The Banana Bag: Small Potatoes against Wernicke’s Encephalopathy

Neha Patel MD, Devika Das MD, Selena Stuart MD, Analia Castiglioni MDThe University of Alabama at Birmingham

References

Case Description

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Kopelman M, Thomson A, Guerrini I. “The Korsakoff Syndrome: Clinical Aspects, Psychology and Treatment.” Alcohol & Alcoholism. Vol. 44, No.2, pp. 148-154, 2009.

G, Pipitone N. “Neuroimaging Findings in Acute Wernicke’s Encephalopathy: Review of the Literature.” American Journal of Roentgenology. Vol. 192, Feb 2009.

Thomson A, Guerrini I, Marshall E. “Wernicke’s Encephalopathy: Role of Thiamine.” Practical Gastroenterology. Series 75, pp. 21-30, 2009.

Martin PR, Singleton CK, Hiller-Sturmhöfel S. “The role of thiamine deficiency in alcoholic brain disease.” Alcohol Res Health. 2003; 27:134.

Heap LC, Pratt OE, Ward RJ, et al. “Individual susceptibility to Wernicke-Korsakoff syndrome and alcoholism-induced cognitive deficit: impaired thiamine utilization found in alcoholics and alcohol abusers.” Psychiatr Genet. 2002; 12:217.

To recognize that Wernicke’s encephalopathy can present with encephalopathy alone

To understand the utility of neuroimaging in the diagnosis of Wernicke’s encephalopathy

To review thiamine repletion guidelines for suspected cases of Wernicke’s encephalopathy

ObjectivesHospitalization #1Hospitalization #1

55 year old man with alcoholism admitted with encephalopathy and ataxia; no neurological deficits

Treated for alcohol intoxication with benzodiazepines prn and “banana bags” with 100mg IV thiamine daily x 7 days

Discharged in usual state of health after 7 days

Hospitalization #2Hospitalization #2

MRI findings of Wernicke’s encephalopathy

Overview of Wernicke’s Encephalopathy

Take Home Points

Wernicke’s encephalopathy (WE) is a serious yet reversible sequelae of alcoholism resulting from profound thiamine depletion

Untreated, up to 20% of cases result in fatality, and 85% of survivors develop irreparable brain damage, i.e. the Korsakoff syndrome

Wernicke’s encephalopathy often manifests as encephalopathy alone, without cerebellar ataxia or ophthalmoplegia

Although MRI neuroimaging may support a diagnosis of WE, it should not be used to exclude a diagnosis of WE given its low sensitivity

Patients at high-risk for WE warrant high-dose thiamine repletion when presenting with encephalopathy – “banana bags” do not suffice

The Classic Triad of Wernicke’s

encephalopathy

ophthalmoplegiace

rebe

llar a

taxia

Only 20% of cases manifest with the “classic triad”

Majority of cases present only with encephalopathy (i.e. hospitalization #1)

TreatmentDiagnosis Usually a clinical diagnosis

Neuroimaging has a limited role: Head CT offers negligible detection MRI only 53% sensitive

Findings suggestive of WE include increased signaling in mamillary bodies, periaqueductal area, and thalamus

For high-risk patients (i.e. alcoholics) presenting with encephalopathy: Thiamine 250mg IM/IV daily for 3-5 days

(banana bags do not suffice)

If a definitive diagnosis of WE is established: Thiamine 500mg IM/IV daily for 2-3 days,

then 250mg daily for 3-5 days, then daily supplementation

(+) EtOH, (-) UDS CBC/CMP wnl Head CT wnl

Readmitted within 48 hrs with encephalopathy and ataxia + new findings of lateral gaze palsy, confabulation, and nystagmus

Treated for WE with 500mg IV thiamine daily with rapid resolution of symptoms in 8 days

(+) EtOH, (-) UDS CBC/CMP wnl Head CT wnl

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