Infection as a predictor of mortality in decompensated liver cirrhosis: exploring the relationship to severity of liver failure

Abstract

Background Infections are common in patients with liver cirrhosis and increase mortality. We explored the relationship between infection and liver dysfunction in their effects on mortality. Methods Single-center data on decompensated liver cirrhosis patients hospitalized between March 2014 and December 2017 (index period) were reviewed until death, liver transplantation or 31 December 2018. Infections were classified as community-acquired infection (CAi) or hospital/healthcare associated infection (HCAi). Child-Pugh, model for the end-stage liver disease (MELD) and chronic liver failure-organ failure (CLiF-OF) scores indicated liver (dys)function. Results We enrolled 155 patients (85% alcoholic liver disease), 65 without infection at first hospitalization, 48 with CAi and 42 with HCAi. Multidrug resistant agents were confirmed in 2/48 (4.2%) CAi and 10/42 (23.8%) HCAi patients. At first hospitalization, infection was independently associated with worse liver dysfunction and vice versa, and with higher 30-day mortality [odds ratio (OR) = 2.73, 95% confidence interval (CI) 1.07–6.94]. The association was reduced with adjustment for MELD/CLiF-OF scores, but mediation analysis detected an indirect (via liver dysfunction) association. Twenty-eight patients were repeatedly hospitalized, 11 with new HCAi. HCAi was independently associated with twice higher risk of medium-term mortality and added an additional risk to any level of liver dysfunction, considering all or patients who survived the first 30 days. In those repeatedly hospitalized, HCAi appeared independently associated with a higher probability of infection and higher MELD scores at subsequent hospitalizations. Conclusion Infection (particularly HCAi) adds mortality risk to any level of liver dysfunction in decompensated liver cirrhosis patients. Mechanisms of long(er)-term effects (in acute episode survivors) seemingly include enhanced deterioration of liver function.

Acute-on-chronic liver failure: a single-centre experience

“…7). This is in agreement with the study from Croatia where infections increased 30-day mortality 2.3-times irrespective of the degree of liver failure [17]. The most prevalent infection site was the peritoneum (spontaneous bacterial peritonitis -SBP), which, together with respective proportions of the other sites, we consider to be a real reflection of the situation in our liver unit.…”

Short‐term outcomes of patients with chronic liver disease hospitalised with COVID‐19

“…6 Interestingly, the observed mortality from COVID-19 is similar to that from bacterial infections as previously recorded in cirrhosis, and they likely share similar pathways in causing liver damage. 26,27 Hence, after contracting COVID-19 cirrhotic patients are at risk of becoming decompensated, with a high mortality as noted. According to a report from Asia, approximately 20% of patients with cirrhosis develop decompensation on the contraction of COVID-19, with a higher mortality among patients with a baseline Child-Turcotte-Pugh score >8.…”

“…This was also confirmed in a multicentric study from the United States ( n = 867 patients with CLD, of whom 134 had compensated and 93 decompensated cirrhosis) that found 2.9 times higher risk of death in decompensated patients as compared to those with compensated cirrhosis and non‐cirrhotic CLD 6 . Interestingly, the observed mortality from COVID‐19 is similar to that from bacterial infections as previously recorded in cirrhosis, and they likely share similar pathways in causing liver damage 26,27 . Hence, after contracting COVID‐19 cirrhotic patients are at risk of becoming decompensated, with a high mortality as noted.…”

Higher levels of neutrophil percentage-to-albumin ratio predict increased mortality risk in patients with liver cirrhosis: a retrospective cohort study

“…Neutrophils played an essential role in mediating inflammatory responses. Previous studies indicated infection increases mortality risk in decompensated liver cirrhosis patients [ 15 ]. As the protein synthesized specifically by the liver, serum albumin concentration was also influenced by inflammation [ 16 ].…”