Critical illness in pregnancy: ICU management and obstetric emergencies

[1] [1] [1]

Exam practice — SAQs

[1] [1]

Clinical pearls

Red flags

Prognosis

[1]

Pathophysiology — physiological adaptations of pregnancy (deep dive)

Pregnancy induces a coordinated, hormonally driven re-engineering of every major organ system so that the maternal body can sustain a second, growing organism. The intensivist must know these adaptations in detail because every "normal" value on a blood test, blood gas or monitor changes — and because they are the substrate on which critical illness is superimposed.[6][9]

The hallmark is a hyperdynamic, low-resistance, hypercoagulable, hypoalbuminaemic, low-FRC circulation. The placenta is a low-resistance arteriovenous shunt, accounting for much of the fall in systemic vascular resistance (SVR) and the rise in cardiac output. Progesterone-mediated smooth-muscle relaxation produces generalised vasodilation, decreased lower oesophageal sphincter tone and reduced gut motility. Oestrogen drives water retention, mucosal oedema and a rise in clotting factors. The combined effect is that the pregnant patient has less physiological reserve at baseline — she desaturates faster, hides blood loss better, thromboses more readily, and tolerates hypotension poorly. [1]

[1]

Cardiovascular adaptation — the hyperdynamic circulation

Cardiac output rises by 30-50% above baseline by the late second trimester and is sustained through term. The rise comes initially from a stroke-volume increase (due to a ~40% rise in plasma volume) and later from a 15-20 bpm rise in heart rate. Simultaneously, SVR falls ~20% under the combined effect of progesterone-mediated vasodilation, the low-resistance uteroplacental shunt, and the fall in visceral vascular tone. The net blood pressure in mid-pregnancy is therefore 10-15 mmHg lower than pre-pregnancy, with a nadir at 16-24 weeks; "normal" pregnancy blood pressure is approximately 100/60. A "normal" community blood pressure of 120/80 in a pregnant woman may already represent gestational hypertension.[6]

Two structural features drive ICU practice. First, the gravid uterus compresses the inferior vena cava and aorta in the supine position from approximately 20 weeks' gestation (uterus at umbilical level), reducing venous return by up to 30% and arterial flow to the uterus and lower limbs — the basis of the mandatory left lateral tilt. Second, an auto-transfusion of 300-500 mL of blood into the maternal circulation occurs at delivery, briefly raising preload and cardiac output — important in PPCM, where this transient load can precipitate pulmonary oedema. [1]

A benign flow murmur is common (hyperdynamic circulation); pathological murmurs (diastolic, loud systolic, radiation) warrant echocardiography. A normal ECG may show slight left-axis deviation and small Q/T-wave changes in lead III — do not over-interpret. [1]

Respiratory adaptation — the precarious airway and oxygen reserve

Respiratory adaptation is the most dangerous system for the intensivist because it produces rapid desaturation on apnoea — the single most important cause of complications at intubation in pregnancy.[7][9]

• Minute ventilation rises 30-50% (mainly via tidal volume), driven by progesterone-mediated sensitivity of the respiratory centre to CO2. PaCO2 falls to 30-32 mmHg — a "normal" PaCO2 of 40 in a pregnant woman is already hypercapnic, and a respiratory acidosis is ominous.
• Functional residual capacity (FRC) falls 20% in the erect position and up to 30% supine in the third trimester (diaphragmatic elevation by the gravid uterus + reduced chest wall compliance).
• Oxygen consumption rises 20-30% (fetoplacental unit, increased cardiac and respiratory work, breast tissue). [1]

The combined effect of low FRC and high oxygen consumption is a marked reduction in the apnoeic reserve: a healthy non-pregnant adult tolerates ~8-9 minutes of apnoea before desaturation; a third-trimester woman desaturates within 2-3 minutes, faster if obese or septic. This is the rationale for the modified RSI, including prolonged pre-oxygenation and the use of apnoeic oxygenation (nasal catheter at 5-15 L/min). [1]

Airway anatomy also changes: mucosal oedema and friability (oestrogen and increased blood volume), breast engorgement interfering with laryngoscopy, and a shortened thyromental distance. Failed intubation is 8 times more common in the obstetric population than in the general surgical population (McDonnell ANZCA study, ~1 in 274 vs 1 in 2230).[7]

Renal and gastrointestinal adaptation

Glomerular filtration rate (GFR) rises by ~50% above baseline by the early second trimester, sustained through term. The serum creatinine falls to approximately 50-60 µmol/L and urea to ~3 mmol/L. A "normal" creatinine of 90 µmol/L in a pregnant woman represents significant renal impairment (approximately 50% loss of function) and is one of the criteria for severe pre-eclampsia. Renal glycosuria and aminoaciduria are physiological, not signs of tubular injury. The upper ureters dilate (smooth-muscle relaxation + compression), predisposing to pyelonephritis — the commonest cause of maternal sepsis. [1]

Gastrointestinal adaptation centres on the progesterone-mediated reduction in lower oesophageal sphincter tone and delayed gastric emptying from mid-pregnancy, both of which combine to make the pregnant patient high-risk for aspiration (Mendelson's syndrome — chemical pneumonitis from acidic gastric contents). This is the rationale for rapid sequence induction with cricoid pressure for any obstetric intubation, despite recent debate about the efficacy of cricoid pressure itself. The stomach is also pushed cephalad by the gravid uterus, increasing intragastric pressure. [1]

Haematological adaptation — dilutional anaemia and the hypercoagulable state

Plasma volume expands ~40-50% while red cell mass expands only ~20-30%, producing a dilutional ("physiological") anaemia — Hb of 105-120 g/L is normal at term. Albumin falls proportionally to ~25-30 g/L, with consequences for drug protein binding, colloid oncotic pressure (predisposition to pulmonary oedema) and the interpretation of "calcium-corrected" tests. [1]

The hypercoagulable state is profound and is the dominant reason pregnancy is a major risk factor for venous thromboembolism (4-5x baseline, peaking postpartum). Fibrinogen rises to 4-6 g/L (a "normal" fibrinogen of 2.5 g/L in late pregnancy is abnormally low and signals DIC), factors VII, VIII, IX, X and XII rise, protein S falls, and acquired activated protein C resistance develops. Platelet count falls mildly (~10%) but generally remains above 100 × 10⁹/L; gestational thrombocytopenia is benign. The clinical correlate: a low fibrinogen in late pregnancy is always pathological and is a key marker of AFE, placental abruption and severe pre-eclampsia/HELLP with DIC. [1]

[1]

ICU admission causes in the obstetric population

The indications for ICU admission cluster into obstetric (direct causes — pre-eclampsia/eclampsia, obstetric haemorrhage, AFE, puerperal sepsis) and non-obstetric (indirect causes — pneumonia, asthma, valvular or ischaemic heart disease, DKA, trauma, drug overdose). Globally, hypertensive disorders of pregnancy and obstetric haemorrhage together account for the majority of obstetric ICU admissions, while indirect (medical) causes increasingly dominate in high-income settings where cardiovascular disease is the leading cause of maternal death.[1][15]

[1]

Globally, the WHO systematic analysis (Say 2014) attributes the majority of maternal deaths to: haemorrhage (27%), sepsis (11%), hypertensive disorders (14%), unsafe abortion (8%), and indirect/medical causes (28%) — with cardiovascular disease increasingly dominant in high-income settings. The intensivist's job is not to deliver the baby (the obstetrician's) but to manage the maternal physiological derangement while the obstetric team plans delivery.[15]

Maternal sepsis — recognition and management

Sepsis is the third leading direct cause of maternal death and is rising. The Sepsis-3 framework applies — sepsis is life-threatening organ dysfunction caused by a dysregulated host response, and septic shock is sepsis with circulatory and cellular/metabolic abnormalities sufficient to substantially increase mortality — but the physiological changes of pregnancy confound the scoring.[12]

The qSOFA score performs poorly in pregnancy because tachypnoea, tachycardia and a confusional state may all be physiological in late pregnancy. A new, persistent fever, an unexplained tachycardia out of proportion to the expected pregnancy rise, a rising lactate, a new oxygen requirement, or a falling platelet count should trigger a maternal sepsis bundle rather than a wait-and-see approach. [1]

Pregnancy-specific sources of sepsis.

• Pyelonephritis — the single most common cause of maternal sepsis; physiological hydronephrosis and glycosuria predispose. Cover with a third-generation cephalosporin or piperacillin-tazobactam.
• Chorioamnionitis (intra-amniotic infection) — fever, maternal and fetal tachycardia, uterine tenderness, foul liquor; treat with ampicillin + gentamicin (or cephalosporin) and deliver.
• Puerperal sepsis (endometritis, wound infection, mastitis, episiotomy infection) — typically post-Caesarean; cover Group A and B streptococcus, anaerobes, gram-negatives; high index for Group A streptococcal (GAS) toxic shock (rapid onset, soft-tissue involvement, multi-organ failure).
• Septic abortion — historically important, still relevant where access to safe termination is limited; cover broadly and evacuate the uterus.
• Pneumonia (including influenza, COVID-19, varicella) — pregnant women are disproportionately affected by viral pneumonitides due to the immunomodulation and reduced FRC; influenza and COVID-19 vaccination are recommended.
• Appendicitis, cholecystitis, bowel obstruction — atypical presentations due to displacement of organs by the gravid uterus. [1]

[1]

Severe pre-eclampsia, eclampsia and HELLP — ICU management summary

(See dedicated topic for detail.) The intensivist's role in hypertensive disorders of pregnancy is: (1) prevent seizure with magnesium sulfate for any severe pre-eclampsia or eclampsia; (2) control severe hypertension (SBP ≥ 160 or DBP ≥ 110) within 30-60 minutes to prevent intracerebral haemorrhage, using IV labetalol or hydralazine, target 140-160/90-105; (3) avoid fluid overload — these patients are oedematous but intravascularly contracted with a leaky endothelium, and pulmonary oedema is the commonest reason for ICU admission; (4) monitor for and treat the catastrophic complications — eclampsia, hepatic rupture (HELLP), DIC, AKI, PRES, pulmonary oedema; (5) plan delivery as the definitive treatment once maternal stabilisation is achieved.[2][5][16]

Obstetric haemorrhage and postpartum haemorrhage (PPH)

Postpartum haemorrhage (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 is loss ≥ 1500 mL (or half the circulating volume) — the threshold for activating a massive transfusion protocol. The pregnant patient tolerates acute blood loss deceptively well (50% plasma volume expansion, tachycardia at baseline) — a systolic BP < 90 in a young pregnant woman is a pre-arrest sign, not an early warning. [1]

The causes are remembered by the "4 Ts": Tone (uterine atony — 70% of cases), Trauma (cervical/vaginal tears, uterine rupture), Tissue (retained placenta, placenta accreta/increta/percreta), and Thrombin (coagulopathy — pre-existing, dilutional, or DIC from abruption/sepsis/AFE). [1]

Amniotic fluid embolism (AFE) — clinical features and management

Amniotic fluid embolism is a rare, catastrophic, unpreventable peripartum syndrome classically presenting with the abrupt onset of hypoxia, hypotension and coagulopathy during labour, delivery, Caesarean section, or within 30 minutes of delivery. UKOSS data report an incidence of approximately 1.7 per 100 000 maternities with a contemporary case-fatality of ~13-20% (much better than older estimates of 60-80%, reflecting earlier recognition and better supportive care).[3]

The pathophysiology is a complement-mediated anaphylactoid response to amniotic fluid entering the maternal circulation during labour — the term "anaphylactoid syndrome of pregnancy" is more accurate. The clinical course is classically biphasic: [1]

• Phase 1 (acute, 0-30 min): Pulmonary vasoconstriction with acute right heart failure, hypoxaemia, hypotension, and often a seizure. The right heart may acutely dilate and fail (visible on POCUS as RV dilation, TR, paradoxical septal motion). Up to a third of women die in this phase.
• Phase 2 (after stabilisation): Left ventricular failure and coagulopathy dominate. Disseminated intravascular coagulation develops in up to 80%, with profuse bleeding from puncture sites, the uterus and surgical wounds. Fibrinogen falls dramatically (recall that pregnancy baseline is 4-6 g/L, so a "normal" value is already abnormal in late pregnancy). [1]

Management is supportive — there is no specific therapy. The cornerstones are: (1) immediate resuscitation with high-flow oxygen, intubation if hypoxic, and vasopressors/inotropes (noradrenaline ± dobutamine or milrinone for LV failure); (2) massive transfusion protocol for the coagulopathy, with aggressive fibrinogen replacement (cryoprecipitate aiming for > 2 g/L), FFP, platelets and red cells; (3) delivery of the fetus if AFE occurs before delivery (often dictated by maternal resuscitation needs, performed at the bedside in extremis); (4) consider VA-ECMO for refractory LV/right heart failure, which has been used successfully in case series.[3]

[1]

Peripartum cardiomyopathy (PPCM)

Peripartum cardiomyopathy is heart failure with reduced ejection fraction (LVEF ≤ 45%) presenting in the last month of pregnancy or within 5 months postpartum, in a woman with no prior heart disease and no other identifiable cause. The incidence is approximately 1 in 1000-4000 live births; risk factors include multiparity, advanced maternal age, pre-eclampsia, African descent, smoking, obesity, and long-term tocolysis.[4][11]

The pathophysiology is a peripartum oxidative stress → cleavage of prolactin into a 16-kDa anti-angiogenic fragment that drives cardiomyocyte apoptosis and endothelial dysfunction. This is the rationale for bromocriptine (a dopamine agonist that suppresses prolactin), which appears to improve LVEF recovery when given early in PPCM.[11]

Management combines standard heart-failure therapy modified for pregnancy: diuretics (furosemide) for congestion, beta-blockers (bisoprolol, metoprolol), hydralazine + nitrates in pregnancy (substitutes for ACEi/ARB, which are contraindicated in pregnancy), then ACEi/ARB + mineralocorticoid receptor antagonist added after delivery, and bromocriptine 2.5 mg BD for 8 weeks (REBICPA showed improved LVEF recovery). Anticoagulation for severe LV dysfunction (LVEF < 30%) due to high thromboembolic risk. Mechanical circulatory support (IABP, Impella, VA-ECMO) as a bridge to recovery or transplant for refractory cardiogenic shock. Breastfeeding is generally discouraged during bromocriptine therapy.[4][11]

Prognosis. Approximately 50% of women recover LVEF to normal within 6-12 months (better than non-ischaemic cardiomyopathy in older patients); 10-15% have persistent severe LV dysfunction; mortality is 5-10% in modern series; ~10% require transplant or LVAD. A subsequent pregnancy in women with persistently reduced LVEF carries a major risk of relapse and death — contraindicated if LVEF < 30% or any persistent dysfunction. [1]

Venous thromboembolism in pregnancy

VTE is the leading direct cause of maternal death in high-income settings (UK and ANZ confidential enquiries); pregnancy confers a 4-5 fold increased risk, peaking in the postpartum period. Risk factors include Caesarean delivery (especially emergency), immobility, obesity, age > 35, pre-eclampsia, previous VTE, thrombophilia, multiparity, dehydration and sepsis. The 9th ACCP guideline provides the framework for risk-stratified prophylaxis and treatment.[13][14]

Diagnosis is challenging. D-dimer is physiologically elevated in pregnancy and not useful. Compression duplex ultrasound of the legs is first-line for suspected DVT; CT pulmonary angiography is the preferred imaging for suspected PE (lower radiation dose than V/Q scan and readily available; the radiation dose to the fetus is well below safety limits). The ECG may show S1Q3T3, RBBB, or T-wave inversion in V1-V4. POCUS may show RV strain. Avoid withholding anticoagulation while awaiting imaging in a haemodynamically unstable patient with a high-suspicion PE — start empirical LMWH. [1]

Treatment is with therapeutic-dose LMWH (e.g. enoxaparin 1 mg/kg BD or 1.5 mg/kg daily) — dose-adjusted with anti-Xa monitoring (target 0.5-1.0 U/mL 4 h post-dose), because the increased GFR and volume of distribution in pregnancy reduce the effective level. LMWH does not cross the placenta (unlike warfarin). Warfarin is teratogenic in the first trimester (fetal warfarin syndrome — nasal hypoplasia, epiphyseal stippling, CNS abnormalities) and causes fetal intracranial haemorrhage in the second and third trimester; it is contraindicated in pregnancy but safe in breastfeeding. Treatment is continued throughout pregnancy and for at least 6 weeks postpartum (minimum total duration 3 months). Mechanical prophylaxis (graduated compression stockings) for all hospitalised pregnant and postpartum women.[14]

Massive PE with haemodynamic compromise is treated with systemic thrombolysis (alteplase 100 mg over 2 h, or 50 mg bolus in cardiac arrest) — the fetal risk of thrombolysis is mainly placental/umbilical bleeding but maternal life takes priority. Catheter-directed thrombolysis or surgical embolectomy are alternatives if thrombolysis is contraindicated. [1]

Maternal cardiac arrest and perimortem Caesarean delivery (PMCD)

Maternal cardiac arrest is rare (1 in 12 000-30 000) but the management is modified standard ACLS with one critical obstetric intervention: perimortem Caesarean delivery (PMCD).[8][1]

The rationale for PMCD is twofold: (1) it may save the fetus if performed early (within 5 minutes of arrest); and (2) it is primarily a maternal resuscitative manoeuvre — emptying the gravid uterus relieves aortocaval compression, restores venous return, and may itself restore maternal cardiac output. The classic Katz paper re-examined the assumption that PMCD was for the fetus and made the case that the 4-minute rule (deliver by 5 minutes) is best understood as a maternal resuscitative intervention.[8]

[1]

Timing of delivery in the critically ill mother

The decision to deliver (or to continue the pregnancy) in a critically ill mother is one of the most complex in obstetric critical care, requiring a multidisciplinary conversation (intensivist, obstetrician, obstetric physician, anaesthetist, neonatologist, the family). The guiding principles are: [1]

1. The mother comes first. Maternal resuscitation always takes priority over fetal salvage. There is no benefit — and substantial harm — in attempting to prolong a pregnancy in a mother who is dying.
2. Delivery is the definitive treatment for the obstetric critical illnesses (severe pre-eclampsia/HELLP, eclampsia, AFE source, chorioamnionitis, refractory obstetric haemorrhage). For these conditions the answer to "should we deliver?" is usually yes, and the question becomes "when and how".
3. Delivery is NOT automatically indicated for non-obstetric critical illness (pneumonia, sepsis from a non-uterine source, DKA, trauma) — manage the maternal condition; continue the pregnancy with monitoring unless there is a separate obstetric indication.
4. Gestational age matters. Before 24 weeks the fetus is generally non-viable and the decision is purely maternal. Between 24 and 34 weeks, corticosteroids for fetal lung maturity (betamethasone 12 mg IM q24h × 2) are given if delivery can be safely delayed 48 h. Beyond 34 weeks the fetus is mature and the balance favours delivery if there is any maternal or fetal indication.
5. Route of delivery — Caesarean vs induction of labour — is an obstetric decision based on the maternal and fetal condition, the indication for delivery, and the gestational age. Caesarean is reserved for obstetric indications or for the patient in extremis (PMCD) — vaginal delivery is generally preferred if time allows. [1]

Pharmacology in pregnancy — vasopressors and teratogenic drugs

Vasopressors in pregnancy

The choice of vasopressor is informed by what little human data exist (mostly observational) plus animal data and an understanding of the uteroplacental circulation, which has no autoregulation — uterine blood flow is directly proportional to uterine perfusion pressure (MAP minus uterine venous pressure). Any drug that raises SVR by vasoconstricting the uterine vasculature may improve maternal BP while worsening placental perfusion.[6]

[1]

Teratogenic and contraindicated drugs in pregnancy

The fetal risk of a drug is graded by FDA pregnancy categories (now replaced by the Pregnancy and Lactation Labeling Rule — PLLR) and Australian categorisation (A, B1, B2, B3, C, D, X). For the intensivist, the practical list of drugs to avoid is short and worth memorising.[6][9]

[1]

Additional clinical pearls

[1] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1]

Additional red flags

[1] [1] [1] [1] [1] [1]

Non-obstetric critical illness in pregnancy

The general principle is that pregnancy is not a contraindication to standard critical care — pregnant women should receive the same investigations, treatments and interventions as non-pregnant patients with the same condition, modified only by the physiological changes and fetal considerations described above. Examples:[9]

• Pneumonia — community-acquired, viral (influenza, COVID-19, varicella), aspiration. Pregnant women are more susceptible to severe viral pneumonitis; influenza and COVID-19 vaccination are recommended in pregnancy. Treat per standard guidelines, with attention to oxygenation (target SpO2 ≥ 94%, because the fetus is vulnerable to maternal hypoxia) and to the lower baseline PaCO2 (a PaCO2 of 40 is hypercapnic).
• Asthma exacerbation — treat per standard guidelines (β2-agonists, steroids, magnesium); the only modification is to avoid prostaglandin F2α (carboprost) in PPH (causes bronchospasm).
• Diabetic ketoacidosis — pregnant women with type 1 diabetes are at increased risk; manage per standard DKA protocol (fluids, insulin, potassium); fetal monitoring is mandatory (DKA causes fetal distress), but delivery is not the answer — fix the maternal DKA and the fetus usually recovers.
• Trauma — major trauma in pregnancy follows ATLS principles with the modifications: left lateral tilt, fetal monitoring if viable, lower threshold for imaging (CT is essential and radiation dose to fetus is acceptable), Rh-negative women with bleeding receive anti-D immunoglobulin, and domestic violence is a leading cause of maternal trauma — screen.
• Acute abdomen — appendicitis (often atypical, displaced by the gravid uterus), cholecystitis (gallstones commoner in pregnancy), pancreatitis (gallstone, hypertriglyceridaemia), bowel obstruction. Operate if indicated — pregnancy is not a contraindication to laparotomy or laparoscopy (in the second trimester if possible). [1]

Outcomes and prognosis

Maternal ICU mortality is lower than general ICU mortality (~2-5% vs 15-20%) because obstetric patients are younger, have fewer comorbidities, and most obstetric critical illnesses are reversible once delivered (pre-eclampsia, eclampsia, HELLP, haemorrhage). The exceptions are AFE (modern case fatality ~13-20%), PPCM (5-10% mortality, with 10% needing transplant), and maternal sepsis (5-10% mortality), which carry higher risk. The long-term legacy of obstetric critical illness is substantial — post-intensive care syndrome (PICS) is increasingly recognised in survivors, with persistent physical, cognitive and psychological morbidity; pregnancy-related PTSD affects up to 30% of survivors of severe obstetric emergencies; and a history of pre-eclampsia, PPCM or gestational diabetes marks a substantially elevated lifelong cardiovascular risk that should be addressed at ICU follow-up.[1][15]

The intensivist's job is to support the maternal physiology while the obstetric team delivers the placenta or treats the underlying cause, to maintain oxygenation and perfusion for both patients, to know the (short) list of contraindicated drugs, and to remember that the young pregnant patient hides blood loss and decompensates abruptly — the threshold for escalation is lower than for a non-pregnant patient with the same derangement. [1]

References

1. [1]Mhyre JM, Bateman BT, Leffert LR. Maternal mortality and the role of the obstetric anesthesiologist Best Pract Res Clin Anaesthesiol, 2017.PMID 28625309
2. [2]Altman D, Carroli G, Duley L, Farrell B, Moodley J, Neilson J, Smith D; Magpie Trial Collaboration Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial Lancet, 2002.PMID 12057549
3. [3]Fitzpatrick KE, Tuffnell D, Kurinczuk JJ, Knight M. Incidence, risk factors, management and outcomes of amniotic-fluid embolism: a population-based cohort and nested case-control study BJOG, 2016.PMID 25683758
4. [4]Elkayam U, Akhter MW, Singh H, Khan S, Bitar F, Hameed A, Shotan A. Clinical Outcomes for Peripartum Cardiomyopathy in North America: Results of the IPAC Study (Investigations of Pregnancy-Associated Cardiomyopathy) J Am Coll Cardiol, 2015.PMID 26293760
5. [5]Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count Obstet Gynecol, 2004.PMID 15121574
6. [6]Neligan PJ, Laffey JG. Clinical review: Special populations--critical illness and pregnancy Crit Care, 2011.PMID 21888683
7. [7]McDonnell NJ, Paech MJ, Clavisi OM, Scott KL; ANZCA Trials Group. Difficult and failed intubation in obstetric anaesthesia: an observational study of airway management and complications associated with general anaesthesia for caesarean section Int J Obstet Anesth, 2008.PMID 18617389
8. [8]Katz V, Balderston K, DeFreest M. Perimortem cesarean delivery: were our assumptions correct? Am J Obstet Gynecol, 2005.PMID 15970850
9. [9]Reitman E, Flood P. Anaesthetic considerations for non-obstetric surgery during pregnancy Br J Anaesth, 2011.PMID 22156272
10. [10]WOMAN Trial Collaborators. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial Lancet, 2017.PMID 28456509
11. [11]Hilfiker-Kleiner D, Haghikia A, Masuko D, Nonhoff J, Held D, Libera M, Marsano-Zambrano I, et al. Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study Eur Heart J, 2017.PMID 28934837
12. [12]Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903338
13. [13]Kane E, Essenmacher S, Weber C, Happe S, Baptist A. Venous thromboembolism as a cause of severe maternal morbidity and mortality in the United States Semin Perinatol, 2019.PMID 30935751
14. [14]Bates SM, Greer IA, Middeldorp S, Veenstra DL, Prabulos AM, Vandvik PO; American College of Chest Physicians. VTE, thrombophilia, antithrombotic therapy, and pregnancy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines Chest, 2012.PMID 22315276
15. [15]Say L, Chou D, Gemmill A, Tunçalp Ö, Moller AB, Daniels J, Gülmezoglu AM, Temmerman M, Alkema L. Global causes of maternal death: a WHO systematic analysis Lancet Glob Health, 2014.PMID 25103301
16. [16]Duley L, Gulmezoglu AM, Henderson-Smart DJ, Chou D. Magnesium sulphate and other anticonvulsants for women with pre-eclampsia Cochrane Database Syst Rev, 2010.PMID 21069663