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Year : 2014  |  Volume : 3  |  Issue : 4  |  Page : 273-275

Mixed beriberi: Sub acute cardiac beriberi with neurological involvement

Department of General Medicine, Guntur Medical College and Government General Hospital, Guntur, Andhra Pradesh, India

Date of Web Publication10-Dec-2014

Correspondence Address:
Pothukuchi Venkata Krishna
57-9-15, New Postal Colony, Patamata, Vijayawada - 520 010, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2277-8632.146645

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We present a case of mixed beriberi, with cardiac and neurological involvement (dry beriberi). Prolonged Thiamine deficiency causes beriberi, which is classically categorized as wet or dry; although, there is considerable overlap. In either form of beriberi, patients may complain of pain and paresthesia. This is a treatable condition sometimes with incomplete recovery, but it is probably under recognized yet increasingly common due to increasing levels of alcohol abuse. The disorder is a metabolic emergency and requires immediate treatment with intravenous thiamine. Sudden cardiac failure is common. Death occurs from right heart failure and the patient usually dies fully conscious. This patient was successfully treated with intravenous thiamine.

Keywords: Acute fulminant, neurological (dry beriberi), subacute cardiac (wet-beriberi)

How to cite this article:
Krishna PV, Ahmed S, Chepuri VR. Mixed beriberi: Sub acute cardiac beriberi with neurological involvement. J NTR Univ Health Sci 2014;3:273-5

How to cite this URL:
Krishna PV, Ahmed S, Chepuri VR. Mixed beriberi: Sub acute cardiac beriberi with neurological involvement. J NTR Univ Health Sci [serial online] 2014 [cited 2023 Feb 4];3:273-5. Available from: https://www.jdrntruhs.org/text.asp?2014/3/4/273/146645

  Introduction Top

Beriberi is a treatable condition, the onset is insidious, but may be acute with death within hours without nervous system symptoms occurring. [1] Now-a-days, because of growing alcohol consumption the occurrence of this type of cases is increasing. There is no documented incidence of beriberi in India after independence in the literature, except for a few case reports, Prakasha et al. reported three cases of dry and wet-beriberi mimicking critical illness polyneuropathy. [2] Rathi reported a case of infantile beriberi. [3] That's why, we are reporting this case.

  Case REPORT Top

A 26-year-old male who was a chronic alcoholic and smoker presented with weakness of both lower l imbs since 1 month, bilateral pedal edema since 1 week and fever since 1 week. Weakness started as feeling of tiredness and exhaustion and cramps in both lower limbs and progressed over 1 month to difficulty in getting up from the sitting position, associated with tingling and numbness of both lower limbs. Pedal edema started in both ankles progressed up to knees over 1 week; breathlessness is New York Heart Association grade 3 and is associated with palpitations.

Physical examination revealed pulse rate was 100/min, regular high volume, collapsing and pistol shot sounds were heard over large arteries, blood pressure was 80/10 mm of Hg, temperature was 100°F, jugular venous pressure was elevated with prominent "V" wave, apical impulse was felt in sixth intercostal space. Cardiovascular system examination revealed a third heart sound along with first and second heart sounds, and a grade 3/6 pansystolic murmur was heard all over precordium. Respiratory system examination revealed tachypnea and on auscultation there were bilateral basal fine crepitations, electrocardiogram showed T wave inversions. Abdominal examination revealed tender hepatomegaly.

Central nervous system examination revealed normal higher mental functions, Glasgow Coma Scale is 15. Motor system examination showed the power of 3/5 in both lower limbs. Sensory examination revealed loss of fine touch, vibration sense in both lower limbs. Plantar reflex was flexor, deep tendon reflexes were absent in both lower limbs and intact in upper limbs.


Hemogram showed normocytic hypochromic anemia and no hemoparasites. Serum electrolytes-sodium-133 meq/L, potassium-5.0 meq/L, chlorides-100 meq/L, bicarbonate-20 meq/L. Thyroid profile was normal. Nerve conduction studies showed mixed sensory and motor axonal neuropathy in lower limbs without changes of demyelination [Figure 1]. Blood thiamine level was <0.07 μg/dl (0.20-2.0).
Figure 1: Nerve conduction studies

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Two-dimensional (2D) echocardiogram [Figure 2] revealed normal valves with moderate tricuspid regurgitation, moderate pulmonary artery hypertension, dilated right atrium and right ventricle, with intact septa, no vegetation, no clots, good ventricular systolic function with ejection fraction >70%. Patient was treated with 100 mg of intravenous thiamine per day and oral paracetamol. Patient improved after 1 day with a sense of wellbeing, decreased shortness of breath and decreased swelling of lower limbs. After 4 days, power improved to 4/5 and started walking, without support. 2D echocardiogram [Figure 3] revealed a completely normal heart, which was dilated previously. After 7 days, patient regained full power of 5/5 and was discharged after 12 days with oral thiamine supplementation.
Figure 2: Two-dimensional echo at admission showing dilated right atrium and ventricle

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Figure 3: Two-dimensional echo after treatment showing normal right atrium and ventricle

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  Discussion Top

Thiamine was the first B vitamin to be identified and therefore is referred to as vitamin B1. Primary food sources for thiamine include yeast, organ meat, pork, legumes, beef, whole grains, and nuts. The germ and bran portions of cereal grains contain the most thiamine. Milled rice and grains contain little thiamine, if any. Thiamine deficiency is therefore more common in cultures that rely heavily on a rice-based diet. [4] Daily requirement of thiamine is 0.25-0.35 mg/1000 kcals of energy intake. [5]

Thiamine acts as a coenzyme for carbohydrate metabolism in the Krebs citric acid cycle and exerts a role in the oxidative breakdown of pyruvic acid. Thiamine is also involved in acetylcholine synthesis and in neurotransmission. The role of thiamine diphosphate in pyruvate dehydrogenase means that in deficiency, there is impaired conversion of pyruvate to acetyl coenzyme A. In subjects on a relatively high carbohydrate diet, this results in increased plasma concentrations of lactate and pyruvate, which may cause life-threatening lactic acidosis. Lactic acid accumulates with a breakdown of the Krebs cycle, producing a metabolic acidosis. Any factor leading to an increased thiamine demand may be etiological. For example, young men are often affected possibly because they work hardest. Since the brain nervous tissue and heart muscle use large amounts of glucose, it is in these tissues that carbohydrate metabolism is especially deranged in thiamine deficiency. [1]

The pathological anatomy of beriberi involves changes in the nervous system, the heart and muscle fibers. Microscopically, the nerve trunks show changes ranging from slight medullary degeneration to complete neural destruction (Wallerian degeneration). In the heart, there is fatty degeneration of varying severity and loss of contractility due to water retention. The essential features of "beriberi heart" are: A hyperkinetic circulation, peripheral vasodilation, right side enlargement and high-output failure. The cause of the hyperkinetic circulation deficiency is low peripheral arterial resistance from vasodilation due to loss of muscular arteriolar tone. [1]

Most dietary deficiency of thiamine worldwide is the result of poor dietary intake. In Asian countries because of increasing alcohol consumption thiamine deficiency is becoming more common. Thiamine should always be replenished when a patient with alcoholism is being re fed, as carbohydrate repletion without adequate thiamine can precipitate acute thiamine deficiency with lactic acidosis. Thiamine deficiency in its early stage induces anorexia and nonspecific symptoms (e.g., irritability, decrease in short-term memory). Prolonged thiamine deficiency causes beriberi, which is classically categorized as wet or dry, although there is considerable overlap. In either form of beriberi, patients may complain of pain and paresthesia. Wet-beriberi presents primarily with cardiovascular symptoms, due to impaired myocardial energy metabolism and dysautonomia, and can occur after 3 months of a thiamine-deficient diet. Patients present with an enlarged heart, tachycardia, high-output congestive heart failure, peripheral edema, and peripheral neuritis. Patients with dry beriberi present with a symmetric peripheral neuropathy of the motor and sensory systems with diminished reflexes. The neuropathy affects the legs most markedly, and these patients have difficulty rising from a squatting position. [4] In our case, the patient had both features of wet and dry beriberi with considerable overlap as described above and improved with intravenous thiamine. We conclude that beriberi is uncommonly encountered and not widely recognized.

  Acknowledgments Top

We acknowledge the support by Dr. Shaik Moulali (Cardiologist), Dr. N. V. Sundarachari (Neurologist) for guiding us in the investigations.

  References Top

Abrams S, Brabin BJ, Coulter JB. Nutrition-associated disease. In: Farrar J, White NJ, Hotez PJ, Junghanss T, Lalloo D, Kang G, editors. Manson's Tropical Diseases. 23 rd ed. USA: Saunders; 2014. p. 1162-4.  Back to cited text no. 1
Prakasha SR, Mustafa AS, Baikunje S, Subramanyam K. "Dry" and "wet" beriberi mimicking critical illness polyneuropathy. Ann Indian Acad Neurol 2013;16:687-9.  Back to cited text no. 2
[PUBMED]  Medknow Journal  
Rathi G. Iatrogenic infantile beriberi. Indian Pediatr 2006;43:1006-7.  Back to cited text no. 3
Russell RM, Suter PM. Vitamin and trace mineral deficiency and excess. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18 th ed. New York: The McGraw-Hill Companies; 2012. p. 595-8.  Back to cited text no. 4
A Report of the Expert Group of the Indian Council of Medical Research. Nutrient Requirements and Recommended Dietary Allowances for Indians. Hyderabad: Indian Council of Medical Research, National Institute of Nutrition; 2009. p. 247-8.  Back to cited text no. 5


  [Figure 1], [Figure 2], [Figure 3]


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