Fulminant hepatitis A in a robust adult: a case report of acute liver failure requiring urgent living donor liver transplantation

Introduction

Hepatitis induced acute liver failure (ALF), a condition marked by abrupt loss of hepatic function without pre-existing liver disease, can develop in a small subset of adults after a virus infection that usually resolves on its own (1). Orthotopic liver transplantation (OLT) is the only proven treatment for patients who will not survive with medical management alone, and its management depends on quick prognostic stratification (2). In order to address the crucial decision-making process in this medical emergency, we present a case of HAV-induced ALF in a young adult who was successfully treated with living donor liver transplantation (LDLT).

In the general adult population, HAV-related ALF is rare (<1%), but in hospitalized or severe cases, incidence may rise to about 10% with outcomes of 55% recovered, 31% transplanted, 14% died (3,4). We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0019/rc).

Case presentation

A 34-year-old Indian male residing in the United Arab Emirates presented to the hospital with a 3-day history of fever, severe abdominal pain, vomiting, diarrhea, and dizziness shortly after returning from India. His vaccination history, including hepatitis A immunization status, was unavailable as no medical records were accessible from India and no family members were present in the United Arab Emirates to provide this information. His weight was 94 kg and height 182 cm, with a calculated body mass index (BMI) of 28.3 kg/m². At the time of presentation, vital signs were as follows: blood pressure 143/83 mmHg, heart rate 111 beats per minute, temperature 37.0 ℃, and respiratory rate 20 breaths per minute. The patient reports a history of frequent consumption of street-vended food, which may predispose to increased risk of foodborne illnesses.

On examination, he was visibly jaundiced and acutely ill, but alert and oriented (Glasgow Coma Scale 15). His medical history was unremarkable, with no evidence of chronic liver disease, significant medication use, or substance abuse.

Initial laboratory investigations revealed profound liver injury: aspartate aminotransferase 4,520 U/L, alanine aminotransferase 3,880 U/L, and direct hyperbilirubinemia (total bilirubin 8.98 mg/dL, direct bilirubin 8.14 mg/dL). The patient presented with significant coagulopathy, with laboratory findings showing prothrombin time (PT) of 79.7 seconds, international normalized ratio (INR) of 7.23, activated partial thromboplastin time (APTT) of 54.3 seconds, and D-dimer of 18.72 mg/L, confirming the presence of coagulopathy supporting the diagnosis of ALF. Further workup indicated severe systemic compromise: lactic acidosis 15.5 mmol/L, acute kidney injury [creatinine 7.11 mg/dL, estimated glomerular filtration rate (eGFR) 9.6 mL/min], thrombocytopenia (platelets 117,000/µL), and elevated ammonia (103 µmol/L). A comprehensive panel for other viral hepatitis [hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis E virus (HEV)] and autoimmune markers was negative. Serology was positive for anti-HAV immunoglobulin M (IgM), confirming acute hepatitis A (Table 1). Abdominal ultrasonography showed no biliary obstruction or chronic liver disease signs, with only non-specific increased bronchovascular markings on chest imaging noted. However, toxicology screening was negative.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent for publication of this case report was not obtained from the patient or the relatives after all possible attempts were made.

Abdominal ultrasonography revealed a normal-sized liver with increased parenchymal echogenicity denoting fatty infiltration and focal geographic areas of normal echogenicity suggestive of fatty sparing. No focal lesions, intrahepatic biliary dilatation, or signs of chronic liver disease were seen. The portal vein was patent, with a thin rim of perihepatic hypoechoic fluid noted.

The patient was transferred to the intensive care unit (ICU) for management. He received aggressive supportive care, including fluid resuscitation and empiric intravenous ceftriaxone. However, he demonstrated rapid clinical deterioration and developed complications including acute renal failure, severe hepatic encephalopathy, coagulopathy, thrombocytopenia, lactic acidosis, hyperbilirubinemia, hypocalcemia, sepsis, and multiple organ dysfunction.

Based on poor prognostic indicators, he was listed for urgent liver transplantation. A living donor was identified, and the patient successfully underwent LDLT after being transferred to a transplantation healthcare center within 96 hours of presentation to the hospital.

The patient’s postoperative course was uncomplicated. His graft function normalized promptly, and he showed remarkable improvement regarding his liver and kidney functions, also improved hepatic encephalopathy symptoms. Then, he was discharged from the transplant healthcare center after arrangement with a specialized medical center in his home country to continue management and follow-up.

Discussion

This case exemplifies the potential severity of HAV infection in adults. While HAV is often mild in children, the risk of progressing to ALF and mortality increases with age (3). Our 34-year-old patient fell within a demographic at significant risk. This rapid decline in this scenario is not solely due to viral cytopathy but is considerably influenced by a dysregulated host immune response (5). Specifically, this includes injury mediated by CD4⁺ T cells and proinflammatory cytokines such as TNF-alpha that result in massive hepatocyte necrosis (6).

This diagnosis was then readily confirmed by the presence of serum IgM anti-HAV antibodies, the gold standard for diagnostic testing in acute infection (7). His clinical presentation consisted of coagulopathy, jaundice, and an episode of encephalopathy, and thus fit into the definition of ALF. The development of multi-organ dysfunction, including acute kidney injury and lactic acidosis, represented a very ominous prognosis. Such patients could be identified with the help of such prognostic models as King’s College Criteria, which are intended to point out the small likelihood of spontaneous survival in patients and hence the need for transplantation of the liver (8).

His management in the ICU was per established guidelines for systemic support, including continuous vasopressors, mechanical ventilation, and other organ-supportive care. N-acetylcysteine administration in non-acetaminophen ALF, as due to HAV, remains controversial, though it is generally used without a proven mortality benefit (9). Given his rapid deterioration, he never had much of a chance to improve with medical therapy and thus required an urgent transplant.

Liver transplantation remains the treatment of choice for irreversible ALF, even today, with 1-year patient survival rates of about 73% (10). The use of LDLT, as in this case, is a critical strategy to overcome the time-sensitive nature of ALF and the shortage of deceased donors. Outcomes for LDLT are almost equivalent to those for deceased donor transplantation at experienced centers (11). Moreover, the survival after transplantation due to HAV-induced ALF is generally favorable because there is no chronic liver disease, and the infection is self-limited in nature, thus leading to excellent recovery (12). The smooth, outstanding recovery of the patient also tallies well with this reported outcome.

Conclusions

The present case illustrates that while rare, HAV-induced ALF can take an acutely fulminant course in healthy adults; a high index of suspicion, prompt diagnosis, and early transfer to a specialized transplant center are essential. Herein, a well-structured multidisciplinary approach with a focus on aggressive care in the ICU and appropriate timing of LDLT is demonstrated to yield excellent outcomes and complete functional recovery.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0019/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0019/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0019/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent for publication of this case report was not obtained from the patient or the relatives after all possible attempts were made.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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