Primary and Secondary Organ Failures Cause Mortality Differentially in Acute Pancreatitis and Should be Distinguished.

OBJECTIVE: The aim of this study was to study the development of early and late organ failure (OF) and their differential impact on mortality in patients with acute pancreatitis (AP). METHODS: Consecutive patients (N = 805) with acute pancreatitis were included in an observational study. Organ failure was categorized as primary if it occurred early due to pancreatitis per se and secondary if it occurred late due to infected pancreatic necrosis (IPN). Primary outcome was a relative contribution of primary OF, secondary OF, and IPN to mortality. RESULTS: Of the 614 patients (mean age, 38.8; standard deviation, 14.6 years; 430 males) in a derivation cohort, 274 (44.6%) developed OF, with 177 having primary OF and 97 secondary OF due to sepsis. Primary OF caused early mortality in 15.8% and was a risk factor for IPN in 76% of patients. Mortality in patients with primary OF and IPN was 49.5% versus 36% in those with IPN and secondary OF (P = 0.06) and 4% in those with IPN but without OF (P < 0.001). The results of the 191 patients in the validation cohort confirmed the relative contribution of primary and secondary OF to mortality. CONCLUSION: Primary and secondary OF contributed to mortality independently and are distinct in their timing, window of opportunity for intervention, and prognosis.

Reduction in mortality in severe acute pancreatitis: A time trend analysis over 16 years.

BACKGROUND: The trend in the outcome of patients with acute pancreatitis (AP) as a result of evolving management practices is not known. OBJECTIVE: To study and compare the outcomes of patients with AP at a tertiary care academic center over a period of 16 years. METHODS: In a retrospective study on a prospectively acquired database of patients with AP, we analyzed time trends of severity and mortality of AP. The influence of determinants of severity [APACHE II score, organ failure (OF), infected pancreatic necrosis (IPN)], and management strategy on the actual and predicted mortality was assessed. The actual mortality was adjusted for severity to analyze the severity-adjusted mortality at different times as a reflection of management practices over time. RESULTS: A total of 1333 patients were studied. The number of patients hospitalized with AP has been increasing over time. The proportion of patients with severe AP also increased from 1997 to 2013 as shown by increasing incidence of organ failure and IPN (Spearman's rank correlation coefficient (ρ): OF ρ(17) = 0.797, p < 0.01; IPN ρ(17) = 0.739, p < 0.001), indicating an increasing referral of sicker patients. Consequently, the overall mortality has been increasing (ρ(17) = 0.584; p = 0.014). However, despite increasing severity of AP, the mortality adjusted for OF has decreased significantly (ρ(17) = -0.55, p = 0.02). CONCLUSION: Even with increasing proportion of patients with severe AP, there has been a significant decrease in organ failure adjusted mortality due to AP suggesting improved management over years.

Acute on chronic liver failure because of acute hepatic insults: Etiologies, course, extrahepatic organ failure and predictors of mortality.

BACKGROUND AND AIM: Acute on chronic liver failure (ACLF) because of precipitating factors (variceal bleed/infections) identifies cirrhotics at risk for high short-term mortality. Information on ACLF because of acute hepatic insults is lacking. The aim of the study was to evaluate acute hepatic insults in ACLF and their effect on the course and outcome. METHODS: In a prospective study, 213 consecutive patients of ACLF because of acute hepatic insults were included. Etiology of acute hepatic insult, frequency of silent, and overt chronic liver disease (CLD), organ failure (OF), and outcomes were assessed. Prognostic models such as model for endstage liver disease (MELD), acute physiology and chronic health evaluation (APACHE II), and chronic liver failure-sequential organ failure (CLIF-SOFA) were evaluated. RESULTS: Etiologies of acute hepatic insult were hepatitis virus(es)- 81 (38%; HBV-42, HEV-39), continuous alcohol consumption-77 (33.3%), antituberculosis drugs-11 (5.2%), autoimmune hepatitis flare-5(2.3%), cryptogenic-44 (20.7%). The common causes of CLD were alcohol (n = 85/40%), HBV(n = 52/24%), and cryptogenic(n = 50/20%). The MELD, APACHE II, and CLIF-SOFA scores were similar among silent and overt CLD and did not influence outcome. Predominant etiologies of ACLF were hepatitis virus(es) reactivation or superinfection in silent CLD(52/112, 46.4%) and alcohol among overt CLD(43/101, 43%). Independent predictors of mortality included hepatic-encephalopathy (early, HR: 4.01; advanced, HR: 6.10), serum creatinine ≥1.5 mg/dl (HR: 4.53), CLIF-SOFA ≥8(HR: 1.69), and etiology of acute hepatic insult (alcohol, HR: 4.08; cryptogenic, HR: 3.18). HEV-ACLF had lower mortality (12.8% vs. 33-54% in other etiologies;P < 0.001). OF was major determinant of mortality. With increasing number of OF, mortality increased linearly(P = 0.001). CONCLUSIONS: Hepatitis virus(es) and continuous alcohol consumption are important causes of ACLF caused by acute hepatic insults. HEV-ACLF has lower mortality. OF is an important prognostic predictor.