Obstetric · Emergency
Hyperemesis Gravidarum Protocol
HG admission protocol with thiamine-before-dextrose rule, antiemetic ladder, VTE prophylaxis, refractory-case steroids. RCOG GTG 69 + ACOG PB 189 + SMFM #67.
Last reviewed 27 May 2026
Hyperemesis Gravidarum
IV thiamine, fluids, antiemetic ladder + VTE
Currently tolerating
Tier
Severe HG — admission
ADMIT. (1) Thiamine 100 mg IV before any dextrose. (2) IV 0.9 % NaCl + KCl 20–40 mmol/L titrated to serum K+. (3) Antiemetic step 3-4: metoclopramide or ondansetron IV; consider step 5 (methylprednisolone 16 mg IV TDS x 3 d then PO taper) if refractory at 48 h. (4) Prophylactic LMWH (e.g. enoxaparin 40 mg SC daily; weight-banded) — dehydration + reduced mobility = VTE risk. (5) PPI (e.g. omeprazole 20 mg PO/IV daily) if reflux. (6) Mental-health screen. (7) Daily weights, fluid balance. Re-feeding syndrome risk if pre-pregnancy underweight — slow advancement of nutrition with electrolyte monitoring.
Labs
FBC, U+E, LFTs, TFTs, urine ketones, calcium, magnesium, phosphate; repeat U+E q12-24h until normalised. cCTG / fetal-medicine input not routinely needed for HG alone.
Troubleshooting + common pitfalls
- Pitfall: Giving dextrose before thiamine.
Solution: ALWAYS thiamine 100 mg IV (or PO if mild) FIRST. Dextrose load on a thiamine-deficient brain precipitates Wernicke’s encephalopathy — permanent neurological injury. Hyperemesis patients on prolonged restricted intake are at high risk. - Pitfall: Treating HG without VTE prophylaxis.
Solution: HG + dehydration + reduced mobility = real VTE risk. RCOG GTG 37a indicates prophylactic LMWH for the admission + 7 days post-discharge. - Pitfall: Missing thyrotoxicosis associated with HG.
Solution: ~50 % of severe HG has biochemical hyperthyroidism (hCG-mediated). Most resolves spontaneously by 18–20 wk — do NOT routinely treat unless TSH-receptor antibody positive (Graves coexistence) or symptoms persist. TFTs at admission to characterise. - Pitfall: Refractory case — corticosteroids forgotten.
Solution: RCOG GTG 69 endorses methylprednisolone 16 mg IV TDS x 3 d then oral prednisolone 40 mg taper for refractory HG. Effect often dramatic. Avoid < 10 wk if possible (theoretical cleft palate signal in animal studies, not consistently seen in humans). - Pitfall: Ondansetron at < 10 wk without informed consent.
Solution: Huybrechts 2018 BMJ — small absolute increase in cleft palate (background 11 per 10,000 → 14 per 10,000). Counsel and document benefit/risk; many women accept given symptom severity. Reserve for step-4 if earlier agents fail. - Pitfall: Re-feeding syndrome in chronically malnourished woman.
Solution: Slow advancement of nutrition. Daily electrolytes (especially phosphate, magnesium, potassium) for the first 5–7 days of re-feeding. Replace before deficiency develops; dietitian input. - Pitfall: Discharging on a single antiemetic that wasn’t controlling symptoms in hospital.
Solution: Discharge meds = the regimen that achieved tolerance + at least a 12-hour observation off IV fluids. Cyclizine + ondansetron combinations are common. - Pitfall: No mental-health screen.
Solution: Severe HG is associated with depression, anxiety, PTSD, and termination considerations — offer EPDS/GAD-7 screening at admission and 2-week post-discharge. - Pitfall: Treating HG as “normal pregnancy sickness”.
Solution: Recognise diagnostic criteria (> 5 % weight loss, dehydration, electrolyte imbalance OR PUQE-24 ≥ 13). Validate the patient’s experience; HG carries real morbidity. - Pitfall: Forgetting to investigate alternative causes.
Solution: Persistent vomiting at > 20 wk, new symptoms (abdominal pain, fever, jaundice), or refractory to standard treatment → rule out cholecystitis, hepatitis, pancreatitis, UTI, surgical causes. HG typically settles by 16–20 wk; persisting suggests another aetiology. - Pitfall: Reflux symptoms not addressed.
Solution: PPI (omeprazole 20 mg) is compatible with pregnancy and improves antiemetic response when reflux is contributing. - Pitfall: Discharge without follow-up.
Solution: Day-unit review at 48 h post-discharge OR home midwife review. Up to 30 % readmission rate within 2 weeks if no structured follow-up. - Pitfall: Liver enzymes elevated — assumed HG.
Solution: ~50 % of severe HG has mildly elevated transaminases (typically < 200 IU/L), settles with hydration. But marked elevation (> 500), jaundice, RUQ pain, or PE features — rule out HELLP, AFLP, hepatitis, cholestasis.
Educational tool only — not medical advice. RCOG GTG 69; ACOG PB 189; SMFM Consult #67. Decisions and dosing by obstetric / day-unit team.
What does this mean?
Hyperemesis gravidarum (HG) is not just bad morning sickness. The diagnosis — persistent vomiting + > 5 % weight loss + dehydration + electrolyte imbalance, or PUQE-24 score ≥ 13 — affects 0.3–2 % of pregnancies and accounts for the most common non-obstetric cause of admission in pregnancy. The single most important practical rule is thiamine before dextrose — giving glucose-containing fluids to a thiamine-deficient woman precipitates Wernicke’s encephalopathy, a permanent neurological injury that is entirely preventable with a 100 mg dose given first. The antiemetic ladder runs from pyridoxine + doxylamine (step 1, outpatient) through cyclizine / promethazine / metoclopramide / ondansetron (steps 2–4) to corticosteroids (step 5, methylprednisolone IV taper) for refractory cases. Two specific risks need active management: VTE prophylaxis (HG + dehydration + immobility = real thrombosis risk; RCOG GTG 37a indicates prophylactic LMWH) and mental-health screening (HG carries elevated depression, anxiety, PTSD, and termination considerations — the suffering is real and frequently underestimated). The biochemical hyperthyroidism seen in ~50 % of severe HG is hCG-mediated and resolves by 18–20 wk without treatment unless TRAb-positive Graves coexists.
Introduction
Hyperemesis gravidarum is the most common non-obstetric cause of hospitalisation in pregnancy. The diagnosis requires > 5 % weight loss, dehydration, and electrolyte imbalance, or PUQE-24 score ≥ 13.
Core admission protocol
- Thiamine 100 mg IV BEFORE any dextrose-containing fluid.
- IV 0.9 % NaCl + KCl 20–40 mmol/L titrated to serum K+.
- Antiemetic ladder steps 1–5.
- Prophylactic LMWH for admission + 7 days.
- PPI for reflux symptoms.
- Mental-health screen.
Troubleshooting — common pitfalls
- Pitfall: Dextrose before thiamine. Solution: Thiamine ALWAYS first.
- Pitfall: No VTE prophylaxis. Solution: LMWH for admission + 7 d.
- Pitfall: Treating biochemical HG-thyrotoxicosis. Solution: Resolves by 18–20 wk; observe unless Graves coexists.
- Pitfall: Corticosteroids forgotten for refractory cases. Solution: Methylprednisolone 16 mg IV TDS x 3 d then oral taper.
- Pitfall: Ondansetron at < 10 wk without counselling. Solution: Discuss small cleft palate signal; document.
- Pitfall: Re-feeding syndrome missed. Solution: Daily PO4, Mg, K during early re-feeding; dietitian.
- Pitfall: Liver enzymes high — assumed HG. Solution: Marked elevation, jaundice, RUQ pain → rule out HELLP / AFLP.
- Pitfall: No mental-health screen. Solution: EPDS / GAD-7 at admission and 2 wk post-discharge.
- Pitfall: No structured discharge follow-up. Solution: Day-unit review at 48 h or home midwife.
Sources
- RCOG Green-top Guideline 69. The Management of Nausea and Vomiting of Pregnancy and Hyperemesis Gravidarum. 2016, reaffirmed 2024.
- ACOG Practice Bulletin 189. Nausea and Vomiting of Pregnancy. 2018, reaffirmed 2024.
- SMFM Consult Series #67. Hyperemesis gravidarum. 2022.
- Huybrechts KF, et al. Ondansetron and oral cleft / cardiac malformations. JAMA 2018, BMJ 2018.
- Koren G. The Pregnancy-Unique Quantification of Emesis (PUQE) scoring system. Am J Obstet Gynecol 2002.
Frequently asked questions
What's the difference between NVP and hyperemesis?
Nausea and vomiting of pregnancy (NVP) affects up to 80 % of pregnant women — typically mild, settles by 16–20 wk, doesn't impair function. Hyperemesis gravidarum (HG) is severe: persistent vomiting + > 5 % weight loss + dehydration + electrolyte imbalance, or PUQE-24 ≥ 13. Affects 0.3–2 % of pregnancies. The two are best thought of as ends of a spectrum, with HG warranting active medical treatment.
Why give thiamine BEFORE dextrose?
Wernicke's encephalopathy prevention. Severe HG patients on prolonged restricted intake are at high risk of thiamine deficiency. Giving glucose-containing fluids before thiamine forces glucose metabolism in the absence of the required cofactor, depleting CNS thiamine acutely and precipitating Wernicke's — confusion, ataxia, ophthalmoplegia, with permanent injury (Korsakoff's syndrome). 100 mg IV thiamine first, then anything.
What's the antiemetic ladder?
Step 1 — pyridoxine (B6) 10–25 mg PO TDS ± doxylamine 12.5 mg. Step 2 — cyclizine 50 mg or promethazine 12.5–25 mg. Step 3 — metoclopramide 10 mg PO/IV TDS or prochlorperazine 5–10 mg. Step 4 — ondansetron 4–8 mg (caution < 10 wk). Step 5 — corticosteroids (methylprednisolone 16 mg IV TDS × 3 d then oral prednisolone 40 mg taper). Climb the ladder until symptoms controlled.
Is ondansetron safe in pregnancy?
Mostly yes, with a small absolute caveat. Huybrechts 2018 BMJ — ondansetron < 10 wk associated with small absolute increase in cleft palate risk (11 per 10,000 background → 14 per 10,000). Cardiac-anomaly signal in earlier studies was not replicated. Reserve for step 4 if earlier agents fail; counsel and document benefit/risk; many women accept given symptom severity.
Do I need VTE prophylaxis?
Yes. RCOG GTG 37a indicates prophylactic LMWH for HG-related admission + 7 days post-discharge. Dehydration + reduced mobility = real VTE risk. Enoxaparin weight-banded (40 mg SC daily for most). Stop if delivery imminent.
What about elevated liver enzymes?
~50 % of severe HG has mildly elevated transaminases (typically < 200 IU/L) that settle with hydration. BUT marked elevation (> 500 IU/L), jaundice, RUQ pain, or pre-eclamptic features — rule out HELLP, acute fatty liver of pregnancy (AFLP), hepatitis, cholestasis. Don't dismiss.
What about thyrotoxicosis?
Common in severe HG — hCG cross-reacts with TSH receptor; biochemical thyrotoxicosis affects ~50 %. Almost always resolves spontaneously by 18–20 wk WITHOUT antithyroid treatment. Don't treat unless TSH-receptor antibody positive (Graves coexisting), persistent past 20 wk, or significant maternal symptoms. Don't use iodine in pregnancy.
How does this relate to other calculators on BumpBites?
Companion: /calculators/puqe-score for the validated severity score; /calculators/vte-prophylaxis-pregnancy for LMWH dosing; /calculators/postpartum-thyroiditis for the different thyroid context; /calculators/postpartum-depression-quiz for the mental-health overlap; /calculators/hellp-classifier for the liver-enzyme differential.