Compartmental Syndromes.

Edited By: Winston J. Warme, MD, Frederick A. Matsen III, M.D.
Last updated Thursday, February 10, 2005

Sequelae

Sequelae of compartmental syndromes

Sequelae of compartmental syndromes may include persistent hypesthesia and dysesthesia, persistent motor weakness, infection, myoglobinuric renal failure, contractures, amputation, and death.

These sequelae are the direct result of nerve and muscle injury and death, and thus their frequency and severity are minimized by prompt diagnosis and treatment of compartmental syndromes.

The potential sequelae of a compartmental syndrome include persistent hypesthesia and dysesthesia, persistent motor weakness, infections of bone and soft tissue, renal failure, contractures, amputation, and death. Early treatment of compartmental syndromes is the best method for preventing these sequelae. This point is well demonstrated by our retrospective review of 46 extremities in 44 patients having surgical decompression of compartments afflicted with compartmental syndromes. 1 Only 7 of the 22 extremities decompressed within 12 hours of the appearance of the compartmental syndrome showed residual deficits at the time of follow-up examination; only 1 had a significant complication. In four of these cases, compartmental syndromes developed after intra-arterial drug injection, a situation in which microembolization also compromises local circulation. 2-4 If these four cases are excluded, residual deficits occurred in only 3 of the remaining 18 extremities that received early decompression. By contrast, 22 of the 24 extremities having late decompression showed residual functional losses (none of these compartmental syndromes resulted from intra-arterial drug injection). In the late decompression group 13 of the 24 extremities had complications, 5 of which required amputation.

It is important to realize that in this study the duration of the compartmental syndrome before surgical decompression was determined retrospectively from the time that the earliest evidence of functional deficits appeared, not the time at which the syndrome was diagnosed by the physician caring for the patient. In many cases, much of the apparent 12-hour "grace period" had elapsed before the diagnosis of a compartmental syndrome was made.

Motor deficits resulting from a compartmental syndrome are initially treated with appropriate orthotic devices, e.g., a drop foot brace when the anterior compartment of the leg is affected. If function does not return in about one year, tendon transfer and other forms of reconstructive surgery may be considered. Hypesthesia and painful dysesthesia can also result from a compartmental syndrome. These may resolve slowly with time. Diphenylhydantoin (Dilantin, Parke-Davis) and carbamazepine (Tegretol, Ciba-Geigy) may be of some value in making the patient more comfortable.

Infection can be a serious complication of a compartmental syndrome. In our retrospective reviews 11 of 24 extremities having late surgical decompression developed infections. Five, or almost one-half, of these infections led to an amputation. One case of osteomyelitis occurred in a patient with an initially closed tibial fracture who underwent fasciotomy and primary closure 28 hours after the onset of the compartmental syndrome. Infection appears to be most frequent in the presence of devitalized muscle, particularly if skin closure has been attempted. Infected compartments are treated by wide opening of dressings, skin, and fascia, thorough lavage of all affected areas, and debridement of infected tissue. The wound is treated open with damp dressings until it is sufficiently clean for closure or skin grafting. In some cases of refractory osteomyelitis associated with severe functional losses, amputation may present the only reasonable treatment.

Myoglobinuric renal failure is another serious and potentially fatal complication of compartmental syndromes. 5-l0 Myoglobin is released from damaged muscle cells in amounts related to the severity of the muscle damage. If the damaged muscle is perfused, myoglobin enters the circulating blood and is filtered by the kidney. Muscle ischemia of 4 hours gives rise to significant myoglobinuria, which reaches a maximum approximately 3 hours after the circulation is restored, but which persists for as long as 12 hours. Significant myoglobinuria produces myoglobinuric renal failure, which may be due to a direct toxic effect of myoglobin, to renal vasoconstriction, to precipitation of myoglobin in the renal tubules, or to a combination of these factors. Most hospitals have sensitive and specific assays for urinary myoglobin. If these are not available, dark urine may usually be attributed to myoglobinuria if the benzidine or hemastix tests are positive in the absence of pink serum and microscopic hematuria. If myoglobinuria is suspected, one should endeavor to maintain a high urinary output to dilute the effect of myoglobin on the kidney. Because myoglobin is less soluble in acid urine, precipitation may be minimized by the maintenance of an alkaline urine through the administration of lactate or bicarbonate. If renal failure ensues, prompt institution of dialysis may be required. Whereas myoglobinuric renal failure may complicate any compartmental syndrome, it appears to be most common after compartmental syndromes produced by prolonged limb compression in a drug-overdosed patient.

Contractures not infrequently complicate compartment syndromes. l 4,11-15 They appear to result from the shortening of ischemically damaged muscle and from associated nerve damage. Contractures appear to be most common after volar compartmental syndromes of the forearm and deep posterior compartmental syndromes of the leg. In both locations the long flexor muscles of the digits and the nerve supply to the intrinsic muscles are affected. Curiously, the muscles of the commonly involved anterior compartment of the leg rarely undergo postischemic contracture.

Contracture from compartmental syndromes is minimized by early compartmental decompression and by appropriate splinting of the limb during the postoperative period. Passive stretching exercises may help maintain muscle length and the range of motion of the joints. If contractures become established, some combination of muscle-releasing procedures, tendon lengthenings, muscle debridement, neurolysis, tendon transfers, and bony procedures may be necessary.

Death has been known to result from compartmental syndromes. In the series reported by Sheridan and Matsen, 1 a patient with brittle diabetes died from overwhelming sepsis after delayed surgical decompression. Coupland 16 reported a case of sudden death after surgical decompression and attributed this to the sudden release of a large quantity of acidotic, hyperkalemic blood that apparently produced a fatal arrhythmia. When the patient's life is threatened by infection, myoglobinuria, or other systemic effects of a compartmental syndrome, emergency amputation may be life saving.

Surgery for Compartmental Syndromes at the University of Washington

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