CLINICAL TYPES

These are arbitrarily leveled as mild, moderate and severe according to the severity of the condition. In mild type, she loses weight as her nutrition suffers but there is no dehydration. In moderate type, there is dehydration with circulatory changes. In severe type, there are dehydration, circulatory and biochemical changes with complications as mentioned below:

Investigation: Urine analysis - daily total output falls; reaction - acid; specific gravity - high; albumin appears; acetone appears, becomes heavy in severe cases; bile may appear; urine chloride falls and can be absent in severe cases, tested by Fantus test.

Blood Values: Haemoglobin, haematocrit and blood urea shows high-levels in a severe case. Daily estimations of serum electrolytes (chloride, sodium and potassium) are done in evaluation of the progress in the treatment.

Fundus oculi examination: Papilloedema or retinal haemorrhages may rarely develop in severe cases without exudates or vascular changes. Thus, such examinations are very necessary.

CLINICAL FEATURES

A small proportion of primigravida develops the condition which may recur in subsequent pregnancies. Multigravida very rarely gets this condition.

Symptoms: (1) Patient can take nothing by mouth as excessive vomiting of the stomach contents with bile, later coffee-ground in character. Severe retching and nausea is often present. Vomiting occurs day and night despite on eating or drinking; (2) Progressive emaciation; (3) Constipation; (4) Oliguria; (5) Mental symptoms – restlessness, sleeplessness, apathy and even coma and confusion with loss of memory; (6) Eye symptoms – diplopia, dimness of vision and even blindness may occur in severe cases.

Signs: Severe case. (1) Patient is emaciated with evidences of dehydration. There is loss of weight; (2) Tongue – dry brown and furred; (3) Pulse – tachycardia, usually soft; (4) Temperature may rise; (5) Blood pressure usually falls due to dehydration; (6) Jaundice may appear; (7) Evidences of Korsakoff’s syndrome, polyneuritis may be evident; (8) Patient shows evidence of early pregnancy. There may be abnormal pregnancy like hydatidiform mole or acute hydramnios with twins. Mild and moderate cases show evidences of lesser severity.

PATHOLOGH

In most severe cases only, pathological changes in organs are observed. Liver becomes yellow in color. Microscopically, necrosis of central part of lobule, fatty change in the lever, are well demonstrated.

Kidneys commonly show nothing abnormal. Heart tends to be small due to myocardial atrophy with subendocardial haemorrhage. In brain, lesions resembling Wernick’s encephalopathy may develop in severe cases. The lesions are petechial haemorrhages, and areas of congestion in the hypothalamic region. The lesions may be due to the metabolic toxaemia, which is possible due to the deficiency of Vitamin B1 and C. Polyneuritis also develops in severe cases.

Biochemical and circulatory changes: Loss of water by excessive vomiting leads to dehydration, haemoconcentration and even oligaemic shock in a severe case. Loss of salt in vomitus causes fall of plasma sodium chloride in a severe case. Likewise as potassium is lost in large amounts in vomitus in a severe case, state of hypokalaemia can develop. Haemoglobin, blood haematocrit values can rise; likewise blood urea, uric acid levels will rise. Thus, hypotension develops. In case of persistent hypotension below 80 mmHg., systolic pressure, oliguria and anuria can develop. Hepatic dysfunction due to starvation leads to ketosis and acidosis. Cerebral symptoms are partly due to petechial haemorrhages and also perhaps due to the water and electrolyte depletion.

Thus in this condition, in a severe case, there are excessive vomiting, starvation, dehydration, hepatic and cerebral dysfunctions. Severe form of this condition is now seldom encountered because of early treatment.

HYPEREMESIS GRAVIDARUM

This is the excessive vomiting of pregnancy, commonly during early months, which causes the deterioration of the health of the woman. Fortunately enough, incidence of this condition is less at present partly due to better antiemetic drugs and partly because of seeking advice earlier by the patient. The condition traditionally classified as a “toxaemia of pregnancy” is no longer tenable because of the better understanding of its underlying morbid changes.

Aetiology: Definitely this is not known. The following theories have been held to be responsible for this:

1. Neurosis theory - certain amount of neurotic element is present especially in mild to moderate cases, as vomiting suddenly ceases when patient is removed from her environment particularly to the hospital.

2. Endocrine theories - excess of chorionic gonadotrophins has been suspected to be the cause of excessive vomiting. However on hormonal assay, this could not be confirmed. Excess of oestrogens from growing trophoblast is also suspected to set up vomiting.

The “trigger mechanism” to initiate vomiting in pregnancy is obscure. It is perhaps initiated by the early trophoblast being aggravated by neurosis. In a fully developed case of hyperemesis gravidarum, manifestations are mainly those for effects of vomiting and starvation. These effects are those of carbohydrate starvation leading to acidosis and ketosis, vitamin deficiencies, and water, electrolytes depletion.

VOMITING IN PREGNANCY

Vomiting in pregnancy is an important symptom and may be encountered as follows:

Vomiting during first half of pregnancy:

(i) Vomiting due to pregnancy:

(a) Occasional vomiting with nausea in the morning is an aliment of normal pregnancy during second and third month. It does not affect the health of the woman and gradually passes off at the end of third month. Marked hormonal and metabolic changes associated with early pregnancy, are considered responsible for physiological nausea and vomiting of pregnancy.

(b) Hypermesis gravidarum - this is pernicious vomiting of pregnancy which can be normal or rarely hydatidiform mole.

(ii) Vomiting due to causes associated with pregnancy viz. gastric ulcer, food poisoning, appendicitis, infective hepatitis and acute hepatic failure, intestinal obstruction, intestinal worms, pyelonephritis, hysteria, cerebral tumour, uraemia, twisted ovarian cyst, pedunculated fibroid or fibroid with red degeneration.

Vomiting during second half of pregnancy:

Vomiting may appear or get aggravated during this period as follows:

(i) Vomiting due to pregnancy:

(a) Slight vomiting of pregnancy, can very rarely extend even upto the second half of pregnancy in some cases.

(b) Severe pre-eclampsia, hydatidiform mole or acute hydramnios can cause vomiting.

(ii) Vomiting due to associated causes: This forms the important cause during the pregnancy period. The causes are medical, surgical, gynaecological as already mentioned above. Hiatus hernia, ketosis and acidosis in diabetes mellitus form important causes of vomiting during this period.