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Brachial Neuropathy After Hemodialysis Shunt Placement Under Axillary Blockade

Hebl, James R. MD; Horlocker, Terese T. MD

doi: 10.1213/00000539-199910000-00037

Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota

June 2, 1999.

Address correspondence and reprint requests to Terese T. Horlocker, MD, Department of Anesthesiology, Mayo Clinic, 200 First St., SW, Rochester, MN 55905. Address e-mail to

Perioperative nerve injury has long been recognized as a complication of axillary brachial plexus blockade, with a frequency ranging from 0.2% (1) to 19% (2). The creation of vascular access for chronic hemodialysis may also be associated with significant neurological injury. Prompt recognition of reversible etiologies, in all cases of neurological injury, is essential to improve outcome. The presence of residual neural block after regional anesthesia, however, may delay diagnosis and intervention of neurological dysfunction postoperatively. We present a case of ischemic monomelic neuropathy (IMN), a postoperative clinical syndrome associated with severe sensorimotor dysfunction, in a patient who underwent dialysis graft placement under axillary blockade.

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Case Report

A 78-yr-old man with a history of hypertension and chronic renal failure secondary to Alport’s Syndrome presented for left upper extremity polytetrafluoroethylene graft placement for chronic hemodialysis. The patient had no history of diabetes or an existing peripheral neuropathy. Axillary blockade was performed using a 25-gauge, 3.8-cm needle and a 1:1 mixture of bupivacaine 0.5% and lidocaine 1.5%. While using a transarterial technique, elicitation of a median nerve paresthesia occurred. A total solution volume of 40 mL was deposited posterior and anterior to the axillary artery. An additional 10 mL of lidocaine 1.5% was deposited into the coracobrachialis musculature for musculocutaneous nerve anesthesia. After establishing successful anesthesia, a brachial artery-axillary vein Gore-Tex graft was placed. Before closure, however, fresh clot was evacuated from the graft and the anastomosis reconstructed because of inadequate flow, palpable at the arterial end of the graft. Initial neurological assessment after regression of the block included a mild decrease in grasp strength attributed to pain and a poor radial pulse.

On the next day, the patient complained of his hand “feeling like a block of wood.” The primary service documented that it was “probably related to (the) axillary block.” However, throughout the day the patient experienced progressive worsening of his sensorimotor deficits. Neurological examination revealed numbness and paresthesias over the radial, median, and ulnar nerve distributions of his hand and a weakened grasp that was markedly worse than immediately postoperatively. The hand was felt to be “slightly cooler,” with mild cyanosis of the digits when compared with the nonoperative side. Radial and ulnar pulses were the same as postoperatively. The patient was surgically reexplored under local anesthesia 21 h after his initial procedure. The entire graft was removed and fresh clot evacuated from the brachial artery. Postoperatively, the hand appeared warmer, and motor function was “clearly improved.” However, paresthesias persisted throughout the hand in a “glove-like distribution.”

The patient experienced no neurological improvement during the next 2 days. Mild signs of ischemia were present, although radial and ulnar pulses were detected by a hand-held doppler probe. An angiogram demonstrated “total occlusion of the left brachial artery with diminished but otherwise normal run-off to the hand.” The patient subsequently underwent reconstruction of the brachial artery using a left saphenous vein graft and was discharged. Two weeks later, the patient still complained of burning paresthesias throughout the volar aspect of his left forearm extending onto the medial aspect, and numbness involving the palmar aspect of the entire hand. He was also found to have a persistently weakened grip on the left. One year later, the patient still suffered from paresthesias of the left forearm and hand.

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IMN is a rare complication of dialysis access, characterized by profound neurologic impairment (3–7). Patients with IMN experience pain, paresthesias, and weakness of the hand and forearm. All major nerve distributions may be affected with a slight predilection for the median nerve (6). Complete paralysis of the intrinsic hand musculature is common with less severe weakness in wrist flexion and extension. Typically, the ischemia is either transient or insufficient to cause muscle or soft tissue necrosis. It is unclear whether temporary arterial occlusion that occurs during graft placement or the resultant low-grade ischemia from diversion of blood flow into the graft is most critical. The generally uniform presence of long-standing diabetes mellitus and diabetic neuropathy suggests that a preexisting neuropathy may be responsible for an increased sensitivity to ischemia. Other associated risk factors include severe distal atherosclerosis documented by angiography, hypertension, and failure of a previous distal shunt (4). The condition has not been described in patients with grafts originating distal to the brachial artery.

The frequency of IMN after graft placement has been estimated to be 0.5% (8). Hye and Wolf (3) describe the largest series, consisting of five patients experiencing postoperative IMN. Most commonly, patients complained of hand pain and numbness, with profound weakness of the intrinsic musculature. Diagnosis was made by electrophysiologic studies in three of the five patients, ranging from one day to six weeks postoperatively. All three had no clinical improvement following graft ligation and/or angioplasty. The remaining two patients were diagnosed by clinical examination on Postoperative Days 4 and 7. One patient underwent graft ligation with significant improvement, while the other underwent embolectomy with no clinical improvement. The neurologic sequelae in two of these patients were initially attributed to complications from axillary blockade, which may have delayed diagnosis and treatment.

Initial symptoms in our patient were thought to be “related to the axillary block” despite evidence of block regression, as demonstrated by the presence of surgical pain immediately postoperatively. It is unclear whether incorrect assessment of this patient’s ischemic symptoms contributed to a delay in surgical intervention and poor neurological outcome. For this reason, practitioners using regional anesthetic techniques for hemodialysis shunt placement should be aware of IMN when asked to evaluate patients who have signs of neurological injury postoperatively. Features that may distinguish IMN from neurological damage caused by needle trauma or direct local anesthetic toxicity are difficult to elicit. However, unlike the abrupt onset and rapid progression of IMN, most cases of nerve injury that result from regional anesthesia occur over days to weeks and rarely involve the entire plexus (9). Therefore, it may be prudent to avoid the use of long-acting local anesthetics for dialysis shunt placement, in an effort to allow a more rapid postoperative neurological assessment. Early recognition of IMN is crucial, so that rapid shunt reversal or banding may be performed to limit ischemia and avoid potentially devastating and irreversible neurological sequelae.

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© 1999 International Anesthesia Research Society