Abstract
We discuss a case of a 58 year old male who presented for left upper extremity steal syndrome including ischemic monomelic neuropathy (IMN) 1.5 months after arteriovenous fistula creation. He presented after three surgical attempts to salvage his fistula with rest pain, complete loss of function with contracture of the 4th and 5th digits, and loss of sensation in the ulnar distribution for more than three weeks. At our institution, he underwent surgical ligation of the distal fistula and creation of a new fistula proximally, resulting in complete resolution of his vascular steal symptoms almost immediately despite the chronicity prior to surgical presentation. Our patient provides a unique perspective regarding dialysis access salvage versus patient quality of life. The patients’ functional status and pain levels should take precedence over salvage of an arteriovenous access site, and early ligation of the access should be completed prior to chronic IMN development. However, if a patient presents late along the IMN course, we recommend strong consideration of access ligation in order to attempt to regain the full neurovascular function of the extremity as we experienced in our patient.
Highlights
We present the case of a 58 year old male with left upper extremity steal syndrome including ischemic monomelic neuropathy (IMN) 1.5 months after arteriovenous fistula creation
He reported burning pain 10/10 radiating from left forearm to left shoulder and presented with contracted left 4th and 5th digits. His past medical history included hypertension, endstage renal disease on hemodialysis, hyperlipidemia, cerebrovascular accident with residual left sided weakness, and insulin dependent diabetes mellitus. His past surgical history included a right internal jugular tunneled dialysis catheter and left forearm fistula, subsequent tunneled dialysis catheter removal, distal revascularization interval ligation (DRIL) to left forearm fistula, and two other salvage procedures to left forearm fistula, the details of which are unknown to our team
Ischemic steal syndrome is caused by a significant decrease or reversal of blood flow through the arterial segment distal to the usually newly created vascular access because of the pressure differential created by the access site
Summary
We present the case of a 58 year old male with left upper extremity steal syndrome including ischemic monomelic neuropathy (IMN) 1.5 months after arteriovenous fistula creation. His past medical history included hypertension, endstage renal disease on hemodialysis, hyperlipidemia, cerebrovascular accident with residual left sided weakness, and insulin dependent diabetes mellitus His past surgical history included a right internal jugular tunneled dialysis catheter and left forearm fistula, subsequent tunneled dialysis catheter removal, distal revascularization interval ligation (DRIL) to left forearm fistula, and two other salvage procedures to left forearm fistula, the details of which are unknown to our team. On physical exam at his initial consultation, our patient had a left forearm arteriovenous fistula with excellent thrill and bruit, exquisite tenderness to palpation, with intact pressure dressing to dialysis puncture sites He had motor weakness with complete loss of active range of motion of 4th and 5th digits on the left hand, and decreased passive range of motion due to contracture of these digits. His venous diameter measurements were as follows: 1. Cephalic vein: Proximal humerus 4.4mm Mid-humerus 5.4mm Antecubital 6.1mm Proximal forearm 5.7mm
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