Case studies

Here are two case studies highlighting the management issues you may encounter when treating hepatic encephalopathy (HE).

Case Study 11

Case history: 56-year-old woman with increased liver enzymes (GPT, GOT), arthralgias, Raynaud’s syndrome and disturbance of sleep and concentration

Findings and diagnosis: Results of serology and liver biopsy found evidence of chronic Hepatitis C infection (HCV) and viral-induced liver cirrhosis with unremarkable liver synthesising parameters. An HCV-triggered cryoglobinaemia was excluded, but highly elevated antinuclear antibodies (ANA) and anti-RNP autoantibodies, typical serological parameters of mixed tissue collagenous (Sharp’s disease) were detectable. Magnetic resonance spectroscopy (H-MRS) was performed to differentiate between cerebral vasculitis and mild HE. This abnormal pattern of cerebral metabolites (myo-inositol and choline), is specific suggesting this patient be diagnosed with HE.

Treatment and course: The patient was started on an antiviral therapy (interferon/ribavirin) and put on a low protein diet with supplementation of L-ornithine-L-aspartate.

Outcome: Following treatment arthralgia and neuropsychiatric symptoms rapidly improved also HCV-RNA PCR became negative. Unfortunately, after cessation of antiviral treatment the patient had a relapse of HCV with a worsening of the arthralgia and the Raynaud symptoms (HCV-triggered Sharp’s disease).

Conclusion: Even in patients with mildly abnormal liver function and liver cirrhosis it is important to consider a diagnosis of mild HE if neuropsychiatric symptoms occur.1

Case Study 22

Case history: 55-year-old man with alcoholic liver cirrhosis who presented with status epilepticus. Laboratory analysis showed markedly elevated blood ammonia. Finding and diagnosis: Brain magnetic resonance imaging (MRI) showed widespread cortical signal changes with restricted diffusion, involving both temporo-fronto-parietal cortex, while the perirolandic regions and occipital cortex were uniquely spared. A follow-up brain MRI demonstrated diffuse cortical atrophy with increased signals on T1-weighted images in both the basal ganglia and temporal lobe cortex, representing cortical laminar necrosis. Conclusion: Clinicians suggested that in this case the brain lesions represent a consequence of toxic effect of ammonia.2


1. Hass HG, Kaiser S. A 56-year-old female patient with Raynaud’s syndrome, increased liver enzymes and neuropsychiatric symptoms. Dtsch Med Wochenschr. 2006;131(40):2213-6.
2. Choi JM et al. Acute hepatic encephalopathy presenting as cortical laminar necrosis: case report. Korean J Radiol. 2013;14(2):324-8.