alexa Neurocirculatory Manifestations of Thiamine Deficiency
ISSN: 2165-7548

Emergency Medicine: Open Access
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Research Article

Neurocirculatory Manifestations of Thiamine Deficiency

Naidoo DP*

Department of Cardiology, University of Kwa Zulu Natal, Durban, South Africa

*Corresponding Author:
Naidoo DP
Department of Cardiology
University of Kwa Zulu Natal
Durban, South Africa
E-mail: [email protected]

Received Date: January 06, 2015; Accepted Date: January 23, 2015; Published Date: January 30, 2015

Citation: Naidoo DP (2015) Neurocirculatory Manifestations of Thiamine Deficiency. Emerg Med (Los Angel) 5:236. doi: 10.4172/2165-7548.1000236

Copyright: © 2015 Naidoo DP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



The diagnosis of thiamine deficiency is essentially made on clinical grounds and may present with neurological deficit such as peripheral neuropathy and Wernicke’s encephalopathy, or with high output heart failure (wet beriberi). This study was done to determine the frequency with which both the neurological and cardiovascular manifestations coexist in states of thiamine deficiency. The hospital records of 186 patients admitted on 200 occasions with a diagnosis of thiamine deficiency due to beriberi or Wernickes encephalopathy were reviewed during the 7-year period (1994-2000). Cases were only included in the analysis if mental changes and neurological deficit (opthalmoplegia, ataxia, nystagmus) resolved rapidly after treatment with thiamine. Similar to the neurological recovery with thiamine, a rapid response in the cardiovascular state and in the metabolic acidosis to treatment with parenteral thiamine was taken as confirmatory evidence of thiamine deficiency. In all but 11 patients, complete recovery ensued within 1-3 days of treatment with parenteral thiamine. The 175 patients who responded dramatically to thiamine (67 Wernicke’s encephalopathy and 108 cardiac beriberi) form the subject of this review. In total, 43/175 (25%) patients exhibited combined neurologic and circulatory manifestations of thiamine deficiency. Eighteen patients presented with overt coexisting neurocardiac manifestations, twelve of whom had acute pernicious beriberi with circulatory shock, metabolic acidosis and accompanying neurological deficit. There was one death due to circulatory shock and metabolic acidosis in patient who arrived in extremis with an unrecordable blood pressure at the emergency room. Cardiovascular/circulatory manifestations in patients presenting with acute neurological deficit are not infrequent and should raise suspicion of thiamine deficiency. Likewise patients with advanced thiamine deficiency states presenting with shock and metabolic acidosis not infrequently have coexistent signs of WE. Empiric therapy with thiamine in advanced stages of thiamine deficiency is life-saving and a rapid therapeutic response is confirmatory of the diagnosis.


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