Abstract

Background and Aim: ACLF is characterized by abrupt onset of severe liver dysfunction with extrahepatic organ failure(s) but with potential for reversal once the acute insult resolves. Although deranged systemic hemodynamics underpins extrahepatic organ failure, especially renal and circulatory failure, changes in systemic hemodynamics after recovery or after complete mobilization of ascites have not been reported. We studied systemic hemodynamics in ACLF before and after complete mobilization of ascites with slow infusion of furosemide and albumin with or without terlipressin [SIFA(T)] and its impact on determining the clinical outcomes. Methods: 25 consecutive patients with ACLF fulfilling the APASL 2014 criteria and with large ascites admitted between April 2016 and March 2017 were enrolled. Patients with active GI bleed, severe comorbidities, malignancy, BCS, <18 yrs, pregnancy were excluded. Besides the standard workup for ACLF, systemic hemodynamic parameters were determined by clinical and echocardiographic examination including cardiac index, systemic vascular resistance index and stroke work. All patients were treated with a response guided protocol with SIFA(T) for mobilization of ascites. Changes in clinical, biochemical, organ failure, hemodynamic parameters measured after resolution of ascites were compared with baseline data. Results: Seven patients died during the hospitalization (28% mortality). Systemic hemodynamics could be reassessed after complete mobilization of ascites in 18 patients using SIFA(T) regimen given for a mean period of 15.1 ± 4.6 days. At discharge there was significant improvement in all the parameters assessed (P = .000 for cardiac index, systemic vascular resistance index) as well as CTP and MELD scores (P = .000 for both). Conclusions: Complete mobilization of ascitic and third space fluid severe ACLF could be successfully achieved in 75% patients SIFA(T) with minimal adverse events. This was associated with significant improvement in liver function, improvement in organ failure), in systemic hemodynamics, and in improved survival. We suggest that improving systemic hemodynamics in ACLF with SIFA(T) therapy may reverse extra-hepatic organ failure and improve survival (Table 1).Table 1VariableAdmissionDischargePRemarksMELD30 (21–46)22 (15–31).000ΔMELD7 (1–17)CTP13 (12–14)10 (9–10.25).000ΔCTP3 (2–4.25)Creatinine1.7 ± 1.270.89 ± 0.23.000Albumin2.5 ± 0.283.3 ± 0.47.000Bilirubin11.2 ± 5.667.6 ± 4.71.000INR2.7 ± 0.802.3 ± 0.67.001UNa (mmol/L)38.9 ± 25.39384.5 ± 209.61 (max).000BSA1.82 ± 0.221.69 ± 0.19.000Heart rate97.2 ± 8.2681.9 ± 8.88.000MAP81.6 ± 6.5293.9 ± 4.98.000Systolic BP109 ± 9122 ± 8.000SV92.1 ± 25.0972.5 ± 24.44.000SVI50.9 ± 13.9543.45 ± 15.4.001Cardiac output8.9 ± 2.626.0 ± 2.28.000Cardiac index4.9 ± 1.413.6 ± 1.42.000SVR668.8 ± 234.131299.5 ± 531.45.000SVRI1206.8 ± 398.82192.7 ± 907.6.000Stroke work14.0 ± 3.9312.4 ± 4.33.013Arterial compliance2.29 ± 0.661.77 ± 0.63.000 Open table in a new tab The authors have none to declare.

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