Vitamin B complex all are important constituents of enzymes. Because many of these enzymes are closely related functionally, lack of single factor can interrupt an entire chain of chemical processes, producing diverse clinical manifestations. Thiamine (Vit. B1), a water soluble vitamin forms the heat labile portion of the vit. B complex is an essential co-enzyme for metabolism of carbohydrates.
It is believed to play a vital, role in the nutrition of heart and peripheral nerves. It is freely distributed in animal and vegetable products such as liver, egg yolk, legumes, yeast, germs of cereals and milk. Home pounded or lightly milled rice, even if not parboiled retains most of its thiamine but polishing the rice considerably destroys the thiamine content. Rural communities are increasingly at risk as the use of small milling machines spreads. . Diets deficient in any one factor of the B complex are quietly poor sources of other B vitamins. It is generally practical to treat the patient with the entire B complex.
Thiamine deficiency (Beriberi):
It is water soluble, function as co-enzyme in carbohydrate metabolism, transketolation and decarboxylation of a-ketoacids, and required for synthesis of acetylcholine.
Breast milk or cow's milk, vegetables, cereals, fruits, and eggs are sources of thiamine.Thiamine is easily destroyed by heat and readily extracted from foodstuffs by cooking water. The polishing of grains reduces the availability as the covering of
cereals contains most of the vitamin. Requirements increase with fever, surgery, or stress. The RDA is 0.5mg/1000kcal consumed.
The lesions are located principally in the heart, peripheral nerves, subcutaneous tissue, and serous cavities. The dilatation of heart and fatty degeneration of the myocardium is common.
Etiology:
Thiamine deficiency leading to beriberi occurs, due to poor intake in the diet, malabsorption states and prolonged illness.
Clinical Features:
Early manifestations include fatigue,apathy, irritability, depression, drowsiness, poor mental concentration, anorexia, nausea, and abdominal discomfort. Signs of progression include peripheral neuritis with tingling, burning, and paresthesias of the toes and feet; decreased tendon reflexes; loss of vibration sense; tenderness and cramping of leg muscles; CCF and psychic disturbances. Hoarseness or aphonia due to paralysis of laryngeal nerve is characteristic sign.
Thiamine deficiency leads to beriberi .There are three kinds of beriberi:
(a) wet or acute and
(b) dry or chronic beriberi
(c) wernike encephalopathy.
The early symptoms occurring in early infancy include restlessness, bouts of excessive crying, vomiting, abdominal distension, flatulence, constipation, insomnia, and anorexia etc.
In the acute cardiac or wet beriberi, the immediate clinical features are evidence of congestive cardiac failure such as tachycardia, gallop rhythm, dyspnoea, hepatomegaly, cardiomegaly, pericardial effusion, and dependent edema. The heart failure is intractable and do not respond to usual therapy.
In wet beriberi, the child is undernourished, pale, and edematous with waxy like skin. The cardiac signs at first are slight, cyanosis and dyspnea may present. Tachycardia, enlargement of the liver, loss of consciousness, and convulsions may develop rapidly. The heart is enlarged, especially to the right. The ECG shows increased Q-T interval, inversion of T waves, and low voltage changes that rapidly revert to normal with treatment. Cardiac failure may lead to death in either chronic or acute beriberi.
In the chronic form (dry beriberi) the manifestations may include, anorexia, weight loss, hoarseness, dysphonia and aphonia give rise to the characteristic noiseless cry with laryngeal nerve paralysis.In dry beriberi, the child may appear plump but is pale flabby, listless, and dyspneic; the heart rate is rapid and the liver enlarged. Peripheral neuritis may be feature. Deep tendon reflexes are usually absent.
Wernicke Encephalopathy: This is characterized by irritability, somnolence, and ocular signs, and less commonly by mental confusion and ataxias. The low level of RBC transketolase and high blood or urinary glyoxylate values are diagnostic. Clinical response to administration of thiamine remains the best test for thiamine deficiency.In the wernike encephalopathy the patient is irritable, mentally confused and ataxic. There may be evidence of raised intracranial pressure such as bulged fontanel, dilated pupil, head retraction and coma. Convulsion may occur. CSF reveals no abnormality. Ataxia may be present in thiamine deficiency.
Diagnosis:
Diagnosis of beriberi is often clinical. But if facilities are available, the following investigation may be helpful.
1. Blood thiamine level less than 4 mg/dl.
2. Low urinary excretion of thiamine.
3. Lowered erythrocyte transketolase activity.
The hallmark of diagnosis is the rapid clinical response to an intramuscular injection of 25 mg of thiamine.
Treatment:
1) If beriberi occurs in a breast-fed infant, both the mother and child should be treated with thiamine. The daily dose for children 10 mg or more. Oral administration is effective. This is both emergency and long term. Dramatic improvement results within a few hours following 50-l(K)mg of thiamine hydrochloride . maintenance dose of 5-10mg of thiamine hydrochloride daily for several days.
2) Thiamine should be given IM or I.V to children with cardiac failure. Such treatment is followed by dramatic improvement, but complete cure requires several weeks.
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