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Presentation: The Patient Who Could Not Stop Falling

A 62-year-old man with a history of remote gastric bypass surgery and chronic alcohol use disorder presented to the emergency department after three days of worsening confusion and repeated falls. His family reported that he had become increasingly drowsy, had difficulty walking, and had begun seeing “flashing lights” in his peripheral vision. On examination, the patient was disoriented to place and time, and exhibited oculomotor abnormalities (specifically horizontal nystagmus) with bilateral lateral rectus weakness. His gait was wide-based and unsteady, and he could not perform tandem walking.

Why This Case Was Nearly Missed

Despite relatively classic features, the initial emergency physician attributed the patient’s condition to alcoholic intoxication and possible withdrawal. The key oversight was ignoring the dietary history: the patient had not eaten for nearly two weeks, surviving only on beer and sugary drinks. His serum thiamine level was returned at 28 nmol/L (normal >70 nmol/L). Chronic alcoholism combined with poor oral intake had precipitated acute thiamine deficiency, the underlying cause of Wernicke’s encephalopathy.

Brain MRI with contrast revealed characteristic symmetric hyperintensities in the mamillary bodies, periaqueductal gray matter, and the thalami. These findings are pathognomonic and should instantly raise suspicion for Wernicke’s encephalopathy, even in the absence of the full triad.

Clinical Clues: The “Hidden” Case 3 Profile

• Oculomotor signs: Nystagmus (horizontal more than vertical), gaze palsy, or diplopia — often the first objective sign.
• Gait ataxia: Usually cerebellar in origin (stance and gait wide, with preserved limb coordination early on).
• Global confusion: Mild disorientation to profound stupor; often mistaken for intoxication or sepsis.
• Risk factor overlap: Bariatric surgery, hyperemesis, starvation, alcoholism, or prolonged IV fluids without thiamine supplementation.

Treatment and Outcome

Intravenous thiamine (500 mg three times daily for three days, then a maintenance dose of 250 mg daily) was administered within two hours of suspicion. Within 48 hours, the patient’s nystagmus resolved completely, and his ataxia improved significantly. The confusion took longer to clear — approximately nine days — but by day 12 he had returned to his baseline cognitive status. This recovery trajectory is typical when treatment is started early; delay in treatment can lead to irreversible memory impairment or Korsakoff syndrome.

Lessons Learned from Case 3

This case illustrates that Wernicke’s encephalopathy remains undiagnosed in up to 80% of patients. The clinical diagnosis relies on a high index of suspicion — especially in patients with any form of malnutrition, malabsorption, or high metabolic demand. The mamillary body involvement on MRI is a crucial confirmatory sign, but imaging should never delay therapy. Every patient with unexplained confusion, ataxia, or eye movement disorder, particularly in the setting of suspected thiamine deficiency, must be treated empirically with parenteral thiamine.

The take-home message: think of Wernicke’s encephalopathy whenever the clinical presentation includes even one element of the classic triad combined with a risk factor for poor nutrition. Case 3 is a reminder that the condition can hide in plain sight.