Obstetric, the reference

A term uterus presses on the aorta and vena cava. This cuts venous return, so chest compressions move little blood. Keeping her flat while an assistant pushes the uterus aside relieves that pressure. Otherwise the arrest is managed as for any adult: standard shock energy, standard adrenaline, and shocks never held back for the fetus. Delivery removes the compressing uterus. So if circulation has not returned after 4 minutes of resuscitation, perimortem caesarean starts where she arrested, aiming to deliver within about 4–5 minutes.

Fifteen-minute caesarean deadline is dangerously late. A quarter-hour deadline sounds urgent, but it is far too late. Caesarean begins when circulation has not returned after 4 minutes, and delivery should follow within about 4–5 minutes. Meanwhile, shocks and adrenaline continue at their usual adult doses.

Keep the woman supine with the uterus manually displaced, give the same shock energy as for a non-pregnant adult, and proceed to caesarean if circulation has not returned after 4 minutes. Reported cases used standard defibrillation and adrenaline, delivering within 4–5 minutes.

Sources: Miller 10eMayo review

The gravid uterus presses on the aorta and vena cava, reducing venous return so compressions generate little output. From the size where the fundus reaches the umbilicus, an assistant pushes it aside by hand while she stays supine. A brief trial of standard CPR comes first while the team prepares. If that fails, emptying the uterus where she lies relieves the compression, aiding the mother first: the guideline's 4-minute trigger leads into Barash's 5-minute delivery target. Keeping her supine is also correct (Miller); the pregnancy-specific key is timely delivery.

Immediate caesarean skips diagnostic CPR trial. It sounds decisive and protective of the fetus. But the operation is done for the mother, to relieve compression of the great vessels. It follows a short trial of CPR with uterine displacement that fails to restore circulation. Operating at once skips that trial and gets the purpose wrong.

The ASA/SOAP guideline says to start standard resuscitation with uterine displacement and have obstetricians perform caesarean delivery if circulation has not returned within 4 minutes; Barash sets delivery ideally within 5 minutes of arrest; Miller explains the vessel compression and supine manual displacement.

Sources: Outside our books: Practice Guidelines for Obstetric Anesthesia: An Updated Report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia and the Society for Obstetric Anesthesia and Perinatology (2016)Barash 9eMiller 10e

A gravid uterus compresses the great vessels and reduces venous return, so chest compressions produce little output. Emptying the uterus improves ACLS effectiveness and benefits a viable fetus. Barash advises delivery ideally within 5 minutes of arrest. Miller advises starting the caesarean if circulation has not returned after 4 minutes, aiming for delivery by 5. These are consistent: 4 minutes is when to cut; 5 is when the baby should be delivered. Operate where she lies, without transfer, and continue compressions.

Prolonged CPR fails without uterine evacuation. This follows ordinary adult ACLS habit: keep compressing and reassess. In late pregnancy, caval compression blunts every compression, so long CPR without emptying the uterus rarely brings circulation back. Delivery is itself part of the resuscitation. Waiting forfeits both mother and baby.

Barash advises perimortem caesarean ideally within 5 minutes of arrest, on the spot rather than in theatre. Miller advises starting at the site if circulation has not returned after 4 minutes, aiming for delivery by 5. The gravid uterus hampers compressions; delivery likely aids ACLS.

Sources: Miller 10eBarash 9e

Barash says bleeding kills more mothers worldwide than any other cause, about 25% of deaths. Miller's US series differs: grouped cardiovascular conditions lead at 15.5%, but that heading pools many heart diseases. Counted alone, cardiomyopathy sits below haemorrhage in every US series: 11% against 11.4% in 2011 to 2013, 10.6% against 11.5% in CDC surveillance for 2005 to 2024, and 8.5% against 13.7% in state reviews for 2017 to 2019. So against cardiomyopathy, pre-eclampsia or aspiration, haemorrhage wins in both sources.

Cardiovascular disease as leading cause. It is tempting because recent texts stress that heart disease now causes the most pregnancy-related deaths in the US. But that figure groups many cardiac conditions together. Cardiomyopathy on its own still ranks just below haemorrhage in US data, and worldwide haemorrhage leads clearly.

Bleeding accounts for roughly 25% of maternal deaths globally, chiefly in low-resource settings. In US data for 2011 to 2013, cardiovascular conditions lead (15.5%), then haemorrhage (11.4%), cardiomyopathy (11%) and hypertensive disorders (7.4%). Haemorrhage deaths are falling; cardiovascular deaths are rising.

Sources: Barash 9eMiller 10eMayo review

Once the placenta separates, the open vessels in the placental bed stop bleeding mainly because the muscle of the uterus contracts around them. Anything that tires, overstretches or inflames that muscle leaves the vessels open. Examples are labour that has been augmented or has gone on a long time, multiple gestation, polyhydramnios and chorioamnionitis. These are common, so atony outnumbers every other cause. It can happen after vaginal or caesarean birth, and the bleeding may be sudden or come hours later.

Retained placenta diagnosis misses atony likelihood. Retained placenta is a real and listed cause, and it also predisposes to atony, so it sounds specific and clever. But nothing in the history points to incomplete delivery of the placenta. A soft, tired uterus after a long labour is far more likely, and atony accounts for most cases.

Textbooks and WHO guidance agree that atony is the leading cause after either vaginal or caesarean birth and accounts for over 70% of cases. Genital tract trauma, rupture, retained tissue and coagulopathy contribute less often.

Sources: FaustBarash 9eOutside our books: WHO Recommendations for the Prevention and Treatment of Postpartum Haemorrhage (2012)

Postpartum haemorrhage most commonly results from a floppy (atonic) uterus, so the first job is to make the uterus contract again. Massage can start at the bedside as soon as the bleeding is recognised and needs no equipment. Oxytocin then keeps the uterus contracted. Crystalloid fluid resuscitation starts at the same time. Tranexamic acid and further measures are only for bleeding that continues after these first steps.

Cross-matching delays urgent uterotonic treatment. Cross-matching is tempting because heavy bleeding makes you think of transfusion. But ordering blood does nothing to make an atonic uterus contract, so the bleeding carries on. The first step that deals with the cause is massage plus a uterotonic. Blood preparation runs alongside it and does not replace it.

Guidance and textbooks agree that atony is the commonest cause of postpartum haemorrhage. Uterine massage should start as soon as haemorrhage is diagnosed, with oxytocin as the first drug and early crystalloid resuscitation. Tranexamic acid is kept for refractory atonic bleeding.

Sources: Outside our books: WHO Recommendations for the Prevention and Treatment of Postpartum Haemorrhage (2012)Miller 10eFaust

Extra oxytocin achieves little in an unresponsive uterus, so switch mechanism. Methylergometrine, an ergot, constricts vessels, causing hypertension and coronary spasm: give 0.2 mg IM, at most 5 doses, and avoid it in pre-eclampsia. Faust calls IV use controversial; the label allows IV only slowly over at least 60 seconds with pressure watched, as a lifesaving measure. Carboprost can cause bronchospasm; Barash repeats it every 15–60 minutes, Mayo allows up to 90 and a 2 mg ceiling. Misoprostol is 600–800 mcg in Miller's; none sets an hourly repeat.

Rapid intravenous methylergometrine 200 mcg. Methylergometrine is a real second-line uterotonic and 200 mcg is the correct dose, so this looks right. The route fails: it is an intramuscular vasoconstrictor, and a rapid IV dose risks hypertensive crisis, stroke or coronary spasm; IV use is reserved for a slow, monitored last resort.

Barash tabulates methylergometrine 0.2 mg IM and carboprost 0.25 mg IM every 15–60 minutes. Miller's names both as second-line agents and adds misoprostol 600–800 mcg. Mayo allows carboprost IM or intramyometrially every 15–90 minutes to 2 mg. Faust calls IV methylergometrine controversial.

Sources: Barash 9eMiller 10eMayo reviewFaust

Stoelting's general-surgical classes reserve red cells for losses far larger than this, but a parturient's bleeding is rapid, can be concealed and consumes clotting factors, so the obstetric chapters of Miller and Barash start replacement on the clinical picture instead of awaiting laboratory results. Abruption makes coagulopathy far likelier and fibrinogen drops early, so fibrinogen or cryoprecipitate begins alongside red cells; coagulation results then decide whether plasma and platelets follow, unless bleeding turns massive or continues, when plasma is given with red cells without waiting.

Fixed ratio package unwarranted at this volume. Abruption's coagulopathy makes a pre-set ratio package look thorough. But this loss is not yet massive, fixed ratios were borrowed from trauma and are questioned in obstetrics, and any ratio used is balanced, not red-cell heavy. Coagulation results decide when plasma and platelets follow.

Obstetric texts say to begin replacement from clinical assessment without awaiting laboratory results and to give fibrinogen or cryoprecipitate early. Prompt component therapy restores oxygenation and corrects coagulopathy. Abruption makes coagulopathy 54 times likelier, so coagulation is monitored closely and massive transfusion is prepared.

Sources: Miller 10eBarash 9e

Obstetric bleeding shares trauma's hypothermia, acidosis and coagulopathy, so Barash carries trauma's mortality-lowering 1:1 red cell to plasma ratio into obstetrics. Red cells alone dilute clotting factors, and fibrinogen falls early, so plasma and fibrinogen must keep pace. Miller's trauma chapter also keeps fixed ratios, but its newer obstetric chapter questions ratios borrowed from non-obstetric settings and prefers clinical and laboratory guidance. Safe under both: in massive bleeding give plasma with red cells early without awaiting results, then move to goal-directed replacement.

Two-to-one ratio under-corrects clotting factor deficit. A ratio of two to one looks like a sensible compromise that saves plasma and echoes older massive-transfusion habits. It fails because it gives too little plasma to offset dilution and consumption of clotting factors; the cited mortality benefit belongs to matched 1:1 replacement.

Barash says obstetric transfusion practice is adapted from trauma, where 1:1 red cells to plasma reduces haemorrhage deaths. Miller's obstetric text says early products follow the clinical picture rather than pending labs, with early fibrinogen; empiric ratios apply only until coagulation-guided therapy is possible.

Sources: Barash 9eMiller 10e

Fibrinogen tends to run low early in obstetric bleeding, so it should be replaced early. The two books set different triggers. Miller's general bleeding guidance replaces fibrinogen at or below 1.5 g/L. Barash's obstetric table replaces it below 150–200 mg/dL at delivery. For a bleed at delivery the obstetric trigger applies, so a level just above the general cut-off still calls for cryoprecipitate. Red cells always run alongside to replace lost blood and keep tissues oxygenated. Using factor VIIa here is off-label, and adverse events have been reported.

Factor VIIa wrong rescue for fibrinogen loss. Factor VIIa is tempting as a rescue drug when INR and aPTT stay prolonged despite plasma. But the deficit here is fibrinogen, which cryoprecipitate replaces directly. Its off-label use in massive haemorrhage has led to adverse-event reports, so it is not universally recommended.

Barash lists obstetric haemorrhage at delivery with fibrinogen below 150–200 mg/dL as an indication for replacement; Miller's general threshold is ≤1.5 g/L. Miller advises early cryoprecipitate or concentrate in obstetric resuscitation, cautioning against factor VIIa. Barash stresses prompt component transfusion for blood loss and oxygenation.

Sources: Miller 10eBarash 9e

Only surgery stops this bleeding, so ICU first, observation or a fixed red-cell-and-plasma order without surgery cannot replace theatre; early operation spares products and limits dilutional coagulopathy. A haemoglobin of 10 lags behind acute loss, so it never excuses blood: resuscitate on the way, warmed crystalloid bridging until red cells arrive. Plasma belongs once clotting fails: obstetric bleeding consumes and dilutes factors, and when haemoglobin has fallen and INR is prolonged after litres of fluid, more crystalloid thins clotting further, so red cells and plasma go in, with early fibrinogen.

Theatre first, withholding blood while giving crystalloid. Tempting because theatre stops the bleeding; it is right when the rivals are ICU first, observation, or plasma without surgery or coagulopathy. But theatre never excuses withholding blood: once haemoglobin has fallen with INR prolonged, more clear fluid deepens the coagulopathy, so red cells and plasma go in.

Obstetric bleeding quickly causes consumptive and dilutional coagulopathy. Prompt component transfusion replaces loss, keeps tissues oxygenated and corrects clotting, guided by the clinical situation rather than awaited labs, with fibrinogen considered early. Operating as soon as possible cuts product needs and dilutional coagulopathy.

Sources: Barash 9eMiller 10e

Uterine flow equals the pressure gradient across the uterine circulation, from its arteries to its veins, divided by the resistance of its vessels. Painful contractions and bearing down set off catecholamine surges. These constrict the uterine vessels, raise resistance and cut flow. Epidural analgesia removes the pain and blunts those surges, so resistance falls and flow improves. The same block can also lower maternal blood pressure. When perfusion pressure falls, flow falls with it, so the benefit depends on keeping maternal pressure up.

Local anaesthetic alone doesn't improve uterine flow. It is tempting because epidural analgesia uses a local anaesthetic and improves uterine flow. The gain comes from losing sympathetic vasoconstriction, not from the drug itself. If the block causes maternal hypotension, uterine flow falls instead.

Epidural analgesia damps the sympathetic surges driven by labour pain. This prevents rises in maternal heart rate and pressure and prevents falls in uterine flow. Flow was reported up to 75% higher after epidural. Hypotension, aortocaval compression, contractions and vasoconstriction all reduce uterine flow.

Sources: Barash 9eMayo review

Vomiting loses acid and hyperventilation blows off carbon dioxide, so the mother's blood becomes alkalaemic. Alkalaemia makes haemoglobin hold oxygen more tightly and shifts the mother's curve left. At the placenta her haemoglobin keeps its oxygen, so less reaches the fetus even when her PaO2 is normal. Alkalosis may also narrow the uterine vessels. Barash states this in general terms. Miller links the fall in uterine blood flow to extreme hypocapnia below 20 mm Hg. So when hypocapnia is only moderate, the curve shift is the surer explanation.

Dehydration assumption misses hyperventilation mechanism. Prolonged vomiting suggests dehydration, and low maternal blood pressure does reduce uterine blood flow. It fails because nothing points to hypotension. The picture is a mother who is alkalaemic and hypocapnic but well oxygenated, and that points to the left-shifted curve, not volume loss.

Barash and Miller both state that maternal alkalosis or hyperventilation shifts the oxyhaemoglobin curve left, reducing fetal oxygen delivery. Both note uterine vasoconstriction; Miller links it to extreme hypocapnia below 20 mm Hg. Maternal hypotension separately reduces uterine flow.

Sources: Miller 10eBarash 9e

Drugs reach the fetus by passive diffusion down the gradient of free drug. A drug under 500 Da that is lipid-soluble and mostly un-ionised passes membranes easily. These are the same properties that let a drug into the brain. So induction agents, volatiles, opioids, benzodiazepines and local anaesthetics reach the fetus. Highly charged drugs stay mostly on the maternal side. These include heparin, glycopyrrolate and every neuromuscular blocker, suxamethonium as well as the non-depolarisers. Little phenylephrine reaches the fetus either.

Molecular charge defeats small suxamethonium transfer. Suxamethonium is a small, fast-acting drug and works differently from the non-depolarising relaxants, so people guess it diffuses freely. It fails because, like every neuromuscular blocker, it is ionised and crosses very poorly. Size alone does not help a charged molecule get through.

Diffusion is helped by low molecular weight, high lipid solubility and little ionisation. Heparin and glycopyrrolate cross minimally because they are charged, while opioids and benzodiazepines cross readily. Both kinds of muscle relaxant cross poorly and so does phenylephrine. Every general anaesthetic drug crosses.

Sources: Mayo reviewMiller 10e

Succinylcholine is highly ionised and poorly lipid soluble, so very little crosses the placenta. It cannot be detected in cord blood unless the mother gets 2–3 mg/kg. Paralysing the neonate needs about 10 mg/kg, far above an intubating dose, so the baby is born with normal tone. Ketamine at the usual induction dose of 1–1.5 mg/kg does not depress the neonate; 2 mg/kg sits above it, where uterine tone rises, uterine flow falls and the seizure threshold drops.

Standard ketamine dose carries no neonatal risk. Hypoxia is tempting because larger ketamine doses can raise uterine tone and cut uterine blood flow, so the fetus looks at risk. But that is a possible effect of higher doses, not the expected finding. Standard ketamine causes no neonatal depression, and succinylcholine barely reaches the fetus.

Succinylcholine crosses the placenta only minimally; it is absent from cord blood below 2–3 mg/kg and blocks the neonate only at about 10 mg/kg, so the baby is not paralysed. Standard-dose ketamine causes no neonatal depression; larger doses affect uterine tone and perfusion.

Sources: Miller 10e

Many women choose drug-free comfort measures for some or all of labour. Her refusal is a valid preference to support, not one to overrule. Miller's links effectiveness with preference. Women rated neuraxial block the most effective method, yet rated hydrotherapy and massage at least as helpful as intravenous opioids. For a woman refusing medication, these are the best-supported low-risk measures. Pressing an epidural or an opioid on her ignores her wishes. Evidence for drug-free methods is mostly weak, so counsel her honestly.

Acupuncture requires specialist training and weak evidence. Acupuncture is also drug-free and has a long history, so it seems to suit a woman refusing medication. It fails because it needs specially trained staff and its evidence varies. No source calls it best. Water immersion and massage are the methods women rated favourably.

Many labouring women prefer drug-free methods for part or all of labour. Women rated neuraxial block most effective but rated water therapy and massage at least as helpful as intravenous opioids. Methods such as acupuncture need specialised training, and evidence varies and lacks rigour.

Sources: Miller 10eBarash 9e

An epidural requires consent, so a competent parturient who declines cannot have one, whatever the clinical case. Miller's and Barash list refusal first. Coagulopathy counts only when real: the obstetric thrombocytopenia consensus sets the low-risk line at 70,000, so a higher count allows a block. Advanced dilation and planned trial of labour after caesarean are absent from Miller's list; that they are allowed is inferred from this absence, as no page states it. For a trial of labour, Miller's asks only for an immediately available obstetric, anaesthetic and nursing team.

Platelet count above seventy thousand permits block. Coagulopathy is on every contraindication list, so a platelet figure in the scenario looks like a reason to refuse. The consensus sets the low-risk line far lower, at 70,000 or more, so this count supports going ahead rather than stopping.

Miller's and Barash name patient refusal as a contraindication to neuraxial block. Consensus rates platelet counts of at least 70,000 as low haematoma risk. For trial of labour after caesarean, Miller's requires only immediate team availability; dilation is not listed.

Sources: Miller 10eBarash 9eOutside our books: The Society for Obstetric Anesthesia and Perinatology Interdisciplinary Consensus Statement on Neuraxial Procedures in Obstetric Patients With Thrombocytopenia (2021)

Epidural analgesia weakens expulsive effort and may favour fetal malposition, so Barash notes a longer second stage in first-time mothers. Miller reports that pooled Cochrane data showed more assisted vaginal births, but a later subgroup analysis found no rise in trials published after 2005, implying modern epidurals spare this outcome. The evidence has weakened rather than reversed, so counselling still mentions a possible instrumental delivery, flagged as uncertain. Caesarean risk is unchanged.

Epidural doesn't increase operative delivery rates proven. Slow, prolonged second stage seems to warrant surgery, and epidurals were long feared to cause dystocia. However, randomised trials and a large Cochrane review found no change in caesarean rates. If a slow second stage ends in intervention, it is an assisted vaginal birth.

Miller states epidural may lengthen the second stage without raising caesarean risk, supported by a 2018 Cochrane review of 33 studies; the pooled assisted-delivery rise disappeared in trials after 2005. Barash links the prolongation in nulliparous women to reduced expulsive forces.

Sources: Miller 10eBarash 9e

If opioids are stopped or antagonised, the patient goes into acute withdrawal. Agonist therapy gives better outcomes than supervised withdrawal, so the aim is to keep the receptors occupied, not to empty them. Methadone and buprenorphine are agonists but act only weakly at the mu receptor, so the daily dose does not cover labour pain. Extra opioids also work less well because the receptors are already occupied. A local anaesthetic-based neuraxial block works without the mu receptor, so it gets round both problems.

Withdrawal from naloxone worse than opioid continuation. It sounds like the proper way to treat drug misuse. But an antagonist such as naloxone pushes opioid off the receptors and triggers acute withdrawal at the worst time. Current practice is to keep her on an agonist and add analgesia, not to reverse the opioid.

Barash says to continue opioids and maintenance therapy through labour and after delivery to prevent withdrawal, and prefers agonist therapy to supervised withdrawal. Faust says maintenance drugs give inadequate labour analgesia and that neuraxial block is safe, effective and should be offered.

Sources: FaustBarash 9e

A tight mitral valve lets the left atrium empty only in diastole. Pain-driven tachycardia and the sympathetic surge of labour shorten filling time, raise atrial and pulmonary pressures, and risk pulmonary oedema. An early neuraxial block blunts that catecholamine response. A catheter already in place can be topped up for pushing without Valsalva. Grading differs by text: Barash's three-band table calls the middle band moderate, whereas Miller and the valve guideline class it severe. An area well below that band is severe on every scheme.

Sympathectomy safer than unopposed catecholamine surge. This is tempting because a fixed-output valve seems unable to tolerate sympathectomy. But withholding the block leaves the tachycardia and catecholamine surge that decompensate the stenotic valve. A slowly titrated epidural is the recommended technique. Avoid it only for coagulopathy or an anatomical problem.

Stoelting's table for severe maternal heart disease prefers vaginal birth with early neuraxial analgesia, arterial monitoring, catheter top-up for second stage and no Valsalva. Nearly all women with major comorbidity should receive early labour analgesia unless coagulopathy or anatomy prevents it.

Sources: Stoelting 8e

Early in the pandemic, obstetric anaesthesia reviewers could not say how much aerosol inhaled nitrous oxide systems produce or how to decontaminate them. They told labour units to weigh the risks and consider stopping it, so calling it contraindicated in labour matches that advice. The infection itself does not rule out an epidural or spinal. Steroids for threatened preterm birth and magnesium for fetal neuroprotection keep their normal indications. None of these sources discusses fetal scalp electrodes.

COVID infection doesn't eliminate fetal steroid benefit. Steroids suppress immunity, so withholding them from a febrile, possibly infected mother feels protective. But pandemic taskforce advice kept antenatal corticosteroids as standard care for threatened preterm birth whether or not COVID-19 is present. Maternal infection does not cancel the benefit to the fetus.

A pandemic-era review found nitrous oxide's aerosol risk and cleaning unknown, advised units to consider suspending it, and stated COVID-19 does not preclude neuraxial analgesia. A taskforce kept antenatal steroids and magnesium neuroprotection as standard care regardless of infection. Fetal scalp monitoring is not addressed.

Sources: Outside our books: COVID-19: Obstetric anesthesia care considerations (2020)Outside our books: The National COVID-19 Clinical Evidence Taskforce: pregnancy and perinatal guidelines (2022)

Late in pregnancy, plasma expansion dilutes platelets and their turnover speeds up. The count therefore drifts down towards term, is normal outside pregnancy, and causes no bleeding. Because the fall is physiological, it is shallow. The SOAP consensus places it above 75,000, and Miller's says it rarely goes below 70,000/mm3; in practice the two cut-offs agree. ITP is immune destruction, so it can begin in any trimester and persist outside pregnancy. ITP and HELLP still need excluding, because gestational thrombocytopenia is a diagnosis of exclusion.

Third-trimester mild thrombocytopenia is pregnancy normal. A clearly low count with no earlier value to compare looks unexplained, so people reach for ITP. But third-trimester onset, a count above the gestational floor and no bruising or gum bleeding fit gestational thrombocytopenia. Earlier onset, a much lower count or bleeding would point to ITP instead.

SOAP consensus: gestational thrombocytopenia arises late in the second or third trimester, with counts above 75,000 and normal counts outside pregnancy; ITP can start in any trimester. Miller's: counts rarely fall below 70,000/mm3, no abnormal bleeding, diagnosed by exclusion.

Sources: Outside our books: The Society for Obstetric Anesthesia and Perinatology Interdisciplinary Consensus Statement on Neuraxial Procedures in Obstetric Patients With Thrombocytopenia (2021)Miller 10e

Spinal epidural haematoma is rare. Almost all evidence comes from pooled case reports linking risk to platelet count: bleeding seems more likely below 50,000 than at 70,000 or more. No study shows any other test can distinguish patients who will bleed from those who will not. PT and aPTT help only when a factor defect is known or suspected. Viscoelastic tests have only small, reassuring reports. The obstetric consensus therefore found too little evidence to recommend any extra test.

TEG cannot predict epidural block safety. TEG is tempting because it measures whole-blood clot strength at the bedside, and small obstetric series report normal traces before blocks with no haematoma. But a few uneventful cases do not show that the test predicts anything. The consensus found too little evidence to use TEG in the decision.

The obstetric consensus says it may be reasonable to avoid a neuraxial block if the platelet count falls under 50,000. PT and aPTT do not predict bleeding unless a factor defect is suspected. There is too little evidence to recommend TEG, ROTEM or PFA.

Sources: Outside our books: The Society for Obstetric Anesthesia and Perinatology Interdisciplinary Consensus Statement on Neuraxial Procedures in Obstetric Patients With Thrombocytopenia (2021)

Type 1 disease is a partial shortfall in the amount of vWF. Pregnancy pushes vWF production up, so by the third trimester most of these women are above the treatment threshold without help, and routine prophylaxis is unnecessary. Type 2 disease is a quality problem: the molecule is there but works poorly. Releasing more of it achieves little, so replacement is needed if levels are low. Childbirth is a major haemostatic challenge, and women with inherited clotting defects commonly bleed heavily after delivery.

Pregnancy-induced vWF rise negates prophylaxis need. Prophylaxis sounds sensible because vWD is a bleeding disorder and delivery carries bleeding risk. But type 1 is only a partial deficit, and the pregnancy rise in vWF usually lifts levels above threshold by term. Most women therefore need no prophylaxis; measure levels rather than treat by default.

In type 1 disease vWF is partly reduced but usually climbs above 50 IU/dL late in pregnancy, so prophylaxis is seldom needed. Type 2 is a functional defect, and boosting release does not help. Postpartum haemorrhage is common in women with bleeding disorders.

Sources: Miller 10e

Type 1 disease is a partial shortage of normal von Willebrand factor. The endothelium still stores the factor, so desmopressin can release it into the blood. That is why type 1 responds best of all the types. Type 3 has no stores, so desmopressin does nothing there. In pregnancy the factor level usually climbs above 50 international units/dL by the third trimester, so many women need no preventive treatment. Desmopressin is kept for those who stay low or who bleed.

Factor VIIa corrects Factor VII not vWF. It sounds like a strong, all-purpose clotting product, and von Willebrand disease feels like a missing-factor problem. But recombinant factor VIIa is for factor VII deficiency. It does not correct the shortage of von Willebrand factor. Desmopressin corrects that shortage by releasing the patient's own stores.

In type 1 disease the factor usually rises by late pregnancy, so preventive treatment is often unnecessary, but desmopressin may be used. Type 1 responds best; type 3, lacking endothelial stores, does not. Factor VIIa is listed for factor VII deficiency.

Sources: Miller 10eStoelting 8eFaust

Inability to intubate and ventilate is the leading anaesthesia-related cause of maternal death, so the danger lies in any plan that makes her apnoeic before her airway is secured. A spinal leaves her breathing spontaneously. The obstetric airway guideline ranks maternal safety above fetal urgency and lists the anaesthetist's seniority among the factors in its airway decisions, hence the most senior anaesthetist. A fresh epidural takes too long to reach surgical block. If general anaesthesia cannot be avoided, intubate awake. Platelets of 70,000 or more carry low haematoma risk.

Awake fibreoptic safe but asleep induction apnoea. Fibreoptic sounds like the difficult-airway answer, but done asleep it induces apnoea first and then searches for the trachea in a patient with little reserve and a full stomach. The fibreoptic only protects her if she is awake and breathing; otherwise choose neuraxial.

Barash advises neuraxial anaesthesia or awake intubation when airway difficulty is foreseen, and rapid sequence only when no such difficulty exists. The OAA/DAS guideline expects a route to summon a second anaesthetist. SOAP judges neuraxial reasonable at platelets of 70,000 or more.

Sources: Barash 9eOutside our books: The Society for Obstetric Anesthesia and Perinatology Interdisciplinary Consensus Statement on Neuraxial Procedures in Obstetric Patients With Thrombocytopenia (2021)Outside our books: Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics (2015)

Pregnancy already congests the upper airway. Preeclampsia makes this oedema worse, so laryngoscopy and passing the tube get harder, and losing the airway is a hazard that applies to every such patient. Separately, the disease can lower platelets, as in HELLP, or cause a coagulopathy, which raises concern about a spinal haematoma. Coagulation status must therefore be assessed before a block. In practice, the screen the sources name is a platelet count and a look for unexplained bleeding. A full clotting panel is not the default test.

Platelet count not full coagulation assessment. It sounds thorough and one review does say coagulation status should be assessed before a block. But the test actually recommended is a platelet count with clinical bleeding signs, not a routine full panel, whereas airway oedema making intubation difficult is true without conditions.

Airway oedema, worse in coexisting preeclampsia, may make tracheal intubation difficult. Before regional anaesthesia in preeclampsia, check the platelet count, as HELLP syndrome can lower it, and assess coagulation status carefully, as coagulopathy may develop.

Sources: Barash 9eMiller 10eMayo review

As body weight rises, cefazolin spreads through a larger volume of distribution, so a fixed dose gives lower tissue concentrations. Barash notes that morbidly obese patients need roughly double the usual dose to reach adequate tissue levels. Guidelines turn this into a single step. The standard 2 g covers most adults, including obese women, and the higher 3 g starts at 120 kg. Later outcome studies asked whether the extra gram really prevents infection. No trial has overturned the cut-off, so the step still applies.

Weight threshold 120kg mandates 3g not 2g. Two grams is the familiar caesarean dose, so 120 kg can feel like the edge of the higher band rather than inside it. The threshold includes 120 kg, so 3 g applies at that weight. A woman of 105 kg stays on 2 g.

International guidelines reserve a raised 3 g cefazolin dose for patients weighing 120 kg or more. Whether 2 g or 3 g suffices at that weight needs large randomised trials. Morbidly obese patients need about double the usual dose for adequate tissue levels.

Sources: Outside our books: 1465. Two- versus Three-Gram Cefazolin Dosing for Surgical Prophylaxis in Colorectal Surgery Procedures (2023)Outside our books: Prophylactic Cefazolin Dosing and Surgical Site Infections: Does the Dose Matter in Obese Patients? (2018)Barash 9e

In pregnancy, the reasons to choose laparoscopy are the same as outside it. Outcome data for appendicectomy show that trimester does not change the complication rate and conversion to open surgery is rarely needed, so gestational age alone is not a reason to avoid it. Absorbed insufflation CO₂ is the main physiological concern because maternal hypercapnia affects the foetus. Ventilate to keep CO₂ normal, and check the foetal heart before and after the procedure.

Fetal heart rate required pre and postoperatively. Fetal assessment really is recommended, so this option sounds correct. It fails because it describes a check after surgery only. The recommendation is to check fetal heart rate both before and after the procedure. The option also misses the main point, which is that surgery is safe in any trimester.

A systematic review of laparoscopic appendicectomy in pregnancy found trimester did not affect complications, and conversion to open surgery occurred in under 1% of cases. Indications are the same as outside pregnancy. Keep carbon dioxide levels normal; check fetal heart rate before and after surgery.

Sources: Miller 10eFaust

An intraoperative tracing is useful only if it can be read and acted on. This depends on fetal viability for emergency caesarean, whether a transducer can sit clear of the surgical field, maternal illness severity and the degree of fetal jeopardy. None follows a set gestational week, so the decision is made with the obstetrician for each case. The fixed minimum is a check before and after the procedure. Any small rise in preterm delivery is linked to the surgery itself, especially abdominal surgery.

Intraoperative monitoring individualised not mandated by week. Cut-offs around this gestational age do appear in pregnancy care for aspiration prophylaxis and uterine displacement, but ACOG sets no week after which intraoperative monitoring becomes compulsory. The only fixed requirement is checking before and after surgery; intraoperative monitoring is decided case by case.

ACOG advises Doppler heart-rate checks before and after surgery in a previable pregnancy. In a viable one it advises electronic heart-rate and contraction monitoring before and after. Intraoperative monitoring is decided with the obstetrician, weighing gestation, type of surgery, maternal disease and fetal jeopardy.

Sources: Miller 10eBarash 9e

Faust treats every woman past the first trimester as having a full stomach, so aspiration at induction is the main danger. Barash makes rapid-sequence induction with a cuffed tube routine after 20 weeks. Stoelting says the risk earlier than that is debated, so the choice depends on the patient and the procedure. Symptomatic reflux is one of those patient factors, and it settles the question in the second trimester. Only a cuffed tracheal tube, placed quickly, guards the lungs against regurgitated gastric contents.

Laryngeal mask inadequate for reflux aspiration risk. Dilatation and curettage (D&C) is short, and a supraglottic device looks enough for a brief case before mid-gestation. But this is a second-trimester woman with active reflux, so she counts as a full stomach. A laryngeal mask gives no protection against aspiration. She needs rapid-sequence induction and a cuffed tube.

One text treats women beyond the first trimester as full stomach, advising intubation with rapid-sequence induction if general anaesthesia is chosen. Another makes cuffed-tube rapid-sequence induction usual after 20 weeks. A third calls the earlier period debated, with the decision depending on patient and procedure.

Sources: FaustBarash 9eStoelting 8e

Laryngoscopy triggers a brief but steep rise in systemic pressure. Faust links that surge to cerebral bleeding in pre-eclamptic parturients and lists blunting agents, lidocaine among them; the list was written for pre-eclampsia, but it matters even more when a cerebral vessel has already bled and a pressure spike could rebleed it. Faust's own recipe pairs propofol with suxamethonium; Barash explains that suxamethonium was the historical favourite, yet with sugammadex available high-dose rocuronium now achieves rapid deep blockade safely, so either keeps the rapid sequence intact.

Standard recipe omits blunting of laryngoscopy surge. It copies the standard obstetric general anaesthetic recipe and protects against aspiration in a vomiting parturient, so it feels safest. It fails because nothing blunts the laryngoscopy pressure surge, and that surge is exactly what threatens a cerebral vessel that has already bled.

Faust warns that the pressor surge of intubation in pre-eclampsia risks cerebral haemorrhage, and reports that pretreatment with lidocaine, esmolol or vasodilators blunts it. Barash states that high-dose rocuronium, reversible with sugammadex, can safely replace suxamethonium for rapid deep blockade.

Sources: FaustBarash 9e

Paracetamol, oral or intravenous, has no known stage-specific harm in pregnancy. NSAID risk depends on timing: repeated early doses are linked to miscarriage and malformation; after 30 weeks they can close the fetal ductus early. Miller's judges limited doses at 20 to 30 weeks likely safe, but the FDA now warns that from 20 weeks NSAIDs can reduce fetal urine output and amniotic fluid, so give only a short, lowest-dose course and check the fluid if prolonged. Systemic opioids can blunt fetal heart rate variability. Only paracetamol is safe throughout.

Ibuprofen for chronic pain throughout pregnancy. Ibuprofen seems natural for chronic joint pain, and a short mid-pregnancy course is tolerated. But this patient needs relief from the first trimester until delivery, risking repeated early exposure, kidney and fluid problems the FDA warns of from 20 weeks, and ductal closure after 30 weeks.

Paracetamol, oral or intravenous, is widely accepted as safe in pregnancy. Repeated early NSAID use risks miscarriage and malformation; after 30 weeks, ductal closure and oligohydramnios. Miller's calls limited doses at 20 to 30 weeks likely safe. Systemic opioids may reduce fetal heart rate variability.

Sources: Miller 10e

Cyclo-oxygenase blockade late in pregnancy makes the fetal ductus constrict while the fetus is still in utero, and it impairs fetal kidney function so amniotic fluid falls. Indomethacin-type tocolytics also risk fetal intracranial haemorrhage and necrotising enterocolitis. Timing decides the risk: repeated early doses risk miscarriage and malformation. Miller places ductal harm after 30 weeks and judges limited doses at 20 to 30 weeks likely safe; the FDA warns the fluid effect can begin from 20 weeks, so in that band use the lowest dose briefly and check the fluid.

Delayed ductal closure or polyhydramnios. People remember the ductus as the signature fetal effect of NSAIDs but reverse its direction. Cyclo-oxygenase blockade shuts the ductus prematurely in utero; it never delays closure. Likewise, the fluid effect is oligohydramnios, not polyhydramnios.

Miller links repeated early use to miscarriage and malformation, and use after 30 weeks to early ductal closure and oligohydramnios, while calling limited doses at 20 to 30 weeks likely safe. Barash notes third-trimester ductal and kidney harm; Faust adds fetal intracranial haemorrhage.

Sources: Miller 10eFaustBarash 9e

Oxytocin contracts the uterus without constricting the airways or raising blood pressure. Its main risk is vasodilation and hypotension after a rapid large bolus, so give it slowly. Carboprost is a prostaglandin F2-alpha analogue. It constricts the bronchi and raises pulmonary vascular resistance, which is dangerous in reactive airways. Methylergometrine is an ergot alkaloid. It causes widespread vasoconstriction and coronary vasospasm, and the resulting hypertension is harmful in pre-eclampsia. Nitroglycerin relaxes the uterus, so it cannot treat atony.

Ergot causes vasospasm contraindicated with hypertension. People remember that prostaglandin F2-alpha is the drug to avoid in asthma. They then assume the ergot, the usual second-line drug, is harmless. But its hazard is hypertension and vasospasm, which rules it out in pre-eclampsia. Only oxytocin is endorsed for both asthma and hypertensive disease.

Mayo calls oxytocin the first-line drug for uterine atony and says it is acceptable in asthma or hypertensive disorders; a large IV bolus causes hypotension. Barash links methylergonovine with hypertension and coronary vasospasm, and carboprost with bronchospasm. Faust also lists bronchospasm for carboprost.

Sources: Mayo reviewBarash 9eFaust

Carboprost is a prostaglandin F2α analogue: it drives smooth muscle to contract, which tightens the atonic uterus but can also constrict bronchi in susceptible airways, so asthmatics wheeze and desaturate. One text lists it after both oxytocin and an ergot have failed, but the ergot is relatively contraindicated in hypertension and is often bypassed, so carboprost may be the second drug given. Identify it by the bronchospasm, not its place in the sequence. One text urges caution in asthma, another calls it contraindicated; reconcile by withholding it unless alternatives fail.

Carboprost causes bronchospasm via airway smooth muscle. Muscarinic stimulation does constrict the airways, so it seems to explain the wheeze. But none of the listed uterotonics works that way. The drug whose listed side effect is bronchospasm is the prostaglandin F2α analogue, which contracts airway smooth muscle as well as the uterus.

The texts list bronchospasm as the leading side effect of the prostaglandin F2α analogue. They advise caution or outright avoidance in asthma and place it after oxytocin and the ergot, which is itself relatively contraindicated in hypertension.

Sources: Mayo reviewMiller 10eFaust

Volatile agents relax uterine smooth muscle the same way they relax vascular smooth muscle. As the concentration rises, spontaneous myometrial contraction falls, and every volatile does this to a similar degree. At low concentrations the effect is small. At 0.5 MAC the relaxation is clear, although the uterus still responds to oxytocin. A relaxed uterus is an atonic uterus, so bleeding risk rises, especially in multiparous women. Nitrous oxide is not halogenated and does not have this relaxing action.

Propofol non-volatile doesn't relax myometrium. It is an inhaled anaesthetic given at a high concentration, so people group it with isoflurane and sevoflurane. It is not a halogenated volatile, though, and it does not relax the myometrium. Uterine activity is unaffected.

The review and textbook sources agree. Every halogenated volatile, including isoflurane and sevoflurane, reduces myometrial contractility in proportion to dose. The relaxation is significant by 0.5 MAC and raises haemorrhage risk, particularly in multiparous women. Nitrous oxide does not change uterine activity.

Sources: Mayo reviewBarash 9eFaust

After the first twin is born, the uterus contracts around the second twin, making breech extraction difficult and risking entrapment of the aftercoming head. The obstetrician needs uterine relaxation, which analgesia alone does not provide. High-concentration volatile anaesthesia formerly achieved this but requires general anaesthesia and a secured airway. Intravenous nitroglycerin now gives rapid, brief relaxation without airway risk. Once the baby is delivered, it is stopped so the uterus can contract again and bleeding is limited.

Local anaesthetic top-up cannot relax uterus. An epidural is already running, so topping it up seems like the natural next step before an operative delivery. But the problem here is a contracted uterus, not pain. A local anaesthetic top-up does not relax uterine muscle, so the second twin can still be trapped.

Barash says volatile agents at high MAC can relax the uterus for second-twin and breech manoeuvres, but IV nitroglycerin 50 to 250 μg has mostly taken over this role. Miller says relaxants are stopped after delivery so the uterus contracts and haemorrhage is reduced.

Sources: Barash 9eMiller 10e

The growing uterus pushes the diaphragm upward, so the lungs sit at a smaller volume once a normal breath has been exhaled. Expiratory reserve and residual volume both shrink. FRC is their sum, so it falls too. Otherwise the static lung volumes are largely kept, and inspiratory reserve rises slightly. The lung tissue does not get stiffer, so intrinsic compliance is unchanged. Bronchial flow on spirometry is unaltered, so airway resistance does not increase. Tidal volume, meanwhile, climbs substantially.

Pregnancy shrinks expiratory not inspiratory reserve. A raised diaphragm looks as if it should shrink every lung volume, including the inspiratory ones. It does not. The loss is at the bottom of the breath, in expiratory reserve and residual volume. Inspiratory reserve is kept and even rises slightly.

At term, tidal volume rises by about 40% to 45% and inspiratory reserve by about 5%, while ERV and residual volume both fall. Apart from the fall in FRC, static lung function is unchanged. Intrinsic compliance is unaffected, and bronchial flow on spirometry is unaltered.

Sources: Mayo reviewStoelting 8eMiller 10e

Hormonal drive makes a pregnant woman breathe about 50% more each minute by term. Carbon dioxide is cleared faster than it is produced, so PaCO2 settles well below the non-pregnant level. This is a chronic respiratory alkalosis. The kidneys compensate by excreting bicarbonate, so serum bicarbonate falls by about 4 mEq/L and pH stays only slightly alkalotic. In labour, pain can push ventilation even higher and drive PaCO2 lower still.

FRC falls at term, which seems to fit the pregnancy answer. However, FRC is a resting lung volume that sets oxygen reserve and the rate of desaturation; it does not govern carbon dioxide clearance. Low PaCO2 with compensatory bicarbonate fall results from increased ventilation, not reduced lung volume.

Hormone-driven hyperventilation, with minute ventilation up by half at term, causes a respiratory alkalosis with PaCO2 of 28-32 mmHg. Renal loss of bicarbonate, averaging about 4 mEq/L, keeps pH only mildly alkalotic. Labour pain can occasionally drop PaCO2 below 20 mmHg.

Sources: Stoelting 8eMiller 10eMayo review

Plasma volume grows by about 45%. Red cell volume also grows, but by less: Stoelting gives 20–25% and Faust 10–15%. The sources differ on how much, but both say it rises. Because plasma outpaces cells, the blood is diluted and haemoglobin and haematocrit fall even though red cell mass is higher. Cardiac output rises about 40% through both stroke volume and heart rate. Systemic vascular resistance falls about 15% at the same time, so arterial pressure stays level or dips. Diastolic pressure dips most.

Systemic vascular resistance falls with increased output. Many people picture pregnancy-induced hypertension and assume resistance climbs along with output. In normal pregnancy resistance actually falls. That is why a much larger cardiac output leaves blood pressure level or slightly lower. A fall in SVR is a real, expected change at term.

The tables show plasma volume, red cell volume, cardiac output, stroke volume and heart rate all rising, while vascular resistance falls. Systolic pressure is unchanged or slightly lower, diastolic pressure falls, and haemoglobin and haematocrit drop because of dilution.

Sources: Stoelting 8eFaust

Pregnancy pushes the balance of clotting towards thrombosis. Most procoagulant factors rise, fibrinogen the most, and natural anticoagulants weaken: protein S and antithrombin fall, and resistance to activated protein C develops even though Miller finds protein C levels unchanged. This imbalance explains why venous thromboembolism is more common in pregnancy. The sources differ on a few factors. One Barash thrombosis list counts II and XIII as raised. Barash's physiology section and Miller both say XI and XIII fall, and Miller keeps II and V unchanged. Use that shared pattern.

Factor XIII falls despite general factor rise. Nearly every clotting factor rises in pregnancy, so it feels safe to assume XIII rises too, and one thrombosis list even includes it. But the obstetric physiology sections of both major texts put XIII with XI as falling, so a rise in XIII is not the expected change.

Miller: factors XI and XIII fall; II and V usually unchanged; protein S and antithrombin fall, protein C holds. Stoelting: anticoagulant activity drops, while fibrinogen and factors XII, X, IX, VIII, VII and I rise. Barash adds acquired protein C resistance.

Sources: Miller 10eStoelting 8eBarash 9e

Pregnancy does not meaningfully change liver perfusion. Options saying flow rises, the liver becomes congested, or compression cuts flow are therefore wrong. What changes is the level of proteins the liver makes. The expanded plasma volume dilutes them, and the liver also makes less cholinesterase. At term albumin is about 25% lower and total protein about 10% lower. Cholinesterase activity falls by roughly 25% to 30% from week 10 until postpartum week 6. That fall is too small to prolong a suxamethonium block.

Cholinesterase reduction insufficient to prolong paralysis. It is tempting because the direction and the timing are right and it sounds like textbook wording. But it overstates the size of the fall. Cholinesterase activity drops by only about a quarter to a third, which is why suxamethonium block is not meaningfully prolonged.

Pregnancy does not significantly change liver blood flow. At term, albumin is 25% lower and total protein 10% lower. Cholinesterase activity falls 25–30% from week 10 to postpartum week 6, from dilution and reduced hepatic synthesis, without needing succinylcholine dose change.

Sources: Miller 10eFaustBarash 9e

Pregnancy increases blood volume and cardiac output. The mitral and tricuspid valves close asynchronously, so S1 becomes louder and more widely split. Extra volume and turbulent flow produce an S3 late in pregnancy and sometimes an S4; neither is significant alone. The enlarged heart stretches the tricuspid annulus, causing mild regurgitation, heard as a benign systolic ejection murmur along the left sternal border. The sources describe no change in the second heart sound.

Diastolic murmur signals valve disease not normal. When asked for a pregnancy murmur, people pick the only murmur on offer, reasoning that a hyperdynamic circulation makes murmurs. But the benign pregnancy murmur is systolic, coming from tricuspid regurgitation during contraction. A diastolic murmur is not among the normal findings and should prompt a search for valve disease.

The obstetric anaesthesia text lists these normal findings: an accentuated S1 with more splitting from out-of-step atrioventricular valve closure; a frequent S3 in the third trimester; an occasional S4; and a benign systolic ejection murmur heard along the left sternal border from mild tricuspid regurgitation.

Sources: Miller 10e

Enlarged breasts crowd the space between chest and chin, so the laryngoscope handle is awkward to insert. The lining of the upper airway becomes engorged, so it swells and bleeds easily. Pre-eclampsia worsens that swelling, so the risk is greater in that patient but the same kind of problem. Separately, a smaller FRC and higher oxygen needs shorten safe apnoea, and weaker sphincter tone favours reflux. These make desaturation and aspiration more dangerous, but they do not physically obstruct intubation.

Pregnancy lowers reserve making difficult airway myth. FRC dominates teaching on obstetric oxygenation, and head-up positioning is recommended partly to raise it, so 'increase' sounds familiar. Pregnancy actually lowers FRC. Even a larger reserve would make airway management easier, not harder.

Enlarged breasts can obstruct insertion of the laryngoscope. The upper airway mucosa becomes vascular and oedematous, with swelling and bleeding risk, and this oedema is worse with pre-eclampsia. Reduced FRC and raised oxygen demand speed desaturation, and sphincter tone falls, promoting reflux.

Sources: Outside our books: Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics (2015)Miller 10e

Most of the aspiration risk in pregnancy comes from hormones. Progesterone lowers lower oesophageal sphincter tone and slows gastric emptying, and the placenta is its main source. Once the placenta is delivered, progesterone starts to fall within hours and is back to normal within a day (Faust). The three sources give different times but agree with each other. Gastric emptying recovers first, by 18 hours (obstetric airway guideline). The rest of the gut follows by one to two days (Barash). None of them gives weeks.

Stomach recovery confused with puerperium. Six weeks is the length of the puerperium, when many other pregnancy changes are taught to resolve, so it feels like the safe default. But the stomach changes depend on placental progesterone, which falls within hours of delivery, so they resolve within about a day.

The obstetric airway guideline says gastric emptying is normal by 18 hours after delivery. Faust says progesterone starts falling 2 hours postpartum and is normal within 24 hours. Barash says the gut changes of pregnancy resolve by 24 to 48 hours postpartum.

Sources: Outside our books: Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics (2015)Barash 9eFaust

During pregnancy, hormones that counter insulin rise: placental lactogen, progesterone, oestrogen and cortisol, which goes up 2.5-fold by term. They reduce how well maternal tissues respond to insulin. This is a problem of insulin action, not of insulin supply. The resistance comes from the placenta and the pregnancy hormonal state, so it resolves soon after birth. Despite the resistance, fasting glucose is lower than outside pregnancy because the fetus takes up a lot of glucose.

Low insulin secretion mistaken for resistance. Too little insulin also raises glucose, so it sounds plausible. But low secretion means insulin deficiency, not resistance. Resistance means the tissues respond poorly to insulin that is there. In pregnancy this comes from placental and other hormones, and it goes away once the placenta is delivered.

Stoelting says pregnancy's insulin resistance comes from more activity of progesterone, oestrogen, cortisol (up 2.5-fold at term) and placental lactogen. It resolves quickly after delivery. Fasting glucose is lower in pregnancy because the fetus uses a lot of glucose.

Sources: Stoelting 8e

With no carbohydrate coming in, the body burns fat instead, and ketone bodies build up. This is starvation ketosis. National intrapartum guidance calls it a normal adaptation to fasting in women without diabetes. It settles on its own once she eats, so the old habit of giving drips for it is unnecessary. The exception is a woman taking an SGLT-inhibitor. Fasting can amplify the same process into ketoacidosis with near-normal glucose, so look for an anion-gap acidosis with ketonaemia.

Gallstone formation from labour fasting. Gallstones are tempting because pregnancy slows bile flow and raises the risk of stones. But stones form over weeks to months. They are not a product of a few hours without food in labour. The immediate metabolic result of fasting is ketone production.

Intrapartum guidance describes ketosis in women without diabetes as a normal, usually self-limiting result of fasting. It clears with oral carbohydrate, and routine intravenous fluids are not needed. Ketoacidosis should be suspected when ketones come with an anion-gap acidosis.

Sources: Outside our books: Intrapartum care, NICE guideline NG235 — [P] Supporting document for the recommendations on fluid balance and peripartum hyponatraemia (2025)AHA/ACC 2024 · §6.3

COX-1 makes thromboxane A2. It causes platelets to clump and narrows blood vessels. Prostacyclin and nitric oxide do the opposite: they dilate vessels and keep uterine perfusion high. A healthy pregnancy depends on these two sides staying in balance. In pre-eclampsia, the damaged endothelium produces fewer dilating eicosanoids and more platelets are activated. The balance then tips further towards thromboxane, so the spiral arteries constrict and uterine flow falls.

Thromboxane vasodilation in pregnancy assumed. Pregnancy is known to raise uterine perfusion, and prostaglandins are often thought of as vasodilators, so this looks like a normal pregnancy effect. Thromboxane actually constricts vessels. Too much of it reduces uterine flow, as in pre-eclampsia. The dilating role belongs to prostacyclin and nitric oxide.

Thromboxane A2 is made by COX-1 and drives platelet aggregation and vasoconstriction. In pre-eclampsia, endothelial injury activates platelets and shifts the prostacyclin–thromboxane balance. With less nitric oxide and fewer dilating eicosanoids, uterine blood flow falls and the spiral arteries constrict.

Sources: Miller 10eFaust

During a contraction, pressure on the fetal head triggers a vagal reflex that slows the heart. The dip is shallow, usually under 20 beats/min, and starts and recovers with the contraction, mirroring it. It does not indicate hypoxaemia or acidosis. A tracing with early decelerations can still be normal if the baseline rate is 110–160 bpm, variability is moderate, and there are no late or variable decelerations. Seeing it straight after a block does not mean the epidural has harmed the fetus.

Normal reflex escalation after block. People escalate when any deceleration appears minutes after a block, fearing epidural fetal harm. But a smooth, shallow dip matching each contraction is a vagal reflex within a normal tracing, so escalation adds nothing. Only late or recurrent variable decelerations need action.

Several texts agree that early decelerations are shallow, usually under 20 beats/min, and track the contraction. They come from vagal slowing caused by head compression and are not linked to fetal compromise, hypoxaemia or acidosis. The three-tier system allows them within a Category I tracing.

Sources: Mayo reviewBarash 9e

Absent variability with recurrent late decelerations marks a category III trace, which signals fetal acidaemia and needs urgent assessment. In-utero resuscitation targets reversible causes, maternal hypotension, aortocaval compression, excess uterine activity, but if the trace fails to recover, delivery, often operative, must follow quickly, and only the obstetrician delivers. So an abnormal trace before siting means the obstetric team must know and plan first. After a bolus, sympathetic block makes maternal hypotension the prime suspect: fresh vital signs detect it, and the obstetrician must be present in case resuscitation fails.

Oxygen as initial fetal resuscitation. Oxygen is tempting because supplemental oxygen is a listed in-utero resuscitation measure. But it neither detects nor corrects the likely culprit after a bolus, maternal hypotension, and it does nothing to bring the obstetrician who must deliver if the trace persists.

Category III traces are abnormal, imply fetal acid–base disturbance and demand prompt evaluation. Resuscitation includes treating maternal hypotension with fluid or vasopressor, oxygen and tocolysis; if the trace does not improve, expedited delivery follows.

Sources: Barash 9eMiller 10e

When the uterine wall tears, blood supply to the placental bed can be cut off and the fetus or placenta may be pushed out of the uterus. Oxygen delivery to the fetus then falls quickly, so the fetal heart trace changes early and in most cases. Maternal signs are less consistent. Breakthrough pain appears in only a minority of women and is not explained by the epidural. Bleeding, hypotension, tachycardia and shock come with haemorrhage. Abnormal presentation, such as breech, is a risk factor.

Breakthrough pain as rupture sign. Review books describe rupture as severe pain with fetal distress, but pain is not the classic sign. Breakthrough pain occurs in only a minority, and its absence is not due to the epidural. A pain-free woman can still have a rupture; the fetal trace detects it more reliably.

Miller lists fetal bradycardia, cessation of contractions, pain, bleeding and loss of station as signs; a non-reassuring fetal heart trace is the most reliable and sensitive. Breakthrough pain is uncommon and unrelated to the epidural. Faust adds hypotension, tachycardia, shock. Malposition is a risk factor.

Sources: Miller 10eFaust

Pre-eclampsia means hypertension plus evidence that organs are being damaged, and proteinuria is only one sign of that damage. Severity depends on which organs are affected, not on how much protein is in the urine. Proteinuria is not on the severe-feature list, and new hypertension with any severe feature counts as pre-eclampsia even when the urine has no protein. Severe-range pressure qualifies on its own. The two readings should ideally be 4 hours apart, but treatment does not have to wait for the second reading.

Pregnancy-induced hypertension despite severe features. Pregnancy-induced hypertension is tempting because the pressure rose for the first time after 20 weeks. That label only applies when there is no proteinuria and no sign of organ damage. Headache, epigastric pain and severe-range pressure are signs of organ damage, so the diagnosis becomes pre-eclampsia with severe features.

Severe features: pressure ≥160 systolic or ≥110 diastolic on two readings 4 hours apart; platelets below 100,000 per microlitre; liver enzymes over twice normal or severe right upper quadrant or epigastric pain; creatinine above 1.1 mg/dL or doubled; pulmonary oedema; new headache or visual disturbance.

Sources: Barash 9eFaustStoelting 8e

HELLP is a severe form of pre-eclampsia defined by the triad; platelet count grades it, and about 100,000/mm3 marks the mild–moderate border. Magnesium sulfate is deliberately titrated above the normal 1.5–2 mEq/L. Being divalent, its millimolar value doubles in milliequivalents, so a typical infusion reading lands in target. Most texts give 4–8 mEq/L; one table narrows this to 4.0–6.0 and starts ECG changes at 5.0, so the bands overlap: an overlap value remains therapeutic, with the ECG watched. No source makes mild hyperkalaemia a separate diagnosis.

Magnesium elevation as separate criterion. Listing every value is tempting because all look abnormal against non-pregnant norms. It is wrong because magnesium is the intended effect of the infusion and lies within the treatment band once converted to milliequivalents. No source treats slightly raised potassium as a separate diagnosis.

HELLP is described as a severe pre-eclampsia variant marked by haemolysis, raised liver enzymes and thrombocytopenia, graded mild to severe by platelet count. Normal magnesium is 1.5–2 mEq/L; treatment aims for 4–8, with one table giving 4.0–6.0 and ECG changes from 5.0.

Sources: Barash 9eMayo reviewFaust

Trophoblast invasion is shallow, so the spiral arteries stay narrow and resist flow. The poorly perfused placenta then releases vasoactive factors that damage the mother's endothelium throughout the body. The result is widespread vasoconstriction and greater sensitivity to catecholamines. Low plasma protein and haemoconcentration mean the circulation is depleted, so the high blood pressure comes from resistance rather than from extra volume. The heart is often hyperdynamic but not in every woman, and some women have myocardial dysfunction.

Raised cardiac index as signature. Many preeclamptic women do have a hyperdynamic heart, so a raised cardiac index seems plausible. But it is not consistent: some women have myocardial dysfunction. The finding that the sources list reliably, and that explains the hypertension, is raised vascular resistance.

One textbook says most preeclamptic women, though not all, have a hyperdynamic heart and moderately raised SVR. Another lists raised SVR alongside hypovolaemia, haemoconcentration and myocardial dysfunction. The first textbook traces this to placental factors that injure the maternal endothelium.

Sources: Stoelting 8eFaust

The cure is delivery of the fetus and placenta, so the disease is tied to the pregnancy itself. Antihypertensives and vasodilators lower the blood pressure but do not reverse the disorder. What needs deciding is when to deliver, not whether. Two things set the timing: how severe the mother's disease is and how mature the fetus is. Without severe features, it is acceptable to wait until term. A preterm fetus justifies symptomatic control under close monitoring. Once the pregnancy reaches term, waiting gains nothing.

Seizure onset predicted from presentation. Hypertension with oedema in an older mother who had little antenatal care sounds alarming, so predicting seizures feels safe. But nothing in the picture shows that seizures are about to happen. The only statement that is always true is that delivery cures the disease.

Every source agrees that delivery is the only curative treatment. Expectant management is allowed until 37 weeks when there are no severe features. For a preterm fetus, symptomatic antihypertensive treatment with close obstetric monitoring is used until delivery.

Sources: Barash 9eFaustStoelting 8e

Normally the decidua provides a plane for placental separation. When it is absent, villi attach to or grow into the uterine wall, named by depth. Accreta: villi only attach. Increta: villi invade the myometrium but remain within it. Percreta: villi penetrate the full thickness of the muscle, can reach the serosa, and may invade organs such as the bladder or bowel. Invasion through the full myometrial thickness is therefore percreta.

Increta as complete myometrial invasion. "Increta" sounds like "into the muscle", so invasion of the whole muscle seems to fit it. But increta stays inside the myometrium. Villi that cross its full thickness have reached the serosa, and that is percreta.

Accreta, the most common type, adheres to the muscle without invading it, with no decidual separation plane. Increta invades the myometrium. Percreta penetrates the uterine wall to the serosa and beyond, and may implant on the bladder, bowel or ovaries.

Sources: FaustMiller 10e

Praevia itself is the main driver of accreta. The number of earlier hysterotomies is the second driver, and the risk rises steeply with each extra uterine scar. Barash and Miller give single figures that climb step by step with each caesarean. The Mayo review gives ranges instead: about 10% to 25% for one scar, and 40% to over 60% for two or more. Those ranges contain the single figures, so the sources agree. When a question wants one number, use the single figure for the exact number of scars.

Parity counted instead of caesarean scars. 40% is the risk with two previous caesareans. A woman who is para 2 has delivered twice, but if only one delivery was a caesarean she has one uterine scar. Counting deliveries instead of hysterotomies overshoots. Her risk is about 11%.

When praevia is known, accreta risk rises from 3% with no previous caesarean to 61% with three. Miller gives the steps in between: 11% with one and 40% with two. The Mayo review quotes ranges that contain these figures.

Sources: Barash 9eMiller 10eMayo review

The lumbosacral trunk joins L4 and L5 fibres and descends into the pelvis, where a fetal head held low through a long second stage can compress it; losing L5 weakens dorsiflexion, numbs the anterolateral leg and drops the foot. Miller ties postpartum lumbosacral injury to nulliparity and prolonged pushing, not epidural use; Barash calls such obstetric palsies commoner than anaesthetic ones. If the trunk is not offered, choose cephalopelvic disproportion, its obstetric cause; femoral and lateral femoral cutaneous neuropathies spare dorsiflexion, and residual block is bilateral and brief.

Lithotomy nerve injury from labour. Common peroneal palsy produces exactly this foot drop, so it looks right. But it is the lithotomy injury, the nerve squeezed against the fibular head by leg supports; after a long second stage without that, the lesion sits higher, in the lumbosacral trunk within the pelvis.

Miller links postpartum lumbosacral injury to first births and a long second stage, not to epidural analgesia, with femoral and lateral femoral cutaneous neuropathies commonest. Barash says obstetric palsies outnumber anaesthetic nerve injuries, partly via fetal-head compression; the lumbosacral trunk unites L4 and L5.

Sources: Miller 10eBarash 9e

The sciatic nerve divides into the tibial and common peroneal nerves. The tibial nerve plantar flexes and inverts the foot. The common peroneal nerve dorsiflexes and everts it, and it also extends the toes. It winds superficially round the fibular head, so a leg brace, stirrup or frame can compress it against bone. That can happen in lithotomy or labour positioning. Losing this nerve therefore removes the muscles that lift the foot and toes. The tibial muscles are untouched, so the foot hangs down and cannot be turned outward.

Tibial nerve weakness in peroneal palsy. This is tempting because the tibial and common peroneal nerves are sister branches of the sciatic nerve and are easily swapped. Plantar flexion belongs to the tibial nerve. A peroneal lesion leaves it intact and does the opposite: the foot cannot be lifted.

The common peroneal nerve is usually damaged where it is pressed against the fibular head by an external support. The injury causes foot drop, with impaired ankle dorsiflexion and loss of eversion and toe extension. The tibial nerve separately mediates plantar flexion and inversion.

Sources: Mayo reviewMiller 10eBarash 9e

The obturator nerve supplies the adductors (longus, brevis, gracilis, pectineus) and the skin of the medial thigh. A lesion causes weak adduction and a strip of inner-thigh numbness, sparing knee extension and the foot. The nerve runs inside the pelvis and exits through the obturator foramen, where forceps delivery or pelvic retraction can compress it. Abducting the hip beyond 30 degrees, or flexing the thigh hard to the groin, stretches it. The epidural does not injure the nerve; delivery and positioning do.

Lumbosacral compression causing adductor weakness. In prolonged labour, the fetal head can compress the lumbosacral trunk against the pelvic brim, the classic obstetric palsy, causing foot drop and lower leg and foot numbness. It does not cause isolated adductor weakness with numbness confined to the medial thigh.

Difficult forceps delivery or strong thigh flexion can damage the obturator nerve, causing loss of adduction and reduced medial thigh sensation. The nerve supplies the adductors and medial thigh skin. Abduction beyond 30 degrees stretches it.

Sources: Mayo reviewBarash 9eFaust

Going up stairs means straightening the knee against body weight, which is the quadriceps' job, and the femoral nerve supplies it. The nerve also carries sensation from the front of the thigh and the inner leg. It is stretched or pinched when the hips stay sharply flexed during long pushing in a semi-sitting position. Sustained compression during a prolonged second stage causes the palsy, not the epidural. Obturator injury looks different: the thigh cannot adduct and numbness is on the inner thigh.

Trunk compression from stair difficulty. The fetal head stuck in the pelvis for hours points toward a pelvic lesion, and fetal head compression is a recognised cause of obstetric palsy. But the complaint to match is failed knee extension, a quadriceps deficit. The sources link that to the femoral nerve, not to a trunk lesion.

Femoral and lateral femoral cutaneous neuropathies are the commonest postpartum nerve injuries, linked to nulliparity and prolonged second stage, not epidural use. Femoral injury weakens knee extension and numbs the anterior thigh; obturator injury causes adduction weakness and medial thigh numbness.

Sources: Mayo reviewMiller 10e

In eclampsia, magnesium is more effective and safer than benzodiazepines or phenytoin, so a breakthrough fit indicates too little magnesium, not the wrong drug. The infusion should hold plasma levels at 4 to 8 mEq/L. A fit on the infusion suggests the level has fallen short: give an extra bolus, then measure the level to confirm the range. If no bolus is offered, raising the infusion rate is the nearest correct move. A seizure alone does not force delivery if mother and fetus are stable.

Benzodiazepine as seizure first-line drug. Midazolam is the reflex first-line drug for a generalised seizure, and a fit on magnesium looks like magnesium has failed. In eclampsia, though, magnesium is more effective and safer than benzodiazepines. The breakthrough fit is treated with more magnesium, so a benzodiazepine is not the first drug.

Magnesium is the anticonvulsant of choice in eclampsia, preferred to benzodiazepines and phenytoin. For a seizure during prophylactic infusion, give a 1–2 g bolus, then check plasma level (target 4–8 mEq/L). Delivery need not be immediate if mother and fetus are stable.

Sources: Stoelting 8eBarash 9e

The infusion is still adding magnesium, so turning it off comes first. Calcium does not remove magnesium. It only blocks its effects for a short time. When signs are life-threatening, such as conduction block or arrhythmia, calcium buys time while the magnesium is cleared. Milder excess is cleared through the kidneys with saline and loop diuretics. Dialysis may be needed if toxicity is severe. Inject calcium slowly, because giving it quickly can remove magnesium's protection against eclamptic seizures.

Fast calcium push or diuretics prioritised. The tempting errors are a fast calcium push, or diuretics first. Diuretics suit milder excess but work too slowly for an arrhythmia, so stopping the infusion and giving calcium must come first. A fast push can remove the anticonvulsant protection, so give calcium slowly.

Stop any magnesium infusion and give 1 g calcium gluconate (10 mL of 10%) slowly over at least 2 minutes when toxicity is suspected. Calcium only temporarily relieves life-threatening signs. Saline with loop diuretics treats milder excess; dialysis may be needed.

Sources: Barash 9eMayo reviewStoelting 8e

Magnesium dilates blood vessels, so blood pressure falls. It also makes existing hypotension worse, a risk named specifically when it is given to protect the preterm fetal brain. It depresses the nervous system and neuromuscular transmission, so tendon reflexes weaken and then disappear. At higher levels breathing is depressed, not stimulated. It causes urinary retention and ileus, not a diuresis. Brisk reflexes are a sign of the underlying pre-eclampsia, which the drug is given to suppress, not a sign of the drug.

Magnesium causing brisk reflex preservation. Brisk reflexes are a classic pre-eclampsia sign and sit next to magnesium in obstetric tables, so the option feels familiar. Magnesium does the opposite: it depresses nerve and muscle function, so reflexes fade. Brisk reflexes during an infusion point to the disease, not the drug.

Barash warns that magnesium given for fetal neuroprotection worsens hypotension and strengthens muscle relaxants. Stoelting links hypotension to vasodilation and lists loss of tendon reflexes as levels rise. Barash adds urinary retention, hyporeflexia and respiratory depression at higher levels.

Sources: Barash 9eStoelting 8e

Magnesium acts at the myoneural junction and strengthens the block that relaxants produce, so each dose has a larger and longer effect. After a 40 mg/kg loading dose, the vecuronium dose needed for half-maximal effect fell by 25%. Onset was almost twice as fast and recovery took about twice as long. Suxamethonium is potentiated as well as non-depolarising agents. Magnesium can also make hypotension worse, so haemodynamic vigilance goes alongside careful dosing of relaxants.

Magnesium reducing neuromuscular block duration. This option names the right drug class and the right interaction, which is why it catches people. But it gets the direction backwards. Magnesium makes the junction more sensitive, so smaller doses are needed and the block lasts longer. Assuming reduced sensitivity leads to overdosing and residual paralysis.

Magnesium given for pre-eclampsia potentiates non-depolarising block, with a lower effective dose, faster onset and longer recovery. It also potentiates depolarising relaxants and prolongs their effect at the myoneural junction. The texts also warn about extubation after magnesium.

Sources: Miller 10eBarash 9e

Both drugs restore maternal blood pressure about equally well, so the choice depends on the baby. Ephedrine crosses the placenta much more (fetal-to-maternal ratio 0.7 against 0.2), which gives beta stimulation in the fetus and more fetal acidosis. The obstetric guideline keeps both drugs as current options. When the mother is not bradycardic, it steers towards phenylephrine, so a mother with a normal or fast heart rate falls on that side. When her heart rate is slow, ephedrine becomes the better choice.

Ephedrine without bradycardia assessment chosen. Ephedrine is familiar and guideline-approved, so it feels like the safe classic answer. Its advantage only applies when the mother is bradycardic. With a normal or fast heart rate, it adds nothing over phenylephrine and crosses the placenta more, leaving the fetus more acidotic.

The obstetric anaesthesia guideline permits either drug for neuraxial hypotension but advises phenylephrine without maternal bradycardia, given better fetal acid–base status. A major text finds them equally effective, with less fetal acidosis from phenylephrine. A review reserves ephedrine for bradycardic hypotension.

Sources: Mayo reviewOutside our books: Practice Guidelines for Obstetric Anesthesia: An Updated Report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia and the Society for Obstetric Anesthesia and Perinatology (2016)Barash 9e

Progesterone raises nitric oxide and prostacyclin output, and vessels respond less to noradrenaline and angiotensin. The pregnant woman is therefore vasodilated from early gestation, with resistance falling by 20% to 50% from about 8 weeks. Her blood pressure depends on reflex sympathetic vasoconstriction, especially when the gravid uterus compresses the vena cava in the supine position. A spinal block abolishes that sympathetic drive. Resistance then falls further from an already low baseline, and the compensation against caval compression is lost, so pressure drops more than in a non-pregnant patient.

Cardiac output increase causing pressure fall. A raised cardiac output is a real and well-known change in pregnancy, so it feels like the right answer. But a higher output supports blood pressure rather than lowering it. The fall after a spinal comes from reduced vascular resistance, not from the heart.

Pregnancy hormones cause peripheral vasodilation and lower systemic resistance from early gestation. Pregnancy is a named risk factor for hypotension after a spinal. Neuraxial block removes the sympathetic vasoconstriction that normally offsets supine caval compression, which makes the hypotension worse.

Sources: Barash 9eStoelting 8eMiller 10e

Lying supine lets the heavy late-pregnancy uterus fall back onto the inferior vena cava, so venous return, preload and cardiac output fall; hypotension, bradycardia and reduced uterine flow with fetal distress can follow. Neuraxial block adds its own fall in pressure, so flat positioning is avoided during spinals. The term 'aortocaval' reflects an older belief, still used by Barash and Miller, that the aorta is squeezed too; Stoelting notes newer evidence spares the aorta. Either way, shifting the uterus leftward restores flow.

Spinal anaesthesia blamed for caval compression. Spinal-induced hypotension is tempting because it is the commonest complication after neuraxial block. But here pressure fell the instant she lay flat and recovered with left tilt; relief by displacing the uterus identifies caval compression as the cause, with the block merely aggravating it.

At term a minority of women develop hypotension and bradycardia within minutes of lying supine, because the enlarged uterus compresses the vena cava and cuts venous return. Left tilt lessens the fall and protects uterine and fetal flow. Newer work suggests the aorta is spared.

Sources: Mayo reviewMiller 10eStoelting 8e

BIS is a processed EEG index with a general anaesthesia target of 40 to 60, so a reading this low is deeper than needed. In propofol–remifentanil anaesthesia the value mainly reflects propofol, as the monitor barely registers opioids; a low reading therefore means excess propofol. First remove the surplus hypnotic. A drug that only speeds the heart leaves the overdose in place. In a term patient, also check for left uterine displacement, as supine caval compression alone can cause hypotension and bradycardia.

Anticholinergic chosen for assumed vagal effect. A heart rate under 60 with soft pressure makes an anticholinergic look like the obvious answer. But the rate is only slightly slow and nothing points to a vagal trigger. The BIS shows the patient is too deep, and glycopyrrolate does nothing to correct that cause.

Barash sets the BIS target for general anaesthesia at 40 to 60. It notes that processed EEG hardly responds to opioids, so under TIVA the reading mainly reflects propofol. The Mayo review notes that supine term patients can develop hypotension with bradycardia from aortocaval compression.

Sources: Barash 9eMayo review

Blood crosses a narrowed mitral orifice only during diastole. A faster heart rate shortens filling time, raising left atrial and pulmonary pressures and lowering output. Tachycardia is more harmful than losing atrial contraction. Phenylephrine restores systemic pressure with little effect on pulmonary artery pressure, and obstetric guidance already prefers it when the mother is not bradycardic. Barash's table grades an intermediate valve area as moderate; Miller and the valve guideline call it severe, with a high gradient and pulmonary pressure. The drug choice is the same either way.

Ephedrine despite heart rate increase risk. Ephedrine is the usual obstetric pressor and would be right if the mother were bradycardic. But its beta-adrenergic action speeds the heart. In mitral stenosis the shorter diastole raises left atrial pressure and risks pulmonary oedema, so it makes the underlying problem worse.

Stoelting favours pure alpha vasoconstrictors such as phenylephrine for hypotension in mitral stenosis, sparing pulmonary pressure. Miller warns tachycardia shortens diastolic filling and is the main cause of decline. Obstetric guidelines prefer phenylephrine unless the mother is bradycardic, as fetal acid–base is better.

Sources: Stoelting 8eMiller 10eOutside our books: Practice Guidelines for Obstetric Anesthesia: An Updated Report by the American Society of Anesthesiologists Task Force on Obstetric Anesthesia and the Society for Obstetric Anesthesia and Perinatology (2016)

A poor first view often has a correctable cause: cricoid force can distort the larynx, and head position or external laryngeal manipulation can improve the view. The obstetric difficult airway guideline therefore expects a second, better-equipped attempt by the senior person. The newer adult difficult airway guideline adds exit branches: stop at once and oxygenate by facemask if she desaturates, and declare failure even after one look if nothing can be changed. A second attempt is justified only if there is an improvement to make and she is well oxygenated.

Rescue airway device before optimisation. A laryngeal mask with cricoid pressure is the standard rescue after failed intubation, but failure has not been declared: she is oxygenating and the poor view is correctable. Use the rescue device only if the optimised second attempt fails.

The obstetric guideline wants a senior second attempt with alternative equipment, after improving a poor view by easing cricoid force, laryngeal manipulation and repositioning. The adult guideline: hypoxaemia ends any attempt; failure may be declared after one attempt if nothing can improve.

Sources: Outside our books: Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics (2015)Difficult Airway Society 2025

A supraglottic airway restores oxygenation; a second-generation drain tube allows gastric suction. If neither device nor mask oxygenates, declare CICO, call an ear, nose and throat surgeon or intensivist, and do scalpel-bougie-tube front-of-neck access: narrow cannulas fail more, especially in obesity; surgical airways succeed more. If that fails, start arrest protocol with caesarean beyond 20 weeks. Once oxygenated by any method, front-of-neck access included, weigh waking against proceeding by maternal and fetal compromise: no urgency, wake; urgent, operate on the device, intubating through it only if required, fibrescope-guided.

Video laryngoscopy retry during desaturation. Video laryngoscopes improve the glottic view and are promoted as a rescue after failed direct laryngoscopy, so another attempt feels logical. But with saturation falling after a failed attempt, priority shifts from intubating to oxygenating; further attempts prolong hypoxia and risk airway trauma, while a supraglottic airway restores oxygenation.

A supraglottic device is advised after failed intubation. The obstetric airway guideline adds drain-tube suction, fibrescope-only intubation through it, a wake-or-proceed review once oxygenated, specialist help once CICO is declared, surgical over cannula access, and arrest protocol with caesarean beyond 20 weeks.

Sources: Miller 10eOutside our books: Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics (2015)Difficult Airway Society 2025

Amniotic material gets into the mother's circulation through open uteroplacental sinusoids or torn endocervical veins. That is why the event is tied to labour and the time just after the placenta separates. Pulmonary vasospasm first causes severe pulmonary hypertension and right heart failure. Left ventricular failure and pulmonary oedema follow, causing hypoxaemia and severe hypotension, and a consumptive coagulopathy develops. None of these features is unique to this condition. So the consensus definition needs all three: abrupt collapse, DIC and the timing, with no better diagnosis.

Uterine atony as embolism criterion. The mother bleeds heavily after delivery, so atony seems to fit. But in this condition the bleeding comes from DIC, not a soft uterus. Atony is an alternative cause of postpartum haemorrhage, and the criteria exclude anything with another obvious diagnosis. Atony plays no part in the definition.

The consensus definition requires sudden cardiorespiratory compromise, documented DIC, and onset in labour or within 30 minutes of placental delivery, with no other obvious diagnosis. The classic triad is hypoxaemia, haemodynamic collapse and coagulopathy with no clear cause.

Sources: Miller 10eMayo review

Amniotic fluid entering the maternal circulation first causes intense pulmonary vasospasm, severe pulmonary hypertension and right ventricular failure. This produces abrupt cardiovascular collapse and hypoxaemia, with consumptive coagulopathy later. The hypoxia is circulatory, not airway-related: high airway pressure is not seen and bronchospasm is rare, under 15%, so it is never the explanation. Seizures occur in roughly half of cases. Breathlessness is the commonest symptom; hypotension and foetal distress lead the signs. AFE can follow second-trimester termination and is a diagnosis of exclusion.

Hypotension sign chosen instead of symptom. Hypotension is the most frequent sign and heads the signs list, so it feels like the answer to any 'most common' question. But it is a sign found on examination. The commonest symptom the patient reports is breathlessness. So first decide whether a symptom or a sign is wanted.

AFE presents dramatically: hypoxaemia, circulatory collapse, DIC, seizures in about 50%; bronchospasm and high airway pressures are not features. Dyspnoea leads symptoms, hypotension signs. Criteria: sudden cardiorespiratory compromise with DIC, in labour or within 30 minutes of placental delivery, with no other diagnosis.

Sources: Mayo reviewOutside our books: Amniotic fluid embolism (2007)Miller 10e

Amniotic fluid can reach the maternal circulation only after the membranes are breached. It also needs an open venous route, either at the placental bed or through torn cervical veins, so amniotomy is the classic trigger. The circulatory insult comes in two phases. First, pulmonary vasospasm causes acute pulmonary hypertension and right heart failure. Left ventricular failure follows. More than 80% progress to cardiopulmonary arrest. Early features include confusion or unresponsiveness, hypoxia and hypotension. The accompanying disseminated intravascular coagulation explains brisk vaginal bleeding.

Abruption with sudden collapse and bleeding. Abruption tempts because vaginal bleeding with shock is its hallmark. However, it presents with a tender, hypertonic uterus and dark clotted blood, and any hypovolaemic changes follow the blood loss. Sudden collapse and altered consciousness triggered by amniotomy, with bleeding from coagulopathy, fit embolism instead.

Embolism needs ruptured membranes plus an open uteroplacental or cervical venous route. Response is biphasic: right heart failure, then left; over 80% arrest. Early signs: altered mentation, hypotension, disseminated intravascular coagulation. Abruption shows a tender, hypertonic uterus and dark clotted blood.

Sources: Mayo reviewMiller 10eBarash 9e

CT angiography has replaced ventilation–perfusion scanning as the first-line test for pulmonary embolism, so a clot seen in the pulmonary arteries confirms the diagnosis. Amniotic fluid embolism has no confirmatory test. It is diagnosed only from the clinical picture: abrupt cardiorespiratory collapse with DIC, starting in labour or within 30 minutes of placental delivery, with no other explanation. A clot shown on CT is that other explanation. A large clot overloads the right ventricle, which produces the strain pattern.

Amniotic embolism despite pulmonary clot. Amniotic fluid embolism is the classic sudden peripartum catastrophe, so breathlessness and tachycardia after delivery point people towards it. But it is a clinical diagnosis. It needs coagulopathy and collapse, and it is excluded once another cause is shown. A clot seen on CT is exactly that other cause.

Chest CT has replaced ventilation–perfusion scanning as the main test for pulmonary embolism. Amniotic fluid embolism has no diagnostic test. It needs sudden cardiorespiratory compromise, DIC, onset in labour or within 30 minutes of placental delivery, and no other obvious diagnosis.

Sources: Barash 9eMiller 10e

Treatment depends on proving a clot anywhere. If leg ultrasound shows a DVT, the woman gets the same anticoagulation, so she needs no chest imaging. If her legs show no signs, her lungs must be imaged. Barash, writing about critically ill patients, says helical CT has replaced V/Q scanning as the main test. The RCOG obstetric guideline instead treats V/Q scan and CTPA as equal options in pregnancy. It prefers CTPA only when the chest film is abnormal.

Catheter angiography as first-line PE test. Catheter angiography sounds like the gold standard, and "highly suspected" tempts towards the most invasive test. However, it is now reserved for narrow situations, such as high PE likelihood with anticoagulation contraindicated and an immediate caval filter needed. It is not the guideline test in pregnancy.

RCOG advises leg duplex ultrasound if DVT signs are present, with no further tests if clot is found. Otherwise it advises V/Q scan or CTPA, favouring CTPA if chest radiograph is abnormal. A critical-care text notes CT has generally overtaken V/Q scanning.

Sources: Outside our books: Thromboembolic Disease in Pregnancy and the Puerperium: Acute Management (2015)Barash 9e

Neuraxial procedures can introduce bacteria into the meninges, usually Streptococcus viridans from the clinician's nasopharynx, via contaminated drugs or needles. Meningeal inflammation causes fever, neck rigidity and falling consciousness. Meningitis may begin as a headache and be mislabelled as a leak headache. A cerebrospinal fluid leak headache worsens sitting up, eases lying flat, has no fever and, in over 90%, begins within 3 days of puncture. A fever-driven illness weeks after delivery therefore suggests infection, not a leak.

Post-dural leak assumed at weeks. Severe postpartum headache with neck pain makes people think of a dural leak, and neck pain can accompany one. However, a leak headache is positional, has no fever and usually starts within days of the puncture. Fever and lethargy weeks later point to meningeal infection instead.

Before labelling postpartum headache a leak headache, Miller advises checking for fever and neck rigidity to exclude meningitis after dural puncture. True leak headache starts within 3 days in over 90%. Barash names streptococcus viridans contamination as the cause.

Sources: Miller 10eBarash 9e

An abscess compresses the spinal cord. It forms slowly, over days after a neuraxial technique, and causes signs of systemic infection such as fever and a raised white count. A haematoma appears early, within 12 hours of the procedure, without these signs. Severe or disproportionate back pain, or weakness returning after the block was wearing off, means cord compression. Only imaging can show whether there is a collection and where it is. That must be established first.

Lumbar puncture without imaging collection. Fever with headache suggests meningitis, so lumbar puncture seems natural. However, fever, leukocytosis and back pain days after delivery suggest a spinal epidural collection, possibly compressing the cord. Image it first; no needle should approach an unimaged collection.

Both haematoma and abscess are rare. A haematoma can develop within 12 hours. An abscess takes days to form and also causes fever and leukocytosis. Disproportionate back pain or returning weakness signals cord compression, and both lesions need imaging such as MRI.

Sources: Mayo review

Around stress and surgery, a brief fall in urine output is often a physiological response that recovers once blood pressure and circulating volume are restored. A sudden fall or stop in flow suggests something is blocking outflow. With a catheter in place, the most likely and most easily fixed block is the catheter itself, through kinking, malposition or blood clot. Confirm that it drains before blaming labour, fluid status or the epidural. The oliguria is described by 0.2 mL/kg/h; it names no cause.

Prerenal azotaemia from labour stress. A long second stage is tempting because it is the event just described, and stress or low volume can briefly reduce urine output. But a long labour does not stop a catheterised bladder from draining. Consider prerenal causes only after the catheter is shown to be patent.

The textbook says that with an indwelling catheter, obstruction from malposition, blood or kinking is the first cause to exclude and correct straight away. Abrupt cessation of flow points to a postrenal block. Catheter obstruction is also listed among the alternative causes of oliguria.

Sources: Miller 10e

Itch after spinal morphine comes from opioid receptors activated in the central nervous system, possibly an itch centre in the medulla reached by the drug spreading upwards. Peripheral histamine release does not cause it. Opioid antagonists and partial agonists relieve it, which supports the central explanation. A partial agonist is the best choice because it acts on the central cause of the itch but, unlike a pure antagonist, does not remove the analgesia.

Antihistamine for morphine histamine release. Itch suggests histamine, and morphine is known to release it, so an antihistamine seems logical. But itch after neuraxial opioids does not come from histamine. It is centrally driven, so diphenhydramine does not treat the cause. Any benefit comes only from its sedative effect.

Both textbooks say itch after neuraxial opioids is centrally mediated and not caused by histamine. It responds to opioid antagonists and to nalbuphine, and nalbuphine keeps analgesia intact. Antihistamines help only by sedating the patient.

Sources: FaustMiller 10e

Local anaesthetic on the S2 to S4 roots weakens the detrusor, so a block can cause retention, but function returns once sensory block recedes below S2–3; a dilute infusion cannot explain symptoms persisting after delivery. Frequency and stress leakage are pelvic floor signs, and a prolonged or instrumental second stage injures the pelvic floor. Epidurals appear in retention risk lists, yet among women who all had one a long second stage still predicts dysfunction; one study linked epidurals to stress incontinence, but prospective cohorts were null. Catheters only treat retention.

Residual local anaesthetic blamed for dysfunction. Local anaesthetic on the sacral roots does weaken the detrusor, so blaming the drug sounds mechanistic. But the effect depends on the block and fades once sensation returns below S2–3. A dilute infusion that has long worn off cannot cause frequency and stress leakage, which point to pelvic floor injury.

Sacral-root blockade weakens the detrusor, but bladder function recovers on its own once the sensory level drops below S2–3. Risk factors for retention after delivery include epidural, protracted labour, instrumental delivery and perineal tear, and forceps raise the chance of pelvic floor dysfunction.

Sources: Miller 10eOutside our books: Prolonged second stage of labor is associated with persistent urinary retention after forceps delivery: An observational study (2023)

A right ventricle facing high pulmonary pressures tolerates little extra afterload. Hypoxia, acidosis and hypercarbia each constrict pulmonary vessels, raising PVR and risking right ventricular failure. Miller notes that in healthy isolated arteries carbon dioxide acts mainly through pH, but diseased pulmonary endothelium strengthens the constriction caused by high carbon dioxide. In pulmonary hypertension, therefore, avoid both high carbon dioxide and low pH. Also support the right ventricle with carefully judged filling and by preventing systemic hypotension.

Fluid loading as initial management. The right ventricle depends on preload, so pushing fluids sounds protective. The sources ask for optimised filling, not more filling. Even so, fluids come second to stopping the triggers that raise PVR. If hypoxia or acidosis drives pulmonary pressure up, extra volume will not rescue the ventricle.

First, prevent rising pulmonary pressure by avoiding hypoxaemia, acidosis, hypercarbia, hypothermia and pain. Next, support the right ventricle with optimised fluids and by avoiding hypotension. Raised PVR or reduced SVR can precipitate right ventricular failure.

Sources: FaustMiller 10eMayo review

The label marks a pregnancy-linked failure of LV contraction, so it needs three things: heart failure arising around delivery, no other explanation (pre-existing heart disease excludes it), and echo proof of systolic impairment. Ejection fraction under 45% and M-mode fractional shortening under 30% are paired measures of the same pump weakness; either suffices. On timing, Barash gives the narrower window, late pregnancy to the first 6 weeks postpartum, while Stoelting and the ESC describe the broader period surrounding delivery; apply the broader one so later postpartum cases are not missed.

Normal range EF as threshold. An ejection fraction near the upper end of normal seems a sensible "abnormal" cut-off, since normal values are quoted around there. However, the threshold for this diagnosis is much lower, below 45%. A value just below the normal range is not systolic dysfunction under these criteria.

StatPearls defines LV systolic impairment as ejection fraction below 45% or M-mode fractional shortening below 30%. Stoelting requires heart failure around delivery, no other cause, and ejection fraction generally below 45%. Barash limits onset to late pregnancy through the first 6 weeks postpartum.

Sources: Outside our books: Peripartum Cardiomyopathy (2024)Stoelting 8eBarash 9e

The link comes from pooled case-control data comparing age at menarche in women with and without endometriosis. Pooling every study at first showed no clear difference, but the studies varied widely. When only studies that adjusted carefully for confounders were combined, the women with endometriosis had consistently reached menarche earlier. Some controls in the original studies may also have had undiagnosed disease. That kind of misclassification hides differences, so the true risk is more likely understated than overstated.

Multiparity reproductive factor not menarche. Multiparity is tempting because, like menarche, it is part of a woman's reproductive history. It fails because the evidence links endometriosis to earlier menarche, not to having had many pregnancies. Choosing it swaps the supported reproductive factor for one the data do not identify.

A meta-analysis of case-control studies found a small but significant increase in endometriosis risk with earlier menarche once it was limited to well-controlled studies. The authors add that misclassification of disease in those studies may mean the real risk is larger.

Sources: Outside our books: Is early age at menarche a risk factor for endometriosis? A systematic review and meta-analysis of case-control studies (2012)

Stoelting groups the risks of pre-eclampsia with vascular disease in general: obesity, chronic hypertension and renal disease. A first pregnancy also adds risk. Age counts only at the extremes. Stoelting names both early and advanced age, and Faust sets the cut-off above 35 years, so 'age' with no value given is not a risk factor. Smoking harms pregnancy in many ways, yet Stoelting says it protects against pre-eclampsia and Barash calls this paradoxical. Faust's risk-factor box is the lone dissent and lists smoking as a risk.

Smoking paradoxically lowers pre-eclampsia risk. Smoking harms so many pregnancy outcomes, and Faust's risk-factor box lists it, so it feels like an obvious vascular risk. However, Stoelting says smoking lowers the risk of pre-eclampsia and Barash agrees. Faust is the lone dissent, so smoking is never the risk factor to choose.

Stoelting lists obesity, nulliparity, very young or older maternal age and general vascular disease as risks, and calls smoking protective. Barash agrees that smoking seems protective. Faust's box lists nulliparity, age over 35 years and obesity, and also lists smoking.

Sources: Stoelting 8eBarash 9eFaust

Zika infection in the mother is often silent or mild. There may be only fever and a rash, so a history of travel or of an outbreak may be the only clue. The harms that are recognised affect the nervous system. Babies of infected mothers are more likely to have a reduced head size, and infected adults show more Guillain–Barré syndrome. The virus also spreads through blood and sexual contact. Pregnant staff are advised to take extra protection because the fetus seems to be at particular risk.

Macrocephaly opposite Zika microcephaly pathology. Macrocephaly differs from the right answer by only one or two letters. A rushed reader who remembers that Zika affects the baby's head picks it on sight. Zika causes the opposite problem: the head is abnormally small, not enlarged.

Most people infected with Zika have no symptoms or only mild ones. However, maternal infection is linked to more microcephaly in newborns and to more Guillain–Barré syndrome. Pregnant carers should use greater protection because of the apparent risk to the fetus.

Sources: Barash 9e