Describe the management of shock (haemorrhagic/hypovolaemic and septic)

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. It is one of the most time-critical recognition tasks in obstetrics: the woman who is going to die of shock often looks deceptively well for a long time and then collapses suddenly.

The two phenotypes that dominate obstetric practice 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 O&G and Basic investigations analysis.

Core knowledge

Classification of shock

Shock is conventionally divided into four physiological categories. In obstetrics two dominate, but all four remain relevant 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.

The classical (ATLS-style) grading of haemorrhage by physiological response is a useful bedside guide, with the caveat that pregnancy masks it — the gravid patient sits one class "better" than her true loss suggests:

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.