Cloudy dialysate as a presenting feature of superior vena cava syndrome

Michael A. Rocklin, Margaret J. Quinn and Isaac Teitelbaum

Division of Renal Disease and Hypertension, Department of Internal Medicine, University of Colorado Health Sciences Center, Denver, CO, USA

Keywords: cloudy dialysate; chylous; peritoneal dialysis; superior vena cava syndrome; triglyceride



   Introduction
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 Introduction
 Case
 Discussion
 References
 
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 [24]. 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
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 Introduction
 Case
 Discussion
 References
 
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 50x106 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.

Eight weeks after starting PD, the patient presented with mid-epigastric abdominal pain, nausea, and vomiting of 2 days duration. Serum lipase was significantly elevated at 6430 U/l (normal range 20–209) and a diagnosis of acute pancreatitis was made. The cell count of the PD fluid revealed only 54x106 leukocytes/l and the culture was again sterile. The triglyceride level in the effluent was again elevated at 33 mg/dl. Over the ensuing 72 h the patient experienced symptomatic improvement concomitant with a fall in her serum lipase to 313 U/l. Yet, her dialysate effluent remained intermittently cloudy.

During the next 4 weeks, the patient's facial and upper extremity oedema worsened causing her new difficulty with speech, swallowing and breathing. Her dialysate effluent continued to be intermittently cloudy, particularly after her long nocturnal dwells. Echocardiography revealed a widely patent foramen ovale and proven right-to-left atrial shunt. The risk of paradoxical embolization was felt to be sufficiently high as to preclude thrombolysis and/or stenting of the SVC. An innominate vein to right atrial bypass was eventually performed utilizing a pericardial tube conduit. In the immediate postoperative period, the patient experienced some waxing and waning upper body oedema and she reported 1 day of cloudy white dialysate. However, in the 18 months since surgery, her symptoms have remained significantly improved and her PD effluent has remained clear. Several repeat triglyceride levels have been less than 10 mg/dl. A postoperative magnetic resonance imaging study with gadolinium demonstrated patency of the graft based on residual internal flow signal and decreased distension of the azygous vein, which had previously served as the major collateral around the obstructed SVC.



   Discussion
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 Introduction
 Case
 Discussion
 References
 
This case exemplifies the challenge of establishing a definitive diagnosis when culture-negative turbid dialysate is encountered. Our patient's dialysate was characterized by normal leukocyte counts, normal red blood cell counts, no organisms, and no malignant cells. Significant fibrin strands were not visible on inspection. The triglyceride level was elevated each time the patient was noted to have cloudy dialysate and it was normal when the dialysate cleared. Therefore, we believe the most likely cause of our patient's cloudy dialysate was the elevated triglyceride content. Certainly, the triglyceride levels we observed do not meet the often used definition of chylous ascites, i.e. a grossly milky fluid with a lipid content greater than that of plasma, a protein content more than half that of plasma, and/or the presence of microscopic fat [7]. However, triglyceride levels comparable to those we observed have been previously reported in association with turbid peritoneal dialysate [5].

Impaired lymphatic drainage in association with SVC syndrome is well recognized. Animal studies have demonstrated the development of chylous effusions in thoraces of dogs following experimental obstruction of the SVC [8]. In man, nontraumatic chylothorax has been reported as a consequence of SVC thrombosis complicating either central venous line or LeVeen shunt placement [9,10]. Similarly, the association of chyloperitoneum with the SVC syndrome (in a non-dialysis patient) was reported by Abadoglu et al. who described a patient with Behcet's disease that presented with, among other manifestations, SVC syndrome and chylous ascites [11].

A basic review of the anatomy and physiology of intestinal lymphatic drainage suggests a plausible mechanism whereby SVC obstruction might result in elevated dialysate triglyceride content. The source of triglyceride in chylous ascites has been shown to be nascent chylomicrons. These are the largest and lowest density lipoproteins produced by intestinal mucosal cells and are characterized by a primarily triglyceride core surrounded by a monolayer of apolipoprotein B [12]. These particles are released into a vast network of intestinal lymphatics that coalesce to form the thoracic duct. This large lymphatic vessel utilizes valves and a thin smooth muscle lining for vasomotion. The thoracic duct empties into the normally low-pressure central venous system at the junction of the left internal jugular and left subclavian veins [13]. SVC thrombosis may impair lymphatic flow by increasing central venous pressure to a level that impedes the relatively weak vasomotion of the lymphatic system. In their report, Abadoglu et al. speculated that the SVC syndrome might produce chyle stasis and possibly even retrograde flow into the peritoneal space resulting in the development of chylous ascites [11]. In our patient, surgical intervention bypassed her venous-outflow obstruction, relieving the high central venous pressure. In the 18 months since her surgery the patient has remained symptomatically improved without recurrence of the severe head, neck, upper truncal, or extremity oedema. During this period her dialysate has remained clear and repeat dialysate triglyceride levels have all been in the normal range.

A number of other potential causes for the elevated peritoneal dialysate triglyceride levels must be considered. Our patient was not taking a calcium channel blocker [6]. Thorough evaluation and follow-up revealed no evidence of a malignancy that might have caused lymphatic obstruction. Our patient did experience a flare of acute pancreatitis. However, turbid dialysate antedated the symptomatic bout of acute pancreatitis by 8 weeks and persisted for more than a month after both clinical and biochemical resolution of her pancreatitis. Therefore, pancreatitis is extremely unlikely to have caused the turbid dialysate. Finally, we must consider the possibility that the turbid dialysate resulted from mild trauma to the lymphatics following Tenckhoff catheter insertion and/or due to repeated catheter movement. It should be noted, however, that at our centre we utilize a ‘buried’ technique for catheter placement. Our patient's catheter was placed 4 weeks before it was externalized. The interval should provide sufficient time for healing of any damaged lymphatic capillaries and reabsorption of leaked chyle. Of course, it is possible that more significant damage to larger lymphatic vessels occurred and leakage may have been ongoing at the time of dialysis initiation. Similarly, repeated mild trauma associated with catheter movement might have contributed to the elevated triglyceride levels. However, these explanations both ignore the temporal correlation of onset and resolution of the patient's cloudy dialysate and her SVC syndrome. Furthermore, no change was made in either PD catheter position or patient technique that might have prevented ongoing lymphatic damage. Yet, the cloudy dialysate ceased almost immediately upon decompression of the central venous system. Therefore, we consider it most probable that our patient's elevated dialysate triglyceride level occurred as a consequence of her SVC thrombosis.

We have described the case of a woman who presented with chylous dialysate concomitant with SVC syndrome and we have offered a plausible mechanism whereby SVC syndrome might result in elevated peritoneal dialysate triglyceride content. To our knowledge this is the first report of chylous dialysate associated with SVC syndrome in a patient performing peritoneal dialysis.



   Notes
 
Correspondence and offprint requests to: Dr Isaac Teitelbaum, Home Dialysis Program, University of Colorado Health Sciences Center, 4200 E. 9th Ave., Denver, CO 80262, USA. Back



   References
 Top
 Introduction
 Case
 Discussion
 References
 

  1. Vas SI. Peritonitis. In: Nolph KD ed. Peritoneal Dialysis, 3rd edn. Kluwer Academic Publishers, Dordrecht: 1989179:
  2. Bargman JM, Zent R, Ellis P, Auger M, Wilson S. Diagnosis of lymphoma in a continuous ambulatory peritoneal dialysis patient by peritoneal fluid cytology. Am J Kid Dis1994; 23: 747–750[ISI][Medline]
  3. Fontan MP, Pombo F, Soto A, Fontan F, Rodriguez-Carmona A. Chylous ascites associated with acute pancreatitis in a patient undergoing continuous ambulatory peritoneal dialysis. Nephron1993; 63: 458–461[ISI][Medline]
  4. Porter J, Wang WM, Oliveira DBG. Chylous ascites and continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant1991; 6: 659–661[ISI][Medline]
  5. Yoshimoto K, Saima S, Echizen H, Nakamura Y, Ishizaki T. A drug-induced turbid peritoneal dialysate in five patients treated with continuous ambulatory peritoneal dialysis. Clin Nephrol1993; 40: 114–117[ISI][Medline]
  6. Yoshimoto K, Saima S, Nakamura Y et al. Dihydropyridine type calcium channel blocker-induced turbid dialysate in patients undergoing peritoneal dialysis. Clin Nephrol1998; 50: 90–93[ISI][Medline]
  7. Goldfarb JP. Chylous effusions secondary to pancreatitis: case report and review of the literature. Am J Gastroenterol1984; 79: 133–135[ISI][Medline]
  8. Hodges CC, Fossum TW, Komkov A, Hightower D. Lymphoscintigraphy in healthy dogs and dogs with experimentally created thoracic duct abnormalities. Am J Veterinary Res1992; 53: 1048–1053[ISI][Medline]
  9. Schiller G. Chylothorax as a complication of central venous catheter-induced superior vena cava thrombosis. Bone Marrow Transplant1992; 9: 302[ISI][Medline]
  10. Warren WH, Altman JS, Gregory SA. Chylothorax secondary to obstruction of the superior vena cava: a complication of the LeVeen shunt. Thorax1990; 45: 978–979[Abstract]
  11. Abadoglu O, Osma E, Ucan ES et al. Behcet's disease with pulmonary involvement, superior vena cava syndrome, chyloptysis, and chylous ascites. Respir Med1996; 90: 429–431[ISI][Medline]
  12. Champe PC, Harvey RA. Lippincott's Illustrated Reviews: Biochemistry. J. B. Lippincott Company, Philadelphia: 1987: 208–209
  13. Junqueira LC, Carneiro J, Kelley RO. Basic Histology, 6th edn. Appleton & Lang, Norwalk, Connecticut: 1989: 227–228
Received for publication: 9. 1.00
Revision received 12. 4.00.



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