Clinical Features of Beriberi

Depletion and repletion studies suggest that intakes >300 mg/4.2MJ are compatible with normal biochemistry and good health, and clinical signs of thiamin deficiency occur at intakes of thiamin below 200 mg/4.2MJ (1000 kcal). The disease as studied from the 1880s onward in Asians subsisting on white rice began typically with weakness, 'wandering pains' in the legs, and lack of feeling in the feet. Some patients then developed oedema (the presence of excessive amounts of fluid in the intercellular tissue spaces of the body) of the legs, trunk, and face. In severe cases, sufferers found it increasingly difficult to catch their breath and would die of heart failure. The clinical features of subacute and acute wet beriberi are summarized in Table 4. The main form was subacute beriberi, which was typically seasonal in endemic areas. There are reports that the peripheral muscles most severely affected were those most frequently used; thus, in male laborers it was the legs. Aching pain, tightness, and cramps in the calf and associated muscles were usually a first cause of complaint, and pain on squeezing the calves was one of the most useful diagnostic tests for beriberi. In women who performed repetitive tasks involving hands and arms, a loss of sensation in the fingers was frequently a first cause of complaint.

Dry beriberi is essentially a chronic condition showing muscular atrophy and polyneuritis and frequently occurring in older adults. Walking is usually difficult because of the weak wasted and painful musculature, and in the later stages feeding and dressing may also become impossible. When bed-ridden and cachetic (extreme state of malnutrition and wasting), patients become very susceptible to infections. Sensory nervous function is impaired (hypoesthesia) almost to the point of anesthesia. Hypoesthesia is particularly evident in the extremities and progressively extends over the outer aspects of the legs, thighs, and forearms. Motor nerve disturbances also begin in the extremities and ascend progressively. Flaccid paralysis of the extensor muscles precedes that affecting the flexors and results in 'wrist drop' and 'foot drop' (Figure 1). Loss of the Achilles tendon reflex usually precedes an impaired patellar reflex.

Mortality from infantile beriberi mainly affected breast-fed infants between the second and fifth months of life, when solid foods were often first introduced. The introduction of white rice porridges, poor in thiamin, to a rapidly growing child and/or the increased exposure to infections when solids are introduced may both have contributed to infantile beriberi. The onset of the disease was rare in the first month and early signs could be mild and somewhat subjective (e.g., vomiting, restlessness, anorexia, and insomnia). Early signs could progress to subacute infantile beriberi, the acute and usually fatal condition, or a chronic form. Features of acute infantile beriberi are presented in Table 5. The subacute form was characterized by slight oedema in the form of puffiness, vomiting, abdominal pain, oliguria, dysphagia, and convulsions. In addition, aphonia (soundless cry) was often a feature of subacute infantile beriberi and may have been due to nerve paralysis or oedema of vocal cords. Vomiting was also a feature of chronic infantile beriberi and could be accompanied by inanition, anemia, aphonia, neck retraction, opisthotonus, oedema, oliguria constipation, and meteorismus (swelling of the abdominal cavity from gas in the intestine). Opisthotonus is a characteristic of acute thiamin deficiency in birds and is described as due to a tetanic spasm in which the spine and extremities are bent backwards.

In alcoholic and other malnourished subjects, one of the early signs of thiamin deficiency is anorexia. In alcohol abuse, the overwhelming desire for alcohol may outweigh all other interest in food, leading to generalized malnutrition. Alcohol specifically blocks the active absorption of thiamin and alcohol abuse can progress to the potentially fatal condition known as Wernicke-Korsakoff syndrome. The typical clinical features of Wernicke's encephalopathy comprise ophthalmoplegia, nystagmus (usually

Table 4 Common features of wet beriberi

Subacute beriberi

Acute fulminating beriberia

Digestive system

Neurological

Cardiac

Urine

Anorexia is common; constipation more frequent than diarrhea

Aching pain, stiffness, tightness, or cramps in calf or associated muscles Increasing muscular tenderness and weakness with fatigue pains resembling muscular ischemia, especially at night Pain on squeezing calves

Inability to rise from squatting position without use of hands

Diminished reflexes of ankle and knees usually bilaterally

Hypoesthesia or paraesthesia presenting as 'pins and needles,' numbness particularly over the tibia, formication (like ants running on the skin) or itching Oedema of feet and legs often appearing first on dorsa of feet and extending up legs but may also appear on back of hands and as puffiness in face Heart enlarged with tachycardia and bounding pulse Raised venous pressure (see Figure 2) with percussion sometimes revealing dilation of right auricle and ventricle Heart murmurs if present are usually systolic Apex beat is downward and outwardly displaced Neck vein possibly distended showing visible pulsations Dyspnea upon exertion Palpations, dizziness, and giddiness Extremities possibly cold and pale with peripheral cyanosis but where circulation is maintained, skin warm due to vasodilatation Electrocardiograms often undisturbed but QRS complex may show low voltage and inversion of T waves indicating disturbed conduction

Nocturia; no albuminuria

Vomiting is common, often with intense thirst Liver enlarged and tender and the epigastric region spontaneously painful Pupils dilated with anxious expression on face Aphonia frequently present and patient moans with cries of a special kind as a result of hoarseness produced by paralysis of laryngeal muscles Reflexes of ankle or knee lost or diminished

Patients severely dyspneic, have violent palpitations of the heart, are extremely restless, experience intense precordial agony but accessory muscles of respiration on slightly brought into action Widespread and powerful undulating pulsations visible in the region of the heart, epigastrium, and neck due to a tumultuous heart action Facial cyanosis more marked during inspiration Pulse is moderately full, regular, even with frequency of 120-150/min A wavelike motion may be felt over the heart On percussion, the heart is enlarged both to the left and right but mainly the latter, and the apex beat may reach the axilla Raised systolic pressure and low diastolic pressure give the 'pistol shot' sound on auscultation over the large arteries Rapidly increasing oedema may extend from legs to trunk and face with associated pericardial, pleural, and other serous effusions Oliguria or anuria; no albuminuria or glycosuria aThe whole picture of acute fulminating beriberi is dominated by insufficiency of heart and blood vessels and this tends to mask all other features of the subacute form, although these are often present and accentuated. Death is accompanied by a systolic pressure falling to 70-80 mm, the pulse becomes thinner, and the veins dilate. The rough whistling respiration deteriorates and rales appear. The patient dies intensely dyspneic but usually fully conscious.

horizontal), ataxic gait, and an abnormal mental state that can range from mild delirium to global confusion. Liver disease and tachycardia occur in more than 50% of cases. Korsakoff's psychosis is characterized by a profound amnesia, disorientation, and often confabulation. The clinical features of Wernicke-Korsakoff syndrome are listed in Table 6.

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  • Isabella
    What is clinical feature of beriberi?
    3 months ago

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