Hemodialysis‐induced acute pancreatitis secondary to kinked hemodialysis blood lines

Introduction: Hemolytic reactions developing during hemodialysis usually are caused by oxidant damage, reduction injury, and osmolar, thermal, and mechanical injury to the red blood cells. Mechanical injury due to maloccluded blood pumps, arterial line collapse, and use of subclavian hemodialysis catheters has been reported. We report one episode of acute hemolysis due to kinked hemodialysis blood lines complicated with pancreatitis. Case Report: An 18‐year‐old man with end‐stage renal failure of unknown origin had been on hemodialysis since 2002. His past medical history included asthma and hypertension. He was admitted to the hospital because of severe abdominal pain, nausea, and vomiting during the dialysis session. Laboratory examination showed hematocrit −30 %, platelet count of 131,000 per cubic mL, LDH −5151 U/L, haptoglobin −0.09 g/L, lipase −919 U/L, CPK‐ 260, ASAT −584 U/L, ALAT‐ 316 U/L, bilirubin −36 μmol/L, and visible schistocytes on smear. Examination of the abdomen revealed diffuse discomfort and tenderness in epigastrium. The patient was diagnosed as having hemolysis‐induced acute pancreatitis. He was treated symptomatically and recovered within a few days. We found the arterial blood line tightly kinked at the dialyser inlet port, and we excluded other reported causes of intravascular hemolysis during hemodialysis. Discussion: Until a critical pressure is exceeded, despite a kink in the post pump predialyser blood tubing, the blood pump can maintain sufficient blood flow to prevent an increase in the arterial pressure with a triggering of the arterial alarm and a decrease in the venous pressure with a triggering of the venous alarm. Thus, an excessively high pressure can be maintained in this silent segment of the dialyser tubing without activating the pressure alarms, exposing the red blood cells to high sheer stresses and resulting in clinically significant hemolysis. Acute hemolysis can cause a life‐threatening acute pancreatitis. The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. The important role of inflammatory cytokines in the pathogenesis of acute pancreatitis is well known. Heme released from hemoglobin after episodes of vascular hemolysis has the potential to act as a signalling molecule involved in the triggering of the inflammatory processes associated with massive hemolysis. Hemolysis itself may induce acute pancreatitis by all or some pathways of neutrophil activation and chemoattraction, such as oxidative burst, direct proinflammatory effect, microcirculatory disturbance, and increased expression of proinflammatory and immunoregulatory cytokines.

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