Minimal hepatic encephalopathy (MHE) is a neurocognitive disorder that affects up to 80% of cirrhotic patients. Similar to overt hepatic encephalopathy, ammonia and oxidative stress play key roles in the pathogenesis of MHE. However, MHE is characterized by subtle deficits and psychomotor abnormalities that can only be elicited by specialized psychometric tests. Although no gold standard exists for the diagnosis, MHE remains an important entity for clinicians to recognize because of its negative impact on a patient's health-related quality of life and association with driving impairment and vehicle accidents. MHE has also been associated with an increased rate in the development of overt hepatic encephalopathy and increased mortality; therefore, identification and treatment should not be delayed. Treatment to date has been focused on reducing serum ammonia levels with agents such as lactulose, probiotics, and synbiotics. MHE is a real and growing problem that is epidemic in cirrhosis, and increasing awareness of this condition is necessary for adequate management of these patients.

A 20-year-old woman presented to the emergency department for evaluation of a wound to left hand (Fig. 1). She admitted having a history of chronic severe headaches requiring daily use of analgesics. She first noted the ulcer approximately 10 months prior to presentation. Her examination was remarkable for a 10-cm by 8-cm ulceration to the dorsum of her left hand with exposed and necrotic metacarpals. Fibrous exudate was present in the wound-bed, and the ulcer was associated with a foul odor. She was afebrile on presentation with a peripheral white blood cell count of 6.4 x109/L, CRP 1.9 mg/dL, and ESR 15 mm/h.

No abstract