Eduovisual
Pregnancy, Childbirth & Puerperium
Hyperemesis gravidarum: outpatient and inpatient management
— Affects 0.3–3% of pregnancies; NVP itself affects ~70–80%.
— Onset typically 4–6 weeks gestation, peaks 9–13 weeks, usually resolves by 16–20 weeks.
— Persists beyond 20 weeks in ~10%.
— Rising β-hCG (stimulates TSH receptor → biochemical hyperthyroidism), estrogen, and altered GI motility.
— Genetic contribution via GDF15 and IGFBP7 signaling at the area postrema.
— Prior HG (recurrence ~15–80%), molar pregnancy, multiple gestation, female fetus, family history, history of motion sickness or migraines, H. pylori infection.
— Pregnant patient in first trimester with persistent vomiting, inability to tolerate PO, orthostasis, ketones in urine, hypokalemia, or hypochloremic metabolic alkalosis.
— Weight documented below pre-pregnancy baseline.
— Mild NVP → lifestyle + first-line antiemetics at home.
— Moderate-severe with ketonuria, ≥5% weight loss, vital sign instability, or failed oral antiemetics → IV hydration in ED or infusion center; admit if refractory.
Board pearl: The combination of first-trimester intractable vomiting + hypokalemic, hypochloremic metabolic alkalosis + ketonuria + ≥5% weight loss is the canonical HG vignette. Always confirm a viable intrauterine pregnancy with ultrasound to exclude molar or multiple gestation, both of which markedly elevate β-hCG and worsen symptoms. HG is a diagnosis of exclusion — rule out alternative causes before labeling.
— Persistent nausea with multiple daily emesis episodes, often unable to keep liquids down.
— Ptyalism (excessive salivation), food aversion, weight loss, fatigue, lightheadedness.
— Hematemesis from Mallory-Weiss tears in severe cases.
— Symptoms beginning after 9–10 weeks gestation that are new — reconsider HG; look for alternative diagnoses (gastroenteritis, appendicitis, pyelonephritis, cholecystitis, DKA, thyroid storm, gastroparesis).
— Symptoms persisting >20 weeks require re-evaluation.
— Number of emesis episodes/24 h, oral intake (ounces of fluid retained), urine output, last solid food.
— PUQE-24 score (Pregnancy-Unique Quantification of Emesis): mild ≤6, moderate 7–12, severe ≥13.
— Pre-pregnancy weight vs current weight (percent loss).
— Abdominal pain prominent → not typical of HG; think surgical abdomen.
— Fever, dysuria, flank pain → pyelonephritis.
— Headache, visual changes, hypertension → preeclampsia (later gestation).
— Heat intolerance, tremor, palpitations → overt hyperthyroidism.
— Diarrhea or sick contacts → gastroenteritis.
— Prior HG, hydatidiform mole, number of fetuses on prior dating ultrasound, last menstrual period, contraception failure timeline.
— Impact on work, ADLs, mood — HG is strongly associated with antenatal depression and anxiety; screen explicitly.
— Food/medication insurance access; ability to fill prescriptions.
Step 3 management: On ambulatory intake, document PUQE-24, percent weight loss, last PO tolerated, urine output, and a depression screen (PHQ-2/9) — these four data points drive the decision between home titration, infusion-center hydration, or admission, and they are routinely tested as the "next best step" trigger.
— Fatigued, dry-appearing, may have acetone (fruity) breath from ketosis.
— Weight loss visible; document current weight against pre-pregnancy baseline.
— Tachycardia (HR >100), orthostatic hypotension (drop ≥20 systolic or ≥10 diastolic on standing, or symptomatic).
— Low-grade fever should prompt search for infection; HG itself is afebrile.
— Tachypnea may reflect compensatory response to metabolic alkalosis or anxiety.
— Dry mucous membranes, sunken eyes, poor skin turgor, capillary refill >2 s.
— Inspect for dental erosion (chronic emesis) and parotid swelling (ptyalism).
— Typically soft, nontender in pure HG.
— Focal tenderness, peritoneal signs, RUQ pain, or CVA tenderness should redirect workup to appendicitis, cholecystitis, pancreatitis, pyelonephritis.
— Fundal height assessment if past 12 weeks; large-for-dates → suspect molar or multiple gestation.
— Confusion, ataxia, ophthalmoplegia (nystagmus, lateral rectus palsy) — Wernicke encephalopathy from thiamine deficiency; emergency.
— Hyporeflexia or weakness — hypokalemia.
Key distinction: A tender abdomen, fever, peritoneal signs, or jaundice are not features of HG — when present, immediately broaden the differential to surgical or infectious etiologies. HG is a clinical diagnosis of a comfortable but dry, tachycardic, weight-losing first-trimester patient without abdominal tenderness; deviation from this picture mandates targeted imaging or labs before anchoring on HG.
— Urinalysis with specific gravity and ketones — large ketones plus concentrated urine confirm dehydration and starvation ketosis.
— Nitrites/leukocyte esterase to exclude UTI/pyelonephritis.
— Urine β-hCG if not already confirmed; quantitative serum β-hCG if molar suspected.
— BMP: classic hypochloremic, hypokalemic metabolic alkalosis; check Na (hyponatremia possible), BUN/Cr ratio elevated from prerenal azotemia.
— Magnesium, phosphorus, calcium — frequently low; replete aggressively.
— Glucose — assess for hypoglycemia from poor intake.
— Mild transaminitis (AST/ALT up to ~300) in up to 50% of severe HG; resolves with rehydration.
— Bilirubin usually normal; if >4 or AST/ALT >1000, look elsewhere (viral hepatitis, AFLP later in pregnancy).
— Lipase if epigastric pain to rule out pancreatitis.
— TSH often suppressed with normal or mildly elevated free T4 — gestational transient thyrotoxicosis from β-hCG cross-reactivity.
— Absence of goiter, ophthalmopathy, and negative TRAb distinguish from Graves.
— Confirm viable intrauterine pregnancy, gestational age, number of fetuses, exclude complete/partial hydatidiform mole ("snowstorm" pattern, theca lutein cysts).
Board pearl: In gestational transient thyrotoxicosis associated with HG, do not start methimazole or PTU. Treatment is supportive — thyroid function normalizes by 18–20 weeks as β-hCG declines. Antithyroid drugs in this setting cause unnecessary fetal exposure to teratogen risk (methimazole embryopathy in T1).
— RUQ ultrasound for cholelithiasis/cholecystitis when RUQ pain or AST/ALT pattern suggests biliary disease.
— H. pylori testing (stool antigen or serology) in refractory HG — eradication may improve symptoms; treat with amoxicillin + metronidazole + PPI (avoid clarithromycin in T1; bismuth/tetracycline contraindicated).
— Upper endoscopy reserved for persistent hematemesis, suspected ulcer, or refractory disease; safe in pregnancy with obstetric coordination.
— TSH, free T4, free T3, TRAb if true Graves suspected (persistent symptoms postpartum or goiter/ophthalmopathy).
— Cortisol if adrenal insufficiency suspected (hyperpigmentation, hyponatremia + hyperkalemia).
— MRI brain (without gadolinium in pregnancy) if Wernicke encephalopathy suspected — mammillary body and periaqueductal changes; do not delay empiric IV thiamine.
— Indicated when K <3.0, Mg low, or QT-prolonging antiemetics (ondansetron, promethazine, droperidol) are used.
— Watch for U waves (hypokalemia) and QTc prolongation.
— Prealbumin, vitamin B1 (thiamine), B6, B12, folate, vitamin D, iron studies.
Step 3 management: Before any first dose of ondansetron, particularly in patients on other QT-prolongers (methadone, antipsychotics, azoles, macrolides) or with hypokalemia/hypomagnesemia, obtain a baseline ECG and correct electrolytes — torsades is a tested adverse event and a documented safety event.
— Mild (PUQE ≤6, no dehydration, weight loss <5%, tolerating some PO): Outpatient lifestyle + first-line oral antiemetics.
— Moderate (PUQE 7–12, ketonuria, poor PO, mild orthostasis): Infusion-center IV hydration, IV antiemetics, then discharge with oral regimen.
— Severe (PUQE ≥13, ≥5% weight loss, refractory vomiting, electrolyte derangement, abnormal mental status): Admit.
— Small frequent meals, bland foods, separate solids and liquids.
— Avoid triggers (strong odors, fatty/spicy foods, prenatal vitamins with iron — switch to folic acid alone temporarily).
— Ginger 250 mg PO QID is evidence-based for mild NVP.
— Acupressure (P6 wristbands) — low-risk adjunct.
— Step 1: Pyridoxine (vitamin B6) 10–25 mg PO q6–8h ± doxylamine 12.5 mg PO (combination available as Diclegis/Bonjesta).
— Step 2: Add dimenhydrinate, diphenhydramine, or meclizine.
— Step 3: Add promethazine or prochlorperazine (PO/PR/IM).
— Step 4: Add metoclopramide, ondansetron (after 10 weeks ideally; weigh risk of cleft palate vs benefit), or trimethobenzamide.
— Step 5: Methylprednisolone for refractory cases — avoid before 10 weeks (oral cleft risk); taper over 2 weeks.
— Normal saline or LR with dextrose for prolonged starvation; add KCl if hypokalemic.
— Always give thiamine 100 mg IV before dextrose if prolonged vomiting (>3 weeks or unclear duration).
CCS pearl: Order set on admission — IV NS with 5% dextrose + KCl, thiamine 100 mg IV daily ×3, IV antiemetic, antiemetic PRN, strict I/Os, daily weights, BMP/Mg/Phos q12–24h, fetal heart tones, DVT prophylaxis (mechanical first).
— Pyridoxine 10–25 mg PO every 6–8 h (max 200 mg/day).
— Add doxylamine 12.5 mg PO at bedtime and morning if needed.
— Combination tablet doxylamine 10 mg/pyridoxine 10 mg (Diclegis) — 2 tabs at bedtime, escalate to 4 tabs/day; Category A; safe throughout pregnancy.
— Sedation is the main adverse effect; counsel about driving.
— Dimenhydrinate 25–50 mg PO/IV q4–6h, diphenhydramine 25–50 mg PO/IV q4–6h, meclizine 25 mg PO q6h.
— Add when B6/doxylamine insufficient.
— Promethazine 12.5–25 mg PO/PR/IM/IV q4–6h — avoid IV push (tissue necrosis with extravasation; dilute and infuse slowly).
— Prochlorperazine 5–10 mg PO/IM q6h or 25 mg PR q12h.
— Watch for extrapyramidal symptoms; treat with diphenhydramine or benztropine.
— Metoclopramide 5–10 mg PO/IV q6–8h — risk of tardive dyskinesia with prolonged use (>12 weeks); EPS.
— Ondansetron 4–8 mg PO/IV q8h — most effective; concerns:
– Small absolute increase in oral clefts with first-trimester exposure (~3 per 10,000); discuss after 10 weeks if possible.
– QT prolongation; check ECG and electrolytes.
– Use lowest effective dose.
— Methylprednisolone 16 mg IV/PO q8h ×3 days, then 2-week taper; defer until after 10 weeks gestation to avoid oral cleft risk.
— Mirtazapine or gabapentin are off-label adjuncts in highly refractory cases.
Board pearl: First-line is B6 ± doxylamine, not ondansetron. A vignette asking for the "best initial pharmacotherapy" in an otherwise stable 8-week patient should select pyridoxine plus doxylamine over ondansetron because of teratogenicity nuance and tested ACOG sequencing.
— Initial bolus: 1–2 L NS or LR for orthostasis/tachycardia.
— Maintenance: D5NS or D5LR + 20–40 mEq KCl/L as needed; avoid pure D5W (risk of rapid hyponatremia and precipitating Wernicke).
— Thiamine 100 mg IV BEFORE dextrose, then daily ×2–3 days minimum, longer in prolonged HG.
— Replete Mg, phos, K, calcium based on labs; recheck q12–24h.
— Promethazine 12.5–25 mg IV q4–6h (slow infusion).
— Metoclopramide 10 mg IV q6h.
— Ondansetron 4–8 mg IV q8h (ECG-guided).
— Combination therapy (different mechanisms) often required.
— Methylprednisolone 16 mg IV q8h ×3 days → oral taper over 2 weeks; if no response in 3 days, discontinue.
— Consider NG enteral nutrition before PN: preferred if gut works.
— Peripheral or central parenteral nutrition (TPN) reserved for failed enteral nutrition with continued weight loss; PICC line carries high thrombosis and sepsis rates in HG — use only when necessary.
— Pregnancy is prothrombotic; immobile, dehydrated HG patients warrant mechanical prophylaxis (SCDs) and prophylactic LMWH (enoxaparin 40 mg SC daily) when admitted and dehydrated.
— PPI or H2 blocker for reflux/gastritis (famotidine preferred; PPIs acceptable).
— Stool softener if constipated.
— Oral care and dental follow-up for enamel erosion.
CCS pearl: Advance the clock in 6–12 h intervals — recheck BMP, Mg, Phos, weight, I/Os, and PUQE score; once tolerating ~1 L PO over 24 h, ketones clear, and electrolytes normalize, transition IV → PO antiemetics 24 h before discharge to ensure tolerance.
— Pre-existing CKD or transplant recipients with HG require careful fluid management to avoid volume overload while correcting prerenal azotemia.
— Metoclopramide is renally cleared — reduce dose 50% if CrCl <40 mL/min; risk of EPS rises.
— Ondansetron — no renal adjustment for single doses; caution with severe impairment.
— Avoid NSAIDs (also pregnancy contraindication after 20 weeks).
— HG itself causes transient transaminitis (AST/ALT up to ~300) that resolves with rehydration — do not stop antiemetics unless markedly abnormal.
— Differentiate from viral hepatitis, AFLP (>20 weeks), HELLP, intrahepatic cholestasis of pregnancy (pruritus, ↑bile acids, usually T3).
— Ondansetron and promethazine hepatically metabolized; use lowest doses if AST/ALT >5× upper limit.
— Type 1 patients with HG are at high risk of DKA even with mild hyperglycemia — check beta-hydroxybutyrate, anion gap; admit early.
— Adjust insulin during poor PO; basal insulin must continue (otherwise DKA); cover with dextrose-containing IVF.
— Distinguish gestational transient thyrotoxicosis (no goiter, no TRAb, resolves) from Graves (treat with PTU in T1, switch to methimazole T2/T3).
— Caution with QT-prolonging antiemetics (ondansetron, droperidol, promethazine) in long QT or structural heart disease.
— Patients on SSRIs and antiemetics — additive serotonergic risk; monitor for serotonin syndrome with ondansetron + SSRI (rare but reported).
Key distinction: Transaminitis in HG normalizes within days of rehydration; persistently elevated LFTs, jaundice, or coagulopathy are NOT HG — investigate viral hepatitis, gallstone disease, or pregnancy-specific liver disease.
— Higher β-hCG → more severe and prolonged HG.
— Confirm with early ultrasound; HG may be the presenting clue.
— Threshold for admission and aggressive nutritional support is lower; weight loss disproportionately affects fetal growth.
— Complete mole: "snowstorm" on US, no fetal parts, β-hCG often >100,000 mIU/mL, theca lutein cysts, early-onset preeclampsia <20 weeks, severe HG, hyperthyroidism.
— Partial mole: less severe; fetal parts with triploidy.
— Management: Suction D&C, anti-D if Rh-negative, serial β-hCG monitoring weekly until undetectable ×3, then monthly ×6 months; contraception during follow-up; refer to GTN specialist if persistent.
— Higher rates of inadequate prenatal care; HG may be first contact.
— Confidentiality nuances: state-specific minor consent for prenatal care; counsel on confidentiality limits.
— Screen for food insecurity, partner violence, depression; involve social work.
— Post–Roux-en-Y or sleeve patients have higher thiamine, B12, iron, and folate deficiency risk; replete proactively.
— Risk of internal hernia presenting as HG-like vomiting — surgical consult if pain.
— Pregnant patients sometimes use cannabis for "morning sickness"; counsel cessation — associated with neurodevelopmental risk.
— Cannabis hyperemesis can mimic HG; hot showers provide symptom relief is a classic clue.
— Recurrence rate 15–80%; start prophylactic B6 + doxylamine before symptom onset in next pregnancy.
Board pearl: Severe first-trimester vomiting + uterine size > dates + β-hCG >100,000 + early preeclampsia features = molar pregnancy until proven otherwise. Order pelvic ultrasound immediately; treatment is suction evacuation with β-hCG surveillance.
— Hypokalemia, hypochloremic metabolic alkalosis, hyponatremia, hypomagnesemia, hypophosphatemia, hypoglycemia.
— Rapid sodium correction → central pontine myelinolysis; correct ≤8–10 mEq/L per 24 h.
— Wernicke encephalopathy: confusion, ataxia, ophthalmoplegia from thiamine deficiency; can cause fetal demise and permanent maternal Korsakoff. Treat empirically with IV thiamine 500 mg TID ×2–3 days, then 250 mg daily.
— Peripheral neuropathy from prolonged B6 excess (>500 mg/day chronically) — rare but reportable.
— Mallory-Weiss tears, esophagitis, GERD, dental enamel erosion, Boerhaave (rare).
— VTE from dehydration, immobility, hypercoagulable pregnancy state; PICC lines compound risk.
— Acute kidney injury (prerenal); usually reverses with rehydration.
— Antenatal depression, anxiety, PTSD related to HG, decision regret, pregnancy termination considered in severe refractory cases.
— Low birth weight, small for gestational age, preterm delivery (especially with significant maternal weight loss or prolonged malnutrition).
— Most pregnancies with adequately managed HG have normal outcomes.
— Increased risk of placental abruption and preeclampsia in severe HG.
— Ondansetron — QT prolongation, torsades; rare oral cleft signal.
— Promethazine — tissue necrosis with extravasation; EPS.
— Steroids — first-trimester oral cleft if used <10 weeks; gestational diabetes, infection with prolonged use.
Step 3 management: Any HG patient with altered mental status, ataxia, or eye movement abnormality gets immediate IV thiamine (high-dose) before glucose, MRI brain (no gadolinium), and neurology consult — Wernicke is reversible if treated within hours, devastating if missed.
— Inability to tolerate PO fluids after ED IV hydration trial (2 L + antiemetics).
— Weight loss ≥5% from pre-pregnancy weight.
— Persistent ketonuria despite hydration.
— Electrolyte abnormalities: K <3.0, Na <130, severe alkalosis (HCO3 >32).
— Hemodynamic instability or AKI.
— Suspected Wernicke, esophageal injury, or other complication.
— Failure of outpatient regimen including stepped antiemetics.
— Psychosocial: unsafe home environment, severe depression, inability to maintain hydration at home.
— Altered mental status concerning for Wernicke.
— Severe electrolyte derangement requiring telemetry (QTc >500, frequent ectopy).
— Hemodynamic compromise requiring vasopressors (rare).
— Severe alkalemia with respiratory compromise.
— Maternal-fetal medicine for refractory HG, comorbid conditions, recurrent HG planning.
— Nutrition (RD) for enteral/parenteral planning, weight tracking, vitamin repletion.
— Psychiatry / behavioral health for depression, anxiety, decision-making support.
— Social work for resources, FMLA paperwork, food/medication insecurity.
— GI if hematemesis, refractory symptoms beyond 20 weeks, or evaluating for H. pylori/endoscopy.
— Endocrine if thyroid status unclear or DM management complex.
— Anesthesia for PICC/central access if TPN considered.
— Tolerating PO ~1 L over 24 h, ketones cleared, electrolytes normal, weight stable or trending up, 24 h on oral regimen, follow-up arranged within 1 week.
CCS pearl: Always arrange OB follow-up within 1 week and ensure prescriptions are filled before discharge — readmission for HG often reflects medication non-fill or inadequate outpatient follow-up rather than disease failure.
— Up to 80% of pregnancies; mild, no weight loss, no electrolyte abnormality, no ketonuria.
— Manage with reassurance, dietary changes, B6 ± doxylamine PRN.
— Markedly elevated β-hCG, uterus larger than dates, "snowstorm" on US, theca lutein cysts, preeclampsia <20 weeks, hyperthyroid symptoms.
— Treatment: suction D&C, serial β-hCG.
— Higher β-hCG → worse HG; identified on US.
— Suppressed TSH, mildly elevated free T4, no TRAb, no goiter, resolves by 18–20 weeks.
— Do not treat with antithyroid medications.
— Nausea/vomiting + headache, RUQ pain, hypertension, proteinuria, thrombocytopenia.
— Different timing (>20 weeks) and additional features.
— Hemolysis, elevated LFTs, low platelets, RUQ pain, vomiting; emergent delivery.
— Nausea, vomiting, RUQ pain, jaundice, hypoglycemia, coagulopathy, encephalopathy.
— Swansea criteria; emergent delivery.
— Pruritus (palms/soles), elevated bile acids, T2–T3; nausea less prominent.
— Pain, bleeding more typical; US distinguishes.
— Sheehan syndrome with hypotension, lactation failure — different timing.
Key distinction: HG is a first-trimester diagnosis with normal vital sign trajectory after rehydration, no proteinuria, no thrombocytopenia, and normal bile acids. Any vomiting that emerges or persists past 20 weeks should pivot the differential toward preeclampsia spectrum, AFLP, HELLP, or cholestasis — not HG.
— Appendicitis — RLQ pain (may be displaced cephalad in pregnancy), fever, leukocytosis; US/MRI to confirm.
— Cholecystitis/cholelithiasis — RUQ pain, Murphy sign, US findings.
— Pancreatitis — epigastric pain, elevated lipase; often gallstone-related in pregnancy.
— Peptic ulcer / gastritis — epigastric pain, hematemesis; consider H. pylori.
— Gastroenteritis — diarrhea, fever, sick contacts.
— Bowel obstruction — distension, no flatus, prior surgeries.
— Pyelonephritis — flank pain, fever, dysuria, pyuria.
— Nephrolithiasis — colicky flank pain, hematuria.
— DKA — even euglycemic DKA in pregnant T1DM; check anion gap and ketones.
— Thyroid storm — beyond gestational transient thyrotoxicosis.
— Adrenal insufficiency — hyponatremia + hyperkalemia, hyperpigmentation.
— Hypercalcemia — primary hyperparathyroidism.
— Migraine, increased ICP, vestibular disease, posterior fossa lesions — headache, focal neuro signs.
— Viral hepatitis (A, B, E — E severe in pregnancy), CMV, HIV.
— Iron from prenatal vitamins, opioids, cannabis hyperemesis, alcohol use, lead, mercury.
— Eating disorder relapse during pregnancy — assess history of bulimia/anorexia.
— Anxiety-driven somatic symptoms.
Board pearl: A pregnant patient on insulin presenting with "HG" who has anion gap, ketones, and "normal" glucose has euglycemic DKA until proven otherwise — pregnancy-specific entity. Treat with IV insulin, dextrose, fluids, and electrolyte repletion; ICU-level care.
— Tolerating PO ≥1 L over 24 h.
— Resolved ketonuria.
— Normal/stable electrolytes for ≥24 h.
— Weight stable or trending up.
— 24 h transition onto oral antiemetic regimen before discharge.
— Outpatient OB follow-up arranged within 1 week.
— Prescriptions filled (verify, especially Diclegis/ondansetron coverage).
— Scheduled (not PRN) B6 + doxylamine combination at therapeutic dose.
— Add second-line antiemetic (promethazine, metoclopramide) as needed.
— Ondansetron sparingly and at lowest effective dose; reassess weekly.
— Wean as symptoms improve, typically by 16–20 weeks.
— Continue prenatal vitamin when tolerated; if iron worsens nausea, use folic acid alone (0.4–1 mg) until T2.
— Small frequent meals, protein-rich snacks, ginger, fluids between meals.
— Resume full prenatal vitamin once tolerated.
— Discuss recurrence risk; consider prophylactic B6 + doxylamine at 4–6 weeks in next pregnancy.
— Document medication tolerance and effective regimens for future reference.
— Screen for postpartum depression and PTSD related to HG experience.
— Connect with HG support groups (HER Foundation).
— Address employment accommodation (FMLA paperwork).
— Most resolve completely without sequelae.
— Rare reports of biliary disease, thyroid dysfunction following severe HG.
Step 3 management: Continue scheduled antiemetics for at least 1 week after symptom resolution before tapering; abrupt discontinuation drives readmissions. Counsel patients to resume the prior effective regimen at first symptom return rather than waiting for severe vomiting.
— Within 1 week of discharge for weight, hydration, symptom reassessment.
— Weekly OB visits during active HG until stable, then routine prenatal schedule.
— Telehealth check-ins between visits acceptable and effective.
— Weight at every visit (vs pre-pregnancy and prior visit).
— Symptom severity (PUQE-24 score documented).
— Urine ketones (home dipsticks reasonable for severe cases).
— Electrolytes if symptoms recur or new medications added.
— Fetal growth assessment by ultrasound in T2 if significant weight loss.
— Document current regimen, doses, side effects at each visit.
— Watch for EPS with metoclopramide/promethazine, QT with ondansetron.
— Discontinue steroids appropriately (no abrupt stop after >2 weeks of use).
— RD referral for severe HG, weight loss >5%, or persistent intake limitations.
— Track gestational weight gain trajectory (IOM guidelines based on pre-pregnancy BMI).
— Iron supplementation reintroduced when nausea allows; check ferritin in T2.
— PHQ-9 screening at first prenatal visit, at 24–28 weeks, and postpartum (USPSTF/ACOG).
— Refer to perinatal mental health if PHQ-9 ≥10 or significant anxiety.
— Discuss reproductive decision-making nonjudgmentally.
— Red flags requiring return: inability to keep fluids down >12 h, weight loss, dizziness, dark urine, confusion, fever, abdominal pain.
— Reassure that HG typically improves by 16–20 weeks; perinatal outcomes generally favorable with treatment.
— Discuss safety of standard antiemetics — most are pregnancy-compatible.
CCS pearl: Always document a PUQE score and weight at each follow-up — this drives objective titration decisions and protects against under-treatment, which is the more common error than over-treatment in HG.
— Counsel on ondansetron's small absolute risk of oral clefts (~3/10,000 with first-trimester use) vs benefits.
— Discuss steroid risk of oral clefts if used <10 weeks; defer methylprednisolone beyond 10 weeks when possible.
— Document shared decision-making; respect patient autonomy in weighing risks.
— Some patients with severe refractory HG consider pregnancy termination; this must be discussed nonjudgmentally with full information about treatment options, prognosis, and legal access.
— Connect with social work and ethics consultation when complex.
— IV promethazine extravasation causes severe tissue injury and necrosis — dilute and infuse slowly in large vein; never give SQ or arterial.
— Wernicke encephalopathy from dextrose without thiamine is a sentinel preventable adverse event — institutional protocols should ensure thiamine first.
— QTc monitoring with ondansetron — sentinel torsades cases reported.
— High-risk transition: ED → home, inpatient → outpatient. Confirm medication reconciliation, prescription fill, and follow-up appointment before discharge.
— Use teach-back to confirm patient understands red flags and regimen.
— Pregnant Workers Fairness Act and FMLA accommodations — provide documentation supporting reasonable accommodations (rest breaks, remote work, leave).
— Avoid medication choices that preclude work without discussion (e.g., heavily sedating regimens).
— Suspected substance use in pregnancy — state-specific reporting laws; counsel and offer treatment; avoid punitive language.
— Black and minoritized patients are under-treated for pain and HG — actively counter implicit bias; use objective severity tools (PUQE, weight loss, ketones) to drive treatment.
Board pearl: Always give IV thiamine before IV dextrose in any pregnant patient with prolonged vomiting — this is a tested patient-safety standard and a never-event when missed.
Step 3 management: A patient calling 3 days post-discharge with mild symptom recurrence — resume the prior effective antiemetic regimen at scheduled (not PRN) dosing, push fluids, ginger, and have her return if unable to keep liquids down for >12 hours or if dizziness, dark urine, or weight loss recur.
— 8-week pregnant patient with nausea/vomiting, mild dehydration, no weight loss, not yet on any antiemetic → Pyridoxine + doxylamine, not ondansetron.
— First-trimester vomiting with pH 7.50, HCO3 32, Cl 90, K 3.0 → hypokalemic hypochloremic metabolic alkalosis; diagnosis HG; next step IV NS with KCl.
— TSH 0.05, free T4 mildly elevated in 10-week pregnant patient with HG, no goiter, no eye signs → gestational transient thyrotoxicosis; do not start antithyroid drugs.
— Severe HG + uterus > dates + β-hCG 200,000 + BP 150/95 at 14 weeks → pelvic ultrasound; suction D&C if molar.
— HG patient given IV D5W without thiamine develops confusion, ataxia, ophthalmoplegia → IV thiamine immediately.
— Patient on methadone receives ondansetron, develops torsades → electrolyte correction (Mg, K), discontinue QT prolongers.
— Vomiting persists at 22 weeks with RUQ pain and pruritus → intrahepatic cholestasis; check bile acids.
— Patient on B6/doxylamine + promethazine + metoclopramide still vomiting, lost 8% weight at 11 weeks → admit; add ondansetron; consider methylprednisolone (after 10 weeks).
— Prior HG planning new pregnancy → start B6 + doxylamine at symptom onset or pre-emptively at 4–6 weeks.
— T1DM patient with "HG" and anion gap, ketones, glucose 140 → euglycemic DKA; insulin drip with dextrose.
Key distinction: Step 3 stems often hinge on what to do NEXT — pick the action that addresses both immediate safety (thiamine before dextrose, ECG before ondansetron, electrolyte correction before refeeding) and longitudinal care (follow-up timing, taper plan, prophylaxis for next pregnancy).
Hyperemesis gravidarum is severe first-trimester vomiting causing ≥5% weight loss, dehydration, and hypokalemic-hypochloremic metabolic alkalosis with ketonuria, managed by a stepwise approach starting with pyridoxine + doxylamine, escalating through antihistamines, dopamine antagonists, ondansetron, and finally methylprednisolone (after 10 weeks), with IV fluids and mandatory thiamine before dextrose to prevent Wernicke encephalopathy.
Board pearl: When the stem describes a first-trimester pregnant patient with intractable vomiting, your reflexes should be — ultrasound to exclude molar/multiples, IV fluids with thiamine before dextrose, electrolyte correction, stepwise antiemetics starting with B6/doxylamine, and follow-up within one week — these five moves capture the high-yield Step 3 management arc.