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← Obstetrics and gynaecology indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Hyperemesis gravidarum

Obstetrics and gynaecology · UK scope · Sources checked 7 Sept 2026 · Clinical review pending

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Neurological change during prolonged vomiting

Confusion, gait disturbance or abnormal eye movements after poor intake may represent thiamine deficiency with Wernicke encephalopathy, even when all three features are not present.

Action: Arrange immediate hospital assessment, give treatment-dose intravenous thiamine through the acute neurological protocol, correct associated magnesium deficiency and do not wait for imaging or a vitamin result. Give thiamine before carbohydrate where feasible, but never delay emergency treatment of hypoglycaemia.

Overview

Recognise disabling pregnancy vomiting, restore fluid and nutritional safety, and escalate antiemetic treatment while investigating features that suggest a different diagnosis.

Nausea and vomiting of pregnancy usually starts early, whereas hyperemesis gravidarum describes the severe end of a clinical spectrum. The practical distinction is inability to eat and drink normally with major restriction of ordinary activities. Weight loss and biochemical abnormalities can support severity but are not prerequisites that a patient must develop before receiving effective treatment. Ask what has actually been retained over the preceding day, how often medicines are vomited, whether urine output has fallen, and how symptoms affect sleep, employment, caregiving and mental health.

A careful chronology protects against diagnostic anchoring. Establish pregnancy dating and whether symptoms began before 16 weeks, ask about previous hyperemesis and response to individual drugs, and check other medicines and substance use. Examine hydration, pulse, blood pressure including postural change when safe, temperature, abdominal tenderness and neurological status. Severity scores support repeated assessment but cannot replace examination. A patient with little vomiting because they have stopped eating may still be severely unwell; similarly, absent urinary ketones must never be used to deny fluids or antiemetics.

Practice

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Obstetrics and gynaecologyOriginal SBA

Severity without urinary ketones

At 10 weeks, a patient cannot retain drinks, passes urine twice daily and becomes dizzy on standing. Urine ketones are negative. What is the best next action?

Choose one answer, then submit
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Sources and review status5 sources · checked 7 Sept 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 7 Sept 2026; clinical approval remains outstanding.

  • RCOG GTG69 nausea vomiting and hyperemesis 2024
  • RCOG GTG69 prescribing correction June 2025
  • RCOG GTG69 intravenous fluid correction June 2026
  • RCOG pregnancy sickness patient information
  • MHRA metoclopramide neurological adverse effects

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Treatment works through several parallel actions: restoring circulating volume and electrolytes, suppressing nausea enough to sustain intake, preventing vitamin deficiency and addressing the consequences of immobility or malnutrition. Ambulatory intravenous treatment is useful when the patient is stable and can return safely. Admission is appropriate for persistent inability to retain oral treatment, significant dehydration or electrolyte disturbance, concurrent illness, or unsuccessful ambulatory care. Discharge depends on a workable oral intake and medicine plan, rather than complete disappearance of nausea or a negative urine ketone test.

Key points

  • Hyperemesis is severe pregnancy nausea and vomiting that prevents normal eating and drinking and substantially impairs daily life.
  • Quantify symptoms with PUQE or HELP alongside oral intake, weight trajectory, hydration, function and psychological distress.
  • Ketonuria is not a reliable measure of dehydration or disease severity and must not determine access to treatment.
  • Use oral or alternative-route antiemetics promptly; combinations from different classes may be necessary when one agent is inadequate.
  • For admitted patients or severely reduced intake, provide thiamine and assess venous thrombosis and refeeding risks.
  • Investigate pain, fever, neurological findings, late onset or major biochemical abnormalities for an alternative or additional disorder.

Aetiology

01

Placental signals

Pregnancy-associated hormonal signalling, including GDF15-related mechanisms and individual sensitivity, contributes to nausea; susceptibility varies substantially between patients and between pregnancies.

02

Predisposition

A previous affected pregnancy and a family history increase recurrence likelihood, while multiple or trophoblastic pregnancy may increase symptom burden through placental factors.

Pathophysiology

  1. 1
    Emetic signalling

    Altered signalling to central nausea pathways can produce persistent queasiness, retching and food aversion even when there is little gastric content to vomit.

  2. 2
    Fluid and electrolyte loss

    Vomiting combined with reduced intake depletes water, sodium and potassium, compromising renal perfusion and increasing weakness, dizziness and arrhythmia vulnerability.

  3. 3
    Starvation and vitamin depletion

    Insufficient carbohydrate and micronutrient intake promotes catabolism and thiamine depletion; rapid nutritional restoration can then precipitate dangerous intracellular electrolyte shifts.

Clinical features and red flags

Functional severity

Ask whether the patient can stand, wash, work, sleep and care for dependants; inability to function is clinically relevant even before substantial weight loss.

Volume depletion

Dry mouth, tachycardia, postural dizziness, scant dark urine and worsening creatinine suggest fluid depletion requiring examination and replacement.

Nutritional vulnerability

Weeks of poor intake, rapid weight loss or repeated admissions raise thiamine deficiency and refeeding concerns that routine antiemetics alone cannot address.

Red flags requiring action

  • Inability to retain fluids or essential medicines, oliguria, syncope or marked postural symptoms requires same-day assessment for dehydration and metabolic disturbance.
  • New focal abdominal pain, fever, haematemesis, jaundice or vomiting that first begins after 16 weeks requires investigation beyond pregnancy sickness.
  • Confusion, ataxia or ophthalmoplegia during prolonged poor intake requires immediate treatment for possible Wernicke encephalopathy.

Investigations

  1. 01
    Urea, electrolytes and creatinineFirst step
    Why
    Measure renal effect and guide safe fluid and potassium replacement.
    Interpretation and limitations
    Hypokalaemia and acute kidney injury change the infusion prescription; repeat daily while intravenous replacement is required, or more frequently for severe abnormalities.
  2. 02
    Full blood count, glucose and targeted liver tests
    Why
    Identify anaemia, infection, hypoglycaemia and important biochemical alternatives.
    Interpretation and limitations
    Mild liver enzyme elevation may accompany hyperemesis, but marked or persistent abnormalities, jaundice or impaired clotting require a broader hepatic assessment.
  3. 03
    Urinalysis and urine culture when indicated
    Why
    Identify urinary infection and interpret urine findings in their clinical context.
    Interpretation and limitations
    Do not treat urinary ketones as a dehydration scale; urinary symptoms or systemic features support culture and pregnancy-appropriate infection treatment.
  4. 04
    Obstetric ultrasound
    Why
    Establish viability, gestation and whether multiple or molar pregnancy is present.
    Interpretation and limitations
    A scan clarifies pregnancy-associated drivers but should not postpone rehydration or antiemetics in a symptomatic patient awaiting the appointment.

Differential diagnosis

01

Gastrointestinal or urinary disease

Gastroenteritis, appendicitis, obstruction, pancreatitis and urinary infection become more plausible with focal pain, fever, bowel change or urinary symptoms rather than isolated early-pregnancy nausea.

02

Endocrine and metabolic illness

Diabetic ketoacidosis, hypercalcaemia and clinically significant thyroid disease require targeted assessment when examination, glucose, acid-base status or history is inconsistent with uncomplicated pregnancy vomiting.

03

Pregnancy liver or hypertensive disease

New vomiting later in gestation with headache, hypertension, epigastric pain, hypoglycaemia or jaundice needs urgent assessment for pre-eclampsia, HELLP or acute fatty liver.

Additional chapter-specific clues

Alternative pathology

Localised pain, urinary symptoms, fever, peritonism, neurological signs or atypical onset should redirect assessment towards concurrent medical or surgical disease.

Management

01Initial treatmentEnable oral intake and symptom controlFirst stepEarly pregnancy nausea is preventing normal meals but assessment shows no physiological instability.+
  1. 1Offer practical food and fluid strategies chosen by the patient, avoiding advice that implies dietary failure caused the illness.
  2. 2Start an appropriate antihistamine or phenothiazine, or licensed doxylamine-pyridoxine; prescribe regularly and change route if tablets are not retained.
  3. 3Review response promptly, combine different drug classes when needed, and provide explicit criteria for same-day reassessment.
02Ambulatory or inpatientRestore hydration and protect nutritionOral treatment has failed or dehydration, biochemical disturbance or severely reduced intake is present.+
  1. 1Prescribe sodium chloride 0.9% with potassium replacement determined by current electrolytes, renal function, fluid status and infusion-safety limits.

Complications

01

Renal and cardiac injury

Profound dehydration can cause acute kidney injury, while potassium and magnesium depletion may provoke arrhythmia, especially alongside medicines that prolong the QT interval.

02

Wernicke and refeeding syndromes

Prolonged undernutrition risks irreversible neurological injury from thiamine deficiency, followed by phosphate, potassium and magnesium depletion when nutrition is restarted too rapidly.

03

Thrombosis and psychosocial harm

Dehydration and immobility increase venous thromboembolism risk, while relentless symptoms may disrupt employment, relationships, mental health and the ability to continue a wanted pregnancy.

Monitoring and follow-up

  • Track fluid balance, orthostatic symptoms and renal function alongside the ability to retain food, fluids and each prescribed medicine.
  • Recheck potassium and other relevant electrolytes during intravenous therapy and refeeding, with ECG monitoring where arrhythmia risk is significant.
  • Review sedation, dystonia, constipation and QT-related interactions when antiemetics are combined or escalated.
  • After discharge, arrange an accessible review and enough medication, and explain where to return if urine output or oral intake deteriorates.

Special situations

Corrected prescribing details

RCOG corrected its guideline in 2025 to remove intravenous prochlorperazine; oral, buccal, rectal or intramuscular alternatives must be prescribed by preparation.

Potassium infusion correction

The June 2026 correction specifies the ambulatory sodium chloride and 20 mmol potassium example over 2 hours, not 1–2 hours; individual renal and fluid assessment remains essential.

Persistent late symptoms

Symptoms continuing into late pregnancy justify reassessment of nutrition and fetal growth, with serial growth assessment when severe illness persists.

Psychological burden is substantial

Listen to the patient’s account of isolation and desperation; compassionate treatment and symptom relief belong alongside any mental health referral.

Common pitfalls

  1. 01

    Requiring ketonuria or five per cent weight loss before accepting that symptoms warrant active treatment.

  2. 02

    Infusing dextrose into a depleted patient without considering thiamine, electrolyte shifts and refeeding risk.

  3. 03

    Repeating ineffective oral tablets despite evidence that the patient vomits every dose.

  4. 04

    Calling late-onset vomiting hyperemesis without checking blood pressure, glucose, abdominal findings and liver function.

  • 05
    Magnesium, phosphate, thyroid tests and ECG selectively
    Why
    Investigate prolonged starvation, refractory symptoms or drug-related cardiac risk.
    Interpretation and limitations
    Refeeding can lower phosphate; vomiting-associated gestational thyrotoxicosis is often transient, whereas clinical Graves disease needs specialist evaluation.
    • 2
    Give thiamine before planned dextrose or nutritional support, assess thrombosis risk and prescribe weight-appropriate LMWH unless contraindicated.
  • 3Measure intake and urine output, repeat electrolytes, assess refeeding risk and involve dietetics when adequate nutrition cannot be re-established.
    • 03Refractory illnessEscalate treatment and supportEscalationRepeated antiemetic combinations and adequate intravenous replacement have not restored tolerable intake.+
    1. 1Reassess the diagnosis, adherence, route and adverse effects before attributing persistent symptoms to refractory hyperemesis.
    2. 2Seek senior obstetric and medical input for corticosteroids and enteral nutrition; parenteral feeding requires multidisciplinary risk assessment.
    3. 3Explore distress and thoughts of self-harm sensitively, involve appropriate mental health support and plan early treatment in future pregnancies.
    Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
    An RCOG initial antiemetic option when its route and adverse-effect profile fit the patient.

    Cyclizine

    Give 50 mg orally, intramuscularly or intravenously every 8 hours when required within a regular symptom-control plan.

    Sedation and anticholinergic effects matter; parenteral administration requires appropriate clinical monitoring and medication-interaction review.

    A subsequent antiemetic option when initial agents fail or are not tolerated.

    Metoclopramide

    Use 5–10 mg orally or by appropriate parenteral route every 8 hours; maximum 30 mg daily or 0.5 mg/kg daily, whichever is lower, usually for no more than 5 days.

    Stop for dystonia or other extrapyramidal symptoms; administer intravenous doses slowly over at least 3 minutes.

    A later antiemetic option after shared discussion when initial treatment has been insufficient.

    Ondansetron

    RCOG Appendix III lists 4 mg orally every 8 hours or 8 mg orally every 12 hours; intravenous treatment is 8 mg over 15 minutes every 12 hours.

    Discuss the small absolute first-trimester oral-cleft signal against untreated hyperemesis; assess QT risk, hypokalaemia, constipation and interacting medicines.

    Prevents depletion while nutrition is restored and before planned carbohydrate loading.

    Thiamine prevention

    Give thiamine 100 mg orally three times daily for admitted vomiting or severely reduced intake; use an appropriate intravenous vitamin preparation if oral absorption is unreliable.

    Suspected Wernicke encephalopathy requires immediate treatment-dose intravenous therapy under an acute protocol; this oral prevention dose is inadequate.