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  1. S. L. Basye,
  2. M. W. Greenwell,
  3. S. R. Acchiardo,
  4. F. D. Parks,
  5. B. M. Wall
  1. Department of Internal Medicine, University of Tennessee-Memphis, and Department of Radiology, Methodist University Hospital, Memphis, TN


Introduction We present an instructive case of bleeding esophageal varices, which occurred as a complication of central venous dialysis catheter (CVC)-induced superior vena cava (SVC) stenosis.

Case Report Our patient is a 34-year-old female with an 11-year history of ESRD, managed recently with hemodialysis via central venous catheters. She presented with shortness of breath and hypotension following 3 days of melenic stools. After stabilization, she underwent endoscopy that uncovered three columns of midesophageal varices with evidence of recent hemorrhage. Six bands were placed. Subsequent evaluation showed no evidence of portal hypertension or liver disease. Physical examination revealed severe swelling of her face, neck, right breast, and right arm, which developed acutely following placement of a right brachioaxillary arteriovenous graft (AVG) 2 weeks previously. CT scan of the chest showed a dialysis catheter inside a thickened SVC with extensive collateral formation. Venography confirmed the diagnosis of SVC stenosis secondary to stricture, with blood being diverted through dilated azygous, intercostal, chest wall, and paraesophageal venous collaterals. Prior to endovascular correction of the SVC stenosis, the patient had another episode of variceal bleeding, necessitating volume resuscitation and banding. After stabilization of her second variceal bleed, the patient underwent percutaneous angioplasty and stenting of a long, fusiform stricture involving the SVC. A post-stent venogram showed collapse of the collateral vessels. Within several weeks, her edema was resolved. She has had no further episodes of overt esophageal bleeding since correction of the SVC stenosis 3 months ago.

Discussion Hemodialysis catheter-induced SVC stenosis is a growing problem in the ESRD community. As in our patient, SVC stenosis is often subclinical (secondary to collateral formation) until a change in hemodynamics occurs, such as increased blood flow across the stenosis via an AVG. We believe our patient developed bleeding esophageal varices secondary to acute dilation of preexisting esophageal collateral veins following placement of the right upper extremity AVG. Percutaneous angioplasty and stent placement led to clinical resolution of the SVC syndrome and prevention of recurrent variceal bleeding.

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