Hyperemesis gravidarum is uncontrollable vomiting during pregnancy that results in dehydration, weight loss, and ketosis. Diagnosis is clinical and by measurement of urine ketones, serum electrolytes, and renal function. Treatment is with temporary suspension of oral intake and with IV fluids, antiemetics if needed, and vitamin and electrolyte repletion.
(See also Nausea and Vomiting During Early Pregnancy.)
Pregnancy frequently causes nausea and vomiting; the cause appears to be rapidly increasing levels of estrogens or the beta subunit of human chorionic gonadotropin (beta-hCG). Vomiting usually develops at about 5 wk gestation, peaks at about 9 wk, and disappears by about 16 or 18 wk. It usually occurs in the morning (as so-called morning sickness), although it can occur any time of day. Women with morning sickness continue to gain weight and do not become dehydrated.
Hyperemesis gravidarum is probably an extreme form of normal nausea and vomiting during pregnancy. It can be distinguished because it causes the following:
Hyperemesis gravidarum may cause mild, transient hyperthyroidism. Hyperemesis gravidarum that persists past 16 to 18 wk is uncommon but may seriously damage the liver, causing severe centrilobular necrosis or widespread fatty degeneration, and may cause Wernicke encephalopathy or esophageal rupture.
Clinicians suspect hyperemesis gravidarum based on symptoms (eg, onset, duration, and frequency of vomiting; exacerbating and relieving factors; type and amount of emesis). Serial weight measurements can support the diagnosis.
If hyperemesis gravidarum is suspected, urine ketones, thyroid-stimulating hormone, serum electrolytes, BUN, creatinine, AST, ALT, magnesium, phosphorus, and sometimes body weight are measured. Obstetric ultrasonography should be done to rule out hydatidiform mole and multifetal pregnancy.
Other disorders that can cause vomiting must be excluded; they include gastroenteritis, hepatitis, appendicitis, cholecystitis, other biliary tract disorders, peptic ulcer disease, intestinal obstruction, hyperthyroidism not caused by hyperemesis gravidarum (eg, caused by Graves disease), gestational trophoblastic disease, nephrolithiasis, pyelonephritis, diabetic ketoacidosis or gastroparesis, benign intracranial hypertension, and migraine headaches.
Prominent symptoms in addition to nausea and vomiting often suggest another cause.
Tests for alternative diagnoses are done based on laboratory, clinical, or ultrasound findings.
At first, patients are given nothing by mouth. Initial treatment is IV fluid resuscitation, beginning with 2 L of Ringer's lactate infused over 3 h to maintain a urine output of > 100 mL/h. If dextrose is given, thiamin 100 mg should be given IV first, to prevent Wernicke encephalopathy. This dose of thiamin should be given daily for 3 days.
Subsequent fluid requirements vary with patient response but may be as much as 1 L q 4 h or so for up to 3 days.
Electrolyte deficiencies are treated; potassium, magnesium, and phosphorus are replaced as needed. Care must be taken not to correct low plasma sodium levels too quickly because too rapid correction can cause osmotic demyelination syndrome.
Vomiting that persists after initial fluid and electrolyte replacement is treated with an antiemetic taken as needed; antiemetics include
After dehydration and acute vomiting resolve, small amounts of oral fluids are given. Patients who cannot tolerate any oral fluids after IV rehydration and antiemetics may need to be hospitalized or given IV therapy at home and take nothing by mouth for a longer period (sometimes several days or more). Once patients tolerate fluids, they can eat small, bland meals, and diet is expanded as tolerated. IV vitamin therapy is required initially and until vitamins can be taken by mouth.
If treatment is ineffective, corticosteroids can be tried; eg, methylprednisolone 16 mg q 8 h po or IV may be given for 3 days, then tapered over 2 wk to the lowest effective dose. Corticosteroids should be used for < 6 wk and with extreme caution. They should not be used during fetal organogenesis (between 20 and 56 days after fertilization); use of these drugs during the 1st trimester is weakly associated with facial clefting. The mechanism for corticosteroids’ effect on nausea is unclear. In extreme cases, TPN has been used, although its use is generally discouraged.
If progressive weight loss, jaundice, or persistent tachycardia occurs despite treatment, termination of the pregnancy can be offered.
Hyperemesis gravidarum, unlike morning sickness, can cause weight loss, ketosis, dehydration, and sometimes electrolyte abnormalities.
Exclude other disorders that can cause vomiting based on the woman's symptoms.
Determine severity by measuring serum electrolytes, urine ketones, BUN, creatinine, and body weight.
Suspend oral intake at first, give fluids and nutrients IV, restore oral intake gradually, and give antiemetics as needed.
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