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Michael A. Rocklin, Margaret J. Quinn, Isaac Teitelbaum, Cloudy dialysate as a presenting feature of superior vena cava syndrome, Nephrology Dialysis Transplantation, Volume 15, Issue 9, September 2000, Pages 1455–1457, https://doi.org/10.1093/ndt/15.9.1455
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Extract
Introduction
The onset of cloudy dialysate fluid in a peritoneal dialysis (PD) patient usually heralds infectious peritonitis [1]. However, infection does not explain all cases of increased dialysate turbidity. When culture‐negative cloudy dialysate is encountered, other aetiologies must be considered. These include the presence of: increased polymorphonuclear cells due to intra‐ or juxtaperitoneal inflammation; eosinophils, seen in association with intraperitoneal free air; red blood cells; malignant cells; and an elevated triglyceride content. The association of chylous ascites with lymphoma, pancreatitis, or catheter‐related trauma in PD patients is well‐recognized [2–4]. Drug‐induced elevations of dialysate triglyceride have been reported also [5,6]. To our knowledge, there have been no reports of chylous peritoneal dialysate associated with progressive superior vena cava (SVC) syndrome.
Case
The patient is a 59‐year‐old woman with end‐stage renal disease (ESRD) secondary to diabetes mellitus. She had been receiving haemodialysis via a right internal jugular Hickman catheter for approximately 2 months when the catheter clotted with associated thrombosis of the SVC. The patient had undergone placement of a subcutaneously tunnelled Tenckhoff catheter 4 weeks earlier in anticipation of a switch to PD. The haemodialysis catheter was removed, anticoagulation medication was started, and PD was initiated. Nevertheless, she developed SVC syndrome, manifested initially by mild facial swelling. During the next 2 weeks, the patient complained of progressively worsening periorbital oedema and bilateral upper extremity swelling. Concomitant with her worsening upper body oedema, she reported intermittent cloudy dialysate. She denied abdominal pain, nausea, vomiting, diarrhoea, fever or chills, and exam revealed no abdominal tenderness. The patient was not taking a calcium channel blocker. Cell counts of the white dialysis effluent revealed fewer than 50×106 leukocytes/l and rare red blood cells. Routine, fungal and AFB cultures revealed no growth. Cytology showed only ‘reactive mesothelial cells’. The triglyceride content of the fluid was elevated at 25 mg/dl.
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