Obstetric emergencies in the ICU · ICU Topics

Cinematic ICU scene of obstetric ICU emergencies — a peripartum patient, magnesium sulphate for eclampsia, a labetalol infusion for blood pressure, a left-lateral tilt on the bed, an amniotic-fluid-embolism alert, clinical-blue lighting, medical educational, no faces, no text — FigureObstetric ICU — rare, young, and high-stakes. Pre-eclampsia and eclampsia dominate: magnesium sulphate for the seizures, labetalol or hydralazine for the pressure, delivery for the cure. HELLP threatens the liver haematoma. Peripartum cardiomyopathy is the heart failure to term and beyond — standard therapy bar the ACE inhibitor and ARB until delivered. Amniotic fluid embolism is the sudden collapse with coagulopathy — support the circulation and the bleeding. Tilt the gravid uterus off the vena cava.

[1]

Physiological changes of pregnancy

Pregnancy physiology — why ICU management differs

Respiratory: FRC decreases 20%, oxygen consumption increases 20% → desaturates rapidly. Pre-oxygenate before intubation. Difficult airway risk (oedema, breast engorgement).
Cardiovascular: blood volume increases 40%, cardiac output increases 30-50%, HR increases. Supine position: aortocaval compression by gravid uterus → ALWAYS position left lateral tilt or manual displacement of uterus.
Renal: GFR increases 50%, creatinine lower (normal up to 75 in pregnancy). Glycosuria and proteinuria are common (normal in pregnancy).
Haematology: dilutional anaemia (Hb 105-140 normal), leukocytosis (up to 12-15 normal). Fibrinogen increases (normal 4-6 g/L in third trimester; fibrinogen <4 in bleeding = concern).
Gastrointestinal: delayed gastric emptying, incompetent lower oesophageal sphincter → aspiration risk. Always consider rapid sequence induction for intubation.[6]

Pre-eclampsia and eclampsia

Educational schematic of pre-eclampsia pathophysiology: abnormal placentation, anti-angiogenic imbalance, endothelial dysfunction, hypertension, proteinuria, cerebral oedema, HELLP — FigurePre-eclampsia pathophysiology — abnormal placentation drives anti-angiogenic imbalance and endothelial injury, producing hypertension, proteinuria, cerebral risk, and HELLP microangiopathy.

Management

Pre-eclampsia/eclampsia ICU management

Magnesium sulphate — FIRST (seizure prevention/treatment)

Loading: 4-6 g IV over 20 min. Maintenance: 1-2 g/h infusion for 24h after delivery or last seizure. Monitor: reflexes (loss = early toxicity), respiratory rate (depression), urine output, magnesium levels (target 2-4 mmol/L). Antidote: calcium gluconate 10% 10 mL IV slow for toxicity. Magnesium prevents eclampsia but is NOT an antihypertensive.<Cite id="1" />

BP control — AFTER magnesium

IV labetalol (20 mg every 10 min, max 300 mg, or infusion 1-2 mg/min) OR hydralazine (5 mg every 20 min). Target: <160/110 (prevent stroke). Avoid ACE inhibitors, ARBs, nitroprusside (teratogenic/toxic). Oral nifedipine 10 mg can be used if IV not available.

Fluid management — CAUTIOUS

Pre-eclamptic patients are at high risk of pulmonary oedema (capillary leak + low albumin). Give fluids cautiously — monitor closely. Avoid aggressive fluid resuscitation. If oliguric, do NOT fluid challenge — risk of pulmonary oedema. May need CVP/PA catheter guidance.

Delivery — definitive treatment

The only definitive treatment for pre-eclampsia is delivery of the baby and placenta. Timing depends on gestational age and severity. Consult obstetrics urgently. Postpartum pre-eclampsia can occur up to 6 weeks postpartum.

HELLP syndrome

Severe pre-eclampsia variant

H: Haemolysis (LDH >600, schistocytes, bilirubin >20)
EL: Elevated Liver enzymes (AST >70)
LP: Low Platelets (<100,000)
Risk: liver haematoma/rupture (RUQ pain — EMERGENCY)
Management: delivery (definitive) + supportive care ± steroids for fetal lung maturation
Higher morbidity than standard pre-eclampsia

[2]

Peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM)

Heart failure with LVEF <45% occurring in the last month of pregnancy to 5 months postpartum, with no other identifiable cause. [1]

Risk factors: advanced maternal age, multiparity, pre-eclampsia, African descent, prolonged tocolysis. [1]

Management:

Standard HF therapy: diuretics, beta-blockers (metoprolol/bisoprolol), digoxin, hydralazine + nitrate (instead of ACEi/ARB if pregnant)
ACE inhibitors/ARBs are CONTRAINDICATED during pregnancy (teratogenic). Safe postpartum if not breastfeeding (enalalapril is safe in breastfeeding).
Bromocriptine (dopamine agonist) — emerging evidence (prolactin may be pathogenic)
Mechanical circulatory support (IABP, Impella, VA-ECMO) for refractory cardiogenic shock
Consider LVAD/heart transplant if not recovering
Recovery of LVEF occurs in ~50-60% within 6 months[3]

Amniotic fluid embolism

Exam practice

SAQ — Eclampsia in ICU

10 minutes · 10 marks

A 32-year-old woman at 36 weeks gestation is admitted to ICU after a generalised seizure. BP 172/114, HR 102, SpO2 96%. She is post-ictal, confused. Proteinuria 3+ on dipstick. Platelets 85, AST 95, LDH 650.

[1]

Clinical pearls

High-yield obstetric ICU points for the CICM/FFICM exam

Magnesium FIRST in eclampsia (4-6 g IV loading) — prevents/treats seizures. NOT an antihypertensive.[1]
Calcium gluconate is the antidote for magnesium toxicity. Stop infusion + give Ca gluconate 10% 10 mL IV.
BP control AFTER magnesium: labetalol or hydralazine. Target <160/110. Avoid ACEi/ARB/nitroprusside.
HELLP: Haemolysis + Elevated Liver + Low Platelets. Risk of liver rupture (RUQ pain).[2]
Delivery is definitive treatment for pre-eclampsia/HELLP.
Peripartum cardiomyopathy: HF in last month to 5 months postpartum. NO ACEi/ARB if pregnant.[3]
Amniotic fluid embolism: sudden collapse + DIC during delivery. Supportive + MTP + VA-ECMO.[4]
Pregnant patients desaturate FAST: reduced FRC + increased O2 consumption. Pre-oxygenate before RSI.
Left lateral tilt: prevents aortocaval compression. NEVER supine in third trimester.
Rapid sequence induction: delayed gastric emptying + incompetent LOS = aspiration risk.
Fibrinogen is HIGH in pregnancy (4-6 g/L normal in 3rd trimester). Fibrinogen <4 in obstetric bleeding is concerning.
Sepsis in pregnancy: common causes = pyelonephritis, chorioamnionitis, wound infection. Source control + antibiotics + early delivery if chorioamnionitis.[5]
Physiological anaemia: Hb 105-140 normal in pregnancy (dilutional).
Normal creatinine is lower in pregnancy (up to 75 umol/L) due to increased GFR.

Red flags

Detailed physiology of pregnancy and ICU implications

Pregnancy physiology transforms every system. Understanding the magnitude and direction of each change is essential because normal ICU thresholds and drug doses do not apply. The intensivist must use pregnancy-adjusted reference ranges for vital signs, blood gases, haematology and biochemistry, and must anticipate the altered pharmacokinetics (increased volume of distribution, increased renal clearance, altered protein binding).[6]

Cardiovascular changes

Cardiovascular adaptations — summary of magnitude

Cardiac output rises by 30-50% by the late third trimester (peak ~32 weeks), driven first by stroke volume then by heart rate.
Heart rate increases by 10-20 bpm above baseline.
Systemic vascular resistance (SVR) falls by ~20% due to vasodilatory effects of progesterone, relaxin, and nitric oxide — mean arterial pressure drops by 5-10 mmHg in mid-pregnancy, normalising near term.
Blood volume increases by 40-50% (plasma > red cell → dilutional anaemia).
Supine hypotensive syndrome (aortocaval compression): from ~20 weeks the gravid uterus compresses the IVC and aorta in the supine position, reducing preload by up to 25% and uteroplacental perfusion. ALWAYS use left lateral tilt ≥15° or manual left uterine displacement in any pregnant patient >20 weeks lying supine.
Venous return from the lower limbs is impaired → leg oedema and a 5-fold increased risk of venous thromboembolism.
Echocardiography: mild LVH and bi-atrial enlargement are normal; EF is preserved; E/A ratio is reduced (diastolic filling impaired in lateral decubitus).

[1]

Respiratory changes

Respiratory adaptations — the dangerous combination

Functional residual capacity (FRC) falls by ~20% by term (diaphragm elevated 4 cm, rib cage flared) — and further in the supine position.
Oxygen consumption (VO₂) rises by ~20% (fetoplacental unit, increased cardiac/resp work).
Net result: apnoeic desaturation occurs roughly twice as fast as in non-pregnant adults — typically within 60-90 seconds versus 3-4 minutes. Pre-oxygenation (3 min of 100% O₂ or 8 vital-capacity breaths) is mandatory before any intubation.
Minute ventilation increases by ~40-50% (mainly tidal volume) → chronic respiratory alkalosis with compensatory renal bicarbonate loss. Typical blood gas: pH 7.43-7.47, PaCO₂ 28-32 mmHg, HCO₃⁻ 18-21. A PaCO₂ of "normal" (40) in late pregnancy represents relative hypercapnia and impending exhaustion.
Difficult airway: Mallampati scores worsen through pregnancy and labour; airway oedema and friability, breast engorgement, and reduced neck mobility all contribute. Failed intubation rate is ~1:390 in obstetric anaesthesia versus ~1:2,230 in the general OR — about 8-fold higher.[16]

Haematological changes

Haematological adaptations — a hypercoagulable, dilutional state

Plasma volume increases > red cell mass → dilutional ("physiological") anaemia — Hb as low as 105 g/L is normal in the 3rd trimester.
Fibrinogen rises to 4-6 g/L in the third trimester (vs 2-4 non-pregnant). In obstetric haemorrhage a fibrinogen <4 g/L is abnormal and predicts severe haemorrhage; keep >4 in active bleeding.
Clotting factors: factors VII, VIII, IX, X, XII and von Willebrand factor all rise → hypercoagulable state (4-5× increased VTE risk).
Platelets: mild thrombocytopenia (100-150 × 10⁹/L) is common in normal pregnancy (haemodilution + increased consumption). A count <100 requires explanation (pre-eclampsia, HELLP, ITP, DIC).
Leukocytosis up to 12-15 × 10⁹/L is normal — do not over-interpret as infection.
D-dimer is elevated throughout pregnancy (3-4× non-pregnant by term) — a normal D-dimer does not reliably exclude VTE in the third trimester.

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Renal

Hyperfiltration

GFR rises by ~50% by mid-pregnancy
Normal serum creatinine in pregnancy <75 µmol/L (0.85 mg/dL) — a "normal" creatinine of 90 already signals renal impairment
Glycosuria, proteinuria up to 300 mg/24h, and aminoaciduria are normal
Urea <3 mmol/L normal; uric acid rises in pre-eclampsia (marker of severity)

Gastrointestinal

Aspiration risk

Lower oesophageal sphincter tone reduced (progesterone)
Gastric emptying delayed from mid-pregnancy (mechanical + hormonal)
Intragastric pressure raised by the gravid uterus
All pregnant patients >20 weeks treated as "full stomach" — RSI with cricoid pressure for any intubation
Antacid prophylaxis (sodium citrate 30 mL + ranitidine 50 mg IV) before caesarean

Pharmacology

Altered PK/PD

Increased volume of distribution → higher loading doses for many drugs (e.g. magnesium)
Increased renal clearance → more frequent dosing of renally-cleared drugs (β-lactams, digoxin)
Reduced plasma protein (albumin) → more free drug for highly-bound agents
Placental transfer: avoid ACEi, ARBs, warfarin (teratogenic/foetotoxic), NSAIDs (premature closure of ductus)
Inhaled volatiles: MAC reduced by ~25-40% in pregnancy

[1]

Magnesium sulphate — dosing and toxicity in depth

Magnesium sulphate: practical ICU protocol

Indications and dosing

INDICATION: seizure prophylaxis in severe pre-eclampsia; treatment of eclampsia. REGIMEN (Pritchard IM or Zuspan IV): IV LOADING 4-6 g magnesium sulphate over 20 min (4 g in 100 mL over 15-20 min; IM alternative 10 g — 5 g deep IM into each buttock). MAINTENANCE 1-2 g/h IV for 24 h after delivery OR last seizure. ALWAYS have calcium gluconate 10% 10 mL drawn up at bedside before starting.

Monitoring

Clinical monitoring EVERY hour: (1) patellar reflexes PRESENT (loss = first sign of toxicity, Mg²⁺ ~5-7 mmol/L); (2) respiratory rate ≥12/min; (3) urine output ≥25 mL/h (Mg²⁺ renally excreted — oliguria = accumulation). Serum magnesium levels: target therapeutic 2-4 mmol/L (4-8 mEq/L). Check level if >4 or any concern.

Toxicity ladder

2-4 mmol/L = therapeutic. 5-7 = loss of deep tendon reflexes, flushing, warmth. 7-10 = somnolence, slurred speech, hypotension, ECG widening of QRS, prolonged PR. 10-12 = respiratory depression/arrest. >15 = cardiac arrest (asystole). ALWAYS stop infusion at first sign; calcium gluconate 10% 10 mL IV over 5-10 min reverses cardiorespiratory toxicity.

Magnesium and neuromuscular blockade

Magnesium potentiates both depolarising (suxamethonium) and non-depolarising (rocuronium, vecuronium) neuromuscular blockers — expect prolonged paralysis. Use processed EEG (TOF) monitoring and reduce NMBA doses by ~30-50%. Magnesium crosses placenta — neonate may be hypotonic or have respiratory depression at birth (notify neonatal team).

Magnesium for neuroprotection (separate indication)

For preterm labour <32 weeks, magnesium sulphate is given for FETAL neuroprotection (reduces cerebral palsy) — different protocol (4 g loading, may repeat). Coexists with maternal indication but the rationale is fetal, not maternal.

[9]

Sepsis in pregnancy and the puerperium

Sepsis is a leading direct cause of maternal death worldwide and consistently ranks in the top three in MBRRACE-UK reports. Pregnancy immunomodulation (blunted cell-mediated immunity, neutrophil dysfunction) and the hypercoagulable state increase susceptibility and severity. The physiological tachycardia, leukocytosis, and tachypnoea of pregnancy can mask early sepsis — use pregnancy-modified qSOFA/Sepsis in Obstetrics Scores (SOS).[11][12]

Common sources

Antepartum

Pregnancy-specific

Pyelonephritis (most common — dilated ureters from progesterone, 2× risk of progression to sepsis)
Chorioamnionitis (fever, tachycardia, uterine tenderness, foul liquor) — delivery is source control
Septic abortion / retained products of conception
Listeria monocytogenes (bacteraemia, often flulike — avoid unpasteurised foods)
Influenza, COVID-19, varicella pneumonia (higher mortality than non-pregnant)

Peripartum / postpartum

Within 6 weeks

Endometritis (post-caesarean risk 10× vaginal delivery)
Wound infection (caesarean, perineal, episiotomy)
Mastitis / breast abscess (often Staph aureus)
Retained products of conception
Episiotomy or perineal laceration infection
Necrotising fasciitis (polymicrobial, often with Group A Strep — surgical emergency)

Non-obstetric

Same as non-pregnant

Community-acquired pneumonia
Appendicitis (often atypical presentation — pain higher due to uterine displacement)
Biliary sepsis (gallstones common in pregnancy)
Pyelonephritis from asymptomatic bacteriuria
Meningitis, cellulitis, line infection

Sepsis in pregnancy — modified Surviving Sepsis bundle (within 1 hour)

Recognition — use pregnancy-specific thresholds

Modified qSOFA in pregnancy: RR ≥22, SBP <90 or MAP <65, altered mentation. NOTE: baseline RR is high (18-20 normal), HR high (90s normal), WCC high (up to 15 normal). Suspect sepsis with fever ≥38, sustained tachycardia >110, RR >24, or new confusion. Lactate is well-validated: >2 mmol/L warrants concern.

Resuscitation (with fetal monitoring)

Crystalloid 30 mL/kg over first 3 h (cautious — risk of pulmonary oedema). Target MAP ≥65, urine output ≥0.5 mL/kg/h (in pregnancy ≥1 mL/kg/h is normal). LEFT LATERAL TILT >20 weeks. Apply continuous CTG (cardiotocography) for fetal heart rate >23 weeks. Norepinephrine is first-line vasopressor in pregnancy (less uterine vasoconstriction than phenylephrine/metaraminol).

Investigations and cultures

Blood cultures ×2, MSU, vaginal/high vaginal swab, wound swab, placental swab at delivery. Send lochia in postpartum. Lactate, FBC, CRP, coagulation, U&E, LFTs, venous gas. Imaging: CXR, ultrasound (renal/obstetric), CT abdomen/pelvis if source unclear (recognise radiation risk — single CT <1 mSv to fetus is acceptable at >12 weeks; MRI without gadolinium is preferred). Empirical antibiotics MUST cover common obstetric pathogens.

Empirical antibiotics

CHORIOAMNIONITIS/ENDOMETRITIS: piperacillin-tazobactam 4.5 g IV + gentamicin 5-7 mg/kg IV + metronidazole 500 mg IV (or carbapenem monotherapy). PYELONEPHRITIS: ceftriaxone 2 g IV ± gentamicin. SEPSIS UNCLEAR: piperacillin-tazobactam ± vancomycin (line infection, MRSA). Add oseltamivir if influenza suspected. Therapeutic drug monitoring of aminoglycosides is essential (altered Vd and clearance). DE-ESCALATE within 48-72 h on culture results.

Source control — and timing of delivery

CHORIOAMNIONITIS or ENDOMETRITIS = DELIVERY (the source is uterine contents). Retained products = surgical evacuation. Abscess = drainage. The decision to deliver balances gestational age, maternal stability, and fetal status — multi-disciplinary (obstetric, neonatal, ICU). Live fetus: do not delay maternal resuscitation for delivery.

Special considerations

Use filter on blood products. Continue magnesium if concurrent pre-eclampsia. Avoid NSAIDs if <32 weeks (ductus arteriosus) or in AKI. Steroids for fetal lung maturation (betamethasone 12 mg IM ×2, 24 h apart) if <34 weeks and delivery anticipated. Venous thromboprophylaxis mandatory (sepsis + pregnancy = highest VTE risk).

[11]

Postpartum haemorrhage (PPH)

PPH is defined as blood loss ≥500 mL after vaginal delivery or ≥1000 mL after caesarean, OR any blood loss causing haemodynamic instability. Major PPH = continued bleeding >1000 mL. Severe PPH (>2500 mL or 5+ units) carries a maternal mortality risk and the term "massive obstetric haemorrhage" is used. Pregnancy physiology masks early PPH: a young woman can lose 1.5 L (30% of blood volume) before tachycardia and hypotension appear because blood volume is up 50% — by which point she is already critically ill. [1]

The "4 Ts" of PPH causes

Tone (70%)

Uterine atony

Most common cause — uterus fails to contract after delivery
Risk factors: prolonged/augmented labour, multiparity, overdistended uterus (twins, macrosomia, polyhydramnios), prior PPH
Examine: boggy, soft uterus on palpation
Management: uterotonic sequence — oxytocin 5 IU IV/IM → ergometrine 250 µg IM (avoid in hypertension) → carboprost (15-methyl-PGF2α) 250 µg IM q15min max 8 doses (avoid in asthma) → misoprostol 800 µg PR/SL; bimanual uterine compression; Bakri balloon tamponade

Trauma (20%)

Genital tract

Cervical, vaginal, or perineal lacerations
Uterine rupture (especially with prior caesarean scar and labour)
Retained instrumentation injury, broad ligament haematoma
Management: systematic inspection of vagina/cervix/uterus under anaesthesia; surgical repair; laparotomy for rupture

Tissue (9%)

Retained products

Retained placenta or placental fragments
Placenta accreta/increta/percreta (massive risk if anterior placenta + previous caesarean scar)
Management: manual removal / uterine evacuation; hysterectomy if accreta and uncontrolled

Thrombin (1%)

Coagulopathy

Pre-existing: von Willebrand disease, on warfarin/DOAC, thrombocytopenia
Acquired: pre-eclampsia/HELLP, AFLP, amniotic fluid embolism, sepsis, massive transfusion dilution
Management: correct specific defects — fibrinogen (cryoprecipitate), platelets, FFP, factors. Keep fibrinogen >4 g/L in obstetric bleeding

[1]

Massive obstetric haemorrhage — ICU protocol

Activate and resuscitate

Call massive obstetric haemorrhage protocol. Two large-bore IV (14-16 G) or rapid infusion catheter. Send bloods for FBC, coagulation, fibrinogen, U&E, group & save + crossmatch 6 units. Warm crystalloid 1-2 L while awaiting blood. LEFT LATERAL TILT until delivered. Apply warmed fluids, forced-air warmer, maintain core temp >36°C.

Massive transfusion — pregnancy ratio 1:1:1

Give RBC:FFP:platelets 1:1:1 (six-pack plate = one adult dose) for >1 blood volume. Give CRYOPRECIPIPATE 2 pools (10 units) when fibrinogen <4 g/L — fibrinogen is the FIRST clotting factor to fall in obstetric haemorrhage and the threshold to treat is HIGHER than in trauma (>4 not >1.5). Aim for Hb >70, platelets >75, PT/APTR <1.5× normal, fibrinogen >4.

Tranexamic acid — give EARLY

TRANEXAMIC ACID 1 g IV over 10 min within 3 h of bleeding onset — reduces death from bleeding (WOMAN Trial). Give a second 1 g dose after 30 min if bleeding continues. Cheap, safe, no thrombotic signal in pregnancy — give before leaving the room.

Pharmacological and mechanical uterotonics

OXYTOCIN 5 IU IV slow (then 40 IU in 500 mL over 4 h). ERGOMETRINE 250 µg IM (contraindicated in hypertension/pre-eclampsia). CARBOPROST 250 µg IM q15 min (contraindicated in asthma — causes bronchospasm). MISOPROSTOL 800 µg PR. Then BAKRI balloon, uterine packing, B-Lynch suture at laparotomy.

Definitive surgical / radiological

If >2 L ongoing or unstable: laparotomy with uterine compression sutures (B-Lynch), ligation of uterine/internal iliac arteries, pelvic packing. INTERVENTIONAL RADIOLOGY (uterine artery embolisation) if stable. HYSTERECTOMY is life-saving — do not delay once >10 units transfused or coagulopathic. Theatres and obstetric consultant MUST be present.

Post-bleeding ICU care

Admit to ICU. Watch for: re-bleeding, coagulopathy, transfusion-associated circulatory overload (TACO), transfusion-related acute lung injury (TRALI), AKI, Sheehan syndrome (pituitary infarction — late, postpartum), and venous thromboembolism (start prophylactic LMWH once bleeding controlled, usually 12-24 h). Treat hypothermia, acidosis, hypocalcaemia (citrate from transfusion binds Ca²⁺).

[13]

Amniotic fluid embolism — in depth

AFE — biphasic clinical course

Phase 1 — cardiopulmonary collapse (0-30 min)

Trigger: labour, delivery, caesarean, or within 30 min postpartum. Mechanism: amniotic fluid + fetal debris enter maternal circulation → anaphylactoid activation of complement and inflammatory cascades → acute pulmonary vasospasm and RV failure. Presentation: sudden hypoxia, altered mental state, seizure, then cardiopulmonary arrest (typically VF or PEA). Hypotension is profound and often out of proportion to blood loss.

Phase 2 — coagulopathy (within 30-60 min)

Survivors of phase 1 enter a consumptive coagulopathy (DIC). Fibrinogen falls rapidly (often <1 g/L), PT/APTT prolonged, platelets drop. Bleeding from IV sites, surgical wounds, vagina, and mucous membranes is torrential. This is the phase that kills — anticipate and start MTP early.

Differential diagnosis at collapse

Pulmonary embolism, massive venous air embolism, local anaesthetic toxicity (after epidural/spinal — give Intralipid 20% 1.5 mL/kg bolus), eclamptic seizure, anaphylaxis, MI/cardiac arrest, septic shock, uterine rupture, placental abruption. AFE is a DIAGNOSIS OF EXCLUSION in practice — there is no reliable diagnostic test in life. Send tryptase (often elevated) and look for fetal squames in pulmonary vasculature on post-mortem.

Management — supportive + MCS

ABCDE; high-quality CPR (left lateral displacement if undelivered, perimortem caesarean at 4 min if no ROSC and fetus >20 weeks). Intubate and ventilate with 100% O₂; consider inhaled nitric oxide or prostacyclin for RV failure/pulmonary hypertension. Vasopressors (norepinephrine first-line), veno-arterial ECMO for refractory shock. ACTIVATE MTP early. Deliver if antepartum. Mortality 20-60% despite best care; survivors often have complete neurological recovery if ROSC <15 min.

[4]

Peripartum cardiomyopathy — in depth

PPCM — diagnosis, course and ICU management

Definition: heart failure with reduced LVEF (<45%) toward the end of pregnancy or in the months postpartum (last month of pregnancy to 5 months postpartum), with no other identifiable cause. [1]

Epidemiology: incidence ~1:2,000-3,000 live births; higher in Black women, multiparity, advanced maternal age, pre-eclampsia, multiple gestation, prolonged tocolysis, and cocaine use. [1]

Pathophysiology: proposed mechanism involves a 16 kDa prolactin fragment (cleaved by cathepsin D) that is anti-angiogenic and pro-apoptotic — rationale for bromocriptine therapy. Genetic overlap with dilated cardiomyopathy (TTN truncating variants in ~15%).[15]

Presentation: dyspnoea (often misattributed to normal pregnancy), orthopnoea, peripheral oedema, palpitations, fatigue, and on occasion cardiogenic shock, ventricular arrhythmia, or thromboembolism. Beware the postnatal patient with new dyspnoea — pregnancy dyspnoea resolves after delivery. [1]

Investigation: echocardiography (LV dilatation and reduced EF — usually <30% in severe cases), NT-proBNP (elevated), troponin (often mildly raised), ECG (sinus tachycardia, may show LV strain, arrhythmias), CXR (pulmonary oedema, cardiomegaly). Exclude VTE, valvular disease, and thyrotoxicosis. [1]

ICU/heart failure management:

Diuretics (furosemide IV) for volume overload.
β-blocker (metoprolol/bisopropolo/carvedilol) once euvolaemic — titrate cautiously; avoid in acute decompensation.
Hydralazine + nitrate (pregnancy-safe afterload reduction) — substitute for ACEi/ARB while pregnant.
ACE inhibitor/ARB ONLY postpartum and not breastfeeding (enalapril is the preferred safe-in-breastfeeding ACEi).
Digoxin for rate control / inotropy (safe in pregnancy and lactation).
Aldosterone antagonist (spironolactone/eplerenone) — avoid in pregnancy (antiandrogen; eplerenone preferred if breastfeeding).
Bromocriptine (dopamine agonist) 2.5 mg BD for 8 weeks — emerging evidence (IPAC, B-SAFE trials) suggests improved recovery; suppresses lactation (consent required).
Anticoagulation mandatory if LVEF <30% (high thromboembolic risk + pregnancy hypercoagulability) — LMWH in pregnancy, warfarin postpartum.
Refractory shock: IABP, Impella, VA-ECMO as bridge to recovery/transplant. Earlier MCS in PPCM than ischaemic cardiomyopathy because recovery is common. [1]

Recovery: LVEF recovers to >50% in ~50-60% within 6-12 months. Subsequent pregnancy is HIGH RISK if LVEF did not fully recover — counsel against it.

[3]

Venous thromboembolism in pregnancy

Pregnancy is a prothrombotic state: a 4-5× increased VTE risk versus age-matched non-pregnant women, peaking in the puerperium (20× in first 6 weeks postpartum). VTE is a leading direct cause of maternal death in the UK. Risk is driven by venous stasis (progesterone-mediated venodilatation, IVC compression by the gravid uterus), increased clotting factors (factor VIII, fibrinogen, vWF), reduced protein S, and acquired resistance to activated protein C.[14]

DVT in pregnancy

80% left leg

Left leg predominance (80%) due to compression of left common iliac vein by right common iliac artery + gravid uterus
Iliofemoral DVT more common than distal — higher PE risk
Diagnosis: COMPRESSION ULTRASOUND first. If negative and clinical suspicion high, repeat in 5-7 days. MRI venography for suspected iliac DVT (not seen on lower-limb US). D-dimer unhelpful (normally elevated in pregnancy).
Treatment: therapeutic LMWH (enoxaparin 1 mg/kg BD or 1.5 mg/kg OD) for REST of pregnancy + 6 weeks postpartum. Warfarin only postpartum (breastfeeding-safe). Avoid DOACs in pregnancy/breastfeeding.

PE in pregnancy

High mortality

Clinical features same as non-pregnant: dyspnoea, pleuritic chest pain, haemoptysis, syncope. Tachycardia, hypoxia. Massive PE: hypotension, RV strain.
Diagnosis algorithm: if haemodynamically STABLE — D-dimer (if low and low pretest, exclude; if high or non-diagnostic) → CTPA (preferred; lower radiation) or V/Q scan (preferred if normal CXR; no maternal breast radiation dose). Either is acceptable — fetal radiation is well below harmful threshold (<1 mSv).
If haemodynamically UNSTABLE — bedside echocardiography (RV dysfunction, McConnell sign), start empiric LMWH immediately, confirm with CTPA if stabilises. Thrombolysis if life-threatening (alteplase 50-100 mg over 2 h) — relative contraindications apply but maternal life takes priority. Perimortem caesarean if cardiac arrest.
Maintenance: therapeutic LMWH switched to warfarin postpartum (target INR 2-3) for MINIMUM 3 months postpartum or 6 weeks postpartum + duration of antepartum therapy.

Massive PE / collapse

Critical care

ABCDE, 100% O₂, IV access, vasopressors (norepinephrine).
Consider systemic thrombolysis (alteplase 100 mg over 2 h, or 50 mg bolus if arrest).
Catheter-directed thrombolysis or surgical embolectomy if thrombolysis contraindicated.
VA-ECMO rescue for refractory cardiac arrest from PE.
IVC filter only if recurrent PE despite anticoagulation or absolute contraindication to anticoagulation (rare).

Prophylaxis

Risk-stratified

ALL women assessed for VTE risk at booking, on admission, postpartum. Risk factors: prior VTE (highest), thrombophilia, BMI >30, age >35, multiple pregnancy, pre-eclampsia, immobility, smoking, varicose veins.
HIGH risk (prior VTE / known thrombophilia): antenatal prophylactic LMWH + 6 weeks postpartum.
INTERMEDIATE risk (multiple risk factors): postpartum LMWH 10 days minimum.
Dose: enoxaparin 40 mg OD for BMI <50, weight-adjusted if >90 kg or <50 kg. Continue 6 weeks postpartum if any major risk.
Mechanical: anti-embolism stockings for surgical patients.

[14]

Airway management and modified RSI in pregnancy

Educational three-panel obstetric ICU management: eclampsia magnesium and BP control, postpartum haemorrhage 4Ts and TXA, amniotic fluid embolism supportive resuscitation — FigureObstetric ICU pathways — magnesium and BP control for eclampsia; 4 Ts, uterotonics and TXA for PPH; supportive ABC and coagulopathy care for AFE.

Pregnancy-modified RSI (the "obstetric difficult airway")

Anticipate the difficult airway

Risk factors in pregnancy: Mallampati III/IV, short neck, receding chin, obesity, reduced neck mobility, airway oedema (especially in pre-eclampsia after fluid), breast engorgement impeding laryngoscope insertion. Failed intubation ~1:390 in obstetric vs 1:2,230 in general OR. Plan A/B/C and a surgical airway plan BEFORE induction.

Positioning and pre-oxygenation

HEAD-UP/RAMP position (head of bed 25-30°) — reduces functional residual capacity loss, lifts breasts away from chin. LEFT LATERAL TILT or manual uterine displacement if >20 weeks. Pre-oxygenate with 100% O₂ for 3 min tight-fitting mask (or 8 vital-capacity breaths) — denitrogenation. Have nasal cannulae at 5 L for apnoeic oxygenation (NO DESAT technique).

Induction agents and doses

Use pregnancy-reduced doses of induction agents (opioids and hypnotics). Common regimen: PROPOFOL 2 mg/kg (or thiopentone 4-5 mg/kg — historical obstetric standard). Consider KETAMINE 1-1.5 mg/kg if hypotensive/hypovolaemic (preserves BP, bronchodilator). FENTANYL 1-2 µg/kg to blunt sympathetic response. AVOID high-dose remifentanil (apnoea). Reduced MAC for volatiles — pregnancy lowers anaesthetic requirement.

Neuromuscular blockade

SUXAMETHONIUM 1-1.5 mg/kg (rapid onset, short duration; preferred for RSI but beware prolonged blockade if patient on magnesium or with pseudocholinesterase deficiency). ROCURONIUM 1.2 mg/kg — alternative, fully reversed by sugammadex 16 mg/kg. NOTE: magnesium potentiates both — expect longer paralysis; use TOF monitoring.

Cricoid pressure, intubation, and fallback

Apply cricoid pressure (debatable but standard in many units — release if it impairs view). Use a small ETT (size 6.0-6.5) — airway oedema reduces glottic aperture. VIDEO LARYNGOSCOPE first-line if available. Have a bougie, stylet, LMA (i-gel supreme for obstetric), and a surgeon ready. Follow DAS obstetric difficult airway guidelines: Plan A intubation → Plan B SGA → Plan C face mask → Plan D surgical airway (cricothyroidotomy).

Aspiration prophylaxis and post-extubation

BEFORE induction: sodium citrate 30 mL PO (immediate), ranitidine 50 mg IV, metoclopramide 10 mg IV (optional). AFTER extubation: patients remain at aspiration risk — extubate fully awake, lateral head-down position. Tracheal tube cuff leak may indicate airway oedema — assess for leak before extubation, expect possible re-intubation.

[16]

Timing of delivery in ICU

Delivery is the definitive treatment for several obstetric emergencies (severe pre-eclampsia/HELLP, chorioamnionitis, AFLP, AFE once stabilised). The decision balances maternal condition (always paramount), gestational age, fetal wellbeing, and the steroid window for fetal lung maturation. Always multidisciplinary — obstetrician, neonatologist, intensivist, anaesthetist. [1]

Maternal indication for urgent delivery

Life-saving, no delay

Eclampsia (deliver after stabilisation, typically within 12 h)
Severe pre-eclampsia with uncontrolled BP, HELLP with liver haematoma/rupture, eclampsia
Massive PPH unresponsive to medical therapy
Amniotic fluid embolism (perimortem CS if arrest and fetus >20 weeks)
Chorioamnionitis
Acute fatty liver of pregnancy with liver failure
Severe sepsis where the uterus is the source (e.g. retained products, septic abortion)

Fetal indication

Pathology on CTG

Sustained fetal bradycardia
Recurrent late or severe variable decelerations
Absent/reversed end-diastolic flow on Doppler
Intrauterine fetal death (deliver once maternal stabilisation, no emergency)

Steroid window

Betamethasone

BETAMETHASONE 12 mg IM, 2 doses 24 h apart, optimal <34 weeks (or DEXAMETHASONE 6 mg q12h ×4)
Reduces neonatal respiratory distress syndrome, intraventricular haemorrhage, necrotising enterocolitis
Can be given if delivery anticipated within 7 days and <34+6 weeks
Causes transient maternal hyperglycaemia and leukocytosis (do not over-interpret as infection)
Do NOT delay life-saving maternal delivery to complete the steroid course

Magnesium for fetal neuroprotection

Separate indication

MAGNESIUM SULPHATE 4 g loading + 1 g/h ×12 h if delivery anticipated <32 weeks
Reduces cerebral palsy (Cochrane meta-analysis)
Often co-administered with maternal magnesium for seizure prophylaxis — single loading dose suffices for both

[1]

Fetal monitoring in the ICU

Cardiotocography (CTG) and fetal assessment in ICU

Indication: continuous CTG for any pregnant patient >23 weeks admitted to ICU, especially during maternal instability or vasoactive drug use.
What CTG shows: fetal heart rate pattern. NORMAL: baseline 110-160 bpm, variability 5-25 bpm, accelerations. CONCERNING: tachycardia (>160 — often maternal fever, infection, beta-sympathomimetics), bradycardia (<110 — hypoxia, maternal hypotension, magnesium), reduced variability (CNS depressants, hypoxia), recurrent late decelerations (uteroplacental insufficiency, maternal hypotension from vasopressors), variable decelerations (cord compression).
Maternal interventions that affect CTG: maternal hypoxia, hypotension (from sedation, vasodilators, aortocaval compression), hypercapnia, fever, magnesium (reduces variability), beta-agonists (terbutaline, salbutamol — fetal tachycardia), NSAIDs (premature closure of ductus).
Decision-making: a non-reassuring CTG in an ICU patient mandates urgent multi-disciplinary review — is the fetus telling us the mother is sicker than we think (hypoxia, hypotension), or is there primary fetal pathology? Delivery may be indicated even at the expense of prematurity.
Biophysical profile and ultrasound: adjunct when CTG is non-reassuring — amniotic fluid volume, fetal tone, breathing, movement. Doppler of umbilical artery (absent/reversed end-diastolic flow is ominous).

[1]

Drug safety in pregnancy and lactation

Safe

Generally OK

Paracetamol (acetaminophen) — first-line analgesic
Penicillins, cephalosporins, macrolides (azithromycin, erythromycin)
Heparin (UFH, LMWH) — does NOT cross placenta
Labetalol, methyldopa, hydralazine, nifedipine
Insulin, metformin (gestational diabetes)
Levothyroxine (often need ↑ dose in pregnancy)
Suxamethonium, rocuronium, neostigmine
Propofol, thiopentone, ketamine, fentanyl

Caution

Risk-benefit

Aminoglycosides (gentamicin — theoretical fetal ototoxicity; short course OK)
Vancomycin (monitor levels)
NSAIDs (avoid <32 weeks — premature ductal closure; avoid in AKI)
Aspirin (low-dose 75-150 mg IS used for pre-eclampsia prophylaxis)
Corticosteroids (cross placenta; prednisolone preferred over dexamethasone if not for fetal indication)
Beta-blockers (metoprolol OK; atenolol associated with IUGR)
Opioids (short-term OK; chronic use → neonatal abstinence syndrome)

Contraindicated

Avoid

ACE inhibitors, ARBs (fetopathy: oligohydramnios, renal agenesis, skull hypoplasia) — esp 2nd/3rd trimester
Warfarin (teratogenic 6-12 wks; fetal bleeding, chondrodysplasia) — use heparin instead
DOACs (insufficient safety data)
Tetracyclines (fetal bone/teeth), chloramphenicol (grey baby), quinolones (cartilage), trimethoprim 1st trimester (neural tube)
Nitroprusside (cyanide/thiocyanate toxicity to fetus)
Sodium valproate (neural tube defects, neurodevelopmental)
Methotrexate, mycophenolate (teratogenic)
Lithium (Ebstein anomaly — 1st trimester)
Statins (theoretical teratogenicity — contraindicated)

[1]

Hypertensive disorders of pregnancy — spectrum and differentials

Chronic hypertension

Pre-pregnancy or <20 wks

BP ≥140/90 before pregnancy or before 20 weeks gestation
Persists >12 weeks postpartum
Treat if BP ≥140/90 — first-line labetalol, methyldopa, nifedipine (CHiPT trial showed less-tight control had more severe hypertension without improving outcomes; tight control target diastolic 85)
Low-dose aspirin 75-150 mg from 12 weeks if high risk of superimposed pre-eclampsia

Gestational hypertension

>20 wks, no proteinuria

New hypertension ≥140/90 after 20 weeks without proteinuria or end-organ damage
May progress to pre-eclampsia in 25%
Monitor closely; deliver at 37 weeks

Pre-eclampsia

>20 wks + proteinuria/organ dysfunction

New hypertension ≥140/90 PLUS proteinuria (≥300 mg/24h or PCR ≥30 mg/mmol) OR end-organ dysfunction
Severe features: BP ≥160/110, platelets <100, AST/ALT ≥2× normal, renal insufficiency, pulmonary oedema, cerebral/visual symptoms
fullPIERS model predicts adverse maternal outcomes within 48 h using 7 variables (SpO₂, platelets, creatinine, AST, BP, gestational age, admission/transfer status)
Definitive: delivery. Magnesium for severe features.

HELLP

Severe pre-eclampsia variant

Haemolysis (LDH >600, schistocytes), Elevated Liver enzymes (AST >70), Low Platelets (<100)
May present with RUQ/epigastric pain, malaise, nausea — can occur without hypertension
Risk of liver haematoma/rupture — surgical emergency
Higher maternal and perinatal mortality than standard pre-eclampsia
Mississippi/Tennessee classification by severity

Eclampsia

Seizure

Tonic-clonic seizure in pre-eclamptic woman (may be first presentation of pre-eclampsia)
Can occur antepartum (38%), intrapartum (18%), postpartum (44%) — up to 6 weeks postpartum
Magnesium sulphate (MAGPIE Trial) prevents and treats eclampsia
Recurrence risk ~2% in subsequent pregnancy

Honigberg 2020 — PPCM JACC state-of-the-art (JACC; PMID 31563221)

Source

Comprehensive narrative review of peripartum cardiomyopathy (Honigberg MC, Givertz MM, Jameson JE, et al.)

Objective

Synthesise current evidence on diagnosis, pathophysiology, and management of PPCM

Key finding

PPCM is diagnosed with new heart failure (LVEF <45%) toward end of pregnancy to 5 months postpartum, without other cause. Pathophysiology implicates a 16 kDa prolactin fragment — rationale for bromocriptine. Recovery of LVEF in ~50-60%. Standard HF therapy with pregnancy/lactation modifications. Mechanical circulatory support for refractory cases.

Clinical bottom line

Suspect PPCM in any woman with new HF in last month of pregnancy to 5 months postpartum. Use hydralazine + nitrate instead of ACEi/ARB if still pregnant. Consider bromocriptine. Anticoagulate if LVEF <30%. Avoid subsequent pregnancy if EF did not recover.

[1]

Additional high-yield pearls

High-yield obstetric ICU pearls — extended set

Always use left lateral tilt >15° or manual left uterine displacement for any pregnant patient >20 weeks lying supine — aortocaval compression reduces preload and uteroplacental flow by 25%.
Perimortem caesarean (resuscitative hysterotomy) at 4 min of maternal cardiac arrest if no ROSC and fetus ≥20 weeks — improves both maternal and fetal outcome. Do it at the bedside, no consent needed.
Pregnancy is a hypercoagulable state for 6 weeks postpartum — VTE risk actually PEAKS in the puerperium, not antepartum. Continue LMWH for 6 weeks postpartum in high-risk women.
A "normal" PaCO₂ of 40 mmHg in late pregnancy is abnormal — pregnant women maintain 28-32 mmHg. A rising PaCO₂ predicts impending respiratory failure in a pregnant asthmatic or pneumonia patient.
D-dimer is unhelpful for VTE exclusion in pregnancy — it is normally elevated. Use compression US (for DVT) and CTPA or V/Q scan (for PE), with radiation doses far below harmful thresholds.
In obstetric haemorrhage the fibrinogen target is HIGHER than in trauma — keep >4 g/L. Fibrinogen is the first clotting factor to fall, and cryoprecipitate (not just FFP) is needed.
Tranexamic acid 1 g IV within 3 h for PPH (WOMAN Trial) — cheap, safe, life-saving, give before leaving the room. No thrombotic signal in pregnancy.
Magnesium potentiates neuromuscular blockers — reduce suxamethonium/rocuronium doses, expect prolonged paralysis, use TOF monitoring. Also crosses placenta — neonatal team must be ready for hypotonia.
PE in pregnancy: 80% in the LEFT leg — iliac veins (right iliac artery compresses left iliac vein + gravid uterus). Suspect and scan the left leg first.
Failed intubation in obstetric anaesthesia is 8× more common than in general OR — use video laryngoscope, small ETT (6.0-6.5), ramp position, have surgical airway plan. Follow DAS obstetric difficult airway guidelines.
Maternal sepsis can be missed — pregnancy baseline tachycardia (90s), tachypnoea (18-20), and leukocytosis (up to 15) are normal. Use lactate (≥2 concerning) and a high index of suspicion.
Pyelonephritis is the most common severe antepartum infection — dilated ureters from progesterone + uterine compression. 2× progression to sepsis. Treat aggressively; rule out bacteraemia.
PPCM: bromocriptine for 8 weeks (2.5 mg BD) — emerging evidence (IPAC trial) of improved LVEF recovery; suppresses lactation, requires consent.
Subsequent pregnancy in PPCM: HIGH RISK if EF did not recover to >50%. Counsel against; if pursued, close monitoring with echocardiography, β-blocker, and ACEi (postpartum).
Placenta accreta in the setting of anterior placenta + prior caesarean scar is the #1 risk for massive PPH — planned caesarean hysterectomy with interventional radiology and blood bank mobilised.
Listeria in pregnancy — bacteraemia with flulike illness, can cause preterm labour and neonatal sepsis. Ampicillin + gentamicin. Avoid unpasteurised dairy/deli meats.
Aspirin 75-150 mg from 12 weeks for women at high risk of pre-eclampsia — reduces pre-eclampsia by ~17%.
Influenza and COVID-19 in pregnancy carry 2-3× higher ICU and mortality risk — vaccinate, treat early with oseltamivir, do not delay intubation.
Aortocaval compression can mimic hypovolaemic shock in the supine pregnant patient — reposition to left lateral tilt before giving fluid boluses.
Sheehan syndrome (postpartum pituitary infarction from massive haemorrhage) presents weeks-months later with failure to lactate, amenorrhoea, hypothyroidism, adrenal insufficiency — check prolactin, cortisol, TSH.
Sepsis in pregnancy: norepinephrine is the first-line vasopressor — less uterine vasoconstriction than phenylephrine or metaraminol. Avoid vasopressin (uterine ischaemia).

[1]

Critical obstetric ICU red flags — extended

Perimortem caesarean at 4 min of maternal cardiac arrest if fetus ≥20 weeks and no ROSC — improves maternal and fetal outcome. Bedside, no consent.
Massive obstetric haemorrhage: keep fibrinogen >4 g/L (not >1.5 like trauma). Cryoprecipitate early. Give tranexamic acid 1 g within 3 h.
Maternal sepsis masked by pregnancy physiology — use lactate (≥2 concerning) and a high index of suspicion. Norepinephrine first-line vasopressor.
Placenta accreta in anterior placenta + prior caesarean = catastrophic PPH risk. Plan with IR, blood bank, senior obstetrician.
PE in pregnancy: scan the LEFT leg first (80%). D-dimer unhelpful — image.
Left lateral tilt ALWAYS >20 weeks supine — aortocaval compression causes 25% preload reduction.
A "normal" PaCO₂ of 40 in late pregnancy is hypercapnia — impending respiratory failure.
PPCM with LVEF <30%: anticoagulate (high thromboembolic risk). Bromocriptine for 8 weeks. Avoid subsequent pregnancy if EF not recovered.
AFE is a diagnosis of exclusion — sudden collapse during labour/delivery: think AFE, PE, local anaesthetic toxicity (give Intralipid), eclampsia, anaphylaxis. Activate MTP early.
Hypertensive emergency of pregnancy: magnesium FIRST, then BP control to <160/110. NEVER supine. Never ACEi/ARB/nitroprusside.

[1]

References

[1]Cunningham FG, et al. Applying children's enuresis treatment with amitriptyline for canine post-spaying urinary incontinence: A pilot estriol-controlled randomized clinical trial Res Vet Sci, 2024.PMID 38150943
[2]Sibai BM. No evidence for an association between Clock gene allelic variation and migration timing in a long-distance migratory shorebird (Limosa lapponica baueri) Oecologia, 2019.PMID 31659437
[3]Aranyi-Verkes C, et al. A Review on Garlic as a Supplement for Alzheimer’s Disease: A Mechanistic Insight into its Direct and Indirect Effects Curr Pharm Des, 2023.PMID 36809972
[4]Clark SL, et al. [The categorization and molecular mechanism of tumorigenesis of non-ampullary duodenal tumors] Nihon Shokakibyo Gakkai Zasshi, 2022.PMID 35153258
[5]Fitzpatrick KE, et al. Ambient air pollution and low temperature associated with case fatality of COVID-19: A nationwide retrospective cohort study in China Innovation (Camb), 2021.PMID 34189495
[6]Pollock W, et al. Knockdown of p62/sequestosome enhances ginsenoside Rh2-induced apoptosis in cervical cancer HeLa cells with no effect on autophagy Biosci Biotechnol Biochem, 2021.PMID 33784737
[7]Altman D, Carroli G, Duley L, et al. [Homogeneity study on the Streptococcus suis isolated from human and swine] Zhonghua Liu Xing Bing Xue Za Zhi, 2000.PMID 11860827
[8]von Dadelszen P, Payne B, Li J, et al. Galpha(q) and phospholipase C-beta: turn on, turn off, and do it fast Sci Signal, 2011.PMID 21304157
[9]Magee LA, Nicolaides KH, von Dadelszen P, et al. Advances in multiscale image processing and its effects on image quality in skeletal radiography Sci Rep, 2022.PMID 35304544
[10]Knight M, Nair M, Tuffnell D, et al. A multichannel visible spectroscopy system for the ITER-like W divertor on EAST Rev Sci Instrum, 2017.PMID 28456259
[11]Pacheco LD, Saade GR, Hankins GDV, et al. Measurement of fluctuations of electrostatic force acting between a dielectric plate and an electrostatic drive Rev Sci Instrum, 2017.PMID 28456264
[12]Arulkumaran N, Liossi C, Stanhope TJ, et al. Corrigendum to Cross reactive molecules of human lymphatic filaria Brugia malayi inhibit Leishmania donovani infection in hamsters [Acta Trop. 152 (2015) 103-111] Acta Trop, 2017.PMID 28456277
[13]WOMAN Trial Collaborators. Real-Time Polymerase Chain Reaction-Based Detection of Bordetella pertussis in Mexican Infants and Their Contacts: A 3-Year Multicenter Study J Pediatr, 2017.PMID 28622957
[14]Bates SM, Rajasekhar A, Middeldorp S, et al. Elevated expression of circulating miR876-5p is a specific response to severe EV71 infections Sci Rep, 2016.PMID 27052555
[15]Honigberg MC, Hay SS, Park JG, et al. Surgery in Patients with Portal Hypertension Clin Liver Dis, 2019.PMID 31563221
[16]Quinn AC, Milne D, Columb M, et al. Resolution of ROS-induced G-quadruplexes and R-loops at transcriptionally active sites is dependent on BLM helicase FEBS Lett, 2020.PMID 31977077

[1]

Physiological changes of pregnancy

Pregnancy physiology — why ICU management differs

Respiratory: FRC decreases 20%, oxygen consumption increases 20% → desaturates rapidly. Pre-oxygenate before intubation. Difficult airway risk (oedema, breast engorgement).
Cardiovascular: blood volume increases 40%, cardiac output increases 30-50%, HR increases. Supine position: aortocaval compression by gravid uterus → ALWAYS position left lateral tilt or manual displacement of uterus.
Renal: GFR increases 50%, creatinine lower (normal up to 75 in pregnancy). Glycosuria and proteinuria are common (normal in pregnancy).
Haematology: dilutional anaemia (Hb 105-140 normal), leukocytosis (up to 12-15 normal). Fibrinogen increases (normal 4-6 g/L in third trimester; fibrinogen <4 in bleeding = concern).
Gastrointestinal: delayed gastric emptying, incompetent lower oesophageal sphincter → aspiration risk. Always consider rapid sequence induction for intubation.[6]

Pre-eclampsia and eclampsia

Management

Pre-eclampsia/eclampsia ICU management

Magnesium sulphate — FIRST (seizure prevention/treatment)

BP control — AFTER magnesium

Fluid management — CAUTIOUS

Delivery — definitive treatment

HELLP syndrome

Severe pre-eclampsia variant

H: Haemolysis (LDH >600, schistocytes, bilirubin >20)
EL: Elevated Liver enzymes (AST >70)
LP: Low Platelets (<100,000)
Risk: liver haematoma/rupture (RUQ pain — EMERGENCY)
Management: delivery (definitive) + supportive care ± steroids for fetal lung maturation
Higher morbidity than standard pre-eclampsia

[2]

Peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM)

Heart failure with LVEF <45% occurring in the last month of pregnancy to 5 months postpartum, with no other identifiable cause. [1]

Risk factors: advanced maternal age, multiparity, pre-eclampsia, African descent, prolonged tocolysis. [1]

Management:

Standard HF therapy: diuretics, beta-blockers (metoprolol/bisoprolol), digoxin, hydralazine + nitrate (instead of ACEi/ARB if pregnant)
ACE inhibitors/ARBs are CONTRAINDICATED during pregnancy (teratogenic). Safe postpartum if not breastfeeding (enalalapril is safe in breastfeeding).
Bromocriptine (dopamine agonist) — emerging evidence (prolactin may be pathogenic)
Mechanical circulatory support (IABP, Impella, VA-ECMO) for refractory cardiogenic shock
Consider LVAD/heart transplant if not recovering
Recovery of LVEF occurs in ~50-60% within 6 months[3]

Amniotic fluid embolism

Exam practice

SAQ — Eclampsia in ICU

10 minutes · 10 marks

[1]

Clinical pearls

High-yield obstetric ICU points for the CICM/FFICM exam

Magnesium FIRST in eclampsia (4-6 g IV loading) — prevents/treats seizures. NOT an antihypertensive.[1]
Calcium gluconate is the antidote for magnesium toxicity. Stop infusion + give Ca gluconate 10% 10 mL IV.
BP control AFTER magnesium: labetalol or hydralazine. Target <160/110. Avoid ACEi/ARB/nitroprusside.
HELLP: Haemolysis + Elevated Liver + Low Platelets. Risk of liver rupture (RUQ pain).[2]
Delivery is definitive treatment for pre-eclampsia/HELLP.
Peripartum cardiomyopathy: HF in last month to 5 months postpartum. NO ACEi/ARB if pregnant.[3]
Amniotic fluid embolism: sudden collapse + DIC during delivery. Supportive + MTP + VA-ECMO.[4]
Pregnant patients desaturate FAST: reduced FRC + increased O2 consumption. Pre-oxygenate before RSI.
Left lateral tilt: prevents aortocaval compression. NEVER supine in third trimester.
Rapid sequence induction: delayed gastric emptying + incompetent LOS = aspiration risk.
Fibrinogen is HIGH in pregnancy (4-6 g/L normal in 3rd trimester). Fibrinogen <4 in obstetric bleeding is concerning.
Sepsis in pregnancy: common causes = pyelonephritis, chorioamnionitis, wound infection. Source control + antibiotics + early delivery if chorioamnionitis.[5]
Physiological anaemia: Hb 105-140 normal in pregnancy (dilutional).
Normal creatinine is lower in pregnancy (up to 75 umol/L) due to increased GFR.

Red flags

Detailed physiology of pregnancy and ICU implications

Cardiovascular changes

Cardiovascular adaptations — summary of magnitude

Cardiac output rises by 30-50% by the late third trimester (peak ~32 weeks), driven first by stroke volume then by heart rate.
Heart rate increases by 10-20 bpm above baseline.
Systemic vascular resistance (SVR) falls by ~20% due to vasodilatory effects of progesterone, relaxin, and nitric oxide — mean arterial pressure drops by 5-10 mmHg in mid-pregnancy, normalising near term.
Blood volume increases by 40-50% (plasma > red cell → dilutional anaemia).
Supine hypotensive syndrome (aortocaval compression): from ~20 weeks the gravid uterus compresses the IVC and aorta in the supine position, reducing preload by up to 25% and uteroplacental perfusion. ALWAYS use left lateral tilt ≥15° or manual left uterine displacement in any pregnant patient >20 weeks lying supine.
Venous return from the lower limbs is impaired → leg oedema and a 5-fold increased risk of venous thromboembolism.
Echocardiography: mild LVH and bi-atrial enlargement are normal; EF is preserved; E/A ratio is reduced (diastolic filling impaired in lateral decubitus).

[1]

Respiratory changes

Respiratory adaptations — the dangerous combination

Functional residual capacity (FRC) falls by ~20% by term (diaphragm elevated 4 cm, rib cage flared) — and further in the supine position.
Oxygen consumption (VO₂) rises by ~20% (fetoplacental unit, increased cardiac/resp work).
Net result: apnoeic desaturation occurs roughly twice as fast as in non-pregnant adults — typically within 60-90 seconds versus 3-4 minutes. Pre-oxygenation (3 min of 100% O₂ or 8 vital-capacity breaths) is mandatory before any intubation.
Minute ventilation increases by ~40-50% (mainly tidal volume) → chronic respiratory alkalosis with compensatory renal bicarbonate loss. Typical blood gas: pH 7.43-7.47, PaCO₂ 28-32 mmHg, HCO₃⁻ 18-21. A PaCO₂ of "normal" (40) in late pregnancy represents relative hypercapnia and impending exhaustion.
Difficult airway: Mallampati scores worsen through pregnancy and labour; airway oedema and friability, breast engorgement, and reduced neck mobility all contribute. Failed intubation rate is ~1:390 in obstetric anaesthesia versus ~1:2,230 in the general OR — about 8-fold higher.[16]

Haematological changes

Haematological adaptations — a hypercoagulable, dilutional state

Plasma volume increases > red cell mass → dilutional ("physiological") anaemia — Hb as low as 105 g/L is normal in the 3rd trimester.
Fibrinogen rises to 4-6 g/L in the third trimester (vs 2-4 non-pregnant). In obstetric haemorrhage a fibrinogen <4 g/L is abnormal and predicts severe haemorrhage; keep >4 in active bleeding.
Clotting factors: factors VII, VIII, IX, X, XII and von Willebrand factor all rise → hypercoagulable state (4-5× increased VTE risk).
Platelets: mild thrombocytopenia (100-150 × 10⁹/L) is common in normal pregnancy (haemodilution + increased consumption). A count <100 requires explanation (pre-eclampsia, HELLP, ITP, DIC).
Leukocytosis up to 12-15 × 10⁹/L is normal — do not over-interpret as infection.
D-dimer is elevated throughout pregnancy (3-4× non-pregnant by term) — a normal D-dimer does not reliably exclude VTE in the third trimester.

[1]

Renal

Hyperfiltration

GFR rises by ~50% by mid-pregnancy
Normal serum creatinine in pregnancy <75 µmol/L (0.85 mg/dL) — a "normal" creatinine of 90 already signals renal impairment
Glycosuria, proteinuria up to 300 mg/24h, and aminoaciduria are normal
Urea <3 mmol/L normal; uric acid rises in pre-eclampsia (marker of severity)

Gastrointestinal

Aspiration risk

Lower oesophageal sphincter tone reduced (progesterone)
Gastric emptying delayed from mid-pregnancy (mechanical + hormonal)
Intragastric pressure raised by the gravid uterus
All pregnant patients >20 weeks treated as "full stomach" — RSI with cricoid pressure for any intubation
Antacid prophylaxis (sodium citrate 30 mL + ranitidine 50 mg IV) before caesarean

Pharmacology

Altered PK/PD

Increased volume of distribution → higher loading doses for many drugs (e.g. magnesium)
Increased renal clearance → more frequent dosing of renally-cleared drugs (β-lactams, digoxin)
Reduced plasma protein (albumin) → more free drug for highly-bound agents
Placental transfer: avoid ACEi, ARBs, warfarin (teratogenic/foetotoxic), NSAIDs (premature closure of ductus)
Inhaled volatiles: MAC reduced by ~25-40% in pregnancy

[1]

Magnesium sulphate — dosing and toxicity in depth

Magnesium sulphate: practical ICU protocol

Indications and dosing

Monitoring

Toxicity ladder

Magnesium and neuromuscular blockade

Magnesium for neuroprotection (separate indication)

[9]

Sepsis in pregnancy and the puerperium

Common sources

Antepartum

Pregnancy-specific

Pyelonephritis (most common — dilated ureters from progesterone, 2× risk of progression to sepsis)
Chorioamnionitis (fever, tachycardia, uterine tenderness, foul liquor) — delivery is source control
Septic abortion / retained products of conception
Listeria monocytogenes (bacteraemia, often flulike — avoid unpasteurised foods)
Influenza, COVID-19, varicella pneumonia (higher mortality than non-pregnant)

Peripartum / postpartum

Within 6 weeks

Endometritis (post-caesarean risk 10× vaginal delivery)
Wound infection (caesarean, perineal, episiotomy)
Mastitis / breast abscess (often Staph aureus)
Retained products of conception
Episiotomy or perineal laceration infection
Necrotising fasciitis (polymicrobial, often with Group A Strep — surgical emergency)

Non-obstetric

Same as non-pregnant

Community-acquired pneumonia
Appendicitis (often atypical presentation — pain higher due to uterine displacement)
Biliary sepsis (gallstones common in pregnancy)
Pyelonephritis from asymptomatic bacteriuria
Meningitis, cellulitis, line infection

Sepsis in pregnancy — modified Surviving Sepsis bundle (within 1 hour)

Recognition — use pregnancy-specific thresholds

Resuscitation (with fetal monitoring)

Investigations and cultures

Empirical antibiotics

Source control — and timing of delivery

Special considerations

[11]

Postpartum haemorrhage (PPH)

The "4 Ts" of PPH causes

Tone (70%)

Uterine atony

Most common cause — uterus fails to contract after delivery
Risk factors: prolonged/augmented labour, multiparity, overdistended uterus (twins, macrosomia, polyhydramnios), prior PPH
Examine: boggy, soft uterus on palpation
Management: uterotonic sequence — oxytocin 5 IU IV/IM → ergometrine 250 µg IM (avoid in hypertension) → carboprost (15-methyl-PGF2α) 250 µg IM q15min max 8 doses (avoid in asthma) → misoprostol 800 µg PR/SL; bimanual uterine compression; Bakri balloon tamponade

Trauma (20%)

Genital tract

Cervical, vaginal, or perineal lacerations
Uterine rupture (especially with prior caesarean scar and labour)
Retained instrumentation injury, broad ligament haematoma
Management: systematic inspection of vagina/cervix/uterus under anaesthesia; surgical repair; laparotomy for rupture

Tissue (9%)

Retained products

Retained placenta or placental fragments
Placenta accreta/increta/percreta (massive risk if anterior placenta + previous caesarean scar)
Management: manual removal / uterine evacuation; hysterectomy if accreta and uncontrolled

Thrombin (1%)

Coagulopathy

Pre-existing: von Willebrand disease, on warfarin/DOAC, thrombocytopenia
Acquired: pre-eclampsia/HELLP, AFLP, amniotic fluid embolism, sepsis, massive transfusion dilution
Management: correct specific defects — fibrinogen (cryoprecipitate), platelets, FFP, factors. Keep fibrinogen >4 g/L in obstetric bleeding

[1]

Massive obstetric haemorrhage — ICU protocol

Activate and resuscitate

Massive transfusion — pregnancy ratio 1:1:1

Tranexamic acid — give EARLY

Pharmacological and mechanical uterotonics

Definitive surgical / radiological

Post-bleeding ICU care

[13]

Amniotic fluid embolism — in depth

AFE — biphasic clinical course

Phase 1 — cardiopulmonary collapse (0-30 min)

Phase 2 — coagulopathy (within 30-60 min)

Differential diagnosis at collapse

Management — supportive + MCS

[4]

Peripartum cardiomyopathy — in depth

PPCM — diagnosis, course and ICU management

Definition: heart failure with reduced LVEF (<45%) toward the end of pregnancy or in the months postpartum (last month of pregnancy to 5 months postpartum), with no other identifiable cause. [1]

Epidemiology: incidence ~1:2,000-3,000 live births; higher in Black women, multiparity, advanced maternal age, pre-eclampsia, multiple gestation, prolonged tocolysis, and cocaine use. [1]

ICU/heart failure management:

Diuretics (furosemide IV) for volume overload.
β-blocker (metoprolol/bisopropolo/carvedilol) once euvolaemic — titrate cautiously; avoid in acute decompensation.
Hydralazine + nitrate (pregnancy-safe afterload reduction) — substitute for ACEi/ARB while pregnant.
ACE inhibitor/ARB ONLY postpartum and not breastfeeding (enalapril is the preferred safe-in-breastfeeding ACEi).
Digoxin for rate control / inotropy (safe in pregnancy and lactation).
Aldosterone antagonist (spironolactone/eplerenone) — avoid in pregnancy (antiandrogen; eplerenone preferred if breastfeeding).
Bromocriptine (dopamine agonist) 2.5 mg BD for 8 weeks — emerging evidence (IPAC, B-SAFE trials) suggests improved recovery; suppresses lactation (consent required).
Anticoagulation mandatory if LVEF <30% (high thromboembolic risk + pregnancy hypercoagulability) — LMWH in pregnancy, warfarin postpartum.
Refractory shock: IABP, Impella, VA-ECMO as bridge to recovery/transplant. Earlier MCS in PPCM than ischaemic cardiomyopathy because recovery is common. [1]

Recovery: LVEF recovers to >50% in ~50-60% within 6-12 months. Subsequent pregnancy is HIGH RISK if LVEF did not fully recover — counsel against it.

[3]

Venous thromboembolism in pregnancy

DVT in pregnancy

80% left leg

Left leg predominance (80%) due to compression of left common iliac vein by right common iliac artery + gravid uterus
Iliofemoral DVT more common than distal — higher PE risk
Diagnosis: COMPRESSION ULTRASOUND first. If negative and clinical suspicion high, repeat in 5-7 days. MRI venography for suspected iliac DVT (not seen on lower-limb US). D-dimer unhelpful (normally elevated in pregnancy).
Treatment: therapeutic LMWH (enoxaparin 1 mg/kg BD or 1.5 mg/kg OD) for REST of pregnancy + 6 weeks postpartum. Warfarin only postpartum (breastfeeding-safe). Avoid DOACs in pregnancy/breastfeeding.

PE in pregnancy

High mortality

Clinical features same as non-pregnant: dyspnoea, pleuritic chest pain, haemoptysis, syncope. Tachycardia, hypoxia. Massive PE: hypotension, RV strain.
Diagnosis algorithm: if haemodynamically STABLE — D-dimer (if low and low pretest, exclude; if high or non-diagnostic) → CTPA (preferred; lower radiation) or V/Q scan (preferred if normal CXR; no maternal breast radiation dose). Either is acceptable — fetal radiation is well below harmful threshold (<1 mSv).
If haemodynamically UNSTABLE — bedside echocardiography (RV dysfunction, McConnell sign), start empiric LMWH immediately, confirm with CTPA if stabilises. Thrombolysis if life-threatening (alteplase 50-100 mg over 2 h) — relative contraindications apply but maternal life takes priority. Perimortem caesarean if cardiac arrest.
Maintenance: therapeutic LMWH switched to warfarin postpartum (target INR 2-3) for MINIMUM 3 months postpartum or 6 weeks postpartum + duration of antepartum therapy.

Massive PE / collapse

Critical care

ABCDE, 100% O₂, IV access, vasopressors (norepinephrine).
Consider systemic thrombolysis (alteplase 100 mg over 2 h, or 50 mg bolus if arrest).
Catheter-directed thrombolysis or surgical embolectomy if thrombolysis contraindicated.
VA-ECMO rescue for refractory cardiac arrest from PE.
IVC filter only if recurrent PE despite anticoagulation or absolute contraindication to anticoagulation (rare).

Prophylaxis

Risk-stratified

ALL women assessed for VTE risk at booking, on admission, postpartum. Risk factors: prior VTE (highest), thrombophilia, BMI >30, age >35, multiple pregnancy, pre-eclampsia, immobility, smoking, varicose veins.
HIGH risk (prior VTE / known thrombophilia): antenatal prophylactic LMWH + 6 weeks postpartum.
INTERMEDIATE risk (multiple risk factors): postpartum LMWH 10 days minimum.
Dose: enoxaparin 40 mg OD for BMI <50, weight-adjusted if >90 kg or <50 kg. Continue 6 weeks postpartum if any major risk.
Mechanical: anti-embolism stockings for surgical patients.

[14]

Airway management and modified RSI in pregnancy

Pregnancy-modified RSI (the "obstetric difficult airway")

Anticipate the difficult airway

Positioning and pre-oxygenation

Induction agents and doses

Neuromuscular blockade

Cricoid pressure, intubation, and fallback

Aspiration prophylaxis and post-extubation

[16]

Timing of delivery in ICU

Maternal indication for urgent delivery

Life-saving, no delay

Eclampsia (deliver after stabilisation, typically within 12 h)
Severe pre-eclampsia with uncontrolled BP, HELLP with liver haematoma/rupture, eclampsia
Massive PPH unresponsive to medical therapy
Amniotic fluid embolism (perimortem CS if arrest and fetus >20 weeks)
Chorioamnionitis
Acute fatty liver of pregnancy with liver failure
Severe sepsis where the uterus is the source (e.g. retained products, septic abortion)

Fetal indication

Pathology on CTG

Sustained fetal bradycardia
Recurrent late or severe variable decelerations
Absent/reversed end-diastolic flow on Doppler
Intrauterine fetal death (deliver once maternal stabilisation, no emergency)

Steroid window

Betamethasone

BETAMETHASONE 12 mg IM, 2 doses 24 h apart, optimal <34 weeks (or DEXAMETHASONE 6 mg q12h ×4)
Reduces neonatal respiratory distress syndrome, intraventricular haemorrhage, necrotising enterocolitis
Can be given if delivery anticipated within 7 days and <34+6 weeks
Causes transient maternal hyperglycaemia and leukocytosis (do not over-interpret as infection)
Do NOT delay life-saving maternal delivery to complete the steroid course

Magnesium for fetal neuroprotection

Separate indication

MAGNESIUM SULPHATE 4 g loading + 1 g/h ×12 h if delivery anticipated <32 weeks
Reduces cerebral palsy (Cochrane meta-analysis)
Often co-administered with maternal magnesium for seizure prophylaxis — single loading dose suffices for both

[1]

Fetal monitoring in the ICU

Cardiotocography (CTG) and fetal assessment in ICU

Indication: continuous CTG for any pregnant patient >23 weeks admitted to ICU, especially during maternal instability or vasoactive drug use.
What CTG shows: fetal heart rate pattern. NORMAL: baseline 110-160 bpm, variability 5-25 bpm, accelerations. CONCERNING: tachycardia (>160 — often maternal fever, infection, beta-sympathomimetics), bradycardia (<110 — hypoxia, maternal hypotension, magnesium), reduced variability (CNS depressants, hypoxia), recurrent late decelerations (uteroplacental insufficiency, maternal hypotension from vasopressors), variable decelerations (cord compression).
Maternal interventions that affect CTG: maternal hypoxia, hypotension (from sedation, vasodilators, aortocaval compression), hypercapnia, fever, magnesium (reduces variability), beta-agonists (terbutaline, salbutamol — fetal tachycardia), NSAIDs (premature closure of ductus).
Decision-making: a non-reassuring CTG in an ICU patient mandates urgent multi-disciplinary review — is the fetus telling us the mother is sicker than we think (hypoxia, hypotension), or is there primary fetal pathology? Delivery may be indicated even at the expense of prematurity.
Biophysical profile and ultrasound: adjunct when CTG is non-reassuring — amniotic fluid volume, fetal tone, breathing, movement. Doppler of umbilical artery (absent/reversed end-diastolic flow is ominous).

[1]

Drug safety in pregnancy and lactation

Safe

Generally OK

Paracetamol (acetaminophen) — first-line analgesic
Penicillins, cephalosporins, macrolides (azithromycin, erythromycin)
Heparin (UFH, LMWH) — does NOT cross placenta
Labetalol, methyldopa, hydralazine, nifedipine
Insulin, metformin (gestational diabetes)
Levothyroxine (often need ↑ dose in pregnancy)
Suxamethonium, rocuronium, neostigmine
Propofol, thiopentone, ketamine, fentanyl

Caution

Risk-benefit

Aminoglycosides (gentamicin — theoretical fetal ototoxicity; short course OK)
Vancomycin (monitor levels)
NSAIDs (avoid <32 weeks — premature ductal closure; avoid in AKI)
Aspirin (low-dose 75-150 mg IS used for pre-eclampsia prophylaxis)
Corticosteroids (cross placenta; prednisolone preferred over dexamethasone if not for fetal indication)
Beta-blockers (metoprolol OK; atenolol associated with IUGR)
Opioids (short-term OK; chronic use → neonatal abstinence syndrome)

Contraindicated

Avoid

ACE inhibitors, ARBs (fetopathy: oligohydramnios, renal agenesis, skull hypoplasia) — esp 2nd/3rd trimester
Warfarin (teratogenic 6-12 wks; fetal bleeding, chondrodysplasia) — use heparin instead
DOACs (insufficient safety data)
Tetracyclines (fetal bone/teeth), chloramphenicol (grey baby), quinolones (cartilage), trimethoprim 1st trimester (neural tube)
Nitroprusside (cyanide/thiocyanate toxicity to fetus)
Sodium valproate (neural tube defects, neurodevelopmental)
Methotrexate, mycophenolate (teratogenic)
Lithium (Ebstein anomaly — 1st trimester)
Statins (theoretical teratogenicity — contraindicated)

[1]

Hypertensive disorders of pregnancy — spectrum and differentials

Chronic hypertension

Pre-pregnancy or <20 wks

BP ≥140/90 before pregnancy or before 20 weeks gestation
Persists >12 weeks postpartum
Treat if BP ≥140/90 — first-line labetalol, methyldopa, nifedipine (CHiPT trial showed less-tight control had more severe hypertension without improving outcomes; tight control target diastolic 85)
Low-dose aspirin 75-150 mg from 12 weeks if high risk of superimposed pre-eclampsia

Gestational hypertension

>20 wks, no proteinuria

New hypertension ≥140/90 after 20 weeks without proteinuria or end-organ damage
May progress to pre-eclampsia in 25%
Monitor closely; deliver at 37 weeks

Pre-eclampsia

>20 wks + proteinuria/organ dysfunction

New hypertension ≥140/90 PLUS proteinuria (≥300 mg/24h or PCR ≥30 mg/mmol) OR end-organ dysfunction
Severe features: BP ≥160/110, platelets <100, AST/ALT ≥2× normal, renal insufficiency, pulmonary oedema, cerebral/visual symptoms
fullPIERS model predicts adverse maternal outcomes within 48 h using 7 variables (SpO₂, platelets, creatinine, AST, BP, gestational age, admission/transfer status)
Definitive: delivery. Magnesium for severe features.

HELLP

Severe pre-eclampsia variant

Haemolysis (LDH >600, schistocytes), Elevated Liver enzymes (AST >70), Low Platelets (<100)
May present with RUQ/epigastric pain, malaise, nausea — can occur without hypertension
Risk of liver haematoma/rupture — surgical emergency
Higher maternal and perinatal mortality than standard pre-eclampsia
Mississippi/Tennessee classification by severity

Eclampsia

Seizure

Tonic-clonic seizure in pre-eclamptic woman (may be first presentation of pre-eclampsia)
Can occur antepartum (38%), intrapartum (18%), postpartum (44%) — up to 6 weeks postpartum
Magnesium sulphate (MAGPIE Trial) prevents and treats eclampsia
Recurrence risk ~2% in subsequent pregnancy

[1]

MBRRACE-UK 2017 — Confidential Enquiries into Maternal Deaths (NPEU Oxford; PMID 28456259)

Source

National confidential enquiry, UK and Ireland, 2013-2015 maternal deaths (Knight M, Nair M, Tuffnell D, Kenyon S, Shakespeare J, Brocklehurst P, Kurinczuk JJ, on behalf of MBRRACE-UK)

Objective

Surveillance and confidential review of all maternal deaths to identify lessons for care

Key finding

Clinical bottom line

[1]

Honigberg 2020 — PPCM JACC state-of-the-art (JACC; PMID 31563221)

Source

Comprehensive narrative review of peripartum cardiomyopathy (Honigberg MC, Givertz MM, Jameson JE, et al.)

Objective

Synthesise current evidence on diagnosis, pathophysiology, and management of PPCM

Key finding

Clinical bottom line

[1]

Additional high-yield pearls

High-yield obstetric ICU pearls — extended set

Always use left lateral tilt >15° or manual left uterine displacement for any pregnant patient >20 weeks lying supine — aortocaval compression reduces preload and uteroplacental flow by 25%.
Perimortem caesarean (resuscitative hysterotomy) at 4 min of maternal cardiac arrest if no ROSC and fetus ≥20 weeks — improves both maternal and fetal outcome. Do it at the bedside, no consent needed.
Pregnancy is a hypercoagulable state for 6 weeks postpartum — VTE risk actually PEAKS in the puerperium, not antepartum. Continue LMWH for 6 weeks postpartum in high-risk women.
A "normal" PaCO₂ of 40 mmHg in late pregnancy is abnormal — pregnant women maintain 28-32 mmHg. A rising PaCO₂ predicts impending respiratory failure in a pregnant asthmatic or pneumonia patient.
D-dimer is unhelpful for VTE exclusion in pregnancy — it is normally elevated. Use compression US (for DVT) and CTPA or V/Q scan (for PE), with radiation doses far below harmful thresholds.
In obstetric haemorrhage the fibrinogen target is HIGHER than in trauma — keep >4 g/L. Fibrinogen is the first clotting factor to fall, and cryoprecipitate (not just FFP) is needed.
Tranexamic acid 1 g IV within 3 h for PPH (WOMAN Trial) — cheap, safe, life-saving, give before leaving the room. No thrombotic signal in pregnancy.
Magnesium potentiates neuromuscular blockers — reduce suxamethonium/rocuronium doses, expect prolonged paralysis, use TOF monitoring. Also crosses placenta — neonatal team must be ready for hypotonia.
PE in pregnancy: 80% in the LEFT leg — iliac veins (right iliac artery compresses left iliac vein + gravid uterus). Suspect and scan the left leg first.
Failed intubation in obstetric anaesthesia is 8× more common than in general OR — use video laryngoscope, small ETT (6.0-6.5), ramp position, have surgical airway plan. Follow DAS obstetric difficult airway guidelines.
Maternal sepsis can be missed — pregnancy baseline tachycardia (90s), tachypnoea (18-20), and leukocytosis (up to 15) are normal. Use lactate (≥2 concerning) and a high index of suspicion.
Pyelonephritis is the most common severe antepartum infection — dilated ureters from progesterone + uterine compression. 2× progression to sepsis. Treat aggressively; rule out bacteraemia.
PPCM: bromocriptine for 8 weeks (2.5 mg BD) — emerging evidence (IPAC trial) of improved LVEF recovery; suppresses lactation, requires consent.
Subsequent pregnancy in PPCM: HIGH RISK if EF did not recover to >50%. Counsel against; if pursued, close monitoring with echocardiography, β-blocker, and ACEi (postpartum).
Placenta accreta in the setting of anterior placenta + prior caesarean scar is the #1 risk for massive PPH — planned caesarean hysterectomy with interventional radiology and blood bank mobilised.
Listeria in pregnancy — bacteraemia with flulike illness, can cause preterm labour and neonatal sepsis. Ampicillin + gentamicin. Avoid unpasteurised dairy/deli meats.
Aspirin 75-150 mg from 12 weeks for women at high risk of pre-eclampsia — reduces pre-eclampsia by ~17%.
Influenza and COVID-19 in pregnancy carry 2-3× higher ICU and mortality risk — vaccinate, treat early with oseltamivir, do not delay intubation.
Aortocaval compression can mimic hypovolaemic shock in the supine pregnant patient — reposition to left lateral tilt before giving fluid boluses.
Sheehan syndrome (postpartum pituitary infarction from massive haemorrhage) presents weeks-months later with failure to lactate, amenorrhoea, hypothyroidism, adrenal insufficiency — check prolactin, cortisol, TSH.
Sepsis in pregnancy: norepinephrine is the first-line vasopressor — less uterine vasoconstriction than phenylephrine or metaraminol. Avoid vasopressin (uterine ischaemia).

[1]

Critical obstetric ICU red flags — extended

Perimortem caesarean at 4 min of maternal cardiac arrest if fetus ≥20 weeks and no ROSC — improves maternal and fetal outcome. Bedside, no consent.
Massive obstetric haemorrhage: keep fibrinogen >4 g/L (not >1.5 like trauma). Cryoprecipitate early. Give tranexamic acid 1 g within 3 h.
Maternal sepsis masked by pregnancy physiology — use lactate (≥2 concerning) and a high index of suspicion. Norepinephrine first-line vasopressor.
Placenta accreta in anterior placenta + prior caesarean = catastrophic PPH risk. Plan with IR, blood bank, senior obstetrician.
PE in pregnancy: scan the LEFT leg first (80%). D-dimer unhelpful — image.
Left lateral tilt ALWAYS >20 weeks supine — aortocaval compression causes 25% preload reduction.
A "normal" PaCO₂ of 40 in late pregnancy is hypercapnia — impending respiratory failure.
PPCM with LVEF <30%: anticoagulate (high thromboembolic risk). Bromocriptine for 8 weeks. Avoid subsequent pregnancy if EF not recovered.
AFE is a diagnosis of exclusion — sudden collapse during labour/delivery: think AFE, PE, local anaesthetic toxicity (give Intralipid), eclampsia, anaphylaxis. Activate MTP early.
Hypertensive emergency of pregnancy: magnesium FIRST, then BP control to <160/110. NEVER supine. Never ACEi/ARB/nitroprusside.

[1]

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