Severe nausea and vomiting of pregnancy with weight loss, dehydration, and electrolyte derangement.
Also known as: hyperemesis gravidarum, HG, severe morning sickness, NVP
Overview
Severe persistent nausea and vomiting in pregnancy producing >5% pre-pregnancy weight loss, dehydration, ketonuria, and electrolyte abnormalities. Distinguished from typical nausea and vomiting of pregnancy (NVP) by severity and functional impairment.
Epidemiology
Affects 0.3-3% of pregnancies; most common cause of antepartum hospitalization in the first half of pregnancy. Onset usually 4-9 weeks; peaks at 9-13 weeks; resolves by 20 weeks in most.
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Multiple gestation, molar pregnancy (very high beta-hCG)
Female fetus, family history
History of motion sickness, migraine, hyperthyroidism
GDF15 genetic variation (emerging evidence)
Pathophysiology
Likely multifactorial. Elevated beta-hCG and estrogen levels are strongly implicated; H. pylori infection, altered GI motility, hepatic dysfunction, and recent evidence implicating placental hormone GDF15 acting on hindbrain receptors all contribute.
Clinical presentation
Symptoms
Persistent vomiting, often unable to tolerate liquids or solids
Weight loss, fatigue, lightheadedness
Hypersalivation (ptyalism), heightened sense of smell
Cholecystitis / pancreatitis — Localized RUQ or epigastric pain, elevated LFTs/lipase, gallstones on US
Hyperthyroidism / thyroid storm — Tachycardia, weight loss, heat intolerance; TSH suppressed; gestational transient hyperthyroidism can co-exist with HG
DKA — Type 1 DM, anion gap acidosis, hyperglycemia, ketonemia
UTI / pyelonephritis — Dysuria, CVA tenderness, UA positive
Increased intracranial process — Headache, focal neuro signs, papilledema
Diagnostic workup
Diagnostic criteria
Clinical: persistent vomiting + >5% pre-pregnancy weight loss + ketonuria/electrolyte derangement, after exclusion of other causes.
Labs
Urinalysis with ketones and specific gravity
BMP: hypokalemia, hyponatremia, hypochloremic metabolic alkalosis (from vomiting); BUN/Cr ratio elevated with dehydration
TSH and free T4: transient gestational hyperthyroidism (suppressed TSH with normal or mildly elevated free T4) common — typically no antithyroid therapy needed
LFTs (mild AST/ALT elevation up to 200 may occur), amylase/lipase if epigastric pain
IV hydration (thiamine FIRST), enteral feeding, rare TPN
Stepwise management of nausea/vomiting of pregnancy and hyperemesis gravidarum (ACOG PB 189).
Treatment
First-line
Step 1 (mild): dietary modification — small frequent bland meals, avoid triggers, ginger 250 mg QID, acupressure wristbands
Step 2: pyridoxine (vitamin B6) 10-25 mg PO every 6-8 h, with or without doxylamine 12.5 mg PO every 6-8 h (combination product Diclegis/Bonjesta is first-line FDA-approved therapy)
Step 4 (severe/refractory): ondansetron (after first-trimester counseling — small association with cleft palate at high doses), or methylprednisolone (use AFTER 10 wk to minimize oral cleft risk)
Hospitalization indication
Inability to tolerate oral intake despite outpatient therapy, dehydration, electrolyte derangement, or >5% weight loss
IV crystalloid (LR or NS), thiamine 100 mg before any dextrose to prevent Wernicke encephalopathy
Repletion of potassium, magnesium
Antiemetics IV/IM until tolerating PO
Second-line / adjunct
Enteral feeding (NG, NJ) if persistent inability to tolerate PO and weight loss continues
Parenteral nutrition reserved for refractory cases — high risk of line sepsis, hepatic dysfunction, thrombosis
Complications
Wernicke encephalopathy (from thiamine deficiency) — confusion, ataxia, ophthalmoplegia; classically precipitated by IV dextrose without prior thiamine
Central pontine myelinolysis from rapid sodium correction
Acute kidney injury from dehydration
Maternal depression and anxiety; reduced fetal growth in severe sustained disease
PANCE pearls
Always give thiamine BEFORE dextrose-containing fluids in any patient with prolonged vomiting — failure to do so can precipitate Wernicke encephalopathy.
Molar pregnancy should be excluded by ultrasound in any patient with severe HG; the very high beta-hCG and hyperthyroidism it causes can mimic primary HG.
Doxylamine + pyridoxine is the first-line, pregnancy-safe (Category A) pharmacotherapy and should be started before ondansetron.
Transient gestational hyperthyroidism in HG resolves spontaneously by 18-20 weeks; antithyroid drugs are generally not indicated.
Methylprednisolone should be avoided before 10 weeks gestation due to a small increase in oral clefts.
References
ACOG PB 189 — ACOG Practice Bulletin 189: Nausea and Vomiting of Pregnancy (Obstet Gynecol 2018)
ACOG CO 814 — ACOG Committee Opinion: Care for Patients with HG
PUQE Score — Koren et al., Pregnancy-Unique Quantification of Emesis (PUQE) score
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