Q: Which of the following contraindicates use of citrate in Continuous Renal Replacement Therapy (CRRT)?
A) Hepatic failure
B) severe Thrombocytopenia
C) DIsseminated Intravascular coagulation (DIC)
D) Requirement of pressor
E) Femoral access for CRRT
Answer: A
Citrate is used in CRRT to provide regional anticoagulation. It works by chelating ionized calcium and consequently prevents coagulation cascade. Though most of the calcium citrate complex is removed by filter, but still clinically significant amount reaches the body. Citrate gets metabolized to bicarbonate by the liver. Each citrate molecule produces three bicarbonate molecules. Citrate should not be used in patients with hepatic failure, because accumulation of citrate may cause life-threatening hypocalcemia by binding to ionized calcium in the body. Instead of LFT, it has been proposed to use prothrombin time or lactate level as predictor of potential citrate toxicity with less than 26 percent and more than 3.4 mmol/L respectively.
All other choices (B, C, D and E) have no effect on citrate.
References:
1. Apsner R, Schwarzenhofer M, Derfler K, et al. Impairment of citrate metabolism in acute hepatic failure. Wien Klin Wochenschr 1997; 109:123.
2. Kramer L, Bauer E, Joukhadar C, et al. Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients. Crit Care Med 2003; 31:2450.
3. Schultheiß C, Saugel B, Phillip V, et al. Continuous venovenous hemodialysis with regional citrate anticoagulation in patients with liver failure: a prospective observational study. Crit Care 2012; 16:R162.
A) Hepatic failure
B) severe Thrombocytopenia
C) DIsseminated Intravascular coagulation (DIC)
D) Requirement of pressor
E) Femoral access for CRRT
Answer: A
Citrate is used in CRRT to provide regional anticoagulation. It works by chelating ionized calcium and consequently prevents coagulation cascade. Though most of the calcium citrate complex is removed by filter, but still clinically significant amount reaches the body. Citrate gets metabolized to bicarbonate by the liver. Each citrate molecule produces three bicarbonate molecules. Citrate should not be used in patients with hepatic failure, because accumulation of citrate may cause life-threatening hypocalcemia by binding to ionized calcium in the body. Instead of LFT, it has been proposed to use prothrombin time or lactate level as predictor of potential citrate toxicity with less than 26 percent and more than 3.4 mmol/L respectively.
All other choices (B, C, D and E) have no effect on citrate.
References:
1. Apsner R, Schwarzenhofer M, Derfler K, et al. Impairment of citrate metabolism in acute hepatic failure. Wien Klin Wochenschr 1997; 109:123.
2. Kramer L, Bauer E, Joukhadar C, et al. Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients. Crit Care Med 2003; 31:2450.
3. Schultheiß C, Saugel B, Phillip V, et al. Continuous venovenous hemodialysis with regional citrate anticoagulation in patients with liver failure: a prospective observational study. Crit Care 2012; 16:R162.
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