Skip to textbook content
Doctor’s PassportTextbook
QuestionsFlashcardsBriefsDashboardAccount
TopicsAll topics

Loading topic navigation…

Textbook navigation
TopicsAll topics

Loading topic navigation…
← Obstetrics and gynaecology indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
Full textbook13 sectionsOpen only what you need
Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Acute fatty liver and HELLP syndrome

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

RapidFull
!
Late pregnancy liver failure or microangiopathy

Vomiting or upper abdominal pain with hypoglycaemia, jaundice, coagulopathy, haemolysis or falling platelets may represent acute fatty liver or HELLP and can deteriorate rapidly.

Action: Call senior obstetrics, anaesthesia and critical care immediately; assess airway, circulation and glucose, obtain urgent blood and coagulation studies, initiate maternal stabilisation and organise birth without delaying for diagnostic certainty or completion of fetal steroids.

Overview

Differentiate overlapping late-pregnancy liver emergencies, recognise organ failure early and coordinate maternal stabilisation, urgent birth and continued postpartum critical care.

Acute fatty liver of pregnancy and HELLP are uncommon but important explanations for a pregnant person who becomes unwell with nausea, vomiting, malaise or upper abdominal pain. Their early symptoms are easily mistaken for gastroenteritis or reflux. HELLP is a microangiopathic syndrome associated with endothelial and placental disease; acute fatty liver reflects hepatic metabolic dysfunction with microvesicular fat accumulation. The distinction matters for investigations, organ support and future counselling, but both demand early senior involvement and a delivery decision rather than prolonged diagnostic observation.

Look for the dominant pattern without forcing the patient into a single label. Haemolysis, markedly falling platelets and the pre-eclampsia phenotype favour HELLP. Recurrent hypoglycaemia, jaundice, impaired coagulation, encephalopathy, renal dysfunction and prominent vomiting suggest acute fatty liver. Neither pattern is exclusive. Blood pressure and proteinuria can be absent or less impressive than expected in HELLP, and acute fatty liver may coexist with hypertensive disease. A single normal platelet count or glucose result early in the presentation cannot exclude an evolving illness.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
Obstetrics and gynaecologyOriginal SBA

Recognising hepatic functional failure

At 36 weeks a patient develops vomiting, jaundice and confusion, glucose 2.2 mmol/L, prolonged prothrombin time and rising creatinine. Platelets are 168 ×10^9/L, with no haemolysis or hypertension. Which diagnosis is most likely?

Choose one answer, then submit
← Rapid synopsisBack to overviewAll Obstetrics and gynaecology topics →
Sources and review status4 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.

  • NICE NG133 severe pre-eclampsia and HELLP management
  • EASL clinical practice guidelines liver diseases in pregnancy
  • NICE NG25 antenatal corticosteroids and preterm birth
  • JBDS hospital hypoglycaemia guideline

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

The Swansea framework can support an AFLP diagnosis when at least six clinical, biochemical, imaging or histological features occur without a better explanation. Features include vomiting, abdominal pain, polydipsia or polyuria, encephalopathy, raised bilirubin or transaminases, hypoglycaemia, leucocytosis, renal impairment, coagulopathy and selected other abnormalities. It is a supportive framework rather than permission to wait for a sixth feature. Imaging may be normal and biopsy is generally unnecessary in a clinically convincing, potentially coagulopathic emergency.

Delivery removes the pregnancy trigger but is not an instantaneous cure. Resuscitation, seizure prevention where indicated, blood-pressure control, glucose replacement and preparation for haemorrhage proceed alongside fetal assessment and planning the safest feasible route of birth. Maternal instability is a reason to expedite care, not to transfer unsafely or defer until a complete steroid course has finished. Continue serial laboratory testing after birth and seek hepatology or transplant-centre advice promptly when acute liver failure does not improve or organ support requirements increase.

Key points

  • HELLP combines haemolysis, elevated liver enzymes and low platelets, usually within the pre-eclampsia spectrum.
  • Acute fatty liver often produces hepatic synthetic and metabolic failure, including hypoglycaemia and coagulopathy.
  • Clinical overlap is common; normotension does not safely exclude HELLP or other serious pregnancy liver disease.
  • Obtain platelet trend, blood film and haemolysis tests together with glucose, renal function, liver tests and coagulation.
  • Stabilise the mother and plan urgent birth through a multidisciplinary team; liver biopsy is rarely needed before action.
  • Continue close postpartum surveillance because laboratory and clinical deterioration can occur after delivery.

Aetiology

01

Placental endothelial disorder

HELLP generally arises within the pre-eclampsia spectrum, where placental dysfunction and maternal endothelial injury promote microvascular damage, haemolysis and platelet consumption.

02

Hepatic metabolic vulnerability

AFLP is linked to disturbed mitochondrial fatty-acid metabolism in pregnancy, sometimes associated with fetal fatty-acid oxidation defects and maternal susceptibility.

Pathophysiology

  1. 1
    Microangiopathic injury

    Endothelial damage and microvascular fibrin deposition shear erythrocytes and consume platelets, while hepatic involvement causes pain and increased circulating liver enzymes.

  2. 2
    Hepatic functional loss

    Microvesicular fatty change can impair glucose production, clotting-factor synthesis and detoxification, explaining the combination of hypoglycaemia, coagulopathy and encephalopathy in severe AFLP.

  3. 3
    Multiorgan consequences

    Renal injury, capillary leak and disordered coagulation compound hepatic illness; circulatory instability and placental dysfunction simultaneously threaten fetal oxygenation and maternal survival.

Clinical features and red flags

HELLP phenotype

Epigastric pain, nausea and malaise with haemolysis and a falling platelet count can precede dramatic hypertension or other classical pre-eclampsia findings.

Metabolic liver failure

Repeated low glucose, confusion, jaundice, renal impairment and prolonged clotting raise particular concern for acute fatty liver with loss of hepatic function.

Hepatic bleeding

Sudden severe upper abdominal or shoulder pain, haemodynamic instability and falling haemoglobin suggest subcapsular haematoma or rupture requiring urgent imaging and intervention.

Neurological emergency

Headache, visual symptoms, seizure or reduced consciousness requires immediate assessment for eclampsia, hepatic encephalopathy, hypoglycaemia and intracranial pathology.

Red flags requiring action

  • Right upper quadrant pain with shock or a falling haemoglobin requires immediate assessment for hepatic haematoma or rupture.
  • Hypoglycaemia, encephalopathy, renal impairment or prolonged clotting in late pregnancy requires urgent consideration of acute liver failure.
  • Severe hypertension, visual disturbance, headache or seizure with liver abnormalities requires immediate pre-eclampsia and eclampsia management.

Investigations

  1. 01
    Urgent full blood count and haemolysis studiesFirst step
    Why
    Identify thrombocytopenia, anaemia and evidence of microangiopathic red-cell destruction.
    Interpretation and limitations
    Blood film fragments, raised LDH and reduced haptoglobin support haemolysis, while serial platelets establish direction and speed of deterioration.
  2. 02
    Glucose, renal profile and blood gas
    Why
    Detect metabolic failure, renal injury and impaired perfusion needing immediate correction.
    Interpretation and limitations
    Treat symptomatic or significant hypoglycaemia promptly; lactate, acid-base disturbance and urine output help assess critical illness rather than merely classify the diagnosis.
  3. 03
    Liver panel and coagulation including fibrinogen
    Why
    Assess hepatic injury, synthetic failure and bleeding risk before birth or procedures.
    Interpretation and limitations
    Transaminases reflect injury rather than functional reserve; prolonged clotting and falling fibrinogen demand haematology and anaesthetic input with blood-component planning.
  4. 04
    Blood pressure and proteinuria assessment
    Why
    Evaluate associated pre-eclampsia and the need for urgent antihypertensive treatment.
    Interpretation and limitations
    Severe hypertension requires treatment, but absence of proteinuria or marked hypertension does not negate an otherwise concerning HELLP presentation.

Differential diagnosis

01

Thrombotic thrombocytopenic purpura

Marked microangiopathic haemolysis and thrombocytopenia with neurological or other organ signs may require urgent plasma-exchange treatment; seek haematology advice before attributing everything to delivery-responsive HELLP.

02

Acute hepatitis or toxic injury

Viral infection, paracetamol toxicity and other drug reactions can cause liver failure during pregnancy and require exposure-specific investigations and treatment alongside obstetric assessment.

03

Biliary or vascular pathology

Gallstone obstruction, cholangitis and hepatic venous thrombosis can cause pain and abnormal liver tests; fever, focal imaging findings or a thrombotic history redirect management.

Management

01Immediate responseTreat maternal deterioration as an emergencyFirst stepA late-pregnancy or recently postpartum patient has hepatic abnormalities with systemic illness.+
  1. 1EscalationEscalate to consultant obstetrics, anaesthesia, critical care and haematology, adding hepatology early when synthetic or metabolic failure is present.
  2. 2Establish intravenous access, frequent observations, bedside glucose checks and strict fluid balance while sending urgent bloods and preparing compatible blood.
  3. 3Correct hypoglycaemia and circulatory disturbance, treat severe hypertension and use magnesium for eclampsia or qualifying severe pre-eclampsia.
02Definitive obstetric actionPlan prompt birth after initial stabilisationDefinitiveAFLP or significant HELLP is suspected and continued pregnancy presents increasing maternal or fetal danger.+

Complications

01

Major bleeding

Disseminated coagulation disturbance, thrombocytopenia and hepatic haematoma or rupture may produce life-threatening haemorrhage requiring coordinated blood components and procedural control.

02

Critical organ failure

Hypoglycaemia, encephalopathy, renal injury, pulmonary oedema and respiratory failure can persist after delivery and may require intensive care or specialist liver-centre support.

03

Adverse perinatal outcome

Placental dysfunction, maternal instability and necessary early birth increase the risks of fetal compromise, stillbirth and complications of prematurity despite appropriate urgent management.

Monitoring and follow-up

  • Use a documented observation frequency with early-warning escalation, including respiratory status, consciousness, pain, blood pressure and oxygenation.
  • Record hourly urine output in severe illness and review cumulative fluid balance to avoid both renal hypoperfusion and pulmonary oedema.
  • Follow laboratory trajectories after birth; a transient improvement in abdominal pain does not prove platelet or coagulation recovery.
  • Before discharge ensure stable glucose without intravenous support, improving organ function, a blood-pressure plan where relevant and an arranged medical follow-up.

Special situations

Corticosteroid distinction

Antenatal steroids may support fetal maturation when preterm birth is expected, but NICE advises against dexamethasone or betamethasone as treatment for HELLP itself.

Reconsider persistent microangiopathy

Ongoing haemolysis, profound thrombocytopenia or neurological and renal abnormalities beyond the expected recovery require urgent consideration of TTP or complement-mediated disease.

AFLP family implications

An association with fetal fatty-acid oxidation disorders supports neonatal metabolic advice and genetic counselling; the relationship is not present in every case.

Anaesthetic decisions are individual

Neuraxial suitability depends on platelet trend, coagulation, bleeding and urgency as well as an absolute count, so an isolated laboratory threshold cannot replace specialist assessment.

Common pitfalls

  1. 01

    Treating epigastric pain as reflux without checking blood pressure, platelets, liver function and the patient’s overall condition.

  2. 02

    Waiting for all Swansea features, liver ultrasound confirmation or biopsy before escalating suspected acute fatty liver.

  3. 03

    Using fetal corticosteroids as a reason to postpone delivery despite progressive maternal organ failure.

  4. 04

    Stopping close observation immediately after birth despite the possibility of postpartum deterioration.

  • 05
    Targeted imaging and alternative-cause tests
    Why
    Investigate rupture, obstruction, thrombosis or another acute hepatic process.
    Interpretation and limitations
    Ultrasound or cross-sectional imaging is selected for the suspected complication; send appropriate viral, drug and other tests without delaying stabilisation and birth.
    • 1
    Agree timing and route with the senior team based on maternal stability, gestation, cervix, fetal status and available operative and neonatal resources.
  • 2Give antenatal corticosteroids if appropriate and feasible, but do not delay medically indicated birth to complete their course.
  • 3Assess coagulation and platelet trajectory before anaesthesia, anticipate haemorrhage and communicate the resuscitation plan to theatre and neonatal teams.
    • 03Postpartum courseContinue organ surveillance after deliveryThe pregnancy has ended but biochemical injury or clinical instability remains.+
    1. 1Repeat blood count, haemolysis markers, glucose, renal function and coagulation at a frequency determined by ongoing severity and trend.
    2. 2EscalationEscalate persistent encephalopathy, acidosis, worsening coagulopathy or organ failure to a liver centre and consider diagnoses requiring additional treatment such as TTP.
    3. 3Arrange a structured follow-up explaining the final diagnosis, recovery, future pregnancy risks and any neonatal metabolic or genetic assessment after AFLP.
    Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
    Treats eclampsia and is considered for qualifying severe pre-eclampsia with planned early birth.

    Magnesium sulfate for eclampsia

    Give 4 g intravenously over 5–15 minutes, then 1 g/hour for 24 hours; after eclampsia continue for 24 hours after the last seizure, with further seizures managed using an additional 2–4 g intravenously over 5–15 minutes.

    Monitor respiration, reflexes and urine output; renal impairment increases toxicity risk and requires dose review and ready access to calcium gluconate.

    Corrects a potentially recurrent and immediately dangerous manifestation of impaired hepatic glucose regulation.

    Glucose for hypoglycaemia

    When oral treatment is unsafe, give intravenous glucose through the hospital hypoglycaemia pathway, for example 150–200 mL of 10% glucose over 10–15 minutes, then recheck and provide continuing replacement if needed.

    Repeat bedside glucose frequently, protect the airway in reduced consciousness and titrate ongoing infusion to measured need and fluid tolerance.