Case Presentation:
A 62‐year‐old African American man with a questionable history of heavy alcohol use was admitted to the urology service for incision and drainage of a scrotal abscess. At the time of incision and drainage, he received D5‐half normal saline, 1 dose of morphine 2 mg intranveously, and empiric antibiotic coverage with vanco‐mycin and Zosyn. The next morning, the patient was found to be combative, tremulous, and not oriented to situation/ place/time. A dose of Ativan was given for suspected alco‐hol/benzodiazepine withdrawal; however, the patient's delirium worsened. Medicine was consulted for acute mental status change. Vitals were 99.6°F, BP 112/70, RR 16, HR 64, 100% O2 saturation on room air. The exam revealed a combative patient who refused interview and physical exam, noted to have an unsteady gait and repeated near falls. Initially the patient had been noted to be appropriate, alert/oriented × 4, and ambulating normally. Extraocular muscles were grossly intact. Labs were: white blood cell count 9.1 × 103/μL, Na 138 mmol/L, K 3.9 mmol/L, blood urea nitrogen 7 mg/dL, creatinine 0.74 mg/dL, glucose 103 mg/dL, magnesium 1.3 mg/dL, calcium 7.8 mg/ dL, thyroid‐stimulating hormone 1.38 UIU/mL. Electrocardiogram showed a normal sinus rhythm. Acetaminophen level was negative. Urine culture (2 days prior) revealed Klebsiella sensitive to Zosyn. CT head was negative for bleed or mass. Our patient was started on intravenous (IV) thiamine, and his symptoms improved overnight. After 2 days of IV thiamine with magnesium fortification, the patient had returned to baseline and was transitioned to oral thia‐mine.
Discussion:
Patients who hide a heavy alcohol history are a common occurrence for the in‐house resident and general internist. Wernicke's encephalopathy (WE) is a less common etiology for acute mental status changes but can lead to serious neurologic morbidity or mortality if missed. It affects as many as one fourth of chronic alcoholics admitted. The diagnosis is clinical and is characterized by ocular abnormalities (nystagmus and paralysis of ocular muscles), mental status changes, and unsteadiness of gait. This classic triad is seen in only a minority of patients. Ocular abnormalities may occur in one third of patients, and as many as a fifth of patients have none of these symptoms at presentation. Accompanying hallucination and behavioral disturbances may mimic acute psychotic disorders. Laboratory confirmation of thiamine deficiency may delay treatment, so empiric IV thiamine is imperative in all patients with suspected alcohol dependence. Magnesium deficiency may exacerbate thiamine deficiency, and magnesium supplementation may reduce a refractory response to therapy. Ocular abnormalities usually respond to treatment in hours to days, confusion may take days, and vestibular imbalances may take days to weeks to recover.
Conclusions:
Given the clinical challenges of diagnosing WE, physicians should maintain a high clinical suspicion of thiamine deficiency and consider prompt treatment in patients who present with unbalanced nutrition or suspicion for alcohol abuse.
Disclosures:
S. Kakoulides ‐ none; K. Wang ‐ none; B. Hymel ‐ none; D. Fotino ‐ none