Hyperemesis Gravidarum Cause, Symptoms, Diet, Treatment, Complications

Hyperemesis gravidarum (Excessive Vomiting in Pregnancy ) is a pregnancy complication characterized by severe nausea, vomiting, weight loss, and possibly dehydration. This post includes everything you want to know about Hyperemesis gravidarum.


At the end of the session, the trainee will be able to diagnose and Manage Hyperemesis Gravidarum.

Definition of Hyperemesis Gravidarum:-

It is a severe type of vomiting of pregnancy which has got a deleterious effect on the health of the mother and/or incapacitates her in day-to-day activities. The adverse effects of severe vomiting are—dehydration, metabolic acidosis (from starvation) or alkalosis (from loss of hydrochloric acid), electrolyte imbalance (hypokalemia), and weight loss.

Incidence of Hyperemesis Gravidarum:-

There has been a marked fall in the incidence during the last 30 years. It is now a rarity in hospital practice (less than 1 in 1,000 pregnancies). The reasons are —

(a) better application of family planning knowledge which reduces the number of unplanned pregnancies,

(b) Early visit to the antenatal clinic and

(c) potent antihistamines and antiemetic drugs.

Etiology of Hyperemesis Gravidarum:-

The etiology is obscure but the following are the known facts:

(1) It is mostly limited to the first trimester;

(2) It is more common in the first pregnancy, with a tendency to recur again in subsequent pregnancies (15%);

(3) Younger age;

(4) Low body mass

(5) History of motion sickness or migraine;

(6) It has got a familial history — mother and sisters also suffer from the same manifestation;

(7) It is more prevalent in hydatidiform mole and multiple pregnancies and

(8) It is more common in unplanned pregnancies but much less amongst illegitimate ones. Women with hyperemesis gravidarum, often suffer from a transient form of hyperthyroidism (clinical or subclinical).

Hyperemesis Gravidarum Theories:-

(1) Hormonal Theory:-

(a) Excess of chorionic gonadotropin or higher biological activity of hCG is associated. This is proved by the frequency of vomiting at the peak level of hCG and also the increased association with hydatidiform mole or multiple pregnancy when the hCG titer is very much raised; 

(b) High serum level of estrogen and

(c) Progesterone excess leading to relaxation of the cardiac sphincter and simultaneous retention of gastric fluids due to impaired gastric motility. Other hormones involved are: thyroxine, prolactin, leptin and adrenocortical hormones.

(2) Psychogenic Theory:

It probably aggravates nausea once it begins. But neurogenic element sometimes plays a role, as evidenced by its subsidence after shifting the patient from the home surroundings. Conversion disorder, somatization, excess perception of sensations by the mother are the other theories.

(3) Dietetic deficiency:-

Probably due to low carbohydrate reserve, as it happens after a night without food. Deficiency of vitamin B6, vitamin B1 and proteins may be the effects rather than the cause.

(4) Allergic or immunological basis.

(5) Decreased gastric motility is found to cause nausea. Whatever may be the cause of the initiation of vomiting, it is probably aggravated by the neurogenic element.

Unless it is not quickly rectified, features of dehydration and carbohydrate starvation supervene and a vicious cycle of vomiting appears — vomiting → carbohydrate starvation → ketoacidosis → vomiting.

Pathology of Hyperemesis Gravidarum:-

There are no specific morbid anatomical findings. The changes in the various organs as described by Sheehan are the generalized manifestations of starvation and severe malnutrition.

  • Liver: Liver enzymes are elevated. There is centrilobular fatty infiltration without necrosis.
  • Kidneys: Usually normal with occasional findings of fatty change in the cells of the first convoluted tubule, which may be related to acidosis.
  • Heart: A small heart is a constant finding. There may be subendocardial hemorrhage.
  • Brain: Small hemorrhages in the hypothalamic region giving the manifestation of Wernicke’sencephalopathy. The lesion may be related to vitamin B1 deficiency.


The changes are due to the combined effect of dehydration and starvation consequent upon vomiting.

Metabolic Changes:-

Inadequate intake of food results in glycogen depletion. For the energy supply, the fat reserve is broken down.

Due to low carbohydrate, there is incomplete oxidation of fat and accumulation of ketone bodies in the blood. The acetone is ultimately excreted through the kidneys and in the breath. 

There is also an increase in endogenous tissue protein metabolism resulting in excessive excretion of nonprotein nitrogen in the urine. Water and electrolyte metabolism is seriously affected leading to biochemical and circulatory changes.

Biochemical Changes:

Patients develop acidosis (due to starvation) and alkalosis from loss of hydrochloric acid and hypokalemia. Loss of water and salts in the vomitus results in a fall in plasma sodium, potassium, and chlorides.

The urinary chloride may be well below the normal 5 g/L or may even be absent. Hepatic dysfunction results in ketosis with a rise in blood urea and uric acid.

The patient suffers from hypoglycemia, hypoproteinemia, and hypovitaminosis.

Circulatory Changes:

There is hemoconcentration leading to a rise in hemoglobin percentage, RBC count, and hematocrit values. There is a slight increase in the white cell count with an increase in eosinophils. There is a concomitant reduction of extracellular fluid.

Hyperemesis Gravidarum Clinical Course:-

From the management and prognostic point of view, the cases are grouped into

  • Early, Late (moderate to severe)
  • The patient is usually a nullipara, in early pregnancy. The onset is insidious.
  • EARLY: Vomiting occurs throughout the day. Normal day-to-day activities are curtailed. There is no evidence of dehydration or starvation.
  • LATE: (Evidence of dehydration and starvation are present).

Symptoms of Hyperemesis Gravidarum:-

Vomiting is increased in frequency with retching. Urine quantity is diminished even to the stage of oliguria. Epigastric pain, constipation may occur. Complications may appear (see below) if not treated.

Signs of Hyperemesis Gravidarum:-

Features of dehydration and ketoacidosis: Dry coated tongue, sunken eyes, acetone smell in the breath, tachycardia, hypotension, rise in temperature may be noted, jaundice is a late feature. Such late cases are rarely seen these days. Vaginal examination and/or ultrasonography is done to confirm the diagnosis of pregnancy.

Investigations for Hyperemesis Gravidarum:-


(1) Quantity—small,

(2) Dark color,

(3) High specific gravity with acid reaction,

(4) Presence of acetone, occasional presence of protein and rarely bile pigments and

(5) Diminished or even absence of chloride.

Biochemical and circulatory changes:-

The changes are mentioned previously. Routine and periodic estimation of the serum electrolytes (sodium, potassium, and chloride) is helpful in the management of the case.

Serum TSH, T3, and Free T4:-

Women may suffer from the transient phase of thyroid dysfunction (clinical or subclinical).

The ophthalmoscopic examination is required if the patient is seriously ill. Retinal hemorrhage and detachment of the retina are the most unfavorable signs.


when there is an abnormal serum potassium level.

Diagnosis of Hyperemesis Gravidarum:-

The pregnancy is to be confirmed first. Thereafter, all the associated causes of vomiting (enumerated before) are to be excluded. Ultrasonography is useful not only to confirm the pregnancy but also to exclude other, obstetric (hydatidiform mole, multiple pregnancies), gynecological, surgical or medical causes of vomiting. Differential diagnosis: When vomiting is persistent in spite of the usual treatment other causes of severe vomiting (medical or surgical) should be considered (p. 181) and investigated.

Complications of Hyperemesis Gravidarum:-

Maternal Complications:-

The majority of the clinical manifestations are due to the effects of dehydration and starvation with resultant ketoacidosis. Leaving aside that symptomatology, the following complications may occur which are fortunately rare nowadays.

(1) Neurologic complications—

(a) Wernicke’s encephalopathy, beriberi due to thiamine deficiency;

(b) Pontine myelinolysis;

(c) Peripheral neuritis;

(d) Korsakoff’s psychosis.

(2) Stress ulcer in stomach;

(3) Esophageal tear (Mallory- Weiss syndrome);

(4) Jaundice, hepatic failure;

(5) Convulsions and coma;

(6) Hypoprothrombinemia due to vitamin K deficiency and

(7) Renal failure.

Effects on the fetus (Foetal Complications):-

A fetus usually remains unaffected once the problem is resolved. Fetal risks may be due to low birth weight.PREVENTION: The only prevention is to impart effective management to correct simple vomiting of pregnancy.

Management of Hyperemesis Gravidarum:-

The principles in the management are:

Maintenance of hydration:-

  • To control vomiting
  • To correct the fluids and electrolytes imbalance
  • To correct metabolic disturbances (acidosis or alkalosis)
  • To prevent the serious complications of severe vomiting
  • Care of pregnancy.


Whenever a patient is diagnosed as a case of hyperemesis gravidarum, she is admitted. Surprisingly, with the same diet and drugs used at home, the patient improves rapidly. The relatives may be too sympathetic or too indifferent.


Oral feeding is withheld for at least 24 hours after the cessation of vomiting. During this period, fluid is given through the intravenous drip method.

The amount of fluid to be infused in 24 hours is calculated as follows:

The total amount of fluid approximates 3 liters, of which half is 5% dextrose and half is Ringer’s solution. An extra amount of crystalloids equal to the amount of vomitus and urine in 24 hours, is to be added.

With this regime — dehydration, ketoacidosis, water, and electrolyte imbalance are likely to be rectified. Serum electrolytes should be estimated and corrected if there is any abnormality. Enteral nutrition through a nasogastric tube may also be given.

Drugs for Hyperemesis Gravidarum:-

(a) Antiemetic drugs:-

  • Promethazine (Phenergan) 25 mg or prochlorperazine (Stemetil) 5 mg or triflupromazine (Siquil) 10 mg may be administered twice or thrice daily intramuscularly.
  • Trifluoperazine (Espazine) 1 mg twice daily intramuscularly is a potent antiemetic therapy. Vitamin B6 and doxylamine are also safe and effective.
  • Metoclopramide stimulates gastric and intestinal motility without stimulating the secretions. It is found useful.

(b) Hydrocortisone:-

Injection Hydrocortisone 100 mg IV in the drip is given in a case with hypotension or in intractable vomiting.

Oral method prednisolone is also used in severe cases.

(c) Nutritional supplementation—

with vitamin B1 (100 mg daily), vitamin B6, vitamin C, and vitamin B12 are given.

Nursing care for Hyperemesis Gravidarum:-

  • Sympathetic but firm handling of the patient is essential. Social and psychological support should be extended.
  • A hyperemesis progress chart is helpful to assess the progress of patients while in hospital.
  • A daily record of pulse, temperature, blood pressure at least twice daily, intake-output, urine for acetone, protein, bile, blood biochemistry, and ECG (when serum potassium is abnormal) are important.

Clinical features of improvement are evidenced by —

(a) subsidence of vomiting

(b) feeling of hunger

(c) better look

(d) normalization of blood biochemistry (electrolytes)

(e) disappearance of acetone from the breath and urine

(f) normal pulse and blood pressure and

(g) normal urine output.

Diet for Hyperemesis Gravidarum:-

Before the intravenous fluid is omitted, the foods are given orally. At first, dry carbohydrate foods like biscuits, bread, and toast are given. Small but frequent feeds are recommended. Gradually full diet is restored.

Termination of pregnancy is rarely indicated. Intractable hyperemesis gravidarum in spite of therapy is rare these days.


  • Excessive vomiting of pregnancy incapacitating day-to-day activities and/or deteriorating the health of the mother is called hyperemesis gravidarum. It is rare nowadays (1 in 1,000). It is common in first birth and limited to early pregnancy.
  • The exact cause is not known but once vomiting starts, probably neurogenic elements aggravate the state. The morbid pathological changes are due to starvation. the clinical manifestations are due to the effect of dehydration, starvation, and ketoacidosis. If not rectified promptly, the condition may turn fatal.
  • Management consists of hospitalization, sympathetic but firm handling of the patient, maintenance of hydration by IV infusion, antiemetic drugs, correction of electrolyte imbalance, and supply of glucose to protect the liver and vitamin supplement. Intractable hyperemesis gravidarum in spite of therapy is rare these days. Termination of pregnancy is rarely indicated.


1. Mention the different causes of vomiting in pregnancy? Write in short the different metabolic changes in a woman due to hyperemesis gravidarum? 

2. Write short notes on complications of hyperemesis gravidarum

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