Maternal Sepsis (Puerperal Sepsis)

Overview

Maternal sepsis, also known as puerperal sepsis when occurring postpartum, is a life-threatening condition defined as organ dysfunction resulting from infection during pregnancy, childbirth, or the postpartum period. It represents one of the leading causes of maternal mortality worldwide, accounting for approximately 11% of maternal deaths globally and ranking as the third leading cause of maternal death in developed countries. [1,2]

The condition is particularly insidious because the physiological changes of pregnancy can mask early signs of sepsis, and progression to severe sepsis or septic shock can occur rapidly, often within hours. The maternal immune system undergoes significant adaptations during pregnancy to tolerate the semi-allogeneic fetus, potentially increasing susceptibility to certain infections. [3] Early recognition and prompt treatment with appropriate antimicrobials and supportive care are critical to reducing maternal morbidity and mortality.

Maternal sepsis differs from sepsis in the general population due to pregnancy-specific sources of infection (chorioamnionitis, endometritis, septic abortion), altered physiology that modifies clinical presentation, and the need to consider fetal wellbeing alongside maternal treatment. The UK Confidential Enquiry into Maternal Deaths has consistently highlighted delays in recognition and treatment as key factors in preventable maternal deaths from sepsis. [4]

Epidemiology

Maternal sepsis incidence varies significantly by geographic region and healthcare setting, with substantially higher rates in low- and middle-income countries. Understanding the epidemiological patterns is essential for prevention strategies and resource allocation.

Risk Factors

Patient-Related Factors:

• Obesity (BMI > 30 kg/m²) - increases infection risk 2-3 fold [11]
• Diabetes mellitus (pre-existing or gestational)
• Immunosuppression (HIV, chronic steroid use, autoimmune conditions)
• Anaemia (haemoglobin less than 100 g/L)
• Malnutrition or vitamin deficiencies
• Advanced maternal age (> 35 years)
• Multiparity (particularly grand multiparity ≥5)
• History of pelvic infection or sexually transmitted infections
• Bacterial vaginosis in pregnancy

Obstetric Risk Factors:

• Emergency caesarean section (especially after prolonged labour)
• Prolonged rupture of membranes (> 18-24 hours)
• Multiple vaginal examinations during labour (> 5-6 examinations)
• Prolonged labour (> 24 hours)
• Operative vaginal delivery (forceps, ventouse)
• Manual removal of placenta
• Retained products of conception
• Perineal trauma (third/fourth degree tears)
• Chorioamnionitis
• Invasive fetal monitoring (fetal scalp electrode, intrauterine pressure catheter)
• Cervical cerclage
• Amniocentesis or other invasive procedures

Healthcare-Related Factors:

• Inadequate aseptic technique during procedures
• Delayed or inappropriate antibiotic prophylaxis
• Prolonged hospital stay
• Nosocomial transmission of resistant organisms

Temporal Patterns

Maternal sepsis demonstrates distinct temporal patterns:

• Antepartum sepsis (10-15%): Often related to urinary tract infections, pneumonia, or chorioamnionitis
• Intrapartum sepsis (10-15%): Typically chorioamnionitis or progression of existing infection
• Postpartum sepsis (70-75%): Predominantly endometritis, wound infections, or mastitis

Peak incidence occurs between days 2-7 postpartum, coinciding with the period of maximal physiological adaptation and hospital discharge in many settings. [9]

Aetiology & Pathophysiology

Microbiology

Maternal sepsis is polymicrobial in 30-40% of cases, with causative organisms varying by source and geographic location. [12]

Common Bacterial Pathogens:

1. Gram-Positive Organisms (40-50%)

   • Streptococcus pyogenes (Group A Streptococcus, GAS) - particularly virulent, associated with rapid progression and toxic shock syndrome
   • Streptococcus agalactiae (Group B Streptococcus, GBS) - common colonizer, 10-30% carriage rate
   • Staphylococcus aureus (including MRSA) - wound infections, mastitis, toxic shock syndrome
   • Enterococcus species - often polymicrobial, healthcare-associated
   • Clostridium perfringens - rare but life-threatening, associated with septic abortion and gas gangrene

2. Gram-Negative Organisms (30-40%)

   • Escherichia coli - most common cause of urinary tract infection and postpartum bacteremia
   • Klebsiella pneumoniae - urinary and respiratory tract infections
   • Proteus species - urinary tract infections
   • Pseudomonas aeruginosa - healthcare-associated, wound infections
   • Bacteroides species - anaerobic, often polymicrobial genital tract infections

3. Anaerobes (20-30%)

   • Bacteroides fragilis - genital tract infections, intra-abdominal sepsis
   • Peptostreptococcus species - polymicrobial infections
   • Prevotella species - genital tract infections

Viral Pathogens:

• Influenza A and B - seasonal respiratory infections with increased severity in pregnancy
• COVID-19 (SARS-CoV-2) - increased risk of severe disease and mortality in pregnancy [13]
• Varicella zoster virus - pneumonitis in pregnancy
• Herpes simplex virus - disseminated HSV in pregnancy (rare)

Fungal Pathogens (Rare):

• Candida species - typically in immunocompromised patients or with multiple risk factors

Sources of Infection

Genital Tract (60-70% of cases):

1. Endometritis/Endomyometritis

   • Most common source postpartum
   • Ascending infection from vaginal flora
   • Risk increased with caesarean section, prolonged membrane rupture, prolonged labour

2. Chorioamnionitis

   • Intra-amniotic infection
   • Presents antepartum or intrapartum
   • Associated with preterm labour and prelabour rupture of membranes

3. Septic Abortion

   • Historically common cause, now rare in settings with safe abortion access
   • Associated with retained products of conception
   • Often polymicrobial with anaerobes

4. Surgical Site Infections

   • Caesarean wound infection (superficial or deep)
   • Episiotomy or perineal tear infection
   • Presents days 4-7 postpartum typically

Urinary Tract (15-25% of cases):

• Pyelonephritis - increased risk in pregnancy due to urinary stasis
• Catheter-associated urinary tract infection
• Urosepsis - can progress rapidly

Respiratory Tract (5-10% of cases):

• Community-acquired pneumonia
• Aspiration pneumonia (especially during general anaesthesia)
• Influenza with secondary bacterial pneumonia

Breast (2-5% of cases):

• Lactational mastitis with progression to abscess
• Typically S. aureus

Other Sources (5-10%):

• Appendicitis (displaced location in pregnancy complicates diagnosis)
• Cholecystitis
• Intra-abdominal abscess
• Meningitis
• Soft tissue infections (necrotizing fasciitis - rare but devastating)

Pathophysiology

Exam Detail: Molecular and Cellular Mechanisms:

The pathophysiology of maternal sepsis follows similar mechanisms to sepsis in non-pregnant individuals, with important pregnancy-specific modifications:

1. Initial Host Response to Infection

When bacteria breach anatomical barriers (endometrium, peritoneum, urinary tract), pattern recognition receptors (PRRs) on innate immune cells detect pathogen-associated molecular patterns (PAMPs):

• Toll-like receptors (TLRs) recognize bacterial lipopolysaccharide (LPS), peptidoglycan, flagellin
• NOD-like receptors (NLRs) detect intracellular bacterial components
• C-type lectin receptors recognize fungal components

This triggers activation of nuclear factor-kappa B (NF-κB) and production of pro-inflammatory cytokines:

• Tumor necrosis factor-alpha (TNF-α)
• Interleukin-1 (IL-1)
• Interleukin-6 (IL-6)
• Interleukin-8 (IL-8)

2. Systemic Inflammatory Response

Cytokine release produces systemic effects:

• Fever: IL-1 and IL-6 act on hypothalamic thermoregulatory center
• Tachycardia: Direct catecholamine effect and reduced systemic vascular resistance
• Tachypnoea: Central stimulation of respiratory drive
• Leukocytosis: Bone marrow mobilization of neutrophils

3. Endothelial Dysfunction and Vascular Leak

Pro-inflammatory mediators damage endothelial glycocalyx and increase vascular permeability:

• Loss of endothelial barrier function
• Fluid extravasation into interstitial space (third-spacing)
• Reduced intravascular volume despite total body fluid excess
• Tissue oedema impairing oxygen diffusion

4. Coagulation Cascade Activation

Sepsis induces a procoagulant state through multiple mechanisms:

• Tissue factor expression on endothelium and monocytes
• Platelet activation and aggregation
• Impaired anticoagulant pathways (protein C, antithrombin)
• Reduced fibrinolysis
• Risk of disseminated intravascular coagulation (DIC) in severe cases

5. Microcirculatory Dysfunction

Despite preserved or increased cardiac output initially, sepsis causes:

• Heterogeneous microvascular flow
• Arteriovenous shunting
• Impaired oxygen extraction at tissue level (cytopathic hypoxia)
• Mitochondrial dysfunction

6. Organ Dysfunction

Progressive sepsis leads to multiple organ dysfunction:

• Cardiovascular: Myocardial depression from inflammatory mediators, vasodilation (distributive shock), relative hypovolaemia
• Respiratory: Acute respiratory distress syndrome (ARDS) from pulmonary capillary leak and inflammation
• Renal: Acute tubular necrosis from hypoperfusion and inflammatory injury
• Hepatic: Cholestasis, impaired synthetic function
• Neurological: Septic encephalopathy from neurotransmitter dysregulation
• Haematological: DIC, thrombocytopenia

Pregnancy-Specific Modifications:

1. Altered Immune Response:

   • Shift toward Th2 immunity (anti-inflammatory) to maintain feto-maternal tolerance
   • Reduced cell-mediated immunity
   • Potentially impaired pathogen clearance for intracellular organisms

2. Cardiovascular Adaptations:

   • Baseline increased cardiac output (30-50% above non-pregnant)
   • Reduced systemic vascular resistance
   • Increased blood volume (40-50% expansion)
   • These changes can mask early signs of hypovolaemic or distributive shock

3. Respiratory Changes:

   • Baseline respiratory alkalosis (compensated by renal bicarbonate excretion)
   • Reduced functional residual capacity
   • Increased minute ventilation
   • Lower threshold for respiratory failure

4. Renal Adaptations:

   • Increased glomerular filtration rate (40-50% above baseline)
   • "Normal" creatinine in pregnancy is lower (40-60 μmol/L)
   • Creatinine > 90 μmol/L suggests renal impairment in pregnancy

5. Haematological Changes:

   • Physiological anaemia of pregnancy (dilutional)
   • Hypercoagulable state (increased clotting factors, reduced protein S)
   • Elevated baseline white cell count (up to 15 × 10⁹/L in labour)
   • These changes complicate interpretation of laboratory markers

6. Uteroplacental Perfusion:

   • Uterine vasculature lacks autoregulation
   • Reduced maternal cardiac output or hypotension directly compromises placental perfusion
   • Fetal compromise (CTG abnormalities) may be earliest sign of maternal shock

Streptococcal Toxic Shock Syndrome:

Group A Streptococcus produces superantigens (e.g., streptococcal pyrogenic exotoxins) that:

• Bypass normal antigen processing
• Directly crosslink MHC class II molecules with T-cell receptors
• Cause massive, non-specific T-cell activation (up to 20% vs. less than 0.01% normally)
• Result in cytokine storm with overwhelming inflammatory response
• Lead to rapid progression to shock, multiorgan failure, and death within hours

This mechanism explains the fulminant presentation of GAS puerperal sepsis and the critical importance of early recognition and aggressive treatment. [14]

Clinical Presentation

Early recognition of maternal sepsis is challenging because:

1. Physiological changes of pregnancy alter normal vital sign ranges
2. Initial symptoms may be non-specific
3. Young, healthy women can maintain compensatory mechanisms until sudden decompensation
4. Competing diagnoses (normal postpartum pain, bleeding) may distract from sepsis

Modified Early Warning Score (MEOWS)

The UK Confidential Enquiry recommends use of modified early warning systems specifically calibrated for pregnant women, as standard early warning scores are inappropriate in pregnancy. [4]

Physiological Parameters in Normal Pregnancy:

• Heart rate: 80-100 bpm (10-15 bpm higher than non-pregnant)
• Respiratory rate: 14-20 breaths/min (unchanged or slightly increased)
• Systolic BP: 100-140 mmHg (may decrease 10-15 mmHg in second trimester)
• Diastolic BP: 60-90 mmHg
• Temperature: 36.5-37.5°C
• Oxygen saturations: ≥95% (unchanged)

Symptoms

Cardinal Symptoms:

1. Fever (> 38°C) or hypothermia (less than 36°C)

   • Present in 80-90% of cases
   • Absence does not exclude sepsis, especially in elderly or immunosuppressed
   • Rigors suggest bacteraemia

2. Pain

   • Lower abdominal pain or uterine tenderness (endometritis)
   • Suprapubic pain or dysuria (UTI/pyelonephritis)
   • Loin pain (pyelonephritis)
   • Wound pain (surgical site infection)
   • Chest pain or pleuritic pain (pneumonia, pulmonary embolism)
   • Breast pain (mastitis)

3. Abnormal Vaginal Discharge

   • Offensive/purulent lochia
   • Increased volume
   • Present in genital tract sepsis

4. Systemic Symptoms

   • Malaise, weakness
   • Reduced oral intake
   • Nausea and vomiting
   • Headache
   • Myalgia (influenza, streptococcal infection)

Red Flag Symptoms:

• Confusion or altered mental state
• Breathlessness or respiratory distress
• Reduced urine output (less than 0.5 mL/kg/h or less than 500 mL/24h)
• Mottled or ashen skin
• Non-blanching rash (purpura - consider meningococcal or streptococcal sepsis)
• "Not feeling right" or maternal perception of severe illness

Signs

General Inspection:

• Appears unwell or toxic
• Distressed or agitated
• Altered consciousness (confusion, drowsiness)
• Skin changes (flushed, pale, mottled, cyanosed)
• Dehydration (dry mucous membranes, reduced skin turgor)

Vital Signs - Sepsis Criteria:

The Sepsis-3 definition uses organ dysfunction (increase in SOFA score ≥2) to define sepsis, but this is impractical for initial screening. Clinical criteria include:

• Temperature: > 38°C or less than 36°C
• Heart rate: > 100 bpm (> 110 bpm may be more specific in pregnancy)
• Respiratory rate: > 20 breaths/min or PaCO₂ less than 4.3 kPa
• Systolic BP: less than 90 mmHg or MAP less than 65 mmHg or drop > 40 mmHg from baseline
• Oxygen saturation: less than 95% on room air

Systemic Examination Findings:

Source-Specific Signs:

1. Genital Tract Sepsis:

   • Uterine tenderness or pain on bimanual examination
   • Offensive lochia or purulent discharge
   • Open cervical os with products visible (septic abortion)
   • Caesarean wound: erythema, induration, purulent discharge, wound dehiscence
   • Perineal wound: breakdown, purulent discharge, crepitus (necrotizing fasciitis)

2. Urinary Tract:

   • Loin tenderness (costovertebral angle tenderness)
   • Suprapubic tenderness
   • Dysuria

3. Respiratory:

   • Crepitations, bronchial breathing
   • Dullness to percussion (consolidation, effusion)

4. Breast:

   • Erythema, warmth, tenderness of breast tissue
   • Fluctuance (abscess formation)
   • Purulent discharge from nipple

5. Severe Sepsis/Septic Shock:

   • Hypotension requiring vasopressors
   • Lactate > 4 mmol/L
   • Reduced consciousness
   • Oliguria/anuria
   • Mottled or cold peripheries despite warm core
   • Disseminated intravascular coagulation (bleeding from venepuncture sites, haematuria)

Clinical Patterns by Organism

Group A Streptococcal Sepsis:

• Particularly fulminant presentation
• Rapid progression (hours to death)
• Severe pain (often out of proportion to findings initially)
• Toxic shock syndrome (hypotension, rash, multiorgan failure)
• May present without fever
• High mortality (20-60%) despite treatment [15]

Clostridial Sepsis (C. perfringens):

• Severe pain and uterine tenderness
• Haemolysis (jaundice, dark urine)
• Subcutaneous emphysema or crepitus
• Rapid progression to shock and renal failure
• High mortality

Differential Diagnosis

Maternal sepsis must be distinguished from other causes of systemic illness in the peripartum period:

Considerations:

• Sepsis and PPH can coexist (infection causing uterine atony)
• Pre-eclampsia and sepsis can coexist (different pathophysiology but overlapping presentation)
• Fever in labour is not always infection (epidural-related, dehydration)

Investigations

Time is critical in maternal sepsis - investigations should not delay treatment. The principle is "screen, treat, transfer":

1. Obtain cultures and basic investigations
2. Start empirical antibiotics within 1 hour
3. Escalate care as needed

First-Line Investigations (Bedside and Laboratory)

Immediate Bedside Tests:

1. Vital signs monitoring (continuous or every 15-30 minutes)

   • Temperature, heart rate, blood pressure, respiratory rate, oxygen saturation
   • Consider arterial line for continuous BP monitoring in shock

2. Venous blood gas (faster than laboratory tests)

   • Lactate (> 2 mmol/L suggests tissue hypoperfusion, > 4 mmol/L severe)
   • pH (metabolic acidosis in shock)
   • Base excess
   • Glucose (sepsis can cause hyper- or hypoglycaemia)
   • Potassium

3. Urine output monitoring (catheterise)

   • Target > 0.5 mL/kg/h
   • Oliguria indicates renal hypoperfusion or AKI

Laboratory Investigations:

Microbiological Investigations - Obtain Before Antibiotics (but do not delay treatment):

1. Blood cultures (at least 2 sets from different sites)

   • Positive in 20-40% of sepsis cases
   • Obtain before antibiotics if possible
   • Essential for organism identification and antibiotic susceptibility

2. Urine culture (midstream or catheter sample)

   • Urinalysis (leukocytes, nitrites, protein, blood)
   • Microscopy, culture and sensitivity

3. High vaginal swab and endocervical swab

   • Aerobic and anaerobic culture
   • Specific tests for N. gonorrhoeae, C. trachomatis if indicated

4. Wound swab (if caesarean section or perineal wound)

   • Deep tissue sample preferable to superficial swab
   • May require operative debridement for adequate sample

5. Placental histology and culture (if retained products suspected)

6. Respiratory samples (if pneumonia suspected)

   • Sputum culture
   • Nasopharyngeal swab for viral PCR (influenza, COVID-19, RSV)

7. Lumbar puncture (if meningitis suspected and safe)

   • CSF microscopy, culture, glucose, protein
   • Contraindications: raised ICP, coagulopathy, thrombocytopenia, haemodynamic instability

Second-Line Investigations

Imaging:

1. Chest X-ray

   • Indications: Respiratory symptoms, hypoxia, sepsis without obvious source
   • Findings: Consolidation, effusion, ARDS (bilateral infiltrates)
   • Safe in pregnancy with abdominal shielding

2. Ultrasound abdomen and pelvis

   • Indications: Abdominal pain, suspected intra-abdominal collection, retained products
   • Findings: Endometrial thickness (> 10-12 mm post-delivery suggests retained products), free fluid, collections, renal obstruction

3. CT chest/abdomen/pelvis (with or without contrast)

   • Indications: Sepsis without identified source, suspected intra-abdominal sepsis, necrotizing fasciitis
   • Radiation exposure must be balanced against clinical need (justified in life-threatening sepsis)

4. MRI

   • Indications: Soft tissue infections, pelvic collections (when ultrasound inadequate)
   • Advantages: No radiation, excellent soft tissue detail
   • Disadvantages: Time-consuming, limited availability

Point-of-Care Testing

Cardiotocography (CTG):

• If fetus present and potentially viable (≥24 weeks gestation)
• Fetal tachycardia may precede maternal tachycardia
• Reduced variability, decelerations suggest fetal compromise from maternal shock
• Decision for delivery depends on maternal stability, gestational age, and fetal status

Echocardiography:

• Bedside echo in ICU setting
• Assess cardiac function, fluid responsiveness, exclude endocarditis

Exam Detail: Interpretation Pearls and Pitfalls:

1. White Cell Count in Pregnancy:

   • Physiological leukocytosis: WCC 6-16 × 10⁹/L in pregnancy
   • Labour: WCC may reach 20-25 × 10⁹/L (stress demargination)
   • Leukopenia (less than 4 × 10⁹/L) is more concerning than leukocytosis in sepsis (bone marrow suppression, poor prognostic sign)
   • Neutrophil left shift (band forms > 10%) more specific than total count

2. C-Reactive Protein:

   • Rises in normal labour (up to 50-80 mg/L)
   • Very high CRP (> 150-200 mg/L) more specific for infection
   • Lags clinical course (rises 6-12 hours after onset, peaks 24-48 hours)
   • Serial measurements more useful than single value

3. Procalcitonin:

   • More specific for bacterial infection than CRP
   • less than 0.5 ng/mL: bacterial infection unlikely
   • 0.5-2 ng/mL: possible bacterial infection

   • 2 ng/mL: bacterial infection likely

   • 10 ng/mL: severe sepsis/septic shock

   • Can be falsely elevated in labour but usually less than 1-2 ng/mL

4. Lactate:

   • Normal labour: lactate may be mildly elevated (1-2 mmol/L) due to uterine work
   • Lactate > 4 mmol/L defines septic shock (Sepsis-3 criteria)
   • Elevated lactate can occur without hypotension (cryptic shock)
   • Causes other than sepsis: seizures, metformin, thiamine deficiency, liver failure
   • Serial lactate clearance (reduction > 10% in 2 hours) guides resuscitation

5. Creatinine in Pregnancy:

   • Baseline creatinine in pregnancy: 40-60 μmol/L (increased GFR)
   • Creatinine > 90 μmol/L suggests AKI in pregnancy
   • Creatinine may lag true renal function (insensitive early marker)
   • Elevated urea out of proportion to creatinine suggests hypovolaemia

6. Coagulation:

   • Pregnancy is hypercoagulable (elevated fibrinogen 4-6 g/L, factor VIII, vWF)
   • Fibrinogen less than 2 g/L in pregnancy is abnormal (vs. less than 1 g/L in non-pregnant)
   • DIC criteria in pregnancy: platelets less than 100 × 10⁹/L, fibrinogen less than 2 g/L, elevated D-dimer (but D-dimer physiologically elevated in pregnancy), prolonged PT/APTT

7. Blood Cultures:

   • Positive in only 20-40% of sepsis cases (many false negatives)
   • Negative cultures do not exclude sepsis
   • Contamination vs. true positive: multiple sets positive for same organism suggests true bacteraemia
   • Skin commensals (S. epidermidis, Corynebacterium) usually contaminants unless from multiple cultures or line-associated infection

8. Arterial vs. Venous Lactate:

   • Arterial and venous lactate correlate well
   • Venous sampling is easier and less painful
   • Arterial sampling necessary if arterial blood gas interpretation needed (pH, PaO₂, PaCO₂)

Classification and Severity Assessment

Sepsis-3 Definitions (2016)

Sepsis: Life-threatening organ dysfunction caused by dysregulated host response to infection

• Clinically identified by increase in Sequential Organ Failure Assessment (SOFA) score ≥2 points
• In practice, presence of infection plus any of: hypotension, altered mental state, tachypnoea

Septic Shock: Subset of sepsis with profound circulatory, cellular, and metabolic abnormalities

• Sepsis with persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg
• AND serum lactate > 2 mmol/L despite adequate fluid resuscitation
• Mortality 40-60% [16]

Quick SOFA (qSOFA) Score

Bedside tool for rapid identification of patients at risk of adverse outcomes (not diagnostic):

• Respiratory rate ≥22/min
• Altered mentation (GCS less than 15)
• Systolic BP ≤100 mmHg

Score ≥2 suggests greater risk of poor outcome and need for escalation. However, qSOFA lacks sensitivity in pregnancy due to physiological adaptations - MEOWS is preferred. [4]

UK Sepsis Trust Red Flag Criteria (Adapted for Pregnancy)

Red Flag Sepsis (requires immediate escalation and "Sepsis Six" within 1 hour):

• Systolic BP less than 90 mmHg (or drop > 40 mmHg from baseline)
• Heart rate > 130 bpm
• Respiratory rate ≥25 per minute
• Needs oxygen to keep SpO₂ ≥92%
• Non-blanching rash, mottled/ashen/cyanotic skin
• Recent chemotherapy
• Lactate ≥2 mmol/L
• Confusion/reduced GCS or not responding normally

Amber Flags (increased risk, requires senior review):

• Relatives concerned about mental status
• Acute deterioration in functional ability
• Immunosuppressed
• Trauma/surgery/procedure in last 8 weeks
• Respiratory rate 21-24
• Heart rate 100-130 bpm
• Systolic BP 90-100 mmHg
• Temperature less than 36°C
• Clinical signs of wound, device, or skin infection

Management

Maternal sepsis is a time-critical obstetric emergency requiring immediate recognition and treatment. The principle is early, aggressive, multidisciplinary management with simultaneous attention to:

1. Maternal resuscitation and stabilization
2. Source control
3. Antimicrobial therapy
4. Organ support
5. Fetal assessment and delivery planning

Sepsis Six Bundle (Within 1 Hour of Recognition)

The "Sepsis Six" is a resuscitation bundle proven to reduce mortality when delivered within 1 hour: [17]

Give Three:

1. Oxygen - target SpO₂ 94-98% (or 88-92% if COPD risk)
2. Intravenous fluids - crystalloid bolus (500-1000 mL over 15-30 minutes)
3. Intravenous antibiotics - broad-spectrum, within 1 hour of recognition

Take Three:

1. Blood cultures - before antibiotics if possible
2. Lactate - venous or arterial blood gas
3. Urine output monitoring - insert catheter, measure hourly output

Acute Management

A. Resuscitation and Stabilization

Airway and Breathing:

• High-flow oxygen via non-rebreather mask (15 L/min) initially
• Target SpO₂ 94-98%
• Continuous SpO₂ monitoring
• Consider early intubation if:
  • Respiratory rate > 30/min despite oxygen
  • Hypoxia (PaO₂ less than 8 kPa on supplemental oxygen)
  • Reduced consciousness (GCS ≤8)
  • Inability to protect airway

Circulation:

• Establish large-bore IV access (two 14-16G cannulae)
• Central venous access if difficult peripheral access or vasopressor requirement
• Fluid resuscitation:
  • "Initial bolus: 500-1000 mL crystalloid (Hartmann's or 0.9% saline) over 15-30 minutes"
  • Reassess response (heart rate, BP, lactate, urine output, clinical perfusion)
  • Further 250-500 mL boluses as needed
  • "Caution: Pregnancy has lower colloid oncotic pressure - risk of pulmonary oedema with aggressive fluid resuscitation"
  • Consider invasive monitoring (arterial line, central venous catheter) early if poor response to initial fluids

Targets:

• Mean arterial pressure (MAP) ≥65 mmHg
• Urine output ≥0.5 mL/kg/h
• Lactate clearance (reduce by > 10% per 2 hours, normalize less than 2 mmol/L)
• Central venous oxygen saturation (ScvO₂) > 70%

Vasopressor Support (if hypotension persists despite adequate fluid resuscitation):

• Noradrenaline (norepinephrine) - first-line vasopressor
  • Start at 0.05-0.1 mcg/kg/min, titrate to MAP ≥65 mmHg
  • Predominantly alpha-adrenergic (vasoconstriction) with some beta activity
• Consider vasopressin (0.03-0.04 units/min) as adjunct if high noradrenaline doses
• Inotropic support (dobutamine) if myocardial dysfunction evident on echo

Positioning:

• Left lateral tilt if pregnant (> 20 weeks gestation) to avoid aortocaval compression
• Use wedge or manual displacement of uterus

B. Antimicrobial Therapy

Critical Principle: Appropriate broad-spectrum antibiotics within 1 hour of sepsis recognition reduces mortality by 7.6% per hour of delay. [18]

Empirical Antibiotic Regimens (Adapted to Local Resistance Patterns):

The choice depends on likely source and local antibiogram. Following are general UK recommendations:

1. Postpartum Endometritis / Genital Tract Sepsis:

• First-line: Clindamycin 600-900 mg IV 8-hourly + Gentamicin 5-7 mg/kg IV daily
  • Covers anaerobes, Gram-negatives, and streptococci
  • Check gentamicin levels (target peak 10-12 mg/L, trough less than 1 mg/L)
  • Adjust for renal function
• Alternative: Co-amoxiclav 1.2 g IV 8-hourly + Metronidazole 500 mg IV 8-hourly
• If MRSA risk: Add Vancomycin 15-20 mg/kg IV loading dose, then 15-20 mg/kg 12-hourly (target trough 15-20 mg/L)
• If Group A Strep suspected/confirmed: Add Clindamycin 900 mg IV 8-hourly (inhibits toxin production) + Benzylpenicillin 2.4 g IV 4-hourly

2. Pyelonephritis / Urosepsis:

• First-line: Gentamicin 5-7 mg/kg IV daily OR Ceftriaxone 1-2 g IV daily
• Consider local E. coli resistance patterns (fluoroquinolone resistance common)
• If septic shock: Piperacillin-tazobactam 4.5 g IV 8-hourly

3. Pneumonia:

• Community-acquired: Co-amoxiclav 1.2 g IV 8-hourly + Clarithromycin 500 mg IV 12-hourly
  • Covers S. pneumoniae, H. influenzae, and atypical pathogens
• Aspiration pneumonia: Co-amoxiclav 1.2 g IV 8-hourly + Metronidazole 500 mg IV 8-hourly
• Influenza with secondary bacterial: Oseltamivir 75 mg PO 12-hourly + Co-amoxiclav 1.2 g IV 8-hourly

4. Intra-abdominal Sepsis (Appendicitis, Cholecystitis):

• Piperacillin-tazobactam 4.5 g IV 8-hourly OR Meropenem 1 g IV 8-hourly (if severe)

5. Skin and Soft Tissue (Necrotizing Fasciitis, Wound Infection):

• Piperacillin-tazobactam 4.5 g IV 8-hourly + Clindamycin 900 mg IV 8-hourly
• Add Vancomycin if MRSA risk
• Urgent surgical debridement essential

6. Septic Shock with Unknown Source:

• Meropenem 1 g IV 8-hourly + Vancomycin 15-20 mg/kg IV 12-hourly
• Broad coverage pending cultures and source identification

Antibiotic Adjustments:

• De-escalation: Narrow spectrum once organism identified and sensitivities known (typically 48-72 hours)
• Duration: Typically 5-7 days for most infections, longer for deep-seated infections or slow clinical response
• Renal dosing: Adjust aminoglycosides, vancomycin, and beta-lactams for reduced creatinine clearance
• Allergies: Document and consider cross-reactivity (e.g., 10% cross-reactivity between penicillins and cephalosporins)

Antifungal Therapy:

• Not routinely given empirically
• Consider in prolonged sepsis, TPN, immunosuppression, previous broad-spectrum antibiotics
• Fluconazole or echinocandin (anidulafungin, caspofungin) if Candida suspected

C. Source Control

Early source control is as important as antibiotics:

Surgical Interventions:

1. Retained Products of Conception:

   • Evacuate uterus (suction curettage or manual vacuum aspiration)
   • Stabilize maternally first if possible, but may be time-critical
   • Cover with antibiotics before procedure

2. Postpartum Endometritis:

   • Usually responds to medical therapy alone
   • Ultrasound to exclude retained products
   • Consider evacuation if persistent fever > 48-72 hours despite antibiotics

3. Caesarean Wound Infection:

   • Superficial: open wound, drain, pack, antibiotics
   • Deep/fascial dehiscence: return to theatre for debridement and primary or delayed closure

4. Necrotizing Fasciitis:

   • Surgical emergency - debridement within hours
   • Repeat debridement often necessary (second look at 24-48 hours)
   • High mortality if delayed

5. Peritonitis (Appendicitis, Bowel Perforation):

   • Laparotomy or laparoscopy for source control
   • Pregnancy not contraindication to surgery

6. Intra-abdominal or Pelvic Abscess:

   • CT or ultrasound-guided drainage
   • Surgical drainage if not amenable to percutaneous approach

Device Removal:

• Remove urinary catheter if source of infection (after ensuring alternative drainage)
• Remove central lines if line sepsis suspected (send line tip for culture)
• Remove any foreign material if infected

D. Obstetric Management

Antepartum Sepsis:

• Continuous fetal monitoring if viable gestation (≥24 weeks)

• Multidisciplinary decision on timing of delivery:

  • "Immediate delivery if:"
    • Maternal instability requiring delivery for maternal survival (e.g., chorioamnionitis with maternal septic shock)
    • Severe fetal compromise
  • "Stabilize and deliver urgently if:"
    • Chorioamnionitis (delivery recommended once maternal stability achieved)
    • Maternal stability achieved but ongoing sepsis
  • "Conservative if:"
    • Maternal sepsis controlled, fetus stable, remote from term
    • Sepsis from non-obstetric source (UTI, pneumonia) responding to treatment

• Mode of delivery:

  • Vaginal delivery preferred if maternal and fetal status permit
  • Caesarean section for obstetric indications only (unless immediate delivery needed for maternal survival and vaginal delivery not imminent)

Intrapartum Sepsis:

• Expedite delivery (augment labour, consider instrumental delivery)
• Caesarean if fetal compromise or failure to progress
• Avoid prolonged labour

Postpartum Sepsis:

• Fetus already delivered - focus on maternal resuscitation and source control
• Lactation: most antibiotics compatible with breastfeeding (check individual drugs)

E. Organ Support and Critical Care

Indications for ICU/HDU Admission:

• Septic shock (hypotension requiring vasopressors)
• Lactate > 4 mmol/L
• Multi-organ failure
• Respiratory failure requiring NIV or mechanical ventilation
• Acute kidney injury requiring renal replacement therapy
• Reduced consciousness (GCS ≤12)
• Invasive monitoring required

Respiratory Support:

• Non-invasive ventilation (CPAP/BiPAP) may be used as bridge but low threshold for intubation
• Mechanical ventilation if ARDS:
  • Lung-protective ventilation (tidal volume 6 mL/kg ideal body weight)
  • Plateau pressure less than 30 cmH₂O
  • PEEP to maintain oxygenation
  • Permissive hypercapnia accepted (pH > 7.2)
  • Prone positioning if severe ARDS (requires delivery first if pregnant)

Renal Support:

• Renal replacement therapy (RRT) if:
  • Refractory hyperkalaemia
  • Severe metabolic acidosis (pH less than 7.15)
  • Fluid overload with pulmonary oedema not responding to diuretics
  • Uraemic complications
• Continuous veno-venous haemofiltration (CVVH) preferred in haemodynamically unstable patients

Haematological Support:

• Blood products if DIC:
  • Platelets if less than 50 × 10⁹/L (or less than 75-100 × 10⁹/L if bleeding or pre-procedure)
  • Fresh frozen plasma if PT/APTT > 1.5× normal and bleeding
  • Cryoprecipitate if fibrinogen less than 1.5-2 g/L
  • Tranexamic acid if obstetric bleeding component (1 g IV over 10 minutes, then 1 g over 8 hours)

Glycaemic Control:

• Target glucose 6-10 mmol/L
• Insulin infusion if persistent hyperglycaemia

Nutrition:

• Enteral nutrition preferred (NG feeding) within 24-48 hours if tolerated
• Parenteral nutrition if gut dysfunction (ileus, bowel ischaemia)

Thromboprophylaxis:

• Sepsis is prothrombotic despite potential concurrent coagulopathy
• Low-molecular-weight heparin once platelets > 50 × 10⁹/L and no active bleeding
• Mechanical prophylaxis (compression stockings, intermittent pneumatic compression) if contraindications to pharmacological

Stress Ulcer Prophylaxis:

• Proton pump inhibitor (omeprazole, lansoprazole) or H2-receptor antagonist (ranitidine) if mechanically ventilated or high risk of GI bleeding

Corticosteroids:

• Not routinely recommended
• Consider hydrocortisone 50 mg IV 6-hourly if refractory septic shock (requiring escalating vasopressor doses)
• Controversial evidence; may reduce time on vasopressors

Special Populations and Considerations

Pregnancy-Specific Considerations:

1. Medication Safety:

   • Most antibiotics safe in pregnancy (penicillins, cephalosporins, carbapenems, clindamycin, metronidazole)
   • Aminoglycosides: potential ototoxicity, use with monitoring
   • Fluoroquinolones: avoid (cartilage damage in animal studies, but may be used if life-threatening and no alternatives)
   • Tetracyclines: avoid (dental staining, bone growth effects)
   • Vancomycin: safe but requires monitoring

2. Fluid Balance:

   • Lower threshold for pulmonary oedema (reduced colloid oncotic pressure)
   • Balance between adequate resuscitation and fluid overload
   • Consider early invasive monitoring

3. Breastfeeding:

   • Most antibiotics compatible with breastfeeding
   • Benefits of breastfeeding usually outweigh minimal drug exposure
   • Advise temporary cessation only if high-dose metronidazole or chloramphenicol

Obesity (BMI > 30 kg/m²):

• Higher infection risk
• Dosing adjustments for antibiotics (use actual or adjusted body weight depending on drug)
• More difficult vascular access - consider ultrasound guidance
• Technical challenges for surgery and imaging

Immunosuppression (HIV, Steroids, Biological Agents):

• Broader differential (opportunistic infections: Pneumocystis jirovecii, Mycobacterium tuberculosis, CMV, fungi)
• Lower threshold for invasive investigations (bronchoscopy, CT)
• Consider empirical broader antimicrobial coverage
• Avoid live vaccines

Monitoring and Follow-up

Acute Phase (First 24-72 hours):

• Continuous vital signs monitoring
• Hourly urine output
• Lactate every 2-4 hours until normalizing
• Blood glucose 4-6 hourly
• FBC, U&E, LFT, CRP daily
• Blood cultures if persistent fever
• Clinical reassessment for source control adequacy

Recovery Phase:

• Transition to oral antibiotics when:
  • Afebrile > 24 hours
  • Haemodynamically stable
  • Tolerating oral intake
  • Improving inflammatory markers
• Total antibiotic duration typically 5-10 days depending on source

Complications to Monitor:

• Acute respiratory distress syndrome (ARDS)
• Acute kidney injury progressing to requiring RRT
• Disseminated intravascular coagulation
• Intensive care unit-acquired weakness
• Venous thromboembolism
• Nosocomial infections (catheter-associated UTI, line sepsis, VAP)

Post-Discharge:

• Outpatient follow-up 1-2 weeks
• Ensure completion of antibiotic course
• Screen for postpartum depression (increased risk after severe illness)
• Debrief and psychological support
• Contraception counselling
• Documentation for future pregnancies (recurrence risk assessment)

Complications

Maternal sepsis can result in significant maternal morbidity and mortality:

Fetal/Neonatal Complications:

• Preterm delivery (iatrogenic or spontaneous)
• Fetal distress and compromise
• Intrauterine growth restriction (if chronic infection)
• Vertical transmission of infection (GBS, CMV, HIV, HSV)
• Neonatal sepsis
• Intrauterine fetal death (severe maternal compromise)

Long-Term Complications:

• Chronic kidney disease (if severe AKI)
• Respiratory complications (pulmonary fibrosis post-ARDS - rare)
• Neurocognitive impairment (septic encephalopathy)
• Post-sepsis syndrome (fatigue, cognitive impairment, physical disability) - seen in up to 50% of sepsis survivors [19]
• Psychological trauma (PTSD, anxiety, depression)
• Uterine synechiae (Asherman syndrome) if severe endometritis

Prognosis

Mortality:

• Overall maternal sepsis mortality: 1-10% depending on severity and resource setting [1]
• Septic shock mortality: 20-40% in high-income countries, up to 60-80% in low-resource settings [8,16]
• Group A Streptococcal sepsis: 20-60% mortality despite treatment [15]
• Clostridial sepsis: 50-80% mortality

Prognostic Factors - Poor Outcome:

• Delayed recognition and treatment (every hour delay in antibiotic administration increases mortality)
• Septic shock (lactate > 4 mmol/L, vasopressor requirement)
• Multi-organ dysfunction (number of organ systems failing correlates with mortality)
• Source not controlled (retained products, ongoing contamination)
• Immunosuppression
• Extremes of age (though less relevant in obstetric population)
• Specific organisms: Group A Streptococcus, Clostridium perfringens, Gram-negative rods
• Pregnancy-specific: Chorioamnionitis with fetal demise, septic abortion, amniotic fluid infection

Prognostic Factors - Good Outcome:

• Early recognition and treatment (antibiotics within 1 hour)
• Prompt source control
• Single organ involvement
• Responsive to initial resuscitation (lactate clearance)
• Identified organism with antibiotic susceptibility

Quality of Life:

• Many survivors return to baseline function
• Post-sepsis syndrome affects 50% - ongoing fatigue, reduced exercise tolerance, cognitive difficulties [19]
• Psychological impact significant - PTSD, anxiety, depression in 30-40%
• Impact on future pregnancies (anxiety, increased surveillance)

Recurrence Risk:

• Low if precipitant removed (e.g., caesarean wound infection)
• Higher if underlying predisposition (diabetes, immunosuppression)
• Counselling for future pregnancies: risk assessment, preventive strategies

Prevention & Screening

Primary Prevention:

1. Antibiotic Prophylaxis:

   • Caesarean section: Single dose co-amoxiclav 1.2 g IV or cefuroxime 1.5 g IV at skin incision (reduces surgical site infection by 50%) [10]
   • Operative vaginal delivery: Consider prophylaxis (evidence less robust than for caesarean)
   • Manual removal of placenta: Consider prophylactic antibiotics
   • Prelabour rupture of membranes (PROM): Erythromycin 250 mg QDS for 10 days reduces maternal and neonatal infection (ORACLE trial) [20]
   • Group B Streptococcus colonization: Intrapartum antibiotic prophylaxis (benzylpenicillin 3 g IV loading, then 1.5 g 4-hourly until delivery) reduces neonatal GBS sepsis [21]

2. Infection Control Measures:

   • Hand hygiene (single most important intervention)
   • Aseptic technique for procedures (vaginal examinations, catheterization, IV cannulation)
   • Limit vaginal examinations in labour
   • Early removal of urinary catheters postpartum
   • Appropriate surgical site skin preparation (chlorhexidine-alcohol)

3. Modifiable Risk Factor Management:

   • Optimize diabetes control
   • Treat anaemia (iron supplementation, investigate cause)
   • Nutritional support if malnourished
   • Smoking cessation
   • Treat bacterial vaginosis if high-risk (previous preterm birth)

4. Vaccination:

   • Influenza vaccine (inactivated) - recommended for all pregnant women
   • Pertussis vaccine (combined with diphtheria and tetanus) - offered at 16-32 weeks gestation
   • COVID-19 vaccination - recommended in pregnancy
   • Pneumococcal vaccine if high-risk (asplenia, immunosuppression)

5. Minimize Interventions:

   • Reduce caesarean section rate (where safe and appropriate)
   • Avoid unnecessary membrane rupture
   • Judicious use of invasive fetal monitoring

Secondary Prevention (Early Detection):

1. Education and Awareness:

   • Educate healthcare professionals on maternal sepsis recognition
   • Sepsis screening tools (MEOWS) for all pregnant/postpartum women
   • "Sepsis Six" training and awareness
   • Public health campaigns educating pregnant women on warning signs

2. Early Warning Systems:

   • Routine vital signs monitoring in labour and postpartum
   • Modified Early Obstetric Warning Scores (MEOWS) charting
   • Escalation protocols for abnormal observations

3. Postnatal Surveillance:

   • Routine postnatal check (day 1-2 and day 5-7)
   • Monitor for fever, wound complications, offensive lochia
   • Low threshold for investigation and treatment

4. Clear Pathways:

   • Sepsis care bundles and protocols
   • Clear escalation pathways
   • Multidisciplinary team involvement (midwifery, obstetrics, anaesthetics, critical care, microbiology)

Screening Programs:

• No formal screening program for maternal sepsis (event-based diagnosis)
• Group B Streptococcus screening varies by country:
  • "Universal screening approach (USA, Canada): Vaginal-rectal swab at 35-37 weeks, intrapartum antibiotic prophylaxis if positive"
  • "Risk-based approach (UK, Australia): Treat based on risk factors (previous GBS-affected baby, GBS bacteriuria in current pregnancy, preterm labour, fever in labour)"

Key Guidelines

International and National Guidelines:

1. Surviving Sepsis Campaign (2021)

   • International consensus guidelines on management of sepsis and septic shock
   • Recommends 1-hour bundle: lactate, blood cultures, antibiotics, fluid resuscitation
   • Level of evidence: Strong recommendation, moderate quality evidence [17]

2. Royal College of Obstetricians and Gynaecologists (RCOG) - Bacterial Sepsis in Pregnancy (Green-top Guideline No. 64a, 2012)

   • UK-specific obstetric sepsis guideline
   • Emphasizes use of MEOWS, early recognition, "Sepsis Six" bundle
   • Recommendations on antibiotic choice for different sources [22]

3. UK Confidential Enquiry into Maternal Deaths (MBRRACE-UK)

   • Ongoing surveillance and recommendations
   • Identifies sepsis as third leading cause of maternal death
   • Highlights importance of early recognition, appropriate antibiotics, escalation [4]

4. WHO Recommendations for Prevention and Treatment of Maternal Peripartum Infections (2015)

   • Global perspective, particularly relevant for low-resource settings
   • Antibiotic prophylaxis for caesarean section
   • Clean birth practices
   • Early recognition and referral [23]

5. NICE Clinical Guideline CG149 - Neonatal Infection: Antibiotics for Prevention and Treatment (2012, updated 2021)

   • Includes guidance on Group B Streptococcus prophylaxis
   • Risk factor-based approach to intrapartum antibiotic prophylaxis [21]

6. Society for Maternal-Fetal Medicine (SMFM) - Sepsis in Pregnancy (2016)

   • US-based guidance on diagnosis and management
   • Adaptation of Sepsis-3 criteria for pregnancy [24]

Key Recommendations Summary:

• Use maternal early warning scores (MEOWS) for all pregnant/postpartum women
• "Sepsis Six" bundle within 1 hour of recognition (oxygen, fluids, antibiotics, cultures, lactate, urine output)
• Broad-spectrum empirical antibiotics (review and de-escalate based on cultures)
• Multidisciplinary involvement (obstetrics, anaesthetics, critical care, microbiology)
• Antibiotic prophylaxis for caesarean section and other high-risk procedures
• Education and awareness for healthcare professionals and pregnant women

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Exam-Focused Sections

Common Exam Questions

MRCOG Part 2 Written (SBA/EMQ Style):

1. "A 28-year-old woman is 36 hours post-emergency caesarean section. Her temperature is 38.5°C, heart rate 115 bpm, BP 95/60 mmHg. What is the most appropriate first-line antibiotic regimen?"

2. "Which organism is most commonly associated with rapidly progressive puerperal sepsis and toxic shock syndrome?"

3. "What is the most important intervention that reduces mortality in maternal sepsis?"

4. "A pregnant woman at 28 weeks gestation presents with pyelonephritis. Her creatinine is 95 μmol/L. Is this normal for pregnancy?"

5. "What is the target for lactate clearance in sepsis resuscitation?"

MRCOG Part 3 OSCE/Structured Discussion:

1. "Describe your immediate management of a postpartum woman presenting with fever, tachycardia, and hypotension."

2. "A woman is in labour with prolonged rupture of membranes and maternal pyrexia. Discuss your management including fetal considerations."

3. "Discuss strategies for prevention of postpartum sepsis."

4. "Explain the physiological changes of pregnancy that modify the presentation of sepsis."

Viva Topics:

• Definition and diagnostic criteria for maternal sepsis vs. septic shock
• Sepsis Six bundle and rationale for each component
• Antibiotic choices for different sources of sepsis
• Multidisciplinary management and escalation pathways
• Lessons from Confidential Enquiries (delays in recognition, inappropriate antibiotics)

Viva Points

Viva Point: Opening Statement: "Maternal sepsis is a life-threatening condition defined as organ dysfunction resulting from infection during pregnancy, childbirth, or the postpartum period. It accounts for approximately 11% of maternal deaths globally and is the third leading cause of maternal death in the UK. Early recognition and prompt treatment with the 'Sepsis Six' bundle within one hour is critical to reducing maternal mortality."

Key Facts to Mention:

1. Epidemiology:

   • Incidence 0.1-0.6 per 1,000 deliveries in high-income countries
   • Mortality 1-10% overall, 20-40% in septic shock
   • 75% of cases occur within 10 days postpartum

2. Definition (Sepsis-3):

   • Life-threatening organ dysfunction from dysregulated host response to infection
   • Septic shock: Persistent hypotension requiring vasopressors + lactate > 2 mmol/L despite adequate fluids

3. Pregnancy-Specific Modifications:

   • Altered vital sign ranges (use MEOWS not standard EWS)
   • Lower threshold for respiratory failure, pulmonary oedema
   • "Normal" creatinine in pregnancy is 40-60 μmol/L (> 90 μmol/L suggests AKI)
   • Physiological leukocytosis and tachycardia can mask sepsis

4. Sepsis Six Bundle (within 1 hour):

   • Give: Oxygen, IV fluids, IV antibiotics
   • Take: Blood cultures, lactate, urine output monitoring
   • Each hour delay in antibiotics increases mortality

5. First-Line Antibiotics:

   • Genital tract sepsis: Clindamycin + Gentamicin
   • Pyelonephritis: Gentamicin or Ceftriaxone
   • Pneumonia: Co-amoxiclav + Clarithromycin
   • Group A Strep suspected: Add Clindamycin (toxin inhibition) + Benzylpenicillin

6. Source Control:

   • As important as antibiotics
   • Evacuate retained products, drain abscesses, debride necrotizing fasciitis
   • Surgical delay increases mortality

7. Prevention:

   • Antibiotic prophylaxis at caesarean section (co-amoxiclav 1.2 g IV at skin incision)
   • GBS intrapartum prophylaxis if indicated
   • Aseptic technique, limit vaginal examinations
   • Early warning systems (MEOWS), education

8. Lessons from Confidential Enquiries:

   • Delays in recognition (failure to appreciate severity)
   • Inappropriate antibiotics (narrow spectrum, delayed administration)
   • Failure to escalate to senior clinicians/critical care
   • Need for multidisciplinary approach

Common Mistakes

❌ Mistakes That Fail Candidates:

1. Delayed recognition:

   • Attributing fever to "normal postpartum" or epidural
   • Not recognizing physiological vital signs in pregnancy mask severity
   • Waiting for multiple criteria before escalating

2. Delayed antibiotics:

   • Waiting for senior review before starting antibiotics
   • Waiting for imaging or investigations before treatment
   • Every hour delay increases mortality - "time is life"

3. Inappropriate antibiotic choice:

   • Narrow-spectrum antibiotics (e.g., single agent for genital sepsis)
   • Not covering anaerobes in genital tract sepsis
   • Forgetting to add clindamycin for suspected Group A Streptococcus

4. Inadequate resuscitation:

   • Underdosing fluids (but also avoid fluid overload in pregnancy)
   • Not monitoring response (lactate, urine output)
   • Delaying vasopressors in septic shock

5. Failure to involve multidisciplinary team:

   • Not calling anaesthetics/critical care early
   • Not involving microbiology for antibiotic advice
   • Not documenting clear escalation plan

6. Obstetric errors:

   • Unnecessary caesarean section for maternal sepsis (vaginal delivery usually preferred unless obstetric indication)
   • Not considering fetal wellbeing (CTG monitoring if viable gestation)
   • Forgetting left lateral tilt if pregnant

7. Missing source control:

   • Giving antibiotics alone without addressing source (retained products, abscess, necrotizing fasciitis)
   • Delay in surgical intervention

8. Interpretation errors:

   • Interpreting "normal" creatinine (80 μmol/L) as reassuring in pregnancy (actually suggests AKI)
   • Dismissing modest WCC elevation as "normal for labour"
   • Not recognizing fetal tachycardia as early sign of maternal compromise

Model Answers

Q1: Describe your immediate approach to a postpartum woman presenting with fever, tachycardia, and hypotension.

Model Answer:

"This presentation suggests possible maternal sepsis, which is a medical emergency requiring immediate assessment and treatment. I would approach this using an ABCDE framework and implement the 'Sepsis Six' bundle within one hour.

Immediate Assessment: I would first assess airway, breathing, and circulation. I would give high-flow oxygen via non-rebreather mask targeting SpO₂ 94-98%, establish large-bore IV access with two 14-16G cannulae, and position the patient with left lateral tilt if still pregnant or recently postpartum.

Sepsis Six - Give Three:

1. Oxygen as above
2. IV fluid bolus - 500-1000 mL crystalloid over 15-30 minutes, reassess response
3. Broad-spectrum IV antibiotics within 1 hour - empirically I would give clindamycin 900 mg IV and gentamicin 5-7 mg/kg IV to cover genital tract sepsis (anaerobes and Gram-negatives), adjusting based on likely source

Sepsis Six - Take Three:

1. Blood cultures - at least two sets from different sites before antibiotics if possible
2. Serum lactate - via venous or arterial blood gas
3. Urine output monitoring - insert urinary catheter, target > 0.5 mL/kg/h

Further Assessment: I would take a focused history including timing relative to delivery, mode of delivery, symptoms suggesting source (abdominal pain, offensive lochia, dysuria, cough, breast pain), and risk factors (prolonged labour, membrane rupture, multiple vaginal examinations).

On examination, I would assess for source: abdominal examination for uterine tenderness, wound inspection for surgical site infection, check for loin tenderness (pyelonephritis), respiratory examination, and breast examination.

Investigations: FBC, U&Es, LFTs, CRP, coagulation screen, and a venous blood gas for lactate and metabolic status. Microbiological samples would include blood cultures, urine culture, high vaginal swab, and wound swab if applicable. I would request a chest X-ray if respiratory symptoms and pelvic ultrasound to assess for retained products.

Escalation: I would escalate immediately to the consultant obstetrician and obstetric anaesthetist. If the patient shows signs of septic shock (persistent hypotension, lactate > 4 mmol/L), I would involve the critical care team for ICU-level care including potential vasopressor support.

Source Control: Based on findings, I would arrange for source control - this might include evacuation of retained products, surgical drainage of abscess, or wound debridement.

Ongoing Management: I would reassess response to treatment every 15-30 minutes, monitoring vital signs, lactate clearance, and urine output. The antibiotic regimen would be reviewed once culture results available and de-escalated based on sensitivities. This would all be managed within a multidisciplinary framework involving obstetrics, anaesthetics, critical care, and microbiology, following local sepsis guidelines and the RCOG Green-top Guideline on bacterial sepsis in pregnancy."

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Q2: A woman is in labour at term with prolonged rupture of membranes (24 hours) and maternal pyrexia of 38.2°C. Discuss your management including fetal considerations.

Model Answer:

"This clinical scenario suggests chorioamnionitis - intra-amniotic infection - which requires prompt diagnosis and treatment to prevent maternal and neonatal sepsis.

Immediate Assessment: I would perform a full maternal assessment including vital signs (heart rate, blood pressure, respiratory rate, temperature, oxygen saturation) plotted on a MEOWS chart. I would also commence continuous electronic fetal monitoring with CTG to assess fetal wellbeing.

Confirming Diagnosis: Chorioamnionitis is a clinical diagnosis based on maternal fever (> 38°C) plus two or more of:

• Maternal tachycardia (> 100 bpm)
• Fetal tachycardia (baseline > 160 bpm)
• Uterine tenderness
• Offensive amniotic fluid
• Maternal leukocytosis (> 15 × 10⁹/L in labour)

I would examine for uterine tenderness, assess liquor if visible (colour, odour), and take appropriate investigations.

Investigations:

• Blood tests: FBC (looking for leukocytosis), CRP, blood cultures (two sets from different sites), venous blood gas for lactate
• Urine analysis and culture (to exclude UTI as source)
• High vaginal swab for microscopy and culture

Immediate Management - Sepsis Six:

1. Give oxygen if hypoxic
2. IV fluid resuscitation if needed
3. Broad-spectrum IV antibiotics - I would give co-amoxiclav 1.2 g IV or ampicillin 2 g IV plus gentamicin 5-7 mg/kg IV to cover the common causative organisms (Group B Streptococcus, E. coli, anaerobes)
4. Obtain blood cultures before antibiotics
5. Monitor lactate and urine output

Obstetric Management - Delivery Planning: The definitive treatment for chorioamnionitis is delivery of the fetus and placenta. I would:

• Expedite delivery: augment labour with oxytocin if not progressing adequately
• Aim for vaginal delivery if safe and imminent (within 4-6 hours)
• Consider caesarean section if failure to progress, fetal compromise, or maternal deterioration
• Avoid prolonged labour which increases maternal and fetal morbidity

Fetal Considerations:

• Continuous CTG monitoring: fetal tachycardia is common with maternal pyrexia but reduced variability or decelerations suggest fetal compromise
• Fetal tachycardia alone (in setting of maternal fever) is not an indication for immediate delivery if otherwise reassuring CTG
• Notify neonatal team of anticipated delivery: the neonate will require assessment for early-onset neonatal sepsis
• Obtain cord blood gases and bloods for neonatal team
• Delayed cord clamping may not be appropriate if immediate neonatal resuscitation needed

Escalation: I would inform the consultant obstetrician and anaesthetist. If the patient develops signs of severe sepsis or septic shock, I would escalate to critical care.

Postpartum:

• Continue antibiotics for 24-48 hours postpartum (or until afebrile for 24 hours and clinically improving)
• Ensure placenta is complete; send for histological examination to confirm chorioamnionitis
• Monitor for postpartum endometritis
• Document clearly for neonatal team regarding maternal sepsis and antibiotics given

Neonatal Management: The neonate is at high risk of early-onset sepsis and will require:

• Full examination by neonatal team
• Blood cultures, FBC, CRP
• Empirical IV antibiotics (typically benzylpenicillin and gentamicin) pending cultures
• Close monitoring for signs of sepsis

This management follows the RCOG guideline on bacterial sepsis in pregnancy and NICE guidance on neonatal infection."

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20. Kenyon S, et al. Broad-spectrum antibiotics for preterm, prelabour rupture of fetal membranes: the ORACLE I randomised trial. Lancet. 2001;357(9261):979-988. doi:10.1016/S0140-6736(00)04233-1

21. National Institute for Health and Care Excellence. Neonatal infection: antibiotics for prevention and treatment. NICE guideline CG149. 2012 (updated 2021).

22. Royal College of Obstetricians and Gynaecologists. Bacterial Sepsis in Pregnancy. Green-top Guideline No. 64a. 2012.

23. World Health Organization. WHO recommendations for prevention and treatment of maternal peripartum infections. WHO Guidelines. 2015.

24. Plummer M, Abdelhafiz I. Incidence of postpartum hemorrhage and methods to decrease blood loss. Obstet Gynecol Clin North Am. 2021;48(1):1-13. doi:10.1016/j.ogc.2020.11.009

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This topic was last updated on 2026-01-06. Clinical guidelines and evidence are subject to change. Always refer to current local protocols and national guidelines for patient care.