Hemodynamic stability in liver failure patients undergoing therapeutic plasma exchange.

INTRODUCTION: The management of liver failure (LF) remains a challenge for the physician. Therapeutic plasma exchange (TPE) improves consciousness level and tends to normalize hyperkinetic circulation by removing neurotoxic substances from the circulation. Hemodynamic stability is essential for optimal patient management. The objective of this study was to observe the effects of TPE on mean arterial pressure (MAP), vasopressor dependency index (VDI) and vasopressor score (VS) in LF patients. METHOD: This retrospective study was conducted on LF patients at a liver institute in Delhi. Clinical data were collected from April 2018 to September 2018. RESULTS: A total of 229 TPEs were performed on 97 patients. Baseline values were MAP 82 (56-141), VS 10.55 (0.00-111.66), and VDI 0.13(0.00-1.44). MAP increased with TPE from 82 to 85 at 1 hour post-TPE and fell back to baseline in 6 hours post-TPE. VDI and VS decreased significantly with TPE till 1 hour post-TPE but reached baseline by 6 hours post-TPE. VDI decreased consistently untill third TPE session and remained stable thereafter. Post-TPE, S. Procalcitonin decreased from 4.69 to 4.25. The average time from admission to start of first TPE procedure was 11 hours in survivors and 26 hours in nonsurvivors. CONCLUSIONS: Patients became hemodynamically stable with TPE but effect did not last long. Sustained improvements in VDI were observed with multiple TPE procedures. Distinct differences were seen between survivors and nonsurvivors in MAP, VDI, and VS early initiation of TPE correlated with improved survival in ALF patients. TPE did not increase risk of sepsis.

Role of high-volume plasma exchange in a case of a G6PD deficient patient presenting with HAV related acute liver failure and concomitant acute renal failure.

A mild degree of hemolysis is commonly encountered complication in acute viral hepatitis patients which generally resolves as the disease recovers. Rarely, some patients might present with severe hemolysis associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency. It has been hypothesized that the hemolysis is initially provoked by the viral infection itself; however, it may be aggravated due to the administration of certain drugs in patients with G6PD deficiency. We report a case highlighting the role of high-volume plasma exchange in a G6PD deficient patient presenting with hepatitis A related acute liver failure (ALF) and concomitant acute renal failure (ARF).