Pregnancy · Emergency

HELLP Syndrome Classifier

Classify HELLP syndrome per Sibai’s Tennessee criteria (1990 — complete vs not) and Martin’s Mississippi three-class system (1991 — severity by platelet count). Educational tool to support obstetric assessment of severe preeclampsia.

Last reviewed 25 May 2026

HELLP syndrome classifier — Tennessee + Mississippi

Haemolysis · Elevated Liver enzymes · Low Platelets

U/L
mg/dL
U/L
/µL
Enter at least LDH (or bilirubin), AST, and platelets to classify.
Educational tool only — not medical advice. HELLP is a medical emergency. Maternal mortality 1-3 %, perinatal mortality 7-20 % depending on gestation. Definitive treatment is DELIVERY. Magnesium sulphate, BP control, transfusion support, and intensive monitoring are the bridges to delivery. Any suspicion of HELLP requires same-day obstetric input.
What does this mean?
HELLP (Hemolysis, Elevated Liver enzymes, Low Platelets) is a severe variant of pre-eclampsia complicating ~0.5 % of pregnancies and ~10–20 % of severe PE. ~30 % of cases occur postpartum, often within 48 h of delivery — that’s why right-upper-quadrant or epigastric pain, nausea, or headache in the first week after birth should never be brushed off. Maternal mortality is 1–3 % overall but rises with delays; perinatal mortality 7–20 %. Major complications: DIC, placental abruption, acute kidney injury, hepatic capsule haematoma/rupture, pulmonary oedema. Treatment is timely delivery + magnesium sulphate seizure prophylaxis + BP control (labetalol, hydralazine, nifedipine) + platelet/RBC support as needed. Some women with class 2/3 (less severe) HELLP < 34 wk can be stabilised for 24–48 h to complete steroids before delivery. Always over- rather than under-react to HELLP suspicion.

Introduction

HELLP — Haemolysis, Elevated Liver enzymes, Low Platelets — is a severe pregnancy-related liver and coagulation disorder considered a variant of preeclampsia. Maternal mortality is 1-3 %; perinatal mortality 7-20 %. First described by Weinstein in 1982 (AJOG). About 0.5-0.9 % of all pregnancies; 10-20 % of women with severe preeclampsia develop HELLP.

The two classification systems

Tennessee (Sibai 1990)

Binary diagnosis — “complete” HELLP requires ALL three of:

  • Haemolysis — LDH > 600 U/L, OR bilirubin > 1.2 mg/dL, OR fragmented red cells on smear.
  • Elevated liver enzymes — AST ≥ 70 U/L.
  • Low platelets — PLT < 100,000 / µL.

Mississippi (Martin 1991)

Three-class severity grading by platelet count, given haemolysis and elevated liver enzymes:

  • Class 1 (severe) — PLT ≤ 50,000 + LDH ≥ 600 + AST ≥ 70. Highest morbidity.
  • Class 2 (moderate) — PLT 50,001-100,000 + LDH ≥ 600 + AST ≥ 70.
  • Class 3 (partial) — PLT 100,001-150,000 + LDH ≥ 600 + AST ≥ 40. “Incomplete” HELLP variant.

Mississippi correlates more closely with maternal outcome severity. Many obstetric teams document both for clarity.

Symptoms — when to suspect HELLP

  • Right-upper-quadrant or epigastric pain (~90 %) — from liver capsule stretch / ischemia.
  • Nausea, vomiting, malaise (~50 %).
  • Headache, visual disturbance (~30 %).
  • Hypertension — usually but not universal; ~12 % normotensive.
  • Generalised oedema — legs, hands, face.
  • “Flu-like” feeling in the days before — non-specific but commonly reported.

Management — delivery is definitive

  1. Stabilisation — BP control with IV labetalol, hydralazine, or oral nifedipine (target SBP < 160, DBP < 110).
  2. Magnesium sulphate — 4-6 g IV load over 20 min, 1-2 g/hour maintenance, continued 24 hours postpartum.
  3. Lab and clinical assessment — FBC, coagulation, U&E, LFTs every 6 hours.
  4. Platelet transfusion if PLT < 20,000 or < 40,000 with bleeding or planned caesarean.
  5. Delivery — mode determined by GA, cervical status, maternal stability. After 34 weeks: deliver immediately. Before 34 weeks: consider 48-hour delay for antenatal steroids if maternal-fetal status allows; ALPS criteria for late preterm.
  6. Postpartum monitoring — LFTs and PLT may worsen for 24-48h before improving. Stay in level-2 care.

Differential diagnosis

  • Acute fatty liver of pregnancy (AFLP) — hypoglycaemia, DIC more prominent.
  • Thrombotic thrombocytopenic purpura (TTP) — neurological prominence, ADAMTS13 deficiency.
  • Atypical haemolytic uraemic syndrome (aHUS) — renal prominence.
  • Antiphospholipid syndrome flare.
  • Drug-induced hepatitis.

These differentials matter because management differs (plasma exchange for TTP, eculizumab for aHUS).

Outcomes

  • Maternal mortality 1-3 %.
  • Maternal morbidity: DIC (20 %), placental abruption (16 %), AKI (8 %), pulmonary oedema (8 %), subcapsular liver hematoma (1 %; can rupture — life-threatening), retinal detachment.
  • Perinatal mortality 7-20 %, mostly related to prematurity and abruption.
  • HELLP typically resolves within 48-96 hours postpartum.

Recurrence and future pregnancies

  • Recurrence rate 5-25 % depending on severity and gestation at index event.
  • Aspirin prophylaxis (75-150 mg) from 12-16 weeks in subsequent pregnancies.
  • Preconception MFM consultation for severe early-onset HELLP.
  • Lifetime cardiovascular risk elevated — annual BP / lipids / lifestyle modification.

Limitations

  • HELLP is a clinical emergency — this tool is educational. Any suspicion warrants same-day obstetric assessment.
  • Lab cutoffs differ slightly across systems; Tennessee remains the most-cited binary criterion.
  • The smear finding (fragmented RBCs / schistocytes) is hard to capture in a calculator; this widget uses LDH and bilirubin as haemolysis surrogates.
  • “Partial” HELLP (Mississippi Class 3) carries similar prognostic implications to severe-features preeclampsia — both warrant intensive management.

Sources

  • Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy. Am J Obstet Gynecol 1982;142:159-67.
  • Sibai BM. The HELLP syndrome: much ado about nothing? Am J Obstet Gynecol 1990;162:311-6.
  • Martin JN Jr, Blake PG, Perry KG Jr, et al. The natural history of HELLP syndrome: patterns of disease progression and regression. Am J Obstet Gynecol 1991;164:1500-9.
  • Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol 2004;103:981-91.
  • ACOG. Practice Bulletin 222: Gestational Hypertension and Preeclampsia. 2020.

Frequently asked questions

What is HELLP syndrome?
HELLP — Haemolysis, Elevated Liver enzymes, Low Platelets — is a severe pregnancy-related liver and coagulation disorder, considered a variant of preeclampsia. About 0.5-0.9 % of all pregnancies; 10-20 % of women with severe preeclampsia develop HELLP. Maternal mortality is 1-3 %; perinatal mortality is 7-20 % depending on gestation. First described by Weinstein 1982 (AJOG).
Tennessee vs Mississippi criteria — what's the difference?
Two complementary classification systems. Sibai's Tennessee (1990) is binary: 'complete' HELLP requires ALL THREE of haemolysis (LDH > 600 or bilirubin > 1.2 or fragmented RBCs), elevated AST ≥ 70, and platelets < 100,000. Martin's Mississippi (1991) is a three-class severity grading by platelet count: Class 1 (PLT ≤ 50K — severe), Class 2 (PLT 50-100K — moderate), Class 3 (PLT 100-150K + AST ≥ 40 — 'partial' HELLP). Mississippi correlates better with maternal outcome severity. Both are used; many obstetricians document both.
What are the symptoms of HELLP?
Right-upper-quadrant or epigastric pain (~90 %) — from liver capsule stretch / hepatic ischemia. Nausea, vomiting, malaise (~50 %). Headache, visual disturbance (~30 %). Hypertension (in most, but not all — some present normotensive). Edema (lower extremity, facial). Many women describe feeling 'like I'm coming down with the flu' in the days before HELLP diagnosis. Any of these symptoms in the second half of pregnancy or postpartum warrants same-day clinical assessment.
How is HELLP managed?
DELIVERY is the only definitive treatment. Magnesium sulphate (4-6 g IV load, 1-2 g/hour maintenance) for seizure prophylaxis. BP control with IV labetalol, hydralazine, or oral nifedipine if SBP ≥ 160 or DBP ≥ 110. Platelet transfusion if PLT < 20,000 (or < 40,000 + bleeding/c-section). Red cell transfusion as needed. Dexamethasone has been tried for platelet improvement (data inconsistent; not standard). Postpartum, HELLP typically resolves within 48-96 hours but liver function and platelets may worsen for 24-48 hours before improving.
Can HELLP develop postpartum?
Yes — about 30 % of HELLP cases present postpartum (most within 48 hours, some up to 7 days). Postpartum HELLP carries similar morbidity to antepartum HELLP and the same urgent management. This is why postpartum BP monitoring matters; some maternity units provide home BP devices for the first 1-2 weeks.
Differential diagnoses to consider?
Acute fatty liver of pregnancy (AFLP) — overlapping presentation; AFLP has hypoglycaemia and DIC out of proportion. Thrombotic thrombocytopenic purpura (TTP) — neurological symptoms more prominent. Atypical haemolytic uraemic syndrome (aHUS) — renal failure prominent. Antiphospholipid syndrome flare. These differentials matter because management differs (plasma exchange for TTP, eculizumab for aHUS); haematology and high-risk MFM input is appropriate.
Will HELLP recur in future pregnancies?
Recurrence rate is roughly 5-25 % depending on severity and gestation of index event. Women with severe early-onset HELLP have higher recurrence. Aspirin prophylaxis is recommended in subsequent pregnancies. Preconception consultation with maternal-fetal medicine is appropriate after any HELLP pregnancy.