Clinical overview
The puerperium — the six weeks from delivery of the placenta to involution of the genital tract — is the most lethal period of the maternity continuum in South Africa, and yet the most clinically neglected. The woman has "delivered safely", goes home (often within hours of a normal vaginal birth), and re-presents days later, frequently to a level-1 clinic, with a complaint that the junior practitioner is tempted to under-read. Sepsis, venous thromboembolism (VTE), and the postpartum psychiatric emergencies kill in this window, and they kill because their early signals are mistaken for the normal discomforts of the early puerperium. The Saving Mothers (NCCEMD) reports repeatedly identify the puerperium as a phase where substandard care — late recognition, late referral, no senior review — converts a survivable complication into a maternal death.
This objective is a HOTS objective: you are asked to appraise — to weigh risk factors, presentation, diagnosis and management together and decide what matters. The exam will not reward a list; it will reward a registrar who can take a woman 8 days postpartum with a fever, a tender breast, a swollen calf and a flat affect, and triage which of those is the emergency. The discipline is to treat every puerperal presentation as guilty until proven innocent: fever is sepsis until excluded, breathlessness is pulmonary embolism until excluded, and a mother who says she might harm her baby is a psychiatric emergency, not a "low mood" to be reviewed next week. Build on the baseline of the Normal puerperium before reading this — you cannot recognise the abnormal without owning the normal involution timeline, lochia pattern and physiological observations.
Figure J3.1 — Red-flag triage dashboard for puerperal presentations, prioritising sepsis, VTE/PE, psychiatric emergency and lactation infection within the 42-day puerperal clock.
Core knowledge
Puerperal sepsis
Maternal sepsis is infection of the genital tract (or any source) occurring between rupture of membranes/delivery and 42 days postpartum, with a systemic inflammatory response. In South Africa, non-pregnancy-related infections (overwhelmingly HIV-associated) plus pregnancy-related sepsis remain leading causes of maternal death per Saving Mothers/NCCEMD, and the immunosuppressed parturient (advanced HIV, low CD4, TB co-infection) presents atypically and deteriorates fast.
The genital-tract source is usually endometritis — ascending polymicrobial infection (group A and B streptococci, E. coli, anaerobes, Staphylococcus aureus; group A Streptococcus pyogenes causes the most fulminant, rapidly fatal puerperal sepsis). Risk factors: caesarean delivery (the single largest), prolonged rupture of membranes, prolonged labour, repeated vaginal examinations, retained products of conception, manual removal of placenta, operative vaginal birth, anaemia, diabetes, and immunosuppression. Non-genital sources that masquerade as puerperal sepsis must be actively sought: mastitis/breast abscess, urinary tract/pyelonephritis, wound (caesarean or perineal) infection, chest (including TB and COVID-class respiratory infection), and septic pelvic thrombophlebitis.
The danger of sepsis is that the classic febrile picture is unreliable: a septic woman may be normo- or hypothermic, and tachycardia or tachypnoea may be the only early sign. Standard teaching is that a sustained maternal tachycardia (>90–100/min) or tachypnoea is a red flag that outranks the temperature.
Venous thromboembolism
Pregnancy and the puerperium are prothrombotic (Virchow's triad: venous stasis, hypercoagulability of pregnancy, endothelial injury at delivery). The postpartum period carries the highest per-day risk of VTE of the whole maternity continuum, concentrated in the first weeks after birth. Deep vein thrombosis (DVT) in pregnancy is left-sided in the great majority (the gravid uterus and right iliac artery compress the left iliac vein) and is more often ilio-femoral/proximal, which both raises embolic risk and confounds the inexperienced who expect calf disease. Pulmonary embolism (PE) is a direct, fast cause of puerperal maternal death.
Risk factors stratify the patient: caesarean (especially emergency), age >35, obesity (BMI ≥30), parity ≥3, immobility, pre-eclampsia, postpartum haemorrhage/transfusion, sepsis, varicose veins, smoking, previous VTE, and known thrombophilia. RCOG Green-top Guideline 37a (risk and prophylaxis) and 37b (acute management) frame the assessment; the principle is a postnatal VTE risk-factor score that drives the duration of low-molecular-weight heparin (LMWH) thromboprophylaxis.
Breast complications
Engorgement (bilateral, days 3–5, physiological), mastitis (a tender, erythematous, wedge-shaped segment with fever and flu-like malaise, usually 2nd–3rd week, commonest organism Staph. aureus, classically from milk stasis ± a cracked nipple) and breast abscess (a fluctuant, pointing collection where mastitis has not resolved) form a continuum. Importantly, mastitis is not an automatic indication to stop breastfeeding — continued drainage of the affected breast is part of the treatment. See Infant feeding for the lactation physiology that underpins this.
