In one line
The puerperium is the single highest-risk period for venous thromboembolism in a woman's reproductive life, so every postnatal woman earns a documented VTE risk assessment and most need prophylactic low-molecular-weight heparin for at least 10 days; secondary postpartum haemorrhage — excessive bleeding from 24 hours to 12 weeks after delivery — is endometritis and retained products until proven otherwise, but the trap is the woman whose bleeding is actually a uterine artery pseudoaneurysm, in whom a curette makes a survivable problem catastrophic.
These two complications are linked by their timing and by a shared clinical discipline: both kill quietly, days after the woman has gone home, and both are managed badly when the early signal is read as trivial.
Mechanism & pathophysiology
Venous thromboembolism in the puerperium is Virchow's triad maximally expressed. Pregnancy is a physiologically prothrombotic state engineered to survive the haemostatic challenge of placental separation, and that protection does not switch off at delivery — it peaks. Hypercoagulability: oestrogen-driven rises in fibrinogen and factors VII, VIII and X, a fall in protein S, and acquired resistance to activated protein C tip the balance towards clot, and these changes persist for roughly six weeks postpartum before returning to baseline. Stasis: venous capacitance and the mechanical compression of the gravid uterus on the iliac veins — worse on the left, because the left iliac vein is crossed by the right iliac artery — slow flow, which is why iliofemoral DVT in pregnancy is overwhelmingly left-sided and often presents with whole-leg rather than calf swelling. Endothelial injury: delivery itself, and caesarean section in particular, traumatises pelvic vasculature and activates the endothelium. The puerperium is when all three are simultaneously maximal, which is why the daily risk of VTE is higher in the weeks after birth than at any point in the antenatal period, and the first week is the most dangerous of all.
This matters because VTE remains a leading direct cause of maternal death across every high-quality confidential enquiry, and almost all of those deaths are from pulmonary embolism in women who were either never risk-assessed or were under-dosed and under-treated. The disease is largely preventable; the deaths are largely failures of a system that did not weigh the risk and act.
Two consequences of this physiology shape every downstream decision. First, the prothrombotic milieu does not respect the artificial line between antenatal and postnatal care, so a woman with antenatal risk factors is more, not less, at risk once delivered — the assessment must be repeated after birth, not assumed to have ended with it. Second, because the changes take roughly six weeks to resolve, prophylaxis pitched to the inpatient stay alone — a few days after a vaginal birth, a little longer after caesarean — leaves the larger part of the high-risk window uncovered. The pathophysiology is the argument for community-prescribed, weeks-long prophylaxis in the women who need it.
Secondary postpartum haemorrhage is a disorder of the involuting placental bed. After delivery the placental site is a raw, vascular wound that heals by thrombosis of the spiral arteries and progressive involution of the uterus. Three things derail that process. Retained products of conception keep the bed open: residual trophoblast and decidua prevent the uterus from contracting down on the placental site and act as a nidus for infection. Endometritis — ascending infection of the decidualised endometrium — inflames the bed, impairs involution and is itself frequently driven by retained products, so the two travel together. Subinvolution of the placental site is failure of the normal thrombosis-and-obliteration of the utero-placental vessels, which then re-bleed days to weeks later even when the cavity looks empty.
The dangerous minority is vascular. A uterine artery pseudoaneurysm is a contained rupture of an arterial wall — classically after the uterine trauma of caesarean section — in which blood is held only by a thin fibrous capsule and surrounding clot rather than a true three-layered vessel wall. Because the wall is incomplete, the lesion enlarges with arterial pressure and ruptures unpredictably, which is why the bleeding it causes is characteristically sudden, heavy and intermittent — quiescent while the capsule holds, then catastrophic when it gives. An arteriovenous malformation is an abnormal direct communication between uterine arteries and veins, either congenital or, more often in this setting, acquired after caesarean, evacuation or other instrumentation; it presents similarly with recurrent heavy bleeding and a uterus that looks structurally normal on greyscale imaging. Both are destroyed by the instrument that treats retained products: passing a curette into a pseudoaneurysm tears the capsule and converts intermittent bleeding into exsanguination. Recognising that a vascular cause can masquerade as ordinary retained products is the whole game.
The link between the two vascular causes and the rest of the topic is the caesarean section. The same operative trauma that injures pelvic veins and drives postpartum VTE also injures the uterine arteries and seeds pseudoaneurysm and AVM — so as caesarean rates rise, both these complications become commoner, and the woman who had a caesarean is simultaneously the woman who most needs thromboprophylaxis and the woman in whom secondary bleeding must never be reflexively curetted. Finally, gestational trophoblastic disease — persistent trophoblast after a molar or even a non-molar pregnancy — can present as secondary PPH and is the reason a βhCG belongs in the workup of bleeding that does not behave (see Gestational trophoblastic disease).
Assessment
Postpartum VTE — assess every woman, suspect clinically, image decisively.
- The risk assessment is the intervention. Every woman has a documented VTE risk assessment at booking, repeated after any admission, and — critically — again after delivery before discharge. Postnatal risk factors are cumulative: caesarean section (especially emergency), class-3 obesity (BMI ≥40), age >35, parity ≥3, smoking, pre-eclampsia, prolonged labour, mid-cavity instrumental delivery, postpartum haemorrhage, immobility, infection, and any personal or strong family history of VTE or known thrombophilia. The number of risk factors drives the decision, so the assessment is not paperwork — it is the treatment decision.
- Suspected DVT. Unilateral (usually left) leg pain and swelling, sometimes whole-leg, sometimes only lower abdominal or buttock pain if the thrombus is iliac. Compression duplex ultrasound is the primary test. If it is negative but clinical suspicion is high, stop anticoagulation and repeat the scan on days 3 and 7 — a negative early scan does not exclude a propagating iliac clot.
- Suspected PE. Breathlessness, pleuritic chest pain, tachycardia, haemoptysis, collapse. An ECG and chest X-ray come first (fetal/maternal radiation from a CXR is negligible and it identifies pneumonia, pneumothorax or other causes). If there are leg symptoms, a duplex showing DVT confirms the need to treat and spares chest imaging. Without leg symptoms, choose V/Q scan or CTPA; if the CXR is abnormal, CTPA is preferred. The choice is a genuine consent conversation, but in a woman who has already delivered the trade-off is not a future child. CTPA delivers a higher radiation dose to her own breast tissue, a lifetime breast-cancer consideration in a young woman. V/Q spares the breast but uses a radiopharmaceutical that means interrupting breastfeeding and expressing and discarding milk per the nuclear-medicine protocol. There is no free option; the woman should be part of the decision.
- The investigation that is wrong in pregnancy. D-dimer is not used to investigate acute VTE in pregnancy or the puerperium. It is physiologically elevated by pregnancy and rises further with delivery, surgery and any inflammation, so a "positive" result is meaningless and a "negative" result cannot be relied upon to rule out. Treating a pregnant woman's leg or chest symptoms on a D-dimer is a category error that either floods imaging with false positives or, worse, falsely reassures.