Postpartum Complications

Hemorrhage — the four Ts

• Tone (atony): the most common cause of early postpartum hemorrhage. Anything that overdistends or exhausts the myometrium blocks the mechanical clamping of spiral arteries — multiple gestation, polyhydramnios, macrosomia, grand multiparity, prolonged or induced labor, prolonged oxytocin exposure (receptor desensitization), chorioamnionitis, and halogenated inhalational anesthetics.
• Trauma: cervical/vaginal lacerations, episiotomy, uterine rupture, operative vaginal delivery (forceps > vacuum), and uterine inversion from excessive cord traction on a fundal placenta.
• Tissue: retained placenta or placental fragments, succenturiate lobe, and the accreta spectrum — driven by prior cesarean scar plus placenta previa, the classic examiner pairing.
• Thrombin: von Willebrand disease, ITP, HELLP, abruption, amniotic fluid embolism, and dilutional coagulopathy from massive crystalloid/red-cell resuscitation.

Infection

• Cesarean delivery is the dominant risk factor for endometritis — the reason ACOG recommends pre-incision antibiotic prophylaxis. Additive risks: prolonged rupture of membranes, chorioamnionitis, prolonged labor, repeated digital exams, internal monitors, manual placental extraction, GBS or bacterial vaginosis colonization.
• Mastitis: milk stasis plus nipple trauma allowing Staphylococcus aureus entry; incomplete emptying, missed feeds, and abrupt weaning are the modifiable drivers.

Perinatal mood disorders

• Non-modifiable: prior major depression, prior postpartum depression, and especially bipolar disorder — the strongest predictor of postpartum psychosis; family history; primiparity for psychosis.
• Modifiable/contextual: absent social support, intimate partner violence, unintended pregnancy, sleep deprivation, breastfeeding difficulty, thyroiditis, and untreated antenatal depression or anxiety — the targets of the USPSTF recommendation for counseling interventions in at-risk pregnant and postpartum persons.

Hemorrhagic Complications

• Uterine atony results from failure of the myometrium to contract adequately after placental delivery, leading to continued bleeding from open placental bed vessels; risk increased by prolonged labor, multiparity, uterine overdistension, and retained products of conception
• Placental abnormalities (placenta accreta/increta/percreta) occur when trophoblastic invasion extends beyond the normal Nitabuch layer into the myometrium or beyond, preventing normal placental separation and increasing hemorrhage risk
• Coagulopathy develops through consumption of clotting factors and platelets (disseminated intravascular coagulation), dilution from massive transfusion, or primary bleeding disorders, creating a vicious cycle of ongoing hemorrhage

Infectious Complications

• Postpartum endometritis results from ascending polymicrobial infection (aerobic and anaerobic bacteria from vaginal flora) into the uterine cavity following loss of cervical barrier and epithelial disruption from placental implantation
• Wound complications occur via direct bacterial contamination during delivery (vaginal laceration, perineal trauma, episiotomy) or cesarean incision; risk elevated by hematoma formation, inadequate hemostasis, and tissue ischemia
• Thrombophlebitis and septic thrombophlebitis develop when infection triggers inflammation of venous walls with secondary thrombosis, particularly in the ovarian and pelvic veins

Hypertensive Complications

• Preeclampsia/eclampsia persistence reflects endothelial dysfunction and placental ischemia that may persist days to weeks postpartum despite placental delivery; involves abnormal placentation, angiogenic imbalance (low PlGF, high sFlt-1), and systemic endothelial activation
• Posterior reversible encephalopathy syndrome (PRES) occurs from hypertensive breakthrough of cerebral autoregulation, leading to vasogenic edema predominantly in posterior cerebral territories

Thromboembolism

• Venous thromboembolism (VTE) pathophysiology follows Virchow's triad: stasis (immobility, uterine compression of iliac vessels), endothelial injury (placental delivery, instrumentation), and hypercoagulability (pregnancy-induced increase in factors II, VII, VIII, X; decreased protein S; endothelial activation)
• Postpartum hypercoagulability is exaggerated compared to pregnancy itself due to tissue factor release from placental separation, platelet activation, and increased inflammatory cytokines

Postpartum Hemorrhage (PPH)

• Early PPH (within 24 hours): heavy vaginal bleeding typically noted immediately after delivery, with soaking of pads, blood pooling, or continued heavy flow despite uterotonic administration; tachycardia, hypotension, and decreased urine output reflect hemodynamic compromise
• Late PPH (24 hours to 1 year): usually presents 1-2 weeks postpartum with prolonged lochia rubra, reinitiation of heavy bleeding after initial decrease, passage of clots, or anemia symptoms (fatigue, dyspnea); often due to retained products of conception or subinvolution
• Classic vital sign findings: orthostatic hypotension, tachycardia disproportionate to apparent blood loss (pregnant women may lose significant volume before decompensating), cool extremities in severe hemorrhage

Postpartum Infection

• Endometritis: fever (typically 38-39°C) appearing 24-72 hours postpartum, purulent/foul-smelling lochia, lower abdominal/uterine tenderness on exam, tachycardia; cervical motion tenderness often present
• Perineal/wound infection: localized warmth, erythema, edema, purulent drainage from laceration, episiotomy, or cesarean incision; abscess formation presents with fluctuance and severe localized pain
• Septic pelvic thrombophlebitis: persistent high fever despite antibiotics, lower abdominal pain, palpable adnexal mass or cord-like fullness in lateral vaginal fornices; may present as "fever of unknown origin" in postpartum patient

Hypertensive Emergencies

• Postpartum preeclampsia/eclampsia: hypertension (≥140/90 mmHg, ideally on repeat measurements), headache, visual disturbances, epigastric/right upper quadrant pain, pulmonary edema presenting as dyspnea or orthopnea
• Eclamptic seizures: generalized tonic-clonic seizures occurring days to weeks postpartum (unusual this late but can occur), typically with severe hypertension and proteinuria
• PRES presentation: headache, altered mental status, visual disturbances, seizures; imaging shows posterior predominant edema

Venous Thromboembolism

• DVT: unilateral leg swelling, pain, warmth, and erythema (though may be subtle); elevated D-dimer; Wells score elevated; classic presentation 1-2 weeks postpartum
• Pulmonary embolism: acute dyspnea, chest pain (pleuritic), syncope, hemoptysis, or sudden cardiovascular collapse; tachycardia and tachypnea out of proportion to exam findings
• Important pearl: hypercoagulability extends beyond 42 days (increased VTE risk up to 12 weeks postpartum and beyond in some studies)

Other Postpartum Complications

• Uterine inversion: extreme postpartum hemorrhage with shock out of proportion to visible bleeding, severe abdominal pain, visible dark mass at introitus; obstetric emergency
• Amniotic fluid embolism: sudden cardiovascular collapse, respiratory distress, DIC, and altered mental status occurring during labor/delivery or immediately postpartum (rare but catastrophic)
• Postpartum psychosis: acute onset of delusions, hallucinations, and disorganized behavior within first 2 weeks postpartum; requires psychiatric evaluation and often hospitalization

Postpartum Hemorrhage

• Clinical assessment: quantified blood loss (weight of soaked pads, collection in under-buttocks drape), vital signs, hemoglobin/hematocrit comparison with antepartum baseline, assessment for ongoing bleeding source
• Laboratory evaluation: CBC (baseline hemoglobin often falsely reassuring initially due to fluid shifts), coagulation studies (PT, aPTT, fibrinogen, D-dimer if DIC suspected), type and cross-match for massive transfusion protocols
• Imaging: transvaginal or transabdominal ultrasound to assess for retained products of conception, intrauterine clots, or gestational trophoblastic disease; CT angiography if arterial bleeding suspected

Postpartum Infection

• Endometritis diagnostic criteria: fever ≥38°C on 2 occasions ≥4 hours apart (or ≥38.5°C once) plus uterine tenderness and/or purulent lochia; consider this diagnosis in any postpartum fever
• CBC: elevated WBC (though often elevated postpartum normally); left shift suggests infection
• Blood and urine cultures: obtained before antibiotic initiation if sepsis suspected, though treatment should not be delayed pending cultures
• Wound cultures: obtained if purulent drainage present, though empiric coverage often initiated before results available

Hypertensive Emergencies

• BP criteria: systolic ≥160 mmHg or diastolic ≥110 mmHg on 2 occasions ≥15 minutes apart (severe range); postpartum preeclampsia requires ≥2 of: proteinuria, thrombocytopenia, elevated liver enzymes, pulmonary edema, cerebral/visual symptoms
• Laboratory studies: CBC (thrombocytopenia <100,000), liver function tests (elevated transaminases indicate HELL

Immediate stabilisation (hemorrhage)

• Call for help, two large-bore IVs, type and cross, quantify blood loss — per the ACOG/AIM Obstetric Hemorrhage bundle. Bimanual uterine massage is simultaneous, not sequential: mechanical compression is what actually occludes the placental bed while drugs take effect.
• Massive transfusion protocol with balanced product ratios if bleeding continues; replace fibrinogen (cryoprecipitate) early, since it falls first in obstetric coagulopathy.

First-line pharmacotherapy (uterotonics, ACOG Practice Bulletin 183)

• Oxytocin (posterior pituitary analogue): 10–40 units in IV crystalloid infusion, or 10 units IM. Never give undiluted rapid IV push — vasodilation and hypotension.
• Ergot alkaloid — methylergonovine 0.2 mg IM: contraindicated in hypertension/preeclampsia (vasoconstriction).
• Prostaglandin F2α — carboprost 250 mcg IM: contraindicated in asthma (bronchospasm).
• Misoprostol 800–1000 mcg (PGE1) when the above are unavailable; expect fever and shivering.
• Tranexamic acid 1 g IV within 3 hours of birth — antifibrinolytic, supported by the WOMAN trial and endorsed by WHO and ACOG as an adjunct, not a substitute for uterotonics.

Escalation and definitive management

• Tamponade: intrauterine balloon (Bakri) or vacuum-induced hemorrhage-control device.
• Uterine artery embolization if hemodynamically stable; **compression sutures (B-Lynch), uterine or hypogastric artery ligation, then hysterectomy** as the definitive lifesaving step.
• Retained tissue: manual extraction or ultrasound-guided curettage. Inversion: replace the fundus first (Johnson maneuver) with a relaxant (nitroglycerin/terbutaline), then resume uterotonics — giving uterotonics first traps the inversion.

Other entities

• Endometritis: IV clindamycin plus gentamicin until afebrile ~24–48 hours; no oral tail needed. Add ampicillin for enterococcal coverage if no response.
• Mastitis: continue emptying the breast; antistaphylococcal penicillin/cephalosporin (dicloxacillin, cephalexin); TMP-SMX or clindamycin if MRSA; drain an abscess.
• Severe-range hypertension: IV labetalol, IV hydralazine, or oral immediate-release nifedipine within 30–60 minutes plus magnesium sulfate for seizure prophylaxis (ACOG Practice Bulletin 222).
• Depression: SSRI (sertraline) with CBT/IPT; neuroactive steroid GABA-A modulators (brexanolone, zuranolone) are FDA-approved specifically for postpartum depression. Postpartum psychosis is an inpatient emergency.
• VTE: low-molecular-weight heparin (enoxaparin); warfarin is breastfeeding-compatible, DOACs generally avoided.

Of hemorrhage

• Hypovolemic shock and DIC — emergency. Consumption of factors and fibrinogen creates a feedback loop; signals are oozing from IV sites, falling fibrinogen, and a rising INR out of proportion to transfusion.
• Sheehan syndrome: hemorrhagic hypotension infarcts the hyperplastic, portal-perfused anterior pituitary. Signalled by failure of lactation (prolactin loss) followed by amenorrhea, fatigue, and hypotension from secondary adrenal insufficiency — sometimes months later.
• Asherman syndrome: intrauterine adhesions after aggressive curettage, presenting as secondary amenorrhea/infertility with a normal hormonal profile.
• Transfusion-related: TRALI (hypoxemia with bilateral infiltrates and normal filling pressures), TACO, citrate-induced hypocalcemia, hyperkalemia, and dilutional coagulopathy.
• Hysterectomy: definitive but ends fertility; ureteral injury is the classic operative complication.

Of infection

• Pelvic abscess or infected hematoma: persistent fever with a palpable mass; imaging-guided drainage required.
• Septic pelvic thrombophlebitis: fever unresponsive to appropriate antibiotics with an otherwise reassuring exam — a diagnosis of exclusion; anticoagulation is added to antibiotics.
• Necrotizing fasciitis of an episiotomy or cesarean wound — surgical emergency; pain out of proportion, crepitus, dusky skin, systemic toxicity.
• Sepsis/septic shock; breast abscess from untreated mastitis (fluctuant mass, ultrasound-confirmed).

Of hypertensive disease

• Hemorrhagic stroke — emergency and the leading cause of death in untreated severe-range hypertension; hence ACOG's 30–60-minute treatment window.
• Eclampsia, PRES, pulmonary edema, hepatic hematoma rupture (HELLP).

Of therapy

• Magnesium toxicity: loss of deep tendon reflexes → respiratory depression → cardiac arrest; treat with IV calcium gluconate.
• Gentamicin: nephrotoxicity and irreversible ototoxicity — monitor renal function.
• Ergots with hypertension → stroke; carboprost with asthma → bronchospasm.

• Atony is the answer until proven otherwise: a boggy, soft, high-riding fundus with brisk bleeding after delivery. Single best next step is bimanual uterine massage with oxytocin, not imaging, not labs. A firm uterus with ongoing bright red bleeding redirects you to laceration (trauma).
• The uterotonic contraindication pair examiners love: methylergonovine in the hypertensive/preeclamptic patient, carboprost in the asthmatic. Choose oxytocin or misoprostol in those stems.
• Shock out of proportion to visible bleeding plus a mass at the introitus = uterine inversion. Replace the fundus first; uterotonics before replacement is the trap.
• Failure of lactation after a hemorrhagic delivery = Sheehan syndrome. Amenorrhea after a postpartum curettage = Asherman syndrome. Do not swap them.
• **Postpartum fever workup — the *five Ws*: womb (endometritis), wind (atelectasis/pneumonia), water (UTI), walking (DVT), wound. Cesarean delivery is the single biggest endometritis risk factor; treat with clindamycin plus gentamicin**.
• Fever persisting despite appropriate antibiotics with an unremarkable exam = septic pelvic thrombophlebitis, a diagnosis of exclusion.
• Mastitis: keep breastfeeding. Milk is not infectious to the infant and emptying is therapeutic; stopping worsens stasis. Fluctuance means abscess and needs drainage.
• Mood timeline is the discriminator: blues are mild, peak around day 4–5, resolve within two weeks, and need reassurance only; depression persists beyond two weeks with functional impairment and warrants an SSRI (sertraline) plus therapy; psychosis appears abruptly in the first two weeks with delusions — hospitalize, and look for underlying bipolar disorder, the association most often tested.
• Tranexamic acid works only if given early (within 3 hours of birth) and is an adjunct to, never a replacement for, uterotonics.