PURPOSE: Ischaemic monomelic neuropathy (IMN) is a rare but serious complication of haemodialysis access procedures, with a highly variable clinical presentation. We present a case of presumed IMN managed with ligation of the prosthetic brachial-axillary access, leading to recovery of neurological function. METHODS: A 75-year-old male who underwent placement of a left prosthetic brachial-axillary access developed a swollen left upper limb following surgery and underwent interventional management for central venous occlusion. RESULTS: Eleven weeks following placement of the access, he presented with gross swelling and loss of function in the left arm. Ultrasonography excluded nerve compression. The brachial-axillary access was urgently ligated, leading to recovery of function in the arm. Electromyography (EMG) studies confirmed an ischaemic cause. CONCLUSIONS: The pathophysiology of IMN is poorly understood. This case is atypical in that the patient suffered from central venous stenosis prior to the development of IMN. This raises the possibility that the gross swelling secondary to recurrent central venous occlusion may have led to an ischaemic neuropathy by altering nerve perfusion. Early management led to a functional recovery of the affected limb, suggesting that an urgent approach in patients with suspected IMN might be associated with the best outcomes.
PURPOSE:Ischaemic monomelic neuropathy (IMN) is a rare but serious complication of haemodialysis access procedures, with a highly variable clinical presentation. We present a case of presumed IMN managed with ligation of the prosthetic brachial-axillary access, leading to recovery of neurological function. METHODS: A 75-year-old male who underwent placement of a left prosthetic brachial-axillary access developed a swollen left upper limb following surgery and underwent interventional management for central venous occlusion. RESULTS: Eleven weeks following placement of the access, he presented with gross swelling and loss of function in the left arm. Ultrasonography excluded nerve compression. The brachial-axillary access was urgently ligated, leading to recovery of function in the arm. Electromyography (EMG) studies confirmed an ischaemic cause. CONCLUSIONS: The pathophysiology of IMN is poorly understood. This case is atypical in that the patient suffered from central venous stenosis prior to the development of IMN. This raises the possibility that the gross swelling secondary to recurrent central venous occlusion may have led to an ischaemic neuropathy by altering nerve perfusion. Early management led to a functional recovery of the affected limb, suggesting that an urgent approach in patients with suspected IMN might be associated with the best outcomes.