Malaria is a major public health problem worldwide.Severe malaria can lead to multiorgan dysfunction syndrome (MODS), with manifestations including cerebral malaria, severe anemia, acute kidney injury, and hepatic impairment.In this case, we present a 34-year-old male who presented with jaundice, decreased urine output, and altered sensorium.He had tachycardia and tachypnea with mild hypoxia, suggestive of an underlying compensatory response to severe anemia and metabolic acidosis.Thrombocytopenia, an elevated international normalized ratio, and prolonged activated partial thromboplastin time were consistent with coagulopathy.Significantly elevated serum urea and creatinine levels were indicative of acute kidney injury.Contrast-enhanced CT of the abdomen demonstrated no radiological evidence of chronic liver disease, supporting an acute hepatic process.Furthermore, the peripheral blood smear demonstrated trophozoites and gametocytes of Plasmodium falciparum, indicating severe falciparum malaria as the underlying cause of the multiorgan dysfunction.The patient was managed with intravenous artesunate as first-line therapy and subsequently received comprehensive multidisciplinary supportive care for multiorgan dysfunction syndrome.This case highlights the rare occurrence of acute hepatic failure with hepatic encephalopathy as a manifestation of severe P. falciparum malaria and emphasizes the importance of early recognition, timely commencement of antimalarial therapy, and multidisciplinary management of malaria-associated multiorgan dysfunction.
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Karthik et al. (2026) studied this question.
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