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O&G SAQsIntrapartum care — obstetric emergencies

O&G SAQs · Intrapartum care — obstetric emergencies

Amniotic fluid embolism — structured SAQ (15 marks)

FRANZCOG-format structured SAQ on amniotic fluid embolism: the discriminating differential, the first-five-minute resuscitation with perimortem caesarean timing, product-targeted correction of the consumptive coagulopathy, and why the diagnosis remains clinical. Per-sub-part marking rubric included.

15 marks20 min4 min readVerification in progress

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Prompt
You are the on-call obstetric registrar. A 34-year-old G3P2 at 39+4 weeks is in the second stage of labour after induction for post-dates. She suddenly becomes agitated, says she cannot breathe and that she is going to die, then loses consciousness. Peripheral oxygen saturation is 76%, blood pressure 68/34 mmHg, heart rate 138 bpm. The CTG shows a terminal bradycardia. (a) Give your differential diagnosis with the feature that distinguishes each from amniotic fluid embolism. (4 marks) (b) Outline your immediate management in the first five minutes, with the reasoning for each step. (5 marks) (c) She is resuscitated but bleeds heavily after birth. Fibrinogen is 0.7 g/L, platelets 62 × 10⁹/L. Outline your haematological management with targets. (4 marks) (d) The consultant asks how you would confirm the diagnosis. Answer. (2 marks)

How this SAQ is marked

Twelve SAQs, 180 marks, two 2-hour papers — roughly 15 marks and 20 minutes each. Marks come from specifics: the discriminating feature, the drug with its dose, the target number, the time window. Write labelled points, not paragraphs, and answer the sub-part asked. [1]

Reveal model answer and mark schemeShowHide

(a) Differential diagnosis with the discriminating feature (4 marks)

One mark per diagnosis with its discriminator. A bare list without discriminators scores half. [1][2]

DiagnosisWhat distinguishes it from amniotic fluid embolism
Pulmonary thromboembolismHypoxia and right heart strain without early consumptive coagulopathy; risk factors usually present
AnaphylaxisIdentifiable trigger minutes before; urticaria, angioedema, bronchospasm; responds to adrenaline; no early DIC
High or total spinal blockTemporally locked to neuraxial dosing; ascending motor and sensory block with bradycardia; normal clotting
Local anaesthetic systemic toxicityFollows a large local anaesthetic dose; perioral tingling and tinnitus precede seizure and arrhythmia; normal clotting
EclampsiaPreceding hypertension and proteinuria; seizure with inter-ictal recovery; no profound hypoxia or DIC
Haemorrhage with dilutional coagulopathyCoagulopathy proportionate to a large measured loss; amniotic fluid embolism produces coagulopathy out of proportion to loss
[1][2][5]

Additional credit for naming peripartum cardiomyopathy, aortic dissection, myocardial infarction, sepsis, air embolism or drug error. [1]

(b) Immediate management, first five minutes (5 marks)

One mark per point with its reasoning, maximum five. [4][6]

  • Declare a maternal collapse and activate the maternal cardiac arrest team, allocating airway, compressions, uterine displacement, drugs, scribe and neonatal roles. A protocolised, role-allocated first ten minutes is the intervention with the best evidence in this condition.[4]
  • Airway and 100% oxygen, with early tracheal intubation by the most experienced operator. Hypoxia is what produces the neurological injury that determines outcome.[6][3]
  • If pulseless: CPR flat on a firm surface, hands on the centre of the sternum, with continuous manual left uterine displacement. Drug doses and defibrillation energies are unchanged in pregnancy.[6]
  • Set the clock and perform perimortem caesarean birth by 4 minutes in this undelivered woman at term. It is done in the room, for maternal benefit, because emptying the uterus relieves aortocaval compression.[6][1]
  • Two large-bore cannulae above the diaphragm, bloods including fibrinogen, and activate the massive haemorrhage protocol pre-emptively. The coagulopathy is coming.[4][5]
  • Vasopressors early and fluid cautiously — noradrenaline and vasopressin support the failing right ventricle; large-volume crystalloid distends it and worsens output.[3]

(c) Haematological management with targets (4 marks)

One mark each for the fibrinogen target and product, the platelet target, the ratio-based plasma and red cell strategy, and one for either tranexamic acid or the factor VIIa caveat. [5][1]

  • Fibrinogen 0.7 g/L: give cryoprecipitate or fibrinogen concentrate immediately, targeting a fibrinogen at or above 2 g/L. Fibrinogen falls first and fastest in obstetric consumptive coagulopathy.[5]
  • Platelets 62 × 10⁹/L: transfuse to keep platelets above 50 × 10⁹/L, with a higher trigger if she is going to theatre.[5][1]
  • Red cells and fresh frozen plasma in a ratio-based massive transfusion pack until laboratory or viscoelastic guidance is available; use ROTEM or TEG to detect hypofibrinogenaemia and hyperfibrinolysis.[5][3]
  • Tranexamic acid 1 g intravenously over 10 minutes for the haemorrhage component; calcium replacement for the citrate load; active warming throughout.[1][5]
  • Recombinant activated factor VII only as a last resort after full conventional replacement — the systematic review of published cases found worse outcomes in treated women.[7]

(d) How the diagnosis is confirmed (2 marks)

One mark for stating that it is a clinical diagnosis of exclusion, one for naming the criteria or explaining why no test confirms it. [2]

  • It is not confirmed by any test. Amniotic fluid embolism is a clinical diagnosis of exclusion made at the bedside. Fetal squames in maternal pulmonary blood are neither sensitive nor specific; tryptase, complement and zinc coproporphyrin are research tools.[1][2]
  • The Clark/SMFM 2016 research criteria define cases for research, not for the bedside: sudden cardiorespiratory arrest, or hypotension with systolic pressure under 90 mmHg plus respiratory compromise; overt disseminated intravascular coagulation documented after the collapse; onset during labour or within 30 minutes of delivery of the placenta; and no fever of 38.0 degrees Celsius or above during labour. All four are required, deliberately trading sensitivity for specificity.[2]
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References7ShowHide
  1. [1]Pacheco LD, Saade G, Hankins GD, Clark SL Amniotic fluid embolism: diagnosis and management Am J Obstet Gynecol, 2016.PMID 26987420
  2. [2]Clark SL, Romero R, Dildy GA, et al. Proposed diagnostic criteria for the case definition of amniotic fluid embolism in research studies Am J Obstet Gynecol, 2016.PMID 27372270
  3. [3]Pacheco LD, Clark SL, Klassen M, Hankins GDV Amniotic fluid embolism: principles of early clinical management Am J Obstet Gynecol, 2020.PMID 31376394
  4. [4]Combs CA, Montgomery DM, Toner LE, Dildy GA Society for Maternal-Fetal Medicine Special Statement: Checklist for initial management of amniotic fluid embolism Am J Obstet Gynecol, 2021.PMID 33417901
  5. [5]Erez O, Mastrolia SA, Thachil J Disseminated intravascular coagulation in pregnancy: insights in pathophysiology, diagnosis and management Am J Obstet Gynecol, 2015.PMID 25840271
  6. [6]Jeejeebhoy FM, Zelop CM, Lipman S, et al. Cardiac Arrest in Pregnancy: A Scientific Statement From the American Heart Association Circulation, 2015.PMID 26443610
  7. [7]Leighton BL, Wall MH, Lockhart EM, Phillips LE, Zatta AJ Use of recombinant factor VIIa in patients with amniotic fluid embolism: a systematic review of case reports Anesthesiology, 2011.PMID 21720243
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