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Postoperative Onset of Idiopathic Brachial Neuritis

1996; Lippincott Williams & Wilkins; Volume: 84; Issue: 2 Linguagem: Inglês

10.1097/00000542-199602000-00028

1528-1175

Eugene E. Fibuch, Janet S. Mertz, Bruce D. Geller,

Orthopedic Surgery and Rehabilitation

(Fibuch) Professor and Vice-Chairman, Department of Anesthesiology.(Mertz) Associate Clinical Professor, Department of Otolaryngology.(Geller) Assistant Clinical Professor, Department of Medicine.Received from Saint Luke's Health System/University of Missouri at Kansas City School of Medicine, Kansas City, Missouri. Submitted for publication August 22, 1995. Accepted for publication October 26, 1995.Address reprint requests to Dr. Fibuch: Department of Anesthesiology, Saint Luke's Hospital, 44th and Wornall Road, Kansas City, Missouri 64111.Key words: Allergy: ganglioside protein. Measurement techniques: electromyography. Neuropathy: autoimmune; idiopathic brachial plexus neuritis; ulnar.THIS report describes a case of postsurgical idiopathic brachial neuritis (IBN) in an otherwise healthy female physician. The recognition of this entity as a potential cause of symptoms of peripheral neuropathy in the postoperative patient is important for anesthesiologists to know because of the possibility that it may be misdiagnosed as a brachial plexus stretch injury or ulnar nerve compressive injury.A 44-yr-old, ASA physical status 1 woman was scheduled to undergo a diagnostic hysteroscopy, dilatation, and curettage because of menometrorrhagia. Preoperatively, there was no history of trauma or viral or bacterial infection. Her review of systems, medical and surgical history, and family history were noncontributory. She had no allergies to medications and was taking only vitamins. She was 162.5 cm tall and weighed 49.9 kg. Her vital signs (blood pressure 124/70 mmHg) and physical examination results were within normal limits.In the operating room, standard monitoring was applied. While breathing oxygen, she was given atropine (0.3 mg), fentanyl (100 micro gram), and ketorolac (60 mg) intramuscularly in the left deltoid muscle and metaclopromide (10 mg) intravenously before induction. Anesthesia was induced with propofol (4 mg/kg) and maintained with a propofol infusion (2 mg *symbol* kg sup -1 *symbol* min sup -1). The head was maintained in a neutral position, with the intravenous catheter in the right arm, abducted to approximately 70 degrees from the thorax. The left arm was tucked to the left side of the patient. At no time did her systolic blood pressure intraoperatively decrease to less than 95 mmHg. Anesthesia and surgery were uneventful. The anesthetic lasted approximately 34 min. The patient emerged from general anesthesia without sequelae and was taken to the recovery room, where she had an uneventful anesthetic recovery.Because the patient was doing well after discharge, she elected to go to a restaurant for dinner that evening (12 h postoperatively). During the course of the dinner, she complained to her husband (a physician) of an acute burning pain in both shoulders, radiating into the neck and scapula. The pain was so uncomfortable that she became nauseated and terminated eating her meal. That evening she could not get comfortable, despite the use of heat, massage, a cervical collar, and analgesics (naproxen sodium and chlorzoxazone). The following morning, the pain persisted, and weakness in the shoulder girdle had devoloped. Later that day, she noticed a tingling sensation radiating into her left lateral posterior arm and into the thumb and first and second fingers. The pain gradually subsided in 2 weeks, but the weakness on the left side persisted. This weakness made it difficult for her to perform certain procedures in the operating room.Approximately 4 weeks after the onset of symptoms, she was evaluated by a neurologist, who noted that her review of systems was unremarkable except for the above noted complaints. On physical examination, her cranial nerves were intact. Manual muscle testing revealed normal trapezii bilaterally (5/5) and diminished strength in the left deltoid (3+/5), left supraspinatus (2/5), left infraspinatus (2+/5), and left teres minor (3-/5) muscles and the left rhomboids (2+ to 3 -/5). The left triceps muscle was slightly weak (5-/5). The remainder of the manual muscle testing was almost normal on the left and normal on the right. There was mild atrophy of the left infraspinatus muscle. Reflexes in the upper and lower extremities were normal and equal bilaterally. Sensory examination to pinprick was normal except for a decreased appreciation of pinprick in the left second digit. Results of coordination and gait testing were unremarkable.Electromyographic and nerve conduction studies demonstrated, approximately 1 month after the onset of pain, a chronic left C7 radiculopathy and an acute and chronic denervation in muscles sharing innervation through the C5 nerve root and the upper trunk of the brachial plexus. The cervical paraspinal muscles did not demonstrate acute denervation. This pattern noted on electromyographic and nerve conduction studies, in view of the clinical history and examination findings, suggested a left neuralgic amyotrophy.Because of the persistence of left upper extremity weakness, approximately 2 months after the onset of symptoms, laboratory evaluation for serum proteins and thyroid function was performed, and results were within normal limits. However, when ganglioside antibody titers were evaluated, they were noted to be increased, suggestive of an ongoing immune phenomenon (Table 1).A magnetic resonance imaging study of the brachial plexus and neck was performed and found to have normal results, except for a mild posterior disc bulge at C5-C6 that caused minimal impingement anteriorally on the thecal sac.Finally, urine evaluation results for heavy metals (arsenic, lead, mercury, and cadmium) were noted to be normal.Based on the above findings, the diagnosis of postoperative IBN was made. At 11 months after the initial onset of pain, the patient has recovered full function and is painfree.Postoperative IBN2is a well recognized clinical syndrome in the orthopaedic and neurologic literature [3-13]but has not received wide attention in the anesthesiology literature.First described by Spillane in 1943, [14]this disorder has had many names, such as