Clinical overview
Shock is the final common pathway by which two of the three leading direct causes of maternal death in South Africa — obstetric haemorrhage and non-pregnancy-related infection (sepsis, much of it HIV-associated) — actually kill. It is a clinical syndrome of acute circulatory failure in which oxygen delivery to the tissues falls below the metabolic demand, driving a shift to anaerobic metabolism, lactate accumulation, cellular dysfunction and, if uncorrected, irreversible multi-organ failure and death. For the registrar this is the most time-critical recognition task in the discipline: the woman who is going to die of shock often looks deceptively well for a long time and then collapses suddenly.
The two phenotypes you must master are hypovolaemic/haemorrhagic shock (a problem of volume and pump-preload — the tank is empty) and septic/distributive shock (a problem of pathological vasodilatation, capillary leak and maldistribution — the pipes are too wide and leaky). They differ in pathophysiology, bedside signs and the specifics of resuscitation, but share the same overriding principle: restore tissue perfusion fast while you find and fix the cause. Pregnancy itself blunts your warning systems — the ~40–50% rise in blood volume and the physiologically high heart rate mean a healthy young gravida compensates remarkably well, then decompensates abruptly. Treat the trajectory, not the single reassuring observation. This chapter sits alongside resuscitation-in-pregnancy, fluids-in-og and basic-investigations-analysis.
Core knowledge
Classification of shock
Shock is conventionally divided into four physiological categories. In obstetrics two dominate, but you must hold all four because the differential at a maternal collapse is wide (see resuscitation-in-pregnancy).
- Hypovolaemic — loss of intravascular volume. In O&G this is overwhelmingly haemorrhagic (antepartum and postpartum haemorrhage, ruptured ectopic, abortion-related, uterine rupture, surgical), but also non-haemorrhagic (hyperemesis with severe dehydration, diabetic ketoacidosis).
- Distributive — pathological vasodilatation. Septic shock is the classic example; also anaphylactic (including to anaesthetic and oxytocic drugs) and neurogenic (high spinal).
- Cardiogenic — pump failure (peripartum cardiomyopathy, MI, severe valvular disease, arrhythmia).
- Obstructive — mechanical obstruction to flow (massive pulmonary embolism, amniotic fluid embolism, tension pneumothorax, cardiac tamponade, aortocaval compression by the gravid uterus).
Pathophysiology of haemorrhagic shock
Acute blood loss reduces venous return and stroke volume. Baroreceptor-driven sympathetic activation produces tachycardia and peripheral vasoconstriction, shunting blood from skin, gut and kidneys to heart and brain — hence the cold, pale, clammy, oliguric but initially "talking and alert" patient. Blood pressure is a late sign: a young woman can lose roughly a quarter to a third of her blood volume before systolic pressure falls, so hypotension signals decompensation, not early shock. As loss continues, perfusion of vital organs fails, lactate rises, and the lethal triad of hypothermia, acidosis and coagulopathy sets in — each worsening the others and driving dilutional and consumptive coagulopathy. The pregnant uterus at term receives some 500–700 mL/min of blood flow, so an atonic uterus or a placental bed can exsanguinate a woman in minutes.
A useful bedside frame is the classical (ATLS-style) grading of haemorrhage by physiological response, remembering that pregnancy masks it — the gravid patient sits one class "better" than her true loss suggests:
| Class | Approx. blood loss | Heart rate | BP | Mental state |
|---|---|---|---|---|
| I | <15% | Normal/mild ↑ | Normal | Slightly anxious |
| II | 15–30% | Tachycardia | Normal (narrow pulse pressure) | Anxious |
| III | 30–40% | Marked tachycardia | Hypotensive | Confused |
| IV | >40% | Severe tachycardia | Severely low | Lethargic/unconscious |
The shock index (heart rate ÷ systolic BP) is a more sensitive bedside tool than either number alone; standard teaching is that a value ≥0.9–1.0 should prompt concern for significant haemorrhage and trigger escalation. Estimating obstetric blood loss visually under-reads true loss — weigh swabs and use calibrated collector drapes where available, as emphasised by the E-MOTIVE bundle for early PPH detection.
Pathophysiology of septic shock
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is the subset with circulatory and cellular/metabolic abnormality profound enough to substantially increase mortality — clinically, sepsis with persisting hypotension requiring vasopressors to maintain a mean arterial pressure (MAP) ≥65 mmHg and a raised lactate despite adequate fluid resuscitation. Microbial products trigger massive cytokine release, nitric-oxide-mediated vasodilatation, capillary leak and microvascular thrombosis. The result is a warm, vasodilated, often initially well-perfused-looking patient who is nonetheless profoundly hypoperfused at tissue level — a trap for the unwary, because her extremities may be warm and her pressure briefly maintained while lactate climbs.
Common obstetric and gynaecological sources are chorioamnionitis, endometritis (especially post-caesarean or after prolonged rupture of membranes), septic abortion, pyelonephritis, wound and pelvic collections, mastitis, and — in the SA context — the heavy contribution of HIV-associated opportunistic infection and tuberculosis. Group A streptococcus (Streptococcus pyogenes) deserves specific mention as a cause of fulminant, rapidly fatal puerperal sepsis. The Saving Mothers/NCCEMD reports have repeatedly flagged non-pregnancy-related infection — dominated by HIV — among the leading causes of maternal death in South Africa, which is why a low threshold for sepsis and for HIV testing/staging is a national imperative.
Figure M5.1 — Shock physiology and recognition traps in pregnancy, contrasting haemorrhagic/hypovolaemic and septic/distributive shock with escalation triggers.
Assessment
Recognise it: structured ABCDE
Assess every shocked or potentially shocked woman with a systematic ABCDE approach and call for senior help immediately (see resuscitation-in-pregnancy). In the obstetric patient from around 20 weeks, left-lateral tilt or manual uterine displacement is part of "C" to relieve aortocaval compression.
- A/B — airway patency, respiratory rate (tachypnoea is an early and sensitive sign of both sepsis and hypovolaemia), oxygen saturation; give high-flow oxygen.
- C — heart rate, blood pressure, pulse pressure, capillary refill, peripheral temperature and colour, shock index; identify the source of bleeding (uterus, genital tract, abdomen).
- D — conscious level (AVPU/GCS); falling consciousness is decompensation.
- E — temperature (fever or hypothermia), full exposure to find rashes, wounds, the uterus, the perineum and any concealed bleeding.
Quantify perfusion failure: persistent tachycardia, narrowed pulse pressure, cool peripheries, capillary refill >2–3 s, oliguria (<0.5 mL/kg/h) and altered mentation. Lactate is the key biochemical marker of tissue hypoperfusion; standard teaching is that a level above ~2 mmol/L is abnormal and ≥4 mmol/L marks severe hypoperfusion warranting aggressive resuscitation. In sepsis, formal severity scoring (such as the SOFA/qSOFA family) is used to define organ dysfunction; the practical message is that hypotension, altered mentation or tachypnoea in a woman with suspected infection means sepsis until proven otherwise.
Investigations
Take bloods as you resuscitate — never delay treatment for results.
- FBC (haemoglobin and platelets — note Hb may be normal early in acute bleeding before haemodilution), U&E and creatinine, LFTs, glucose.
- Coagulation — PT/INR, aPTT, fibrinogen (a fibrinogen below ~2 g/L in obstetric haemorrhage predicts severe PPH; falling fibrinogen is an early warning).
- Group and crossmatch urgently; activate the massive transfusion protocol early in major haemorrhage.
- Arterial/venous blood gas with lactate (see arterial-blood-gas and basic-investigations-analysis) — guides both the metabolic picture and resuscitation adequacy.
- Septic screen — blood cultures (ideally before antibiotics but never delay antibiotics beyond the first hour), urine, high vaginal/endocervical swabs, wound swabs, sputum/CXR, and a point-of-care HIV test with CD4 if positive in the SA setting.
- Imaging — bedside ultrasound for free fluid, retained products, collections; CXR; consider CT once stabilised.
- β-hCG in any woman of reproductive age with shock and no obvious cause — ruptured ectopic pregnancy presents as haemorrhagic shock and is missed at peril.
Management
The unifying drill is restore perfusion + stop the cause + support the organs, with the obstetric team, anaesthetist, haematology/blood bank and senior nursing all mobilised at once. Two large-bore (14–16 G) cannulae, oxygen, monitoring, and a urinary catheter to track output are the universal opening moves. Resuscitation principles are developed further in fluids-in-og and fluids-electrolytes-og.
Haemorrhagic / hypovolaemic shock — the drill
MAJOR OBSTETRIC HAEMORRHAGE — CALL FOR HELP, ACTIVATE THE MASSIVE TRANSFUSION PROTOCOL.
- Shout for senior help — obstetrician, anaesthetist, blood bank, extra hands. Note the time.
- Airway + high-flow oxygen; left-lateral tilt/manual uterine displacement if undelivered and ≳20 weeks.
- Two large-bore IV lines (14–16 G); take crossmatch, FBC, coagulation, fibrinogen, lactate as you cannulate.
- Stop the bleeding — treat the cause. For PPH this is the E-MOTIVE / "four T's" drill — uterine massage and bimanual compression, uterotonics (oxytocin first-line, then ergometrine, then misoprostol; consider carbetocin), IV fluids, examine the genital tract and escalate — proceeding to balloon tamponade, examination under anaesthesia, compression sutures, uterine/internal iliac artery ligation and hysterectomy as needed (see postpartum-haemorrhage and antepartum-haemorrhage).
- Tranexamic acid 1 g IV as early as possible — within 3 hours of onset of obstetric haemorrhage (WOMAN trial); a second 1 g dose may be given if bleeding continues.
- Resuscitate with blood, not endless crystalloid. Warmed fluids; move early to red cells and a balanced ratio of blood products per the massive transfusion protocol; aim to maintain fibrinogen and correct coagulopathy (cryoprecipitate/fibrinogen concentrate, FFP, platelets) guided by results / viscoelastic testing where available.
- Keep her warm, monitor continuously, reassess (the lethal triad is hypothermia + acidosis + coagulopathy).
Fluid strategy in haemorrhage has shifted away from large-volume crystalloid towards early blood-product, damage-control resuscitation and permissive/controlled volume until the source is controlled, to avoid dilutional coagulopathy and clot disruption. Crystalloid (warmed balanced solution) is the immediate bridge while blood is fetched — give it in measured aliquots and reassess, rather than flooding. Definitive control of the bleeding source is the only thing that ultimately reverses haemorrhagic shock; everything else buys time. In the SA system, recognise the level-of-care reality: a district facility must resuscitate, give TXA, give the uterotonic ladder, apply tamponade, give whatever blood is available and arrange urgent stabilised transfer to a facility with theatre, blood and senior obstetric/anaesthetic cover — escalation must not wait for the patient to deteriorate further.
Figure M5.2 — Major obstetric haemorrhage drill: call help, oxygen and tilt, large-bore access, bleeding control, early tranexamic acid, blood-product resuscitation and reassessment.
Septic shock — the drill
SEPSIS — "give 3, take 3" within the first hour ("Sepsis Six"-style bundle). GIVE: high-flow oxygen; IV broad-spectrum antibiotics (per local protocol/EML, source-appropriate, do not delay for cultures); IV fluid resuscitation. TAKE: blood cultures (before antibiotics if it causes no delay); lactate; urine output (catheterise and measure hourly). Then: find and control the source.
- Antibiotics within the first hour of recognising septic shock, broad-spectrum and source-directed, narrowed once cultures return. Cover the likely obstetric organisms (including Gram-negatives, anaerobes and, where relevant, Group A streptococcus); follow the SA EML / local antimicrobial guidance.
- Fluid resuscitation with a balanced crystalloid — an initial bolus titrated to response (standard sepsis teaching is around 30 mL/kg given as fluid challenges with frequent reassessment), watching for fluid overload, which the leaky septic circulation and the pregnant patient tolerate poorly. Reassess perfusion (MAP, lactate clearance, urine output) after each challenge rather than giving a fixed large volume blindly.
- Vasopressors if hypotension persists despite adequate fluid — noradrenaline is the first-line vasopressor to target a MAP ≥65 mmHg; this requires escalation to a high-care/ICU environment with invasive monitoring.
- Source control is mandatory and time-critical — evacuate retained/infected products of conception (septic abortion), drain collections, debride/wash out infected wounds, deliver in chorioamnionitis once the mother is stabilised, and consider hysterectomy for an infected uterus that cannot otherwise be controlled. Antibiotics without source control will fail.
- Organ support — oxygen/ventilation, correct electrolytes and glucose, consider stress-dose steroids in vasopressor-refractory shock per protocol, and involve critical care early.
- SA context — test for and stage HIV (initiate/continue ART per the national consolidated guidelines), have a high index of suspicion for tuberculosis and other opportunistic infection, and use the Saving Mothers lessons (early recognition, the obstetric early-warning chart, timely referral) to drive your response.
Figure M5.3 — Septic shock first-hour bundle and source-control pathway, including give-three/take-three actions, noradrenaline escalation and South African infection context.
Red flags / pitfalls
- "Her blood pressure is fine" is not reassurance. Hypotension is a late, decompensated sign in a young gravida; act on tachycardia, tachypnoea, a rising shock index, narrowing pulse pressure and oliguria before the pressure drops.
- Visually under-estimating obstetric blood loss. Estimated loss is routinely far below true loss; weigh swabs, use calibrated drapes, and let the physiology (and shock index), not the eyeball, drive escalation.
- Drowning the bleeding patient in crystalloid — large-volume clear fluid dilutes clotting factors, worsens coagulopathy and hypothermia, and disrupts clot. Resuscitate haemorrhage with blood products early, not litres of saline.
- Forgetting tranexamic acid, or giving it late. TXA reduces death from bleeding only when given early (within 3 hours); make it part of the reflex drill.
- Missing ruptured ectopic pregnancy as the cause of unexplained shock in a woman of reproductive age — always check a β-hCG and think of it (see ectopic-pregnancy-management).
- The "warm and well-looking" septic patient. Distributive shock can preserve peripheral warmth and briefly maintain pressure while lactate climbs — trust the lactate, mentation and respiratory rate.
- Delaying antibiotics or source control in sepsis. Every hour of delayed effective antibiotics in septic shock costs lives, and antibiotics without source control (retained products, abscess, infected uterus) will not work.
- Aortocaval compression — failing to tilt/displace the uterus in an undelivered woman ≳20 weeks reduces venous return and undermines every other resuscitation effort.
- Failing to escalate the level of care. At district level, resuscitate and stabilise, then refer urgently with continued resuscitation in transit — do not hold a deteriorating patient hoping she will turn the corner.
- Not anticipating coagulopathy — monitor fibrinogen; a falling fibrinogen in obstetric haemorrhage is an early warning of severe PPH and impending coagulopathic collapse.
Evidence anchors
- National Integrated Maternal and Perinatal Care Guideline (NDoH, 2024) (SA NDoH) — the South African obstetric source of truth for haemorrhage and maternal sepsis management, uterotonic choices and referral pathways.
- Saving Mothers / NCCEMD (latest triennial report) — obstetric haemorrhage and non-pregnancy-related infection (largely HIV-associated) remain leading causes of maternal death in South Africa; emphasises early recognition, early-warning observation charts and timely referral.
- RCOG Green-top Guideline No. 52 — Prevention and Management of Postpartum Haemorrhage.
- RCOG Green-top Guideline No. 63 — Antepartum Haemorrhage.
- RCOG Green-top Guideline No. 47 — Blood Transfusions in Obstetrics (massive transfusion and blood-product use).
- RCOG Green-top Guideline No. 64 — Maternal Sepsis.
- RCOG Green-top Guideline No. 56 — Maternal Collapse in Pregnancy and the Puerperium.
- WOMAN trial (Lancet 2017) — tranexamic acid 1 g IV within 3 hours of onset reduces death due to bleeding in PPH; E-MOTIVE bundle (NEJM 2023) — calibrated drape early detection + Massage, Oxytocic, TXA, IV fluids, Examine/escalate; WHO updated PPH recommendations (2025).
- South African National HIV / ART Consolidated Guidelines (2023) and 2023 SAHCS Adult ART Guidelines — HIV testing, staging and ART in the septic/critically ill obstetric patient.
- South African EML — Hospital Level (Adults), current edition — antimicrobial choices and uterotonic/TXA availability.
Note on hedged facts: shock-index thresholds (~0.9–1.0), lactate cut-offs (~2 and ~4 mmol/L), the ~30 mL/kg sepsis fluid figure, the MAP ≥65 mmHg target, noradrenaline as first-line vasopressor, ATLS haemorrhage classes, the fibrinogen <2 g/L PPH predictor and the first-hour antibiotic principle are stated as standard critical-care/resuscitation teaching — they are not line-itemed in VERIFIED-SOURCES.md and are therefore hedged rather than attached to a specific citation.