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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Question 1ReproductiveEasy
A 28-year-old female at 10 weeks gestation has nausea and vomiting that has failed lifestyle modifications and vitamin B6. She has lost 6% of her pre-pregnancy weight. She is now vomiting 8-10 times per day and is dehydrated with ketones in urine. Which of the following is the most likely diagnosis?
AGastroparesis
BViral gastroenteritis
CHyperemesis gravidarum
DMolar pregnancy
ENormal pregnancy nausea
Reveal answer & full explanation
Correct answer: C — Hyperemesis gravidarum
AGastroparesis
BViral gastroenteritis
CHyperemesis gravidarum✓
DMolar pregnancy
ENormal pregnancy nausea
Why Hyperemesis gravidarum is correct
Hyperemesis gravidarum is defined by intractable vomiting causing weight loss over 5%, dehydration, and ketonuria in pregnancy — all present here (6% weight loss, 8–10 vomiting episodes/day, dehydration, ketonuria)
Failure of lifestyle modifications and vitamin B6 further supports this diagnosis over normal pregnancy nausea
Why the others are wrong
Viral gastroenteritis — an acute, self-limited illness usually accompanied by diarrhea and often fever; it does not explain vomiting that has persisted long enough for lifestyle measures and vitamin B6 to be tried and to fail in the first trimester
Gastroparesis — chronic delayed gastric emptying, not specific to pregnancy; typically has no ketonuria in the acute setting and does not follow the pattern of pregnancy-related emesis
Normal pregnancy nausea — does not cause >5% weight loss, significant dehydration, or ketonuria; responds to lifestyle changes and vitamin B6
Molar pregnancy — very high hCG from a hydatidiform mole is a classic cause of severe vomiting, but most hyperemesis gravidarum occurs in normal pregnancies; nothing here, such as vaginal bleeding or a uterus large for dates, points to a mole, although ultrasound is still used to exclude it
Additional high-yield points
IV fluids: normal saline (NS) or lactated Ringer's (LR) — avoid dextrose until thiamine is given to prevent Wernicke encephalopathy
Thiamine 100 mg IV must be given before dextrose
Antiemetics: ondansetron (small absolute increase in oral clefts with first-trimester use; counsel before starting), promethazine, metoclopramide, prochlorperazine
Vitamin B6 (pyridoxine) plus doxylamine (Diclegis) is FDA-approved for nausea and vomiting of pregnancy (NVP)
Refractory cases: short course methylprednisolone
Severe cases unresponsive to treatment: total parenteral nutrition
Question 2EndocrineMedium
A 28-year-old woman in her first trimester of pregnancy is found to have TSH 0.2 mIU/L (low) with free T4 1.9 ng/dL (mildly elevated). She has no symptoms of hyperthyroidism. thyroid stimulating immunoglobulin (TSI) is negative. Which of the following is the most likely diagnosis?
AGraves' disease
BGestational hyperthyroidism
CSubacute thyroiditis
DToxic multinodular goiter
EPainless thyroiditis
Reveal answer & full explanation
Correct answer: B — Gestational hyperthyroidism
AGraves' disease
BGestational hyperthyroidism✓
CSubacute thyroiditis
DToxic multinodular goiter
EPainless thyroiditis
Why Gestational hyperthyroidism is correct
Gestational hyperthyroidism is caused by human chorionic gonadotropin (hCG) cross-reacting with TSH receptors; hCG peaks at 10–12 weeks, causing transient TSH suppression with mildly elevated free T4
thyroid stimulating immunoglobulin (TSI) negative rules out Graves' disease
It is typically transient, resolving by 20 weeks, requires no antithyroid therapy unless symptomatic, and does not cause fetal harm
It is associated with hyperemesis gravidarum
Why the others are wrong
Graves' disease — has positive thyroid stimulating immunoglobulin (TSI) / TSH receptor antibodies (TRAb) and may require propylthiouracil (PTU) or methimazole
Subacute thyroiditis — is painful and post-inflammatory in etiology
Toxic multinodular goiter (MNG) — is rare at this patient's age of 28
Painless thyroiditis — like gestational hyperthyroidism it is painless and TSI-negative, but painless (silent) lymphocytic thyroiditis is uncommon during pregnancy, when autoimmune activity is dampened, and its pregnancy-related form, postpartum thyroiditis, typically appears within the first year after delivery; transient TSH suppression at the first-trimester hCG peak points to gestational hyperthyroidism
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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 hCG and estrogen levels are strongly implicated (hCG shares an alpha subunit with TSH and has a similar beta subunit, so high levels weakly stimulate the TSH receptor and cause transient gestational thyrotoxicosis that resolves by about 20 wk; Graves disease instead has TRAb, goiter or orbitopathy and persists); 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 (counsel about a small absolute increase in oral clefts with first-trimester exposure), 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, FDA-approved pharmacotherapy for NVP with reassuring fetal safety data 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)
Fejzo 2024 (Nature) — Fejzo M, et al. GDF15 linked to maternal risk of nausea and vomiting during pregnancy. Nature 2024;625:760-7
PUQE Score — Koren et al., Pregnancy-Unique Quantification of Emesis (PUQE) score
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