FRCA Notes

Maternal Sepsis

One might wish to view this page alongside the one on sepsis in adults.

The topic was a CRQ in February 2024, and was 'generally well answered'.

Resources

  • The incidence of mortality from maternal sepsis is rising
  • Issues include:
    • The normal physiological changes in pregnancy can mask clinical signs of sepsis
    • The obstetric population are generally young and not heavily co-morbid, so compensate well before collapsing

Maternal Pregnancy-associated
Diabetes Prolonged rupture of membranes
Obesity Cervical cerclage / amniocentesis
Immunosuppression Instrumental delivery
Close contact with people with Group A Strep. LSCS delivery
PV bleeding or discharge Retained products of conception ± their removal surgically


Causative organisms

  • Group A Streptococcus (Strep. pyogenes)
  • E. coli
  • Staphylococcus aureus inc. MRSA
  • Group B Streptococcus (Strep. agalactiae)
  • Streptococcus pneumoniae

Sources of sepsis

Obstetric - genital tract Obstetric - non-genital tract Other
Wound infection e.g. post-episiotomy/tear/LSCS Lower urinary tract infection Pneumonia
Septic abortion Pyelonephritis TB
Endometritis Mastitis/breast abscess Malaria
Chorioamnionitis Septic pelvic thrombophlebitis HIV
Cellulitis


  • The onset may be non-specific and insidious
  • Reduced SVR leads to hypotension and consequent:
    • Tachycardia
    • Metabolic (lactic) acidosis
    • Tachypnoea

  • There is normally a raised WCC in pregnancy, particularly labour, which may mask a raised WCC associated with sepsis
  • Conversely a low or declining WCC may be a worrisome feature

  • Pyrexia or hypothermia
  • Oligura
  • Impaired consciousness

  • Failure to respond to treatment
  • Widespread rash (toxic shock syndrome)

Maternal red flags

  • The presence of any should prompt instigation of sepsis 6 bundle

  • Respiratory: RR >25bpm | Oxygen to keep sats >92% | cyanosis
  • Cardiovascular: SBP <90mmHg (or >40mmHg drop from normal) | HR >130bpm | Lactate >2mmol/L
  • Neurological: unresponsive or only responding to pain
  • Renal: UO <0.5ml/kg/hr | Not passed urine in 18hrs
  • Other: non-blanching rash | mottled appearance | ashen appearance

  • The management principles of sepsis in the obstetric population are similar to that in the non-obstetric one:
    • Resuscitation
    • Identification of source and source control
    • Consider early delivery
    • Management of complications including hypotension and organ failure

Initial steps - 'sepsis six'

  1. Measure serum lactate
  2. Obtain cultures, swabs (esp. throat for GAS) and sampling of othre potential sources e.g. urine
  3. Measure urine output, which may require catheterisation
  4. Administer early broad-spectrum IV antibiotics followed by microbiology-guided specific therapies
  5. Administer crystalloid ± vasopressor to achieve target MAP
  6. Give oxygen to SpO2 94 - 98%

Fluid therapy

  • Aggressive fluid therapy remains controversial; growing evidence in non-obstetric sepsis that liberal fluid administration is not superior to a restrictive strategy and may be harmful
  • Reduced serum albumin concentration and decreased capillary oncotic pressure leave maternal patients at an increased risk of fluid overload, pulmonary oedema & myocardial dysfunction

Ongoing management

  • HDU monitoring with MEOWS scoring
  • Named consultant anaesthetist and consultant obstetrician responsible for woman's care 24/7
  • Critical care support
    • Appropriate training for midwives
    • If critical care in a non-Obstetric facility needs daily Obstetric review
    • Where possible, do not separate mother and baby when accessing critical care facility

Neuraxial anaesthesia

  • One might be required to provide anaesthesia to a septic parturient e.g. to facilitate foetal delivery due to distress, or to allow surgical intervention for source control
  • Theoretical risks of neuraxial anaesthesia in such a patient include:
    • Cardiovascular instability
    • Infective complications including epidural abscess/meningitis
    • Haematoma risk from sepsis-induced coagulopathy

  • Joint AAGBI, RA-UK and OAA guidelines suggest:
    • Neuraxial intervention in the obstetric patient with overt sepsis carries 'very high risk' for causing intra-uterine foetal death
    • It should be avoided due to the potential risk of CNS infection

  • Yet there's little direct evidence concerning use of neuraxial anaesthesia in obstetric sepsis
  • There's no known relationship between use of neuraxial techniques and subsequent development of meningitis or epidural abscess
  • The incidence of CNS infection after neuraxial intervention in the bacteraemic patient in one review was 0.007% - 0.6%
  • There is a low incidence of CNS infection after neuraxial anaesthesia anyway, particularly so in obstetric patients

  • As ever, it's a risk-benefit balance which needs to be struck in conjunction with the patient's wishes
  • If one chooses a neuraxial technique then spinal anaesthesia is preferred

Cell salvage

  • Intra-myometrial infection is a potent cause of uterine atony and therefore PPH
  • One might therefore wish to have cell salvage in use during any surgical intervention

  • Intra-uterine infection, however, is a relative contraindication to cell salvage use
  • (Systemic sepsis is not a contraindication to cell salvage)

  • Risk-benefit decision must be made