Management of Hyperemesis includes differential diagnosis, routine investigations and treatment of the underlying cause.

Differential Diagnosis

Hyperemesis gravidarum may be a result of underlying disease.

Differential diagnosis includes –

• Pyelonephritis

• Hydatidiform mole

• Red degeneration of fibroids

• Increased intra-cranial pressure

• An acute abdominal emergency

• Hysterical vomiting

In Hysterical vomiting, the patient is likely to complain of vomiting after every meal and of not being able to retain a drop of water. However, she manages to look well physically and her weight is appropriate. Both the patient and her partner are convinced that there is a physical explanation to her symptoms. Psychological explanation may not succeed because of denial of underlying emotional conflict.


Management of hyperemesis includes confirmation of the cause by doing routine investigations.

Routine investigation should include –

• FBC [ Packed cell volume (PCV)]

• Urea and electrolytes to help guide the intravenous (IV) fluid regime in addition to an input and output chart.

• Thyroid function tests (TFTs) may help to identify thyroid dysfunction.

• Exclude urinary tract infection by midstream urine (MSU) for culture.

• In protracted or severe cases liver function tests (LFTs) may be deranged.

• Ultrasound will be useful to confirm an intrauterine pregnancy, identify a multiple pregnancy, and exclude a molar pregnancy.


Management of hyperemesis depends on the following principles of treatment -

• Development of ketonuria in a pregnant woman with severe vomiting should indicate admission to hospital.

• Time should be spent optimizing the woman’s psychological well-being.

• Intravenous fluid replacement in the form of normal saline or 5% dextrose saline is required until ketonuria clears and vomiting subsides.

• Potassium and other electrolytes are replaced in the body, guided by daily or twice daily urea and electrolytes estimation.

• Too rapid reversal of hypernatraemia can cause fetal pontine myelinosis.

• Thiamine (vitamin B1) supplementation may be required to prevent Wernicke’s encephalopathy.

Most patients improve with the help of the above measures without long term sequelae.

Conventional anti-emetics are not usually prescribed, especially before 12 weeks of gestation, but in these women with hyperemesis it is necessary to wean them to oral feeds. The reluctance to use anti-emetics relates to fears concerning their teratogenic effects. Anti emetic medication reduces the frequency of nausea and vomiting in early pregnancy. There is some evidence of adverse effects, but there is little information about the effects on fetal outcome.

• Traditional anti-emetics, such as metoclopramide 10 mg every 8 hours IV, may be tried followed by oral anti-emetics.

• Treatment with pyridoxine (vitamin B1) appears to be effective in reducing the severity of nausea.

• The results from trials of P6 acupressure are equivocal.

• Those resistant to conventional therapy may respond to steroid treatment. There is some evidence that a course of methyl prednisolone is more effective than promethazine for treatment of hyperemesis.

• Placing a Dobbhoff nasogastric tube for enteral feeding has proponents. Isomolar feeds are recommended. Parenteral nutrition may be needed in rare instances. Regular aspiration of the stomach may also be needed if there is continued vomiting due to delayed gastric emptying.

• When symptoms of hyperemesis gravidarum persist into the second trimester, active peptic ulcer disease from Helicobacter pylori should be included in the differential diagnosis.

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