Differentiation of delirium from dementia requires the utmost care, especially when the symptoms lack some core features.1 Detection becomes even more difficult with the absence of suggestive medical history or laboratory findings, which occurs in nonalcoholic steatohepatitis (NASH).2 We report the case of an elderly woman who developed delirium after an emergency shelter stay. She was originally misdiagnosed with dementia with disuse syndrome. In June 2011, an 87-year-old woman's son admitted her, claiming that she had become “senile” after a month-long emergency shelter stay due to damage caused by the March 2011 earthquake and tsunami. Because of the destruction, water was unavailable for flushing toilets. Therefore, most of the evacuees limited food and liquid intake to minimize stool and urine production. After returning home, the woman manifested functional decline; she often mistook the time and forgot to take her medication, her gait became somewhat unstable, and slight edema developed in both legs. She had consulted doctors at several hospitals, where access to detailed tests were limited because of the destruction. Because her brain computed tomography (CT) scan and blood screening tests were normal, she was repeatedly diagnosed with dementia, reinforced by the effect of the disaster and lack of exercise.3 One day, her hands were noted to be shaking briefly. Although this symptom appeared only once, her son decided to admit her to the hospital. The woman's only significant medical history was hypertension, controlled with daily candesartan and nilvadipine (8 mg each); she had no significant family history of disease. No abnormalities, except obesity (body mass index (BMI) 29.4 kg/m2), had been noted over several years of regular examinations. Her edema, which expanded to her upper and lower extremities, was classified as pitting and fast, indicating hypoalbuminemia as the major cause.4 Pyramidal and extra-pyramidal signs and ataxia were not manifested; her muscle strength was well preserved. Mini-Mental State Examination revealed immediate recall failure. The forward and backward digit span test showed lower score, suggesting that her forgetfulness was inattention rather than memory impairment.5 She spoke slowly and showed careless behavior, such as leaving the toilet without flushing after excretion. Because most of her symptoms seemed to be related to inattention, it was speculated that she had delirium rather than dementia, although fluctuation of symptoms or hyperactivity was unapparent. The concomitance of “subsyndromal delirium”1 and edema caused by hypoalbuminemia with mild throm;?>bocytopenia (Figure 1A) suggested hepatic encephalopathy (HE),6 which a blood ammonia level of 194 pg/mL and electroencephalographic findings confirmed. Abdominal ultrasonography showed cirrhosis without fluid retention (Child Class B). CT showed that her liver and spleen were of almost the same density (Figure 1B). Autoantibodies were negative. Her history and CT findings strongly indicated that cirrhosis occurred due to NASH, which often occurs in people with obesity or diabetes mellitus.5 Insulin resistance was detected later; it had been missed in her annual examinations.7 Her transaminase levels were normal in her regular examinations, suggesting that she had developed compensated cirrhosis several years earlier. Her nutrition had already improved by the time she developed HE, but sanitary water remained unavailable. These facts suggested that constipation, rather than malnutrition, was the likely cause of her encephalopathy. After 20 days of lactulose (19.5 g/d) and branched-chain amino acid (12 g/d) administration, her behavior and her performance on neuropsychological tests improved markedly (Figure 1A). Comprehensive evaluation of edema, cognition, and behavior played a major role in diagnosis. Even without full access to detailed examinations, detection of subsyndromal delirium and speculation regarding its etiology were achieved through comprehensive assessment. The major cause of misdiagnosis was NASH, which tends to be missed in the absence of suggestive history (e.g., excessive alcohol intake or hepatitis infection) and normal transaminase levels. Furthermore, if NASH has developed into cirrhosis, diabetes mellitus and insulin resistance (both causes of NASH) might be obscured. Its diagnosis should not depend heavily on laboratory findings or medical history alone. Another cause of misdiagnosis was the subacute progression and lack of fluctuation of symptoms, which resulted from a variation in clinical progression of HE and difficulties in detecting fluctuation within low-stage HE.6 Acute onset and fluctuation of symptoms are considered essential features of delirium,8 but the possibility of delirium should not be excluded if any one of the core features exists. The present case also indicates that maintaining appropriate lavatory conditions at emergency shelters is important not only for preventing infections,9 but also for maintaining good excretory habits. Conflict of Interest: None. Author Contributions: Naoki Tomita: patient diagnosis and care and manuscript preparation. Kaori Une and Takashi Ohrui: patient diagnosis and advice on the manuscript. Takae Ebihara, Youichi Kosaka, Shoji Okinaga, Katsutoshi Furukawa, Hiroyuki Arai: patient diagnosis. All of the authors read the final version of the manuscript. Sponsor's Role: None.
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Jan 1, 2019
Alexander Khoruts + 2
Open Access