Abstract This report describes a 4-month-old infant with multisystem organ failure who developed severe hypernatremia (sodium 168 mEq/l) due to rapid free water removal associated with acute peritoneal dialysis instituted for fluid overload. The current report describes the pathophysiology of the hypernatremia, and its correc- tion by low-sodium hypertonic peritoneal dialysis with- out compromising ultrafiltration or supplementing with free water. Although peritoneal dialysis can cause hyper- natremia, a modified solute concentration in the dialy- sate can treat the hypernatremia successfully. Keywords Hypernatremia · Peritoneal dialysis · Infant · Edema · Critically ill · Sodium Introduction Hypernatremia is a serious condition that can lead to per- manent neurological damage and even death [1, 2, 3, 4, 5, 6, 7]. The majority of children who develop hyperna- tremia do so following admission to the hospital, with a significant percentage being critically ill with multi- system organ failure [8]. These children usually develop hypernatremia either from (1) excess sodium in the form of bicarbonate to treat acidosis or (2) excess free water losses due to polyuria that occurs during the recovery phase of acute renal failure (without a corresponding in- crease in free water intake) [8]. Peritoneal dialysis is not generally considered a risk factor for developing hyper- natremia in the critically ill child with multisystem organ failure. This report describes a child with multi-system organ failure due to cardiogenic shock who developed severe hypernatremia secondary to aggressive fluid removal from acute peritoneal dialysis to treat anasarca. A mech- anism for the development of hypernatremia is proposed. In addition, a method to adjust the solute concentration of the dialysate is proposed to effect successful therapy without compromising fluid removal or providing addi- tional free water. Case report A 3.5-month-old female weighing 3.11 kg was admitted to Monte- fiore Medical Center for corrective surgery of a truncus arteriosus type 2 anomaly. Her preoperative serum sodium was 134 mEq/l, glucose 81 mg/dl, and creatinine 0.5 mg/dl. The infant underwent a modified Rastelli repair of the truncus arteriosus. The intraoper- ative course was complicated by two episodes of circulatory arrest, and the postoperative course was complicated by cardiac compression syndrome. Multisystem organ failure ensued due to hypotension/hypoxic injury requiring pressors and volume sup- port. The patient developed oliguric acute renal failure (serum creatinine 1.6 mg/dl, urine output less than 0.8 ml/kg per hour while receiving a 0.1 mg/kg per hour Lasix infusion). Twenty- four hours following surgery the patient was massively fluid over- loaded in positive fluid balance of 1.9 l. Acute peritoneal dialysis was initiated. Her course on dialysis is shown in Table 1. Following the start of dialysis the patient became progressively hypernatremic and hyperglycemic. An insulin drip was started. The serum sodium rose to 168 mEq/l, despite a small reduction in the dialysate sodium concentration from 140 mEq/l to 130 mEq/l and a reduction in the dwell time for each dialysis exchange from 60 min to 40 min. The renal service was consulted to assist in the dialysis and fluid management. An analysis of the electrolyte con- centration from one exchange of peritoneal dialysis revealed that the peritoneal ultrafiltrate was essentially free water with an ultra- filtrate sieving coefficient of 0.09 (Table 2). This represents a peri- toneal dialysate ultrafiltrate sodium concentration that is 9% of the serum sodium concentration. The recommendation was to correct the serum sodium to no less than 150 mEq/l in 24 h without giving additional free water and without a significant compromise in ultrafiltration. This was achieved by performing low-sodium hypertonic peritoneal dialy- sis. The dialysis dwell time was increased to 120 min to allow suf- ficient time for sodium to diffuse into the dialysate and to main- tain adequate ultrafiltration. The dialysis sodium concentration was decreased to 70 mEq/l as determined by the formula shown in M.L. Moritz ( ✉ ) Division of Nephrology, Children’s Hospital of Pittsburgh, 3705 Fifth Avenue, Pittsburgh, PA 15213–2538, USA e-mail: moritzm@chplink.chp.edu Tel.: +1-412-6925182, Fax: +1-412-6927443 M.L. Moritz · M. del Rio · G.A. Crooke · L.P. Singer Department of Pediatrics, Albert Einstein College of Medicine-Montefiore Medical Center, Bronx, New York, USA Pediatr Nephrol (2001) 16:697–700 © IPNA 2001 DIALYSIS / BRIEF REPORT Michael L. Moritz · Marcella del Rio Gregory A. Crooke · Lewis P. Singer Acute peritoneal dialysis as both cause and treatment of hypernatremia in an infant Received: 2 January 2001 / Revised: 24 April 2001 / Accepted: 24 April 2001