Hepatic encephalopathy secondary to acute viral Hepatitis A

INTRODUCTION

Hepatic encephalopathy (HE) is a reversible neuropsychiatric syndrome resulting from acute or chronic liver dysfunction, leading to accumulation of neurotoxic substances, particularly ammonia, that impair cerebral function. It manifests as a spectrum ranging from subtle cognitive deficits to coma. Hepatic encephalopathy occurs due to failure of hepatic detoxification and portosystemic shunting, resulting in metabolic disturbances affecting the brain.^1-4

Hepatitis A virus (HAV) infection is one of the most common causes of acute viral hepatitis, especially in developing countries. Although HAV infection is usually self-limiting, a very small proportion of patients progress to acute liver failure, among whom hepatic encephalopathy is a rare but serious complication.¹

CASE REPORT

A 14-year-old male presented with fever and yellowish discoloration of the sclera for five days, followed by generalized tonic–colonic seizures and altered sensorium. There was no history of headaches, vomiting, bleeding from any site, or focal neurological deficits. On neurological examination, the patient was drowsy, not oriented to time and place. Pupils were bilaterally normal and reactive to light. Motor examination showed normal tone, exaggerated deep tendon reflexes, and extensor plantar response. Fundus examination was normal. The rest of the systemic examination was normal.

The patient had a history of recent travel to Rajasthan and had a chickenpox infection two months prior. Differential diagnoses were considered as acute fulminant hepatitis with hepatic encephalopathy, complicated malaria, dengue encephalitis, scrub typhus, enteric encephalopathy, and the rare possibility of viral encephalitis and autoimmune encephalitis.

Routine blood investigations, including random blood sugar (RBS), complete blood count, renal function tests, electrolytes, coagulation profile, and thyroid function tests, were within normal limits. Malarial parasite (MP) by card, Dengue NS1 & IgMki, and Widal were negative. Liver enzymes were markedly elevated, suggestive of acute hepatitis. Serum ammonia level was elevated. HBsAg, anti-HCV, and anti-HEV antibodies were non-reactive. Hepatitis A IgM and IgG antibodies were positive. MRI brain with contrast showed no abnormalities. Cerebrospinal fluid (CSF) routine microscopy was normal.

Based on the presence of acute hepatitis, hyperammonemia, and altered mental status with normal neuroimaging and CSF, a diagnosis of hepatic encephalopathy secondary to acute Hepatitis A virus infection was made.

DISCUSSION

Hepatitis A virus infection is predominantly a self-limiting disease; however, a small subset of patients develops acute liver failure, among whom hepatic encephalopathy represents a severe neurological complication. The reported incidence of HAV-related encephalopathy is extremely low, making such presentations uncommon and clinically significant.¹

Risk factors of hepatic encephalopathy include advanced age; prior episodes of hepatic encephalopathy; hypoalbuminemia; elevated total bilirubin levels; higher Child–Pugh class/score and model for end-stage liver disease (MELD)/MELDNa scores; presence of ascites; co-infection; elevated venous ammonia levels; reduced critical flicker frequency; frailty; proton pump inhibitor use; presence of portosystemic shunts; elevated neutrophil count; hyponatremia; acute kidney injury; and acute-on-chronic liver failure.^1-4

The pathogenesis of hepatic encephalopathy is multifactorial, with hyperammonemia playing a central role. In acute hepatic dysfunction, impaired detoxification of ammonia through the urea cycle leads to elevated systemic ammonia levels. Ammonia crosses the blood–brain barrier and is metabolized within astrocytes to glutamine, resulting in astrocytic swelling, cerebral edema, and impaired neuronal signaling. Additional contributors include inflammatory cytokines, oxidative stress, and alterations in cerebral energy metabolism.^2-4

Clinically, hepatic encephalopathy presents as a spectrum of neuropsychiatric manifestations ranging from subtle cognitive changes to seizures, stupor, and coma. In this patient, seizures and altered sensorium in the setting of acute hepatitis and hyperammonemia strongly suggested hepatic encephalopathy. Infectious encephalitis, autoimmune encephalitis, and structural brain lesions were excluded due to the absence of focal neurological deficits and normal brain MRI and cerebrospinal fluid findings, favoring a metabolic etiology.²

Precipitating factors for hepatic encephalopathy include infections, excessive use of diuretics, gastrointestinal fluid losses (diarrhea and vomiting), acute kidney injury or renal failure, acute hepatic insult, portosystemic shunting, electrolyte and metabolic disturbances, constipation, gastrointestinal bleeding, and excessive dietary protein intake.^1-4

Although rare, HAV infection has been associated with other neurological complications such as encephalitis, acute disseminated encephalomyelitis, transverse myelitis, and Guillain-Barré syndrome. These conditions typically demonstrate abnormal neuroimaging or CSF findings, which were not present in this case, further reinforcing the diagnosis of hepatic encephalopathy.

Early recognition and prompt supportive management are crucial, as hepatic encephalopathy in acute viral hepatitis is potentially reversible and carries a favorable prognosis when managed appropriately.⁴

CONCLUSION

Hepatic encephalopathy is a rare but important neurological complication of acute Hepatitis A virus infection, particularly in pediatric and adolescent populations. This case highlights the importance of maintaining a high index of suspicion when patients with acute hepatitis present with altered mental status or seizures.

A comprehensive clinical evaluation supported by laboratory investigations and neuroimaging is essential to differentiate hepatic encephalopathy from other causes of acute encephalopathy. With early diagnosis and timely supportive care, patients can achieve complete neurological recovery without long-term sequelae, as demonstrated in this case.