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© 1996 The Journal of Bone and Joint Surgery, Inc. Septic Arthritis Associated with Brachial Plexus Neuropathy. A Case Report*  , MILWAUKEE, WISCONSINInvestigation performed at the Medical College of Wisconsin, Milwaukee
Pseudoparalysis or apparent weakness of a limb associated with septic arthritis or osteomyelitis is a well documented phenomenon. Muscular spasm associated with pain caused by the infection can lead to the apparent weakness. In contrast, true nerve paralysis associated with osteomyelitis is uncommon, and documentation of the electromyographic changes is rare. We describe a five-week-old male infant who had a brachial plexus neuropathy and paralysis of the right upper extremity secondary to septic arthritis of the glenohumeral joint and osteomyelitis of the proximal part of the humerus.
A male infant was delivered by cesarean section after thirty-six weeks of gestation to a primiparous thirty-five-year-old woman. No problems with the use of the upper extremities were noted at birth. At the age of three weeks, the infant had projectile vomiting and was admitted to the hospital for the operative correction of pyloric stenosis. The hospital course was uneventful, and he was discharged. One week later, he was admitted to the pediatric service for evaluation of a loss of movement of the right upper extremity of several days' duration. There was no history of fever or signs of constitutional illness while the infant was at home, but the mother reported that he had had mild upper respiratory symptoms for two days. The rectal temperature on admission was 37.2 degrees Celsius, and the vital signs were stable. The physical examination revealed a palpable mass in the right axilla, and the right upper extremity was flaccid. The patient had poor grasp, active flexion of the elbow was decreased, and active abduction of the shoulder was absent. Laboratory evaluation revealed a white blood-cell count of 20,800 per cubic millimeter (20.8 x 109 per liter) with a differential of 60 per cent segmented neutrophils, 2 per cent bands, 2 per cent lymphocytes, 16 per cent monocytes, and 5 per cent eosinophils. The erythrocyte sedimentation rate was not determined. Plain radiographs of the shoulder and chest were interpreted as normal, with the exception of mild soft-tissue swelling in the shoulder. A magnetic resonance imaging scan of the shoulder and upper part of the torso revealed soft-tissue swelling extending into the axilla inferiorly and medially (Fig. 1). A focal lesion in the anteroinferior aspect of the axilla was contiguous with the medial aspect of the subclavian and axillary vessels and nerves, but it did not displace them to a substantial degree. The increased signal intensity on T2-weighted images suggested edema, and a lymphangiomatous type of lesion was initially suspected. The cervical and thoracic parts of the spinal cord appeared normal. Suspicion of a superior vena cava syndrome led to an ultrasound evaluation of the subclavian, axillary, and brachial vessels, which showed normal flow. A rounded mass with mixed echo characteristics was evident in the axilla, but no discrete fluid collection was noted.
Nerve-conduction studies showed decreased sensory amplitudes of the median and ulnar nerves in the right upper extremity as compared with those in the left. A needle electromyogram demonstrated an absence of motor-unit action potentials in the deltoid, biceps, and first dorsal interosseous muscles on the right, severely decreased recruitment in the units in the flexor digitorum profundus and extensor digitorum communis, and mildly decreased recruitment in the rhomboids. Fibrillation potentials were present in all of the muscles of the right upper extremity that were tested. No abnormalities were seen in the cervical paraspinal muscles. The findings of the electromyogram were interpreted as being indicative of a neuropathy of the right brachial plexus involving all trunks, with severe motor denervation out of proportion to the sensory involvement. At the time of discharge from the pediatric service, approximately one week after the onset of paralysis, the diagnosis was brachial plexopathy that was possibly secondary to a hygroma. The neurological condition was stable, and an outpatient orthopaedic consultation was scheduled. Approximately two weeks later, the patient was admitted to the orthopaedic service for evaluation of weakness of the right upper extremity, which had been present for approximately seventeen days, and for pain with movement of the right shoulder. The rectal temperature on admission was 38.2 degrees Celsius, the white blood-cell count was 44,000 per cubic millimeter (44.0 x 109 per liter), and the erythrocyte sedimentation rate was sixty millimeters per hour. The right shoulder was edematous, an axillary mass was present, and passive motion of the right arm appeared to be painful. Plain radiographs at that time showed distention of the shoulder joint and lucency in the proximal metaphysis of the humerus, consistent with osteomyelitis (Fig. 2). Three milliliters of purulent material was aspirated from the glenohumeral joint, and the patient was immediately taken to the operating room for irrigation and débridement of the joint and the proximal part of the humerus. More than fifteen milliliters of purulent, thick, yellow material was expressed from the shoulder joint and surrounding tissues during the operation. The lucent defect was debrided. Penicillin-sensitive Staphylococcus aureus grew on culture of both the aspiration and the intraoperative specimens. The patient was given 250,000 units of penicillin G intravenously every six hours for six weeks. The clinical course improved, with a decreasing white blood-cell count, erythrocyte sedimentation rate, and temperature, and with increased active and passive ranges of motion of the right upper extremity. A repeat needle electromyogram, made three and one-half weeks after the first study, demonstrated some reinnervating motor-unit action potentials proximally, indicating axonal regeneration.
At the first follow-up visit, four months after discharge, the patient still had weakness of active abduction of the shoulder and had only minor improvement in active flexion of the elbow and in grasp. The patient was not brought for several follow-up appointments after the initial follow-up examination. Three years later, a physical examination demonstrated persistent muscular weakness about the right shoulder, with active abduction of only 80 degrees and flexion of 160 degrees. Inferior subluxation of the shoulder was clinically evident. Nerve-conduction studies were normal except for slight slowing of the sensory conduction velocity of the median nerve. Repeat needle electromyography at this time showed a few residual fibrillation potentials and mild polyphasic activity in the right biceps and deltoid. The motor units were normal. There were slight residual abnormalities in the biceps, triceps, and deltoid, and the infraspinatus was normal. Plain radiographs made at that time, especially those made with the shoulder in internal rotation, demonstrated the subluxation of the shoulder that had been seen clinically and the considerable destruction of the proximal humeral physis and metaphysis (Fig. 3).
Clay reported on two neonates who had had osteomyelitis in the proximal part of the humerus as well as neurological changes that did not resolve until as long as one year after treatment of the infection. Several other authors have described brachial plexus neuropathy associated with septic arthritis and osteomyelitis about the shoulder1,12,14 and the cervical vertebrae4. Although only one patient had electromyographic documentation, the neuropathy improved in all of the patients as a result of operative decompression. Young and Hawkes described this as a "pseudopseudoparalysis" or true neuropathy, which necessitates early decompression if full recovery is to be expected. Several causes for the pathophysiology of brachial plexus neuropathy due to infection have been proposed. As Clay described, electromyographic changes may be related to an ischemic neuropathy resulting from thrombophlebitis of the vasa nervorum. Arterial embolism can cause ischemia and nerve damage. However, when they are chronic, peripheral nerve lesions after an embolism are often associated with skin changes, muscular necrosis, and flaccid paresis of the most distal muscles3. Jones and Siekert reported on embolic mononeuropathy due to bacterial endocarditis. The findings of Doppler studies in our patient were normal, but that does not rule out microvascular disease completely. Although certain viral infections can directly affect the nerve plexus, most parainfectious plexopathies are thought to be hyperergic or hypersensitivity reactions rather than conditions directly related to infection or direct compression of the nerve. In our patient, the proximity of the infection to the brachial plexus in the axilla suggested direct compression as the predominant cause of the involvement of the cords of the brachial plexus. White et al. provided a detailed description of sciatic and femoral nerve palsy caused by septic arthritis of the hip. The cause of the nerve palsies in their patient was thought to be compression from capsular distention resulting in either impingement of the femoral nerve beneath the inguinal ligament or direct contact of the sciatic nerve with the iliopectineal bursa (which communicated with the hip joint). Also, the sciatic nerve may have become entrapped between the gemelli and piriformis because of the distension of the infected hip capsule. In conclusion, brachial plexopathy with a prolonged neurological deficit can occur in infants who have septic arthritis and osteomyelitis. Infants often do not respond to infection with obvious subjective and objective signs. Examination can be difficult, and elevation of the temperature, white blood-cell count, and erythrocyte sedimentation rate may not be marked. Paralysis of an extremity or pain with passive motion in a previously healthy infant should prompt the treating physician to rule out septic arthritis and osteomyelitis. Early intensive management may decrease not only the complications of joint destruction and growth arrest, but may also diminish the potential for neurological damage.
*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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