Diagnose and manage puerperal sepsis and complications

In one line

Puerperal sepsis is the genital-tract face of maternal sepsis in the six weeks after birth — the historical "childbed fever", now read within the source-agnostic Sepsis-3 framework set out in Maternal sepsis, where sepsis is organ dysfunction from a dysregulated host response to infection rather than a site or a severity of fever. The consultant task is to recognise the deteriorating mother early — before the observations look frightening — name the source (the genital tract is only the commonest one), and combine prompt broad-spectrum antibiotics with the one intervention antibiotics cannot substitute for: source control.

Mechanism & pathophysiology

The puerperium is, in effect, a fresh wound. After delivery the placental bed is a raw, vascular surface the size of a palm, the cervix is patulous, and the lochia draining through it is an excellent culture medium; the involuting uterus, the breast establishing lactation, any caesarean or perineal wound, and a bladder emptied through a recently catheterised urethra are all portals. Normal involution is the background against which infection is read: the uterus descends roughly a fingerbreadth a day and is no longer palpable abdominally by about day 10–14, and lochia moves predictably from rubra (red, 3–4 days) to serosa (pink-brown) to alba (yellow-white) over a few weeks. A uterus that stays high and tender, lochia that turns heavy, offensive or reverts to red, and a fever that will not settle are involution going wrong. The Intermediate groundwork on the normal puerperium and its complications is assumed here; the focus is the consultant-level reasoning that turns a fever into a diagnosis and a plan.

Most puerperal sepsis is polymicrobial and ascends from the lower genital tract. Endometritis is the commonest source — colonisation of the decidua and myometrium by vaginal flora, dramatically more likely after caesarean section (the single biggest risk factor), and worse when products of conception are retained, because devitalised tissue is a protected nidus that antibiotics penetrate poorly. The organisms are the predictable mix of a gut-and-genital field: Escherichia coli and other Gram-negative aerobes, anaerobes (Bacteroides, peptostreptococci), enterococci, and staphylococci including community-acquired MRSA in wounds. Group B streptococcus and genital mycoplasmas contribute.

The organism that dominates the consultant's risk calculus is out of proportion to its frequency. Group A streptococcus (Streptococcus pyogenes) is the pathogen of "childbed fever" — the disease Semmelweis halted with hand-washing — and it behaves differently from the polymicrobial ascending infections. It is exotoxin-driven: streptococcal pyrogenic exotoxins act as superantigens, triggering massive non-specific T-cell activation and a cytokine storm that produces streptococcal toxic shock syndrome and tissue-destroying necrotising fasciitis. Invasive GAS is roughly twenty times more common in postpartum women than in the non-pregnant, can be acquired from the patient's own throat or from a household contact with a sore throat, and kills fast: once shock is established, mortality is of the order of 30–50%. The teaching point that falls out of the mechanism is that GAS can produce profound illness — pain out of proportion to signs, then hypotension — while the local findings are still unimpressive, because the damage is toxin-mediated and deep rather than a visible collection.

The other sources each have their own mechanism. Wound infection after caesarean or of a perineal repair follows the general surgical logic of contamination, haematoma and devitalised tissue; dehiscence is its structural consequence, and the dreaded version is fascial dehiscence with burst abdomen. Mastitis is milk stasis plus a skin organism (usually Staphylococcus aureus entering through a cracked nipple) — an inflammatory cellulitis of a lactating segment that becomes a breast abscess when a walled-off collection forms. Urinary tract infection exploits catheterisation and incomplete bladder emptying, and ascends to pyelonephritis in a ureteric system still dilated from pregnancy. Septic pelvic thrombophlebitis is the subtle one: bacterial seeding of the venous endothelium of the ovarian or deep pelvic veins, where thrombus and infection sustain each other and an antibiotic-resistant "enigmatic fever" persists despite an apparently treated source. Understanding that infection and clot are co-dependent in SPT is what justifies adding anticoagulation to antibiotics — the single counter-intuitive move in this whole topic.

A point of definition keeps the differential honest. The old puerperal pyrexia label — a temperature ≥38°C on any two of the first ten days after delivery (excluding the first 24 hours) — is a screening flag, not a diagnosis, and the modern habit is to treat any sustained postpartum fever as a sepsis screen pointing at a source rather than to wait for it to "declare itself". The timing of onset is a clue: GAS and other streptococcal disease tends to be early and fulminant (within the first day or two), classic ascending endometritis a few days in, wound infection towards the end of the first week, breast abscess as lactation establishes, and septic pelvic thrombophlebitis later still, as the fever that will not resolve.

Two host factors reshape this picture in South Africa. HIV — especially advanced disease with a low CD4 count — blunts the inflammatory response, broadens the organism list, and is associated with more severe and atypical puerperal infection; co-existing tuberculosis must be considered in the puerpera with persistent fever, weight loss or an atypical course, because genital and disseminated TB are part of the SA differential in a way they are not elsewhere. The general principle is that the immunosuppressed host both mounts a quieter signal and tolerates sepsis worse, so the threshold to investigate and to escalate falls. The severe end of any of these sources converges on the same final common pathway — the systemic inflammatory cascade, endothelial injury, capillary leak, and, in the worst cases, disseminated intravascular coagulation and multi-organ dysfunction — which is why the recognition and resuscitation are shared across sources even though the definitive treatment is source-specific.

Assessment

The first task is to recognise the deteriorating puerpera, and the trap is that a young, previously fit woman compensates well and then collapses. Numbers drift before they crash; tachycardia and tachypnoea precede hypotension, and a fall in urine output and a rising lactate are early. Tachypnoea is the single most under-weighted sign — a respiratory rate climbing above 20–24 is often the first marker of compensated metabolic acidosis and is exactly the observation a postnatal ward forgets to count. A structured MEOWS (Modified Early Obstetric Warning System) chart is the system safeguard — it is designed to catch the trending-but-not-yet-alarming observation set that a busy postnatal ward otherwise normalises, and it accounts for the fact that the normal ranges of pulse, blood pressure and respiratory rate shift in the puerperium so that a generic adult early-warning score misreads them. A single red MEOWS trigger, or two yellow triggers, in a febrile puerpera is a reason to escalate, not to recheck in an hour. Lactate carries the same weight here as in any sepsis: a level above 2 mmol/L signals hypoperfusion and above 4 mmol/L marks the patient who needs aggressive resuscitation and critical-care review.

• History: mode of delivery (caesarean and operative vaginal birth raise risk; ANODE-era practice now gives a single prophylactic dose after operative vaginal birth), prolonged rupture of membranes, retained products or manual removal of placenta, the character and odour of lochia, breast symptoms, urinary symptoms, wound pain or discharge, and a sore throat in the patient or a household child (the GAS clue). Pain that seems disproportionate to the wound, or that is rapidly worsening, is the necrotising-fasciitis history until disproven.
• Examination: temperature, the full observation set fed into MEOWS, and a deliberate search for the source — uterine height and tenderness, the caesarean and perineal wounds (erythema, induration, discharge, separation, and crucially crepitus, dusky skin or skin anaesthesia that signal necrotising infection), both breasts (a tender, red, wedge-shaped segment is mastitis; a fluctuant mass is abscess), the renal angles and suprapubic region, and the calves and chest because postpartum venous thromboembolism is the differential that masquerades as sepsis. Examine the throat.
• Investigations: blood cultures before antibiotics (but do not let drawing them delay the first dose), full blood count, CRP, U&E and creatinine, lactate and venous blood gas, and clotting if the picture is severe. A high vaginal and any wound swab, a midstream or catheter urine, and — when GAS or invasive infection is suspected — a throat swab. The bedside numbers that matter are the sepsis-screen physiology: lactate, urine output, and the trend.
• Imaging by question. Pelvic ultrasound to look for retained products (an echogenic endometrial mass with vascularity) or a pelvic or wound collection. CT is the workhorse for the deep and the occult: it shows the gas and fascial-plane fluid of necrotising fasciitis, the thrombosed enlarged ovarian or pelvic veins of septic pelvic thrombophlebitis, and a deep pelvic abscess the ultrasound misses. SPT is in large part a diagnosis reached when a fever persists despite adequate antibiotics and source control, with CT lending support rather than the other way round.