TREATMENT OF SEVERE HYPOPHOSPHA TEMIA WITH INTRAPERITONEAL PHOSPHATE Hypophosphatemia is encountered in a variety of acute and chronic disease states. In most instances, hypophosphatemia reflects either inadequate intake, increased intestinal loss, or transcellular shift of phosphate (1, 2). Severe hypophosphatemia with serum levels below 0.5 mg/dL can be life-threatening and urgent treatment is necessary. We report a case of severe hypophosphatemia treated with intraperitoneal administration of phosphate. CASE REPORT DISCUSSION Phosphate replacement therapy is empiric since it is difficult to determine total body PO4 stores like other intracellular solutes. Phosphate can be given orally in divided doses totalling 30 to 90 mmoles/day (1-3 gm) (1). However, intravenous administration is recommended in patients who are severely hypophosphatemic, symptomatic, or unable to tolerate oral treatment (1, 4-6). Intravenous phosphate is given at a dose of 0.08 mmol/kg (2.5 mg/kg) every 6 hours if patient is asymptomatic and hypophosphatemia is of recent onset and 0.16 mmol/kg (5 mg/kg) if hypophosphatemia developed from multiple causes over a period of time and 0.24 mmol/kg (7.5 mg/kg) ifcondition is symptomatic (1). Our patient should have received 12 mmol (375 mg) of Phosphate intravenously every 6 hours if venous access was available. Our pa George Dy Stephen J. Goldstein Rasib M. Raja Kraftsow Division of Nephrology Department of Medicine Albert Einstein Medical Center Philadelphia, Pennsylvania 19141 REFERENCES 1. Berkelhammer C, Beon RA. A clinical approach to common electrolyte problems: Hypophosphatemia. Can Med Assoc J. 1984; 130:17-23. 2. Lentz RD, Brown DM, Kjellstrand CM. Treatment of severe hypophosphatemia. Ann Intern Med. 1978; 89:941-944. 3. Kramer MS, Koolpe HA, Goldstein SJ, Mendez M, Raja RM. Retroperitoneal feeding tube for peritoneal dialysis patients. Trans Am Soc for Art Intern Organs. 1989; 35:593-595. 4. Kingston M, AI-Siba'l B. Treatment of severe hypo phosphatemia. Crit Care Med. 1985; 13:16-18. 5. Andress DL, Vanatta JB, Whang R. Treatment of re fractory hypophosphatemia. South Med J. 1982; 75:766-767. 6. Vannatta JB, Whang R, Papper S. Efficacy of intrave nous phosphorus therapy in the severely hypophospha temic patient. Arch Intern Med. 1981; 141:885-887. 7. Stoff JS, Phosphate homestasis and hypophosphate mia. Am J Med. 1982; 72:489-495. 8. Knochel JP. The pathophysiology and clinical charac teristics of severe hypophosphatemia. Arch Intern Med. 1977; 137:203-220. 9. Kleeman CR. Metabolic Coma. Kidney Int. 1989; 36:1142-1158. 10. Hebert LA, Lemann J, Petersen JR, Lennon EJ. Studies of the mechanism by which phosphate infusion lowers serum calcium concentration. J Clin Invest. 1966: 45: 1886-1894. Downloaded from http://www.pdiconnect.com/ by guest on September 9, 2014 A 51-year-old female had a past medical history of noninsulin dependent diabetes mellitus, hypertension, and end-stage renal disease. She was on chronic hemodialysis for 5 years but she was switched to continuous ambulatory peritoneal dialysis (CAPD) because of multiple vascular access problems. She had chronic hypophosphatemia and malnutrition because of nausea and vomiting attributed to uremic and/or diabetic autonomic dysfunction. She required a feeding tube inserted transduodenally as reported earlier (3). The present admission was for nausea, vomiting, diarrhea, and peritonitis. Pertinent physical examination on admission showed a blood pressure of lOO/60 mm Hg, heart rate of 88 beats/min, respiratory rate of 20/min, and temperature of 37°C. Heart and lung examination were unremarkable. There was a slight costochondral tenderness. Abdomen was soft with diffuse tenderness. Peritoneal fluid was cloudy. Pertinent laboratory data showed a hematocrit of 31 %, WBC of 18.2 with a left shift, total protein 4.7 gm/dL, albumin 1.1 gm/dL, alkaline phosphatase 243 units, BUN 10 mg/dL, creatinine 6.1 mg/dL, Na 134 mEq/L, K 2.5 mEq/L, Ca++ 7.2 mg/dL (not corrected for albumin), phosphorus 1.8 mg/dL. The patient was started on intraperitoneal Vancomycin for her peritonitis. Other medications were calcium carbonate, Calcitriol, and Metoclopramide. Feeding through retroperitoneal duodenal tube was resumed with Osmolite HN; Aluminum phosphate (11.4 mmole or 354 mg) was added to her feed every six hours. The patient, however, was not able to tolerate this because of vomiting and diarrhea. Her hospital course was complicated by obtundation and lethargy, muscle weakness and myalgia, tremors and bone pain. Serum phosphate was <0.5 mg/dL, CPK was normal, serum glucose was 102 mg/dL. There was no evidence of hemolytic anemia. Since there was no peripheral venous access and she refused to have central venous access, sodium phosphate (15 mmoles or 465 mg of PO4), or potassium phosphate (13 mmoles or 466 mg of PO4) were added to alternate 1500 mL of 1.5% dianeal given every 8 hours. Serial serum PO4 and peritoneal dialysate PO4 were measured after the end of each exchange. Peritoneal fluid PO4 concentration 20 min after dwelling was 15.3 mg/dL. The peritoneal fluid PO4 concentration in the drainage fluid were 3.8, 3.1, 7.4, 6.0, and 7.1 mg/ dL for the first 5 consecutive exchanges. Percent PO4 absorption with each exchange was 88%, 90%, 76%, 81 %, and 77% respectively. Serum PO4 increased to 2.0 mg/dL after the second exchange and 4.3 after the 5th exchange. Ionized calcium decreased to 2.8 mg/dL after the 5th exchange. Peritoneal fluid calcium was measured on one 1 exchange at 5 min, 1, 2, 3, 4, and 8 h of dwell time. We did not observe decrease in any peritoneal fluid calcium concentration. tient's symptoms of hypophosphatemia resolved after phosphate correction. The biochemical abnormality is due to depletion of intracellular adenosine triphosphate which leads to impaired cellular production of energy and depletion of erythrocyte 2,3 diphosphoglycerate with resultant tissue hypoxia (8, 9). To the best of our knowledge, this is the first description of using intraperitoneal PO4 for treatment of severe hypophosphatemia. We believe that the treatment is effective, safe, and well tolerated by the patient. It can rapidly correct severe hypophosphatemia. The side effect of intravenous phosphate administration is avoided. Lentz cautions the use of intraperitoneal addition of phosphate into the dialysate because of calcium precipitation (2). This did not occur. The decrease in serum calcium can be attributed to the rise in serum phosphate (10). Because we anticipated 80-90% intraperitoneal phosphate absorption, we administer 1-3 mmoles of phosphate more than the recommended intravenous dose. Lower dosage of intraperitoneal phosphate should be considered for lesser degree of hypophosphatemia. Intraperitoneal phosphate is well absorbed and can be used in peritoneal dialysis patients who may need replacement. It is an alternate route of phosphate replacement in patients unable to take phosphate by mouth or intravenously. Downloaded from http://www.pdiconnect.com/ by guest on September 9, 2014