A Possible Case of Minimal Hepatic Encephalopathy Treated Successfully With Lactulose

Our patient is a 62-year-old woman who was incidentally found to have cirrhosis of the liver during surgery for endometrial cancer in 2005. She has multiple hepatic cysts on CT scan, but a full serologic workup has been negative and the patient reports never abusing alcohol.

Our patient was admitted to our teaching hospital after a fall, but CT of the head revealed a scalp contusion and no evidence of intracranial hemorrhage. After she was hemodynamically stabilized, we were consulted because of “altered mental status.”

On initial interview, she had psychomotor slowing but denied dysphoria, auditory/visual hallucinations, or delusions. The Vigilant A section of the Confusion Assessment Method-Intensive Care Unit was intact, and The Richmond Agitation Sedation Scale score was zero; however, on The Blessed Short Orientation-Memory-Concentration Scale (SOMC), she scored 24/28 (“cognitive impairment consistent with dementia”), with concentration, and short-term memory deficits. Laboratory data were unremarkable except for a blood ammonia level 112 μg/100 ml (normal range=19–65 μg/100 ml) on admission and 192 μg/100 ml on the day of our consultation.

Our patient was treated with lactulose, 15 ml b.i.d. One day later, her SOMC score was 12 with improvement in orientation and short-term memory, and her ammonia level was 145 μg/100 ml. Lactulose was increased to 30 ml b.i.d.; on the next day, she scored 8 on the SOMC, with improvement in all modalities, and her ammonia level fell to 101 μg/100 ml. Her SOMC score had improved to 6 (“questionable cognitive impairment”) 1 day later and she was discharged with lactulose, 30 ml b.i.d. On follow-up, 6 weeks later, our patient's functioning improved and she was able to perform household tasks that she was unable to perform 6 months earlier.

Minimal hepatic encephalopathy presents with cognitive deficits including attention deficit, memory loss, disorientation, and impaired reasoning, which can lead to significant impairment in daily functioning² (hepatic encephalopathy involves clinically obvious compromise of consciousness/arousal, behavior, and motor functions).¹ The pathogenesis of minimal hepatic encephalopathy may involve increased permeability of the blood–brain barrier, permitting ammonia to diffuse across into the brain more freely, causing ammonia-induced encephalopathy.³ Thus, treatment strategies involve the reduction of blood ammonia levels via the use of oral lactulose⁴ which can improve cognitive function and health-related quality of life.²

The preservation of communication skills and lack of awareness of cognitive symptoms make minimal hepatic encephalopathy patients difficult to identify. Patients with cirrhosis who are engaged in professions that require constant vigilance and coordination (e.g., machinery operators and drivers) are disproportionately affected by minimal hepatic encephalopathy. Therefore, minimal hepatic encephalopathy has the potential to endanger patients and others during occupational tasks.⁵ We feel that it is important to consider minimal hepatic encephalopathy in patients with cirrhosis, as a potentially treatable neurocognitive condition, with medications like lactulose which could improve quality of life.