Severe metabolic alkalosis in pregnant patient due to citrate load with plasma exchange

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Conference Proceeding

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Am J Kidney Dis


Sodium citrate has been widely utilized as an anticoagulant in plasmapheresis (PP). Metabolic alkalosis is a well-known complication of PP in patients with impaired ability to excrete byproducts of citrate metabolism. We report a rare case of iatrogenic citrate toxicity leading to profound metabolic alkalosis in a pregnant patient. A 22-year-old pregnant female, gestational age 16 weeks, was admitted with fever, rash and myalgias. She was intubated due to respiratory failure with diffuse alveolar hemorrhage. Autoimmune studies and skin biopsy were consistent with a new diagnosis of lupus. Steroids and daily PP were initiated. On admission, patient's height was 150 cm and she weighed 71 kg. Lab data showed serum creatinine levels between 0.21 and 0.51 mg/dL. Patient received six daily PP treatments. Three days after initiation of PP, she was noted to have an increase in serum bicarbonate (TCO2) level from 23 to 42 mmol/L. ABG showed pH of 7.55, pCO2 46.2 mm Hg. Peak pH was 7.62, following which she received one dose of acetazolamide. Her TCO2 levels returned to baseline upon completion of apheresis. Volume of distribution of hydrophilic substances is increased in pregnancy. The patient received 10 L of plasma replacement with total citrate load of 294 mmol in the first three days. Under normal conditions citrate is rapidly metabolized to bicarbonate in the liver. One molecule of citrate can be converted to three molecules of bicarbonate, therefore total bicarbonate load was approximately 882 mmol. Iatrogenic bicarbonate load with plasma exchange led to elevation of TCO2 to a critical level. Contributing factors include hypocapnic state of pregnancy and delayed renal compensation. This case also highlights the utility of acetazolamide in such circumstances. Citrate delivery needs to be protocolized and monitored closely to make it safe and effective.





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