The case against the "temporary" peritoneal dialysis catheter.
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Biomedical subjects
Publications and source records attributed to T S Ing.
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In 5 patients who were receiving maintenance hemodialysis, ascites developed that was refractory to treatment by ultrafiltration during hemodialysis. Use of sequential isolated ultrafiltration and hemodialysis therapy either precipitated side effects or else required prolongation of total treatment time which the patients declined to accept. In 4 of the patients, ascites was believed to be primarily responsible for severe, progressive cachexia. Maintenance peritoneal dialysis was instituted in all patients, and abdominal fluid was removed gradually, over a period of 2 to 3 days. Ascites resolved promptly in each case. Three patients noted a dramatic improvement in appetite after relief of abdominal distension. Follow-up periods ranged from 6 to 4 1/2 years. Our results suggest that maintenance peritoneal dialysis can successfully control hemodialysis ascites.
Six maintenance hemodialysis patients are described in whom ascites was encountered at a time when they were anephric. No etiology for ascites could be found, and it was presumed that these patients were manifesting so-called "hemodialysis ascites". Our findings suggest that the use of bilateral nephrectomy in the treatment of hemodialysis ascites should be re-evaluated.
The effect of negative-pressure isolated ultrafiltration on leucocytes, platelets, and clotting factors was evaluated in maintenance hemodialysis patients. A significant decrease in the number of leucocytes was observed during the first 45 minutes of ultrafiltration. However, by one hour, leucocyte counts had returned to pre-ultrafiltration values. A slight, of haptoglobin, free hemoglobin, or fibrinogen after one hour of isolated ultrafiltration. Levels of fibrin degradation products and fibrin monomers similarly showed no change. Heparin administration alone had no effect on the above hematologic values. We suggest that isolated ultrafiltration, as clinically practised, has little acute effect on the coagulation system, and does not cause detectable hemolysis. The transient decrease in leucocyte count, and the modest fall in platelet count that were found are in keeping with changes previously reported to occur during hemodialysis.
In ten patients undergoing maintenance peritoneal dialysis, large numbers of eosinophils were found in the peritoneal fluid. A few of the affected patients complained of episodic abdominal pains, but there was no correlation between abdominal symptoms and the number of peritoneal fluid eosinophils. Microorganisms failed to grow on cultures of the peritoneal fluids, and results of tests for endotoxin were negative. The cause of eosinophilia could not be determined. Peritoneal fluid eosinophil counts were noted to be elevated soon after catheter insertion and initiation of peritoneal dialysis. In some patients, peritoneal fluid eosinophil counts spontaneously returned to normal despite continued peritoneal dialysis.
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Ten alert, non-uraemic, splenectomised dogs were subjected to isolated ultrafiltration until mean arterial pressure decreased to less than 80mmHg. On a separate occasion, in the same dogs, ultrafiltration was performed in the course of haemodialysis. Whether or not dialysate was circulated, ultrafiltration resulted in marked increases in total peripheral vascular resistance, and large increases in plasma concentrations of vasoactive hormones, including norepinephrine. Our results suggest that, in the non-uraemic dog, the haemodynamic responses to ultrafiltration during dialysis and to isolated ultrafiltration are similar.
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In 52 unselected patients maintained in intermittent hemodialysis, protein calorie malnutrition was present in 10 patients (19%). Complete cutaneous anergy to four intradermal skin antigens. (Candida, tuberculin, Streptokinase-dornase, and mumps) and failure to respond to contact sensitization to dinitrochlorobenzene was present in 60% of the patients. No correlation between cutaneous anergy and protein calorie malnutrition could be demonstrated.
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Twelve patients underwent hemodialysis using dialysate containing 130 mEq/L sodium, and, on a separate occasion, dialysis using a dialysate of constantly decreasing sodium concentration (from 150 to 133 mEq/L). Hydrostatic ultra-filtration during dialysis was performed at a constant rate (900 ml/hr) during both treatments, and was continued until a substantial drop in mean arterial pressure (-15%) or symptoms were observed. A double-blind comparison of the two treatment modalities was thus achieved. At the end of ultrafiltration, significantly more fluid had been removed using decreasing sodium dialysate (2.9 +/- 0.3 kg) than when using the low-sodium dialysate (1.9 +/- 0.2 kg, P<0.001). Plasma sodium concentration at the end of ultrafiltration using decreasing sodium dialysate was not significantly different from the predialysis level. Hydrostatic ultrafiltration using a dialysate of decreasing sodium level may prove to be a useful means of removing excess fluid asymptomatically from dialysis patients.
Seven maintenance hemodialysis patients suffering from intractable uremic pericardial effusion were treated with instillation of a non-absorbable steroid, triamcinolone hexacetonide, into the pericardial sac via a large-bore catheter. The latter was placed under direct vision by subxiphoid pericardiotomy. All patients responded to the treatment while complications of the procedure were few and minor.
To study the fate of amantadine hydrochloride in patients with renal failure, we gave 100 mg orally to 12 such patients immediately after hemodialysis. Plasma levels did not decrease between 24 and 44 hours after drug ingestion, suggesting an extremely poor total body clearance. Apparent volume of distribution was 5.1 +/- 0.2 (SEM) L/kg of body weight. Between 44 and 48 hours, as a result of 4 hours of hemodialysis, the mean plasma drug level decreased from 268 to 225 ng/mL (P less than 0.001). Dialyzer clearance was 67.0 +/- 3.9 mL of plasma per minute. The total quantity of drug removed by the dialysis treatment, however, was only 3.9 +/- 0.25 mg. The average half-life of amantadine in eight patients studied while receiving maintenance hemodialysis was 24.3 +/- 2.4 h of dialysis administered over approximately 13 days. Plasma half-life in six nonuremic control subjects was 12.2 +/- 1.6 h. Amantadine is poorly excreted in dialysis patients and has a large volume of distribution. The amount removed by a single dialysis is only a small fraction of the total body store.