We report a case of fulminant liver failure in a patient with acute active hepatitis B infection who was found to have COVID-19 without lung involvement. A 24-year-old male was brought by ambulance service to Hamad General Hospital, Emergency Department (ED), in Doha on April 8, 2020, with chief complaints of fever and cough for 3 days. Upon initial evaluation, the patient was febrile (39.4°C), jaundiced, and disoriented regarding time, place, and person, with an unremarkable past medical history. Initial blood tests showed severely elevated urea, creatinine, transaminases, and ammonium in addition to an impaired coagulation profile consistent with fulminant liver failure. A swab was taken for COVID-19 PCR testing and found to be positive. Serological tests revealed hepatitis B surface antigen positivity and other serology indicating acute hepatitis B. Initial X-ray and repeat chest X-rays did not show lung infiltrates. On the 6^th day after admission, the patient developed fixed dilated pupils, with brain edema on CT; cardiac arrest occurred on the 10^th day after admission, and the patient died. Although it is still largely unclear, HBV0-activated sudden-onset strong cytotoxic T lymphocyte response and enhanced viral replication and/or retention of the viral capsid in infected hepatocytes may cause the pathogenesis of FH. These pathophysiological events cause extensive hepatocyte apoptosis and necrosis, which results in deadly severe liver failure. Our findings support that the liver damage occurring in COVID-19 is caused by an impaired innate immune system rather than by direct cell damage caused by SARS-CoV-2. We think that more consideration should be given to the presence of acute hepatitis B, especially in COVID-19 patients.

This systematic review and meta-analysis aimed to evaluate clinical outcomes associated with different systemic heparin protocols (conservative v standard intensity) during extracorporeal membrane oxygenation (ECMO) support. Included studies comprised both venovenous and venoarterial ECMO modalities. A systematic review and meta-analysis were conducted per Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. The PubMed, Cochrane Library, and Scopus databases were searched through November 15, 2024, for studies comparing conservative anticoagulation (no or low-target activated partial thromboplastin time [aPTT] of 40-60 seconds, anticoagulation monitoring) with standard anticoagulation (standard heparin target aPTT of 60-80 seconds). Studies were conducted in intensive care units across multiple international centers. Eight studies (601 patients; 280 in the conservative group and 321 in the standard group) were included in the meta-analysis. Conservative (no or low-target aPTT of 40-60 seconds, anticoagulation monitoring) versus standard anticoagulation (standard heparin target aPTT of 60-80 seconds). Primary outcomes included mortality, major bleeding, and thrombosis; secondary outcomes were stroke, limb ischemia, and circuit thrombosis. Random-effects models assessed outcomes, with heterogeneity evaluated using the Q test and I² statistic. A total of 698 studies were identified (PubMed, 461; Cochrane Library, 94; Scopus, 143). After removal of duplicates, 358 records were screened, and 245 studies were excluded. Twenty-seven studies underwent full-text review, with 13 meeting the inclusion criteria. Eight studies (601 patients; 280 in the conservative group and 321 in the standard group) were included in the meta-analysis. Mortality was similar between the conservative group (131 of 280 patients [46.8%]) and the standard group (159 of 321 [49.5%]) (odds ratio [OR], 1.04 [95% confidence interval (CI), 0.53-2.05]; I² = 64%). Thrombotic events were assessed in 4 studies (26 of 123 in the conservative group [21.1%] v 47 of 178 in the standard group [26.4%]; OR, 0.60 [95% CI, 0.33-1.09]; I² = 0%). Stroke (5 of 127 v 5 of 178), limb ischemia (10 of 87 v 20 of 147), and circuit thrombosis (15 of 141 v 15 of 191) did not differ between groups. However, major bleeding significantly favored conservative strategies (7 studies; 74 of 251 [29.5%] v 157 of 297 [52.9%]; OR, 0.40 [95% CI, 0.18-0.91]; p = 0.03; I² = 72%). The findings of this systematic review and meta-analysis indicate a potential association between conservative anticoagulation strategies during ECMO and reduced bleeding events without increased mortality or thrombotic complications, including stroke, limb ischemia, and circuit thrombosis. Given the low event rates, wide CIs, and absence of a formal power calculation, these null findings should not be interpreted as evidence of equivalence.

Background/Objectives: Reported infection rates during extracorporeal membrane oxygenation (ECMO) vary widely, partly because case definitions are applied inconsistently. We synthesized the prevalence and prognostic association of nosocomial and bloodstream infection (BSI) acquired during adult ECMO. Methods: PubMed/MEDLINE, Embase, Scopus and CENTRAL were searched through December 2025 for observational studies of at least 10 adults on ECMO with an explicit infection definition. We classified case definitions by the criteria actually applied. We pooled crude mortality odds ratios (ORs) and patient-level BSI prevalence in studies applying laboratory-confirmed criteria, assessed risk of bias with ROBINS-I and the JBI checklist, and rated certainty with GRADE. Results: Forty-seven reports (46 cohorts; 11,573 patients) were included. Pooled BSI prevalence was 25.8% (95% CI 17.3–36.5%; 7 studies, 1193 patients), 18.2% in pre-pandemic and 39.2% in COVID-19 cohorts (post hoc). Infection was associated with higher crude odds of death (OR 1.65, 1.33–2.04; prediction interval 0.95–2.85; 24 studies), but analyses modeling infection as time-varying were inconsistent, including no association in a multistate model (adjusted hazard ratio 1.00, 0.79–1.26), and small-study effects were suggested. Certainty was very low for both outcomes. Conclusions: Roughly one in four adults on ECMO developed laboratory-confirmed BSI, more often in COVID-19 cohorts. Whether infection acquired on ECMO increases mortality remains uncertain.