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In this essay we will discuss about the Beriberi:- 1. Meaning of Beriberi 2. Clinical Features of Beriberi 3. Types 4. Differential Diagnosis 5. Treatment 6. Prevention 7. Wernicke-Korsakoff Syndrome 8. Comment.
Contents:
- Essay on the Meaning of Beriberi
- Essay on the Clinical Features of Beriberi
- Essay on the Types of Beriberi
- Essay on the Differential Diagnosis of Beriberi
- Essay on the Treatment of Beriberi
- Essay on the Prevention of Beriberi
- Essay on the Wernicke-Korsakoff Syndrome
- Comment on Beriberi
Essay # 1. Meaning of Beriberi:
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Beriberi is a nutritional disorder formerly widespread in the rice-eating people of the East. ‘Beri’ means weak. The main features of beriberi are due to deficiency of thiamine. Three forms of the disease occur.
a. Wet beriberi, characterised by oedema often associated with high-output cardiac failure.
b. Dry beriberi, a polyneuropathy.
c. The infantile form.
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Raw fermented fish which contains thiaminase and fermented tea leaves both reduce the availability of the small amount of thiamine in the diet.
Essay # 2. Clinical Features of Beriberi:
a. At first there is anorexia and ill-defined malaise, associated with heaviness and weakness of the legs. This may cause some difficulty in walking.
b. There may be a little oedema of the legs or face and the patient may complain of precordial pain and palpitation.
c. The pulse is usually full and moderately increased in rate.
d. There may be tenderness of the calf muscles on pressure and complains of ‘pins and needles’ and numbness in the legs.
e. The tendon jerks are usually sluggish, but occasionally slightly exaggerate.
f. Anesthesia of the skin, especially over the tibiae, are common.
Such conditions may persist for months or even years with only minor alterations in the symptoms. Patipnts can work to earn their living with low efficiency. At any time this chronic malady may develop into severe forms.
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Essay # 3. Types of Beriberi:
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Wet Beriberi:
a. Oedema is the most prominent feature and may develop rapidly in the legs as well as in the face, in the trunk and also in the serous cavities.
b. Palpitations are marked and there may be breathlessness.
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c. Anorexia and dyspepsia are commonly present.
d. There may be pains in the legs after walking.
e. The calf muscles are frequently tense, slightly swollen and tender on pressure.
f. The neck veins become distended and show visible pulsations.
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g. The apex beat of the heart is displaced outwards.
h. In the arteries there is often a lowered diastolic pressure and systolic pressure is disproportionately higher; hence on auscultation over the femoral and other large arteries, a curious ‘pistol shot’ sound may be heard.
i. The pulse is generally fast.
j. If the circulation is well maintained, the skin is warm to the touch owing to the associated vasodilatation.
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k. When the heart begins to fail, the skin becomes cold and cyanotic, particularly on the face.
l. ECG often shows no changes but in some cases there are low voltage of the QRS complex, inverted T waves or evidence of disturbed conduction.
m. The urinary volume is diminished, but there is no albuminuria.
n. The mind is usually clear.
o. The patient is in danger of sudden increase in the oedema, acute circulatory failure, extreme dyspnoea and death.
Dry Beriberi:
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a. The essential feature is a polyneuropathy.
b. The muscles become progressively more wasted and weak, and walking becomes increasingly difficult.
c. The thin patients need at first one stick, then two and finally become bedridden.
d. The disease is a chronic malady, which may be arrested at any stage by improving the diet.
e. Bedridden patients are very susceptible to infections.
f. Dysentery or tuberculosis are often fatal unless prompt and efficient treatment is given.
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Infantile Beriberi:
a. This occurs in breast-fed infants, usually between the second and fifth months.
b. The mother may have no clinical signs of beriberi although they must have been eating a diet and secreting milk with a low thiamine content.
c. Frank beriberi can develop in late pregnancy and the puerperium.
d. It exists in an acute and chronic form.
e. In acute form cardiac failure may develop abruptly; the mother may have noticed that the infant is restless, cries a lot, is passing less urine than normal and shows signs of puffiness. The infant then may suddenly become cyanosed with dyspnoea and tachycardia and die within 24 to 48 hours. Other serious signs are convulsions and coma.
f. In the chronic form, which is much less common, the main symptoms are due to gastrointestinal disturbances. There is constipation and vomiting. The child is fretful and sleeps poorly. The muscles are soft and toneless, but not markedly wasted. There is often intense pallor of the skin with cyanosis round the mouth. Cardiac failure and sudden death are common.
g. Infantile beriberi is the chief cause of death between the ages of 2 and 5 months in rice-eating rural areas.
Essay # 4. Differential Diagnosis of Beriberi:
a. In mild and chronic cases of beriberi, there may be few or no physical sings and the diagnosis fully depends on the interpretation of symptoms and the dietary history.
b. The oedema of wet beriberi has to be distinguished from that associated with hepatic and renal disease and heart failure. The warm extremities in cardiac beriberi and the absence of protein in the urine are useful diagnostic points. Famine oedema should seldom be a diagnostic difficulty if a proper dietary history is taken.
c. Cardiovascular beriberi has to be distinguished from other causes of high output cardiac failure, notably hyperthyroidism and severe anemia.
d. In all doubtful cases of wet beriberi the therapeutic response to thiamine usually settles the diagnosis.
e. The diagnosis of dry beriberi is mainly based on the dietary history. In endemic areas the disease may be confused with neuritic leprosy, but this is characterized by palpable, cord-like superficial nerves and areas of skin anesthesia. These two diseases do not infrequently occur together and when they do, dry beriberi, if mild, may be overlooked.
f. The diagnosis of infantile beriberi may be difficult. Neither oedema nor paralysis is an early sign and sudden death may occur before either is present. A history of sudden death of a previous child between the ages of 2 and 5 months is suggestive. Infantile beriberi may be confused with PEM and the two may occur together.
Essay # 5. Treatment of Beriberi:
Wet Beriberi:
a. Treatment must be started as soon as the diagnosis is made because of the sudden fatal heart failure.
b. Complete rest is essential and thiamine should be given at once intramuscularly 25 mg twice daily for three days. Thereafter an oral dose of 10 mg two or three times a day should be continued until convalescence is established.
c. Thiamine treatment to a patient with cardiovascular beriberi is the most effective in medical science. Within a few hours the breathing is easier, the pulse rate slower, the extremities cooler and a rapid diuresis begins to dispose of the oedema. Within a few days the size of the heart is restored to normal. Muscular pain and tenderness are also dramatically improved.
d. During convalescence and rehabilitation, a good mixed diet with less rice is needed. Another cereal should be substituted for part of the rice in the diet. Pulses have a well-deserved reputation for curing and preventing beriberi.
Dry Beriberi:
a. Patients are generally undernourished and, if they take sufficient of a good mixed diet to enable them to gain weight, slow improvement may be expected.
b. If the dietary intake is adequate, there is no need to continue with supplementary thiamine.
c. Infections and inter-current disease should be treated and appropriate physiotherapy given.
Infantile Beriberi:
a. The mother’s milk is the simplest way of treatment. The mother should receive 10 mg thiamine twice daily-in severe cases this should be administered by injection.
b. The infant should be given thiamine in doses of up to 10 to 20 mg intramuscularly once a day for three days. This should be followed by 5 to 10 mg orally twice a day.
c. In severe heart failure of convulsions and coma the initial dose may be increased to 25 to 50 mg given intravenously very slowly.
Essay # 6. Prevention of Beriberi:
a. Beriberi can be prevented by the use of under-milled, home pounded or parboiled rice or by increased use of pulses and other foods containing thiamine. Medicinal preparations of thiamine are also available and cheap.
b. Changed milling practices are probably the most important, and in many areas rice is not so highly polished as to remove all the bran.
c. Changed milling practice of rice is the most important without removing all the bran.
d. Improvement in social and economic conditions and the consumption of a better diet with more thiamine-containing foods are essential.
e. The establishment of maternal and child Health Centres has led to many pregnant and lactating women getting good advice on diet as well as vitamin supplements ; infants may also receive them or extracts of rice bran.
Thiamine deficiency in those whose staple diet is not rice:
Thiamine deficiency, in countries where rice is not the staple food, arises in the great majority of cases in persons whose diet has been greatly restricted usually as a result of chronic alcoholism. It also arises, but rarely, secondary to carcinoma of the stomach and other conditions associated with prolonged partial starvation. Hence there is always a lack of other essential nutrients.
A. Alcoholic Neuropathy:
Alcoholics who have restricted their food intake for many weeks often develop a disorder of peripheral nerves, sometimes indistinguishable from dry beriberi. The administration of thiamine leads to no dramatic improvement, but if the patient takes a good diet and gives up alcohol completely a slow diminution of the symptoms may be expected.
The nerves of the lower limbs are affected more severely than those in the upper limbs. There is dysfunction of both sensory and motor fibres. The effects on sensory nerves may be paraesthesiae (pins and nee-dies) or sometimes severe nerve pains, as in the burning feet syndrome; there may be loss of sensation, either numbness of the extremities or loss of position sense.
Signs of motor nerve involvement are foot drop, muscle wasting and impaired knee and ankle jerks.
Other causes of polyneuropathy are:
i. Deficiency diseases:
Pellagra, sub-acute combined degeneration, burning feet syndrome and pyridoxine deficiency.
ii. Metabolic diseases:
Diabetes Mellitus, Uremia, Porphyria etc.
iii. Chemical poisoning:
Heavy metals (lead, arsenic, mercury) and some drugs.
iv. Infective:
Diphtheria, Leprosy etc.
v. In association with carcinoma.
vi. Rare genetic types:
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Refsum’s disease.
B. Occidental Beriberi Heart Disease:
Cardiac failure with generalized oedema, pulmonary congestion and dyspnoea sometimes develop in chronic alcoholics. Damage to the myocardium may be due to direct action of ethanol or thiamine deficiency.
Less frequently there is a sudden circulatory collapse with lactic acidosis. It is wise to give all alcoholics with evidence of heart failure and sufficient thiamine to replenish their tissues; in most cases no benefit is likely but it will do no harm and in few may be life-saving.
Essay # 7. Wernicke-Korsakoff Syndrome:
Wernicke in 1881 described a neurological disorder in three patients, two of them alcoholics and the third a seamstress who had persistent vomiting after ingestion of sulphuric acid. It is characterised by weakness of eye muscles, so that the patient cannot look upwards or sideways and a state of disorientation and apathy.
Sometimes there is jerky, rhythmical movements of the eyes (nystagmus) and if the patient can stand he is unsteady (ataxia). It was found that many of the cases recovered dramatically after large doses.
Korsakoff in 1887 described a psychosis, also occurring in alcoholics, characterised by a severe defect in memory and learning. Confabulation is a characteristic feature, though not always present. The patient can remember past events with verifiable accuracy. He cannot remember what he did earlier in the same day but tends to provide a superficially convincing tale rather than say he has forgotten.
Wernicke’s disease and Korsakoff s psychosis are manifestations of thiamine deficiency. After carrying out 82 postmortem cases it had been found out that there were symmetrical lesions in various parts of the brain stem, diencephalon and cerebellum, the areas commonly affected being the mammillary bodies, the nuclei of the thalamus and the periaqueductal grey matter.
In the most advanced lesions there was virtually complete tissue necrosis; the less severe lesions were characterised by destruction of myelin with less damage to neurones. Small haemorrhages are characteristic but not always present.
The same histological features were seen in cases of Wernicke’s disease and of Korsakoff s psychosis. Most of the patients who recovered from the acute confusional state subsequently developed some memory defect.
Treatment with thiamine is effective in these cases when given promptly. Large doses are also needed. Diagnosis is confirmed by the RBC transketolase test. Although the syndromes occur in alcoholics, it may arise secondary to any disorder which seriously impairs nutrition.
Essay # 8. Comment on Beriberi:
Thiamine deficiency can thus lead to an encephalopathy or a cardiomyopathy or a peripheral neuropathy. Two or rarely all three diseases can occur together in a patient but it is surprising how often they do not. We cannot yet explain why the brain is affected in one person, the heart in another and the peripheral nerves in a third.
Alcoholism is widespread and body stores of thiamine in alcoholics are likely to be small, but thiamine deficiency should be registered. There are still many unsolved problems in the relation between ethanol, thiamine and brain damage.
