In one line
Pregnancy converts a healthy woman into a hypercoagulable one on purpose, to protect her from bleeding to death at delivery, and the price of that protection is a four to five-fold rise in thrombosis that peaks after the baby is born. Almost every maternal death from pulmonary embolism follows a woman who was never formally risk-scored, so the intervention that saves lives here is a piece of paper at booking rather than a drug at the bedside.
Where this sits. The clotting cascade, the natural anticoagulants and fibrinolysis are taught in the Primary chapter on haemostasis, coagulation, thrombogenesis and fibrinolysis. The collapsed woman and her organ support are the Finals chapter on obstetric critical care.
The clot that pregnancy is trying to make
Every woman who delivers loses blood from a raw placental bed the size of a saucer, supplied by vessels carrying most of her cardiac output. Uterine contraction closes those vessels mechanically. Clotting seals them.
Pregnancy therefore prepares for delivery by shifting the entire haemostatic balance towards clotting, and it starts doing so in the first trimester. Held against Virchow's triad, pregnancy satisfies all three limbs simultaneously, which almost nothing else in medicine does.
Hypercoagulability. Procoagulant factors rise: factors VII, VIII, X and XII, von Willebrand factor, and fibrinogen, which roughly doubles by term. Natural anticoagulants fall or are neutralised: free protein S falls substantially, and an acquired resistance to activated protein C develops even in women with no Factor V Leiden mutation. Fibrinolysis is suppressed by rising plasminogen activator inhibitor 1, and by PAI-2, which is produced by the placenta and is essentially absent outside pregnancy. So the clot forms faster and is dismantled more slowly.
Venous stasis. Progesterone relaxes venous smooth muscle, capacitance rises and flow slows from early pregnancy, before the uterus is big enough to compress anything. Later the gravid uterus compresses the inferior vena cava and the iliac veins directly.
Endothelial injury. Delivery, and above all caesarean section, provides it. So does instrumentation, infection and prolonged pressure.
That combination explains the shape of the risk. VTE in pregnancy and the puerperium has an overall incidence of about 1 to 2 per 1000 maternities, and the relative risk postpartum is about five-fold higher than antenatally. The pregnancy prepares the clotting system across nine months; the delivery supplies the endothelial trigger; the clot arrives in the puerperium. A woman is at her most thrombotic when she has gone home.
Why the clot is on the left, and high up
Two features of pregnancy-associated deep vein thrombosis are so consistent that they are diagnostic clues in their own right.
It is usually on the left. The left common iliac vein is crossed and compressed by the right common iliac artery where they meet over the fifth lumbar vertebra. This is the anatomy behind May-Thurner compression, and pregnancy exaggerates it. The great majority of pregnancy DVT is left-sided.
It is usually iliofemoral rather than calf. Outside pregnancy most DVT begins in the calf veins. In pregnancy the compression is proximal, so the thrombus is proximal, and an iliofemoral clot is both more likely to embolise and more likely to be missed on a standard below-knee compression duplex.
Both observations are captured in the LEFt rule, which is worth carrying: Left leg symptoms, calf circumference difference of 2 cm or more (E for oedema), and first-trimester presentation. A woman with none of those three has a low probability of DVT.
The practical consequence is what to say when you request the scan. Ask for the iliac veins to be imaged, not just a below-knee study, because a negative calf duplex in a woman with buttock, back or whole-leg pain does not exclude the diagnosis that is actually likely.
What actually kills
Pulmonary embolism kills by obstructing right ventricular outflow. The right ventricle is a thin-walled chamber built for a low-pressure circuit; it cannot acutely generate the pressure needed to push blood past a large clot. It dilates, its wall tension rises, its own coronary perfusion falls, and it fails. Left ventricular filling collapses because nothing is reaching it, and the woman becomes hypotensive with a raised jugular venous pressure and clear lungs.
That mechanism explains the presentation. Sudden breathlessness with an entirely normal chest examination and a normal chest X-ray is the classic picture, and it is exactly the picture that gets attributed to anxiety, to anaemia, or to the normal breathlessness of pregnancy. Pleuritic chest pain, haemoptysis and a pleural rub occur when a smaller embolus infarcts peripheral lung, which is a less dangerous embolus with more dramatic symptoms.
Add to this that breathlessness, tachycardia and leg swelling are all normal in late pregnancy, and you have the reason thromboembolism is missed. The threshold for investigating must be lower in pregnancy than outside it, not higher.
In South Africa thromboembolism has consistently appeared among the causes of maternal death in successive Saving Mothers reports, and the assessors' recurring finding is the same one reported internationally: the deaths occur in women who were never formally risk-assessed and never offered prophylaxis. This is a systems failure, not a diagnostic one.
Risk assessment is the intervention
The single most effective act in this chapter is completing a structured VTE risk assessment at booking, on any antenatal admission, and again immediately after delivery. RCOG Green-top Guideline 37a gives a scoring tool, and the arithmetic is simple.
Each risk factor scores between 1 and 4, and the thresholds are:
| Total antenatal score | Action |
|---|---|
| 4 or more | Prophylactic LMWH from the first trimester |
| 3 | Prophylactic LMWH from 28 weeks |
| Fewer than 3 | Mobilisation, avoid dehydration, reassess if anything changes |
| Total postnatal score | Action |
|---|---|
| 2 or more | Prophylactic LMWH for at least 10 days |
| Fewer than 2 | Early mobilisation, avoid dehydration |
The high-scoring items are the ones that decide most cases:
- Previous VTE, other than a single event related to major surgery, is the strongest factor of all, with an adjusted odds ratio around 25. Any previous VTE means prophylaxis from the first trimester.
- High-risk thrombophilia: antithrombin deficiency, protein C or protein S deficiency, compound or homozygous low-risk thrombophilias.
- Medical comorbidity: cancer, heart failure, active SLE, inflammatory bowel disease or inflammatory polyarthropathy, nephrotic syndrome, type 1 diabetes with nephropathy, sickle cell disease, current intravenous drug use.
Then the common ones that accumulate quietly, each scoring 1: age over 35, BMI 30 or more, parity 3 or more, smoking, gross varicose veins, current pre-eclampsia, immobility, family history of unprovoked or oestrogen-provoked VTE in a first-degree relative, low-risk thrombophilia, multiple pregnancy, and IVF or assisted reproduction. Transient factors: dehydration or hyperemesis, current systemic infection, long-distance travel over four hours.
Postnatally, add caesarean section, particularly emergency, preterm delivery before 37 weeks, stillbirth, mid-cavity rotational or operative delivery, prolonged labour over 24 hours, and postpartum haemorrhage over 1 litre or requiring transfusion.