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ABSTRACT |
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CASE REPORT |
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Three months later, the next physical examination showed atrophy of left forearm and hand. Trophic changes of the thumb were prominent (Figure 1). On neurologic examination, pain and pinprick sensation were decreased and motor power was graded 3/5 distally. Brachioradialis muscle stretch reflex was decreased in comparison to the other side. Nerve conduction studies showed decreased amplitude of compound motor action potentials, decreased conduction velocities, and increased distal latencies of both median and ulnar nerves. Electromyography (EMG) showed long duration polyphasic motor unit potentials (MUPs), with single MUP recruitment pattern in the ulnar and median innervated muscles of the forearm and hand. Severe axonal damage of the median nerve after innervation of the pronator teres and axonal injury of the ulnar nerve before innervation of the flexor carpi ulnaris without presence of reinnervation MUPs were the other major EMG findings.
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DISCUSSION |
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Compartment syndromes are characterized by increased tissue pressure within the confined space of the fascial sheaths. The lower extremities are affected more commonly than the upper extremities. Loss of integrity of the microcirculation with fluid exudation into the interstitial space results in edema formation, muscle swelling, and raised intracompartmental pressure, eventually leading to compression of blood vessels and nerves.6 Varieties of non-traumatic conditions have been described as etiologic factors in the development of compartment syndrome.7
Acute compartment syndrome is of particular concern because the diagnosis must be made essentially on clinical grounds and must be acted upon promptly if serious and potentially irreversible injury to the relevant compartment is to be avoided. It is progressive and irreversible unless surgical decompression is performed.8 Continuous tissue pressure greater than 30–40 mm of Hg lead to irreversible nerve and muscle damage after 6–12 hours.6 Fryberg has reported that a tissue pressure 30 mm of Hg less than patient’s diastolic pressure is diagnostic.9
Increased intracompartmental pressure may be common due to hemorrhage between fascial sheaths but may evade recognition as a compartment syndrome because it reflects only a transient response to altered intracompartmental pressure that resolves spontaneously, especially with successful treatment of the basic condition. Physical examination, including passive stretching of muscle groups, should be conducted frequently to detect early signs of compartment syndrome, especially in the limbs with widespread ecchymoses.
Direct percutaneous monitoring of patients with intracompartmental pressure has been proposed although criteria have varied regarding the accepted useful diagnostic readings.10,11 Surgical decompression is impossible or very difficult in these patients because of thrombocytopenia, disordered coagulation, and presence of a highly transmissible infection. Blood sampling is an important cause of interfascial hemorrhage. Venipuncture sites should be controlled and compressed carefully to prevent continuous bleeding. Reducing blood sampling and controlling venipuncture sites are useful measures for deceasing interfascial hemorrhage in viral hemorrhagic fevers. Progressive increase in muscle compartment pressure may be prevented by early recognition, conservative therapy, and elevation of the affected compartment. Measuring of blood pressure using the involved limb especially with diffuse echymoses could be an inducing factor, especially when venous pressure is less than tissue pressure.
Patients that are at the risk of developing compartment syndromes especially in the forearm. We emphasize the importance of clinical signs in the early diagnosis of this potentially serious complication of viral hemorrhagic fevers. With greater awareness among physicians, patients with bleeding diatheses, especially secondary to transmissible viral infections, are more likely to have a mild disease course.
Received October 1, 2004. Accepted for publication February 16, 2005.
* Address correspondence to Dr. Ali Moghtaderi, Neurology Department, Zahedan University of Medical Sciences, Zahedan, Iran. E-mail: moghtaderi{at}zdmu.ac.ir 
Authors’ addresses: Ali Moghtaderi, Neurology Department, Zahedan University of Medical Sciences, Zahedan, Iran, E-mail: moghtaderi{at}zdmu.ac.ir. Roya Alavi-Naini, Department of Infectious Diseases, Zahedan University of Medical Sciences, Zahedan, Iran, E-mail: ranaini{at}zdmu.ac.ir. Hadi Azimi, Department of Operative Orthopedics, Zahedan University of Medical Sciences, Zahedan, Iran.
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