Beriberi cardiac failure

Acute infantile beriberi in infants breast-fed by deficient mothers may involve high-output cardiac failure, as in shoshin beriberi, as well as signs of central nervous system involvement similar to those seen in Wernicke s encephalopathy (Section 6.4.4). 

Severe multisystem trauma, endotoxemia, or situations in which there is a raised metabolic demand for thiamin, such as pregnancy, thyrotoxicosis, and intercurrent illness or impaired absorption (e.g., alcohol abuse or gastrointestinal disease or resection), can produce subclinical evidence of thiamin deficiency or more severe life-threatening aspects of beriberi, such as renal and/or cardiovascular failure. The elderly may be particularly at risk of subclinical thiamin deficiency. One Belgian study on patients with a mean age of 83 years reported that 40% had a raised TDP effect (>15%), in whom there was a high proportion of Alzheimer s disease, depression, cardiac failure, and falls. The diuretic furosemide was also more frequently taken by the thiamin-deficient patients. 

High-output" failure is a rare form of heart failure. In this condition, the demands of the body are so great that even increased cardiac output is insufficient. High-output failure can result from hyperthyroidism, beriberi, anemia, and arteriovenous shunts. This form of failure responds poorly to the drugs discussed in this chapter and should be treated by correcting the underlying cause. 

Heart failure without increased cardiac output, and no peripheral edema, may also occur acutely, associated with severe lactic acidosis. This was a common presentation of deficiency in Japan, where it was called shoshin (= acute) beriberi in the 1920s, nearly 26,000 deaths a year were recorded. 

Al Martini. A1 Martini presents a second time with an alcohol-related J high output form of heart failure sometimes referred to as wet beriberi, or as the beriberi heart (see Chapter 9). The term wet refers to the fluid retention which may eventually occur when left ventricular contractility is so compromised that cardiac output, although initially relatively high, cannot meet the demands of the peripheral vascular beds, which have dilated in response to the thiamine deficiency. 

Symptoms of overt beriberi are usually abrupt with presentation of left ventricular cardiac and peripheral vascular failure yielding water retention due to stimulation of the renin-angiotensin-aldosterone axis by hypovolemia, as well as striated and smooth muscles weakness in the wet form of the disease. At this stage of the disease, the clinical diagnosis is usually apparent but outcome of the supplementary treatment with thiamine may be poor, due to irreversible alterations in muscles and the central nervous system (CNS). 

Wet Beriberi. The presence of edema distinguishes this form from dry beriberi. Other features are extreme loss of appetite, breathlessness, and disorders of the heart which range from palpitation and rapid heart rate to dilation of the heart muscle (myocardium) and congestive heart failure. When the cardiac disorders are severe, the disease may be called cardiac beriberi, or Shoshin beriberi (a name us in Asia). 

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