Acute ETOH intoxication vs thiamine deficiency

[apmiller21]

This has come up a few times for me with this general scenario:

50 year old male (ALCOHOLIC) presents to the ER with smell of alcohol on his breath, ataxic, confused, horizontal nystagmus.

A) acute ETOH intoxication
B) Thiamine deficiency

Can't find a good answer distinguishing between the two, so any insight would be of tremendous help.

Thanks!

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[Morsetlis]

Thiamine deficiency, in addition to those, would also show Wernicke-Korsakoff encephalopathy (confabulation, cerebellar signs, and then amnesia, due to degeneration of mammillary bodies) and peripheral neuropathy (paresthesia, anesthesia due to demyelination).

The nystagmus in acute EtOH intoxication is due to Positional Alcohol Nystagmus and changing the viscosity / whatever of the semicircular canals. The ataxia in Thiamine deficiency is due to degeneration of the cerebellum vermis, and nystagmus due to degeneration of floc/nod or any lower brainstem part of the pathway of the VOR.

Plus there's the history.

 

[shan564]

Also depends on when he developed the symptoms. If he had the symptoms upon arrival, it's more likely to be acute intoxication. If he developed the symptoms after you gave him dextrose or glucose, it's definitely thiamine deficiency.

 

[CrimsonMirage]

What about alcoholic cerebellar degeneration/atrophy versus Wenicke Korsakoff (mamillary bodies)? Both are caused by thiamine deficiency and both cause ataxia. I had at least two questions on this.

Also, one of the question explanations said that W-K is caused due to mamillary bodies and temporal lobe deficits. I thought only the mamillary bodies were affected...

Please help!! Thanks.

 

[Morsetlis]

Wernicke encephalopathy: ophthalmoplegia, nystagmus, gait ataxia, derangement of mental function (global confusion, apathy, listlessness, disorientation).

Korsakoff psychosis/syndrome: retrograde amnesia (recall), inability to acquire new information => confabulation.

W-K are not distinct syndromes but rather are successive stages of a single CNS disease with the same pathophysiologic substrate. The CNS lesions affect the mammillary bodies, the periventricular regions of the thalamus, the floor of the fourth ventricle, and the anterior region of the cerebellum. There are hemorrhages and degenerative changes in the neurons.

Typically, W-K follow polyneuropathy (dry beriberi), cardiovascular syndrome (wet beriberi, or dilated cardiomyopathy), in the sequence of alcoholic nervous damage.