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Practice Essentials

Hyperemesis gravidarum is the most severe form of nausea and vomiting in pregnancy,
characterized by persistent nausea and vomiting associated with ketosis and weight loss (>5% of
prepregnancy weight). This condition may cause volume depletion, electrolytes and acid-base
imbalances, nutritional deficiencies, and even death. Severe hyperemesis requiring hospital
admission occurs in 0.3-2% of pregnancies.[1]

Signs and symptoms

The defining symptoms of hyperemesis gravidarum are gastrointestinal in nature and include
nausea and vomiting. Other common symptoms include ptyalism (excessive salivation), fatigue,
weakness, and dizziness.
Patients may also experience the following:

Sleep disturbance



Decreased gustatory discernment




Mood changes

Decreased concentration

See Clinical Presentation for more detail.

Physical examination in women with suspected hyperemesis gravidarum is usually
unremarkable. Findings may be more helpful if the patient has unusual complaints suggestive of
other disorders (eg, bleeding, abdominal pain).
Examination includes the following:

Vital signs, including standing and lying blood pressure and pulse

Volume status (eg, mucous membrane condition, skin turgor, neck veins, mental status)

General appearance (eg, nutrition, weight)

Thyroid evaluation

Abdominal evaluation

Cardiac evaluation

Neurologic evaluation

Laboratory tests
Initial laboratory studies used in the evaluation of women with hyperemesis gravidarum should
include the following:

Urinalysis for ketones and specific gravity

Serum levels of electrolytes and ketones

Liver enzymes and bilirubin levels [2]

Amylase/lipase levels

Thyroid stimulating hormone, free thyroxine levels [3]

Urine culture

Calcium level

Hematocrit level

Hepatitis panel [1]

Imaging studies
The following imaging studies may be used to assess women with hyperemesis gravidarum:

Obstetric ultrasonography: Usually warranted to evaluate for multiple gestations or

trophoblastic disease

Upper abdominal ultrasonography: If clinically indicated, to evaluate the pancreas and/or

biliary tree

Abdominal computed tomography scanning or magnetic resonance imaging: If

appendicitis is suspected as a cause of nausea and vomiting in pregnancy

Additional imaging studies may be warranted if the patients clinical presentation is atypical (eg,
nausea and/or vomiting beginning after 9-10 wk of gestation, nausea and/or vomiting persisting
after 20-22 wk, acute severe exacerbation) or if another disorder is suggested based on the
history or physical examination findings.
In patients with abdominal pain or upper gastrointestinal bleeding, upper gastrointestinal
endoscopy appears to be safe in pregnancy, although careful monitoring is suggested.
See Workup for more detail.

Initial management in pregnant women with hyperemesis gravidarum should be conservative and
may include reassurance, dietary recommendations, and support. Alternative therapies may
include acupressure and hypnosis.[4]
The only FDA-approved drug for treating nausea and vomiting in pregnancy is
doxylamine/pyridoxine. However, antihistamines, antiemetics of the phenothiazine class, and
promotility agents (eg, metoclopramide) have also been used to manage nausea and vomiting
during pregnancy. In cases refractory to standard therapy, ondansetron and steroids may be
The following medications may be used in women with hyperemesis gravidarum:

Vitamins (eg, pyridoxine)

Herbal medications (eg, ginger)

Antiemetics (eg, doxylamine-pyridoxine, prochlorperazine, promethazine,

chlorpromazine, trimethobenzamide, metoclopramide, ondansetron)

corticosteroids (eg, methylprednisolone)

Antihistamines (eg, meclizine, diphenhydramine)

In some refractory severe cases of hyperemesis gravidarum, if maternal survival is threatened, or
if hyperemesis gravidarum is causing severe physical and psychological burden, termination of
the pregnancy should be considered.[5]
Pharmacologic therapy

If pharmacologic therapy is necessary, treatment may be initiated by giving vitamin B-6 10-25
mg 3-4 times daily; doxylamine 12.5 mg 3-4 times daily can be used in addition. Ginger capsules
250 mg 4 times daily can be added at this point if the patient is still vomiting; this has been
shown to be effective in randomized trials.[39]
Metoclopramide 5-10 mg orally every 8 hours may be used next. Promethazine 12.5 mg orally or
rectally q4h or dimenhydrinate 50-100 mg orally q4-6h may be added as well. Ondansetron 4-8
mg orally or IV q8h can be used for further refractory cases. Methylprednisolone 16 mg orally or
IV q8h for 3 days, tapered to the lowest effective dose, can be used if persistent vomiting occurs
despite the above therapy. Steroids seem to increase risk for oral clefts in first 10 weeks of
gestation.[1, 40]
The only FDA-approved drug for treating nausea and vomiting in pregnancy is doxylaminepyridoxine (Diclegis).[41, 42] Originally sold between 1956 and 1983 under a different brand name,
it was pulled from the market because of safety concerns, which have since been disproved. The
new dosage form approved in April 2013 is a delayed-release tablet that, when taken at bedtime,
is at its peak serum concentrations in the morning, when nausea and vomiting may be worse.
Approval of the new formulation of doxylamine-pyridoxine was based on a study of pregnant
women between 7 and 14 weeks' gestation who were suffering from nausea and vomiting.
Compared with placebo, doxylamine-pyridoxine significantly improved both the PregnancyUnique Quantication of Emesis and Nausea (PUQE) scores and quality of life of the trial
Doxylamine-pyridoxines approval did not include hyperemesis gravidarum, but a study by
Koren and Maltepe showed that the drug may work best when administered before the onset of
symptoms. A greater reduction in the recurrence of hyperemesis gravidarum was observed in
those who used the doxylamine-pyridoxine combination preemptively compared to those who
took the drug at symptom onset (43% vs 17%).[44]
Metoclopramide is widely used for nausea and vomiting during pregnancy, but information
regarding human teratogenicity has been lacking. Matok et al found no increased risk for major
congenital malformations, low birth weight, preterm delivery, Apgar scores, or perinatal death
between infants of mothers who took metoclopramide within the first trimester compared with

infants mothers who did not take metoclopramide. The retrospective cohort study included a
total of 81,703 infants who were born to women registered in a single health system with
computerized maternal and infant hospital records. Of these, 3458 (4.2%) had first trimester
exposure to metoclopramide.[45]
Since confirmation of adherence was unavailable, a secondary analysis was performed on infants
of mothers who refilled their prescription for metoclopramide at least once (n=758), and no
increased risk was found in this subpopulation exposed to metoclopramide compared with
infants not exposed. Additionally, the results of the study were unchanged when therapeutic
abortions of exposed and unexposed fetuses were included in the analysis.
The study provides clinicians reassurance that metoclopramide does not cause congenital
malformations; although, dopamine antagonists can cause maternal extrapyramidal symptoms
(ie, acute dystonic reactions, tardive dyskinesia).
If hypokalemia is severe or symptomatic, potassium should be replaced parenterally. Before
administering IV potassium, renal function should be evaluated. Potassium is usually added to
intravenous fluid to achieve a concentration of 40 mEq/L (and not >80 mEq/L). An infusion rate
of 10 mEq of potassium per hour should be safe as long as urine output is adequate.
When administrating intravenous hydration to a patient who has severe volume depletion in an
effort to prevent the development of Wernicke encephalopathy, avoid intravenous glucose until
intravenous thiamine has been administered.
If persistent dehydration, electrolyte loss, and/or weight loss occur despite above therapy,
nutrition supplementation by either the parenteral or enteral route is indicated. The standard
method has been via total parenteral nutrition (TPN). However, documented risks of bacteremia,
sepsis, and thrombosis have been associated with the PICC lines required for TPN
supplementation. Nasogastric tube placement and subsequent enteral feeding has been shown in
small series and reports to be a valid alternative, with less complication risks, similar efficacy,
and similar outcomes in regard to neonatal outcome when compared with TPN.[46]