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© 1998 The Journal of Bone and Joint Surgery, Inc. Delayed Onset of Anterior Tibial Compartment Syndrome in a Patient Receiving Low-Molecular-Weight Heparin. A Case Report*  , NEW HYDE PARK, NEW YORKInvestigation performed at the Department of Orthopaedic Surgery, Long Island Jewish Medical Center, New Hyde Park
Patients who have sustained a major traumatic injury of a lower extremity are at high risk for the development of deep-vein thrombosis. The use of low-molecular-weight heparin for prophylaxis against deep-vein thrombosis in such patients has been advocated by several authors2,4,5,7,9,12. Major complications attributed to the use of low-molecular-weight heparin have included hemorrhage2,8 and spinal epidural hematoma13. Compartment syndrome usually is associated with high-energy or crush injuries. The symptoms of compartment syndrome usually present within twenty-four to forty-eight hours. Compartment syndromes occurring in the absence of an underlying osseous injury are unusual. We describe a case of delayed-onset compartment syndrome of the leg in a patient who was receiving low-molecular-weight heparin.
A thirty-three-year-old man sustained injuries of the left lower extremity in a motor-vehicle accident. The patient was otherwise healthy and had no known hepatic, clotting, or bleeding abnormalities. Physical and radiographic examination revealed closed segmental fractures of the left femur and tibia. Physical examination of the right lower extremity revealed several small, superficial abrasions. There was no swelling or ecchymosis. The compartments of the right thigh and leg were soft, and neurovascular function was intact. Anteroposterior and lateral radiographs of the right tibia revealed normal findings. The patient was managed with emergent retrograde intra-medullary nailing of the left femur and external fixation of the left tibia. Approximately twenty-four hours after the operation, low-molecular-weight heparin, or enoxaparin (Lovenox), was administered subcutaneously at a dose of thirty milligrams every twelve hours for prophylaxis against deep-vein thrombosis. In addition, a sequential compression device was used on the right leg during the first few postoperative days. The postoperative course was uneventful, and the patient remained in the hospital pending transfer to a rehabilitation facility. He was able to walk with assistance. On the twelfth postoperative day, the patient reported pain in the anterior aspect of the right (uninjured) leg. Physical examination revealed a tense, tender anterior compartment and increased pain with passive plantar flexion of the ankle. The posterior compartments of the right leg were soft, and the patient reported no pain with passive dorsiflexion of the ankle. The patient had decreased sensation in the distribution of the deep peroneal nerve, and the strength of the extensor hallucis longus was decreased to grade 2 of 5. The remainder of the neurological examination was unremarkable. Compartment pressures were measured with use of the technique described by Whitesides et al.14 The pressure in the anterior compartment was 110 millimeters of mercury (14.66 kilopascals), and the pressures in the deep and superficial posterior compartments were both approximately thirty-five millimeters of mercury (4.67 kilopascals). At the time of measurement of the compartment pressures, the blood pressure was 124/86 millimeters of mercury (16.53/11.46 kilopascals). Coagulation studies performed at this time revealed a prothrombin time of 15.3 seconds (normal, 11.0 to 13.0 seconds) and a partial thromboplastin time of 31.7 seconds (normal, 20.1 to 31.4 seconds), with an international normalized ratio of 1.34. The administration of low-molecular-weight heparin was immediately discontinued. An urgent four-compartment fasciotomy was performed through medial and lateral incisions. A large volume of clotted blood was removed from the anterior compartment. The superficial posterior, deep posterior, and lateral compartments appeared to be normal. There was no evidence of active bleeding or muscle necrosis. Within twenty-four hours after the fasciotomy, motor and sensory function returned completely. Within forty-eight hours after the discontinuation of the low-molecular-weight heparin, the prothrombin and partial thromboplastin times returned to normal. On the second day after the fasciotomy, the medial and lateral incisions were closed without complication. The early closure of the incisions was possible because of the removal of a large volume of clotted blood at the time of the fasciotomy. Approximately seven days after the fasciotomy, the patient was able to bear full weight on the right lower extremity without pain. After approximately five months of follow-up, the fasciotomy incisions were fully healed, the neurovasculature of the right lower extremity was intact, and the function of the right lower extremity was normal.
Compartment syndrome commonly results from soft-tissue edema or a space-occupying hematoma within the fascial confines of the compartment. Most compartment syndromes of the leg are secondary to a high-energy or crush injury. The onset of symptoms is generally noted within the first twenty-four to forty-eight hours after the injury. Compartment syndrome has been described following blunt trauma or invasive procedures in patients receiving anticoagulation therapy1,3,10,11. We are not aware of any report in which compartment syndrome has been attributed solely to the use of low-molecular-weight heparin or to any other anticoagulant commonly prescribed for prophylaxis against deep-vein thrombosis. Although several investigators have supported the use of low-molecular-weight heparin for prophylaxis against thromboembolism in patients who have sustained a traumatic injury2,4,5,7,9,12, such treatment has not yet been approved by the Food and Drug Administration. Compartment syndrome of the leg is usually associated with an underlying fracture of the tibia. In the case of our patient, the twelve-day delay in the onset of symptoms, the lack of underlying fracture or major soft-tissue trauma, and the intracompartmental hematoma observed at the time of the fasciotomy all were suggestive of the role of low-molecular-weight heparin in the development of compartment syndrome. A high index of suspicion and the measurement of compartment pressures are often necessary for the diagnosis of compartment syndrome, especially when the onset of symptoms is delayed. Early decompressive fasciotomy is necessary to correct this situation. We are not aware of a report of a similar patient despite the widespread use of low-molecular-weight heparin for prophylaxis against deep-vein thrombosis in patients who have sustained a traumatic injury to the lower extremity. Nonetheless, there is a slight chance that its use may be complicated by major hemorrhage and the development of compartment syndrome.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
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