emergency transport, the number of surviving stroke and brain injury patients continues to increase. Aggressive rehabilitation of appropriate candidates is justified. In the period of spontaneous recovery, efforts are made to prevent fixed contractures using passive mobilization, splinting, nerve blocks, and electrical stimulation. If deformity persists and the patient is no longer recovering, operative management can help alleviate the functional and hygiene problems associated with these limb deformities.

Increased tissue pressure within the confines of a nondistensible anatomic compartment increases venous pressure, causes vascular compression, decreases the arteriovenous gradient, and results in a compartment syndrome. The decreased blood flow and hypoxia result in cellular damage of muscles, nerves, and vascular endothelium. Richard von Volkmann's legacy has taught us that a patient's overall status must be monitored to follow the systemic determinants of peripheral blood flow and oxygen transport. Limbs must also be monitored with vigilance. A high index of suspicion must always be present, and compartment pressures can be measured directly to aid in clinical decision making regarding the status of a compartment. The remaining articles in this issue describe and explore von Volkmann's syndrome using the terms and concepts introduced here.

Crush syndrome is the severe systemic manifestation of prolonged muscle compression and compartment syndrome. Careful patient assessment, early diagnosis, and aggressive treatment are vital to prevent multiorgan failure and death. Medical management of systemic complications, along with operative procedures of fasciotomy and debridement, are indicated with accompanying compartment syndrome. Debridement of necrotic and nonviable tissue is necessary; significant risks of infection and hemorrhage remain until the wounds can be subsequently closed or covered with skin graft. Crush syndrome and muscle necrosis in a closed injury without compartment syndrome may be followed clinically until healing or demarcation of a gangrenous part occurs, providing the patient's general medical condition, including renal function, can be maintained. Fasciotomy and hyperbaric oxygen will not reverse necrosis of muscle in the absence of compartment syndrome and therefore do not affect outcome of the extremity. Overall, prognosis is improved by early diagnosis and treatment, but outcome of the crushed extremity is poor and Volkmann's contracture often results.

The forearm is the most common site for compartment syndrome in the upper extremity. The three compartments of the forearm include the volar (anterior or flexor), the dorsal (posterior or extensor), and the mobile wad. Both-bone forearm fractures and distal radius fractures are common initial injuries in adults that lead to acute forearm compartment syndrome. Supracondylar fractures, especially those with associated vascular injuries, are frequent causes of compartment syndrome in children. The flexor digitorum profundus and flexor pollicis longus are among the most severely affected muscles because of their deep location, adjacent to bone. Initial treatment consists of removal of occlusive dressings or splitting or removal of casts. If symptoms do not resolve rapidly, fasciotomy is indicated. Decompression fasciotomy of the forearm is performed through volar or dorsal approaches. The medial nerve is decompressed throughout its course, including high-risk areas deep to the lacertus fibrosus; between the humeral and ulnar heads of the pronator teres, the proximal arch, and deep fascial surface of the flexor digitorum superficialis; and the carpal tunnel.

Exertional compartment syndrome is characterized by intracompartmental pressures that rise transiently following repetitive motion or exercise, thereby producing temporary, reversible ischemia, pain, weakness, and, occasionally, neurologic deficits. The exact cause or pathogenesis remains unclear; a disturbance of microvascular flow caused by elevated intramuscular pressure leads to tissue ischemia, depletion of high-energy phosphate stores, and cellular acidosis. Anatomic contributing factors may include a limited compartment size, increased intracompartmental volume, constricted fascia, loss of compartment elasticity, poor venous return, or increased muscle bulk. The diagnosis is suspected based on history and confirmed with physical examination and intramuscular pressure evaluation before and after exercise (stress test). Differential diagnosis includes claudication or other vascular abnormalities, myositis, tendinitis, periostitis, chronic strains or sprains, stress fracture, other compression or systemic neuropathies, and cardiac abnormalities with angina or referred extremity pain. Initial treatment includes activity modification; refractory symptoms can be managed with elective fasciotomy.

Upper extremity deformity of ischemic contracture usually includes elbow flexion, forearm pronation, wrist flexion, thumb flexion and adduction, digital metacarpophalangeal joint extension, and interphalangeal joint flexion. Treatment of mild contractures consists of either nonoperative management with a comprehensive rehabilitation program (to increase range of motion and strenght) or operative management consisting of infarct excision or tendon lengthening. Treatment of moderate-to-severe contractures consists of release of secondary nerve compression, treatment of contractures (with tendon lengthening or recession), tendon or free-tissue transfers to restore lost function, and/or salvage procedures for the severely contracted or neglected extremity.

The complexity and intricacy of hand function are reflected by the anatomy. Extensor muscles have a relatively consistent architecture but also have notable anatomic variations of their tendons, particularly on the ulnar side of the hand. The extensor tendons, juncturae tendinum, intertendinous fascia, and soft tissue function as a plexiform construct to provide stability during power grip and allow for laxity in performing independent fine finger tasks. The greater independence of index finger motion relates to its two tendons, one (EDC-index) with a thin transverse juncturae tendinum, the other (EIP) without a junctural connection. It is also more independent because of a more mobile metatarsal, and because it is confined by only one web. The first dorsal interosseous also functions to rotate the index finger. The lumbrical to the index finger has only a single origin on the flexor profundus tendon. The elaborate tendon plexus on the dorsum of the hand is repeated in the complexity of the dorsal aponeurosis on the dorsum of the fingers. Finger motion is a balance of flexor muscles and intrinsics and extensor muscles that provides incredible versatility. This versatility and delicate balance of function is easily jeopardized by trauma and disease. The hand is among the most frequently injured parts of the body. An appreciation and understanding of its complex anatomy is of importance to hand assessment, repair, and reconstruction.

CTS is a common upper extremity problem that has an increasing incidence and poorly understood causes. Radiographs and electrodiagnostic tests are helpful, but the diagnosis remains based on clinical symptoms and signs. The several sites of median nerve compression must be considered. Splinting and steroid injections are often effective. Carpal tunnel release is indicated in refractory or acute problems, and both open and endoscopic methods remain popular. Each has specific advantages.

Recurrent symptoms of CTS have been shown to occur in 0% to 19% of patients following CTR, with up to 12% requiring re-exploration. Common causes of recurrent CTS are incomplete release of the TCL, fibrous proliferation, or recurrent tenosynovitis. The prognosis for re-exploration is fair; improvement can be achieved in many cases, but prognosis is not as favorable as in primary CTR. The most predictable improvement seems to be in patients with CTS caused by granulomatous infections, in which proper surgery and medical therapy can usually result in a satisfactory outcome. For the heavily scarred carpal tunnel with fibrous proliferation, many operative options are available. These procedures include external nerve lysis and mobilization, followed by application of local muscle flaps, fat grafts, or vein wrapping. There appear to be higher recurrence rates and poorer outcomes in patients with occupation-related CTS.

The purpose of this study was to delineate the motor point region of the gluteus medius muscle to aid in placing epimysial electrodes for functional electrical stimulation. Seven surgically dissected gluteus medius muscles were studied in five patients. The lateral surface of the muscle was sequentially probed with an electrical stimulator. The motor point region, which responded maximally to an applied electric current, was located on the posterolateral aspect of the muscle, adjacent to the superior margin of the piriformis, 3 cm lateral to the greater sciatic notch; it was rectangular or oval, measuring approximately 3.5 cm by 3.0 cm. The mean threshold current that produced a contraction was 14 mA (range = 2 to 26 mA). The mean minimum current required to produce a maximum contraction was 34 mA (range = 11 to 60 mA). This information provides guidelines for the placement of electrodes for functional electrical stimulation of this deeply situated muscle, and it provides electrical stimulation parameters required for adequate muscle activation.

Carpal bone fractures comprise an important group of injuries that present difficulties in both diagnosis and treatment. These fractures may be missed for the following reasons: physician's low index of suspicion, the carpal bones' irregular contours and degree of overlap on radiographs making the fractures difficult to visualize, and the common occurrence of concomitant fractures of neighboring metacarpals, distal radius, or scaphoid, which misdirects the examiner. A high index of suspicion with careful clinical examination and elicitation of point tenderness is key to making the correct diagnosis (Fig. 14). Swelling, loss of motion, deformity, and crepitus are often minimal and are not reliable in distinguishing carpal fractures. Specific radiographic projections, tomograms, computerized tomographic scans, or bone scans are often required and should be considered in any wrist injury where the diagnosis is in question. A greater awareness of the fracture types, methods of diagnosis, and choices of treatment is essential for optimal management of these injuries.

Malunions of the distal radius are common. Although the best treatment is prevention, symptomatic malunions can be salvaged through more careful fracture management, by corrective osteotomy or, in the presence of post-traumatic arthritis, radiocarpal arthrodesis. Dynamic midcarpal instability following radius malunion does not respond as well to ligament repair or intercarpal arthrodesis as it does to osteotomy of the radius and correction of the malunion deformity.