Genital Infection after Child Birth ‘the risk of sepsis is higher following Caesarean section, particularly when performed after onset of labour’

‘Increased awareness of the principles of general hygiene, a good surgical approach and the use of aseptic techniques will be paramount in combating severe puerperal sepsis’

Genital tract infection following delivery is referred to as puerperal sepsis and is synonymous with older descriptions of puerperal fever, milk fever and childbed fever. It was not realized until the mid-nineteenth century that the high maternal mortality and morbidity were due to poor hygiene of the birth attendants; the establishment of lying-in hospitals and overcrowding perpetuated the condition to epidemic proportion. Puerperal sepsis was the major cause of maternal mortality up until 1937. The discovery of sulphonamides in 1935 and the simultaneous reduction in the virulence of haemolytic streptococcus resulted in a dramatic fall in maternal mortality.

Following delivery, natural barriers to infection are temporarily removed and therefore organisms with a pathogenic potential can ascend from the lower genital tract into the uterine cavity. Placental separation exposes a large raw area equivalent to an open wound, and retained products of conception and blood clots within the uterus can provide an excellent culture medium for infection. Furthermore, vaginal delivery is almost invariably associated with lacerations of the genital tract (uterus, cervix and vagina). Although these lacerations may not need surgical repair, they can become a focus for infection similar to iatrogenic wounds, such as Caesarean section and episiotomy.

Common risk factors for puerperal infection are antenatal intrauterine infection, caesarean section, cervical cerclage for cervical incompetence, prolonged rupture of membranes, prolonged labour, multiple vaginal examinations, instrumental delivery, manual removal of placenta, retained products of conception, non-obstetric such as obesity, diabetes, human immunodeficiency virus (HIV). Symptoms of puerperal pelvic infection include malaise, headache, fever, rigors, abdominal discomfort, vomiting, diarrhoea, offensive lochia and bleeding per vaginam 24 hours after delivery. Signs of puerperal pelvic infection include pyrexia and tachycardia; boggy, tender and larger uterus; infected wounds; peritonism; paralytic ileus; indurated adnexae and bogginess in pelvis (abscess).

Increased awareness of the principles of general hygiene, a good surgical approach and the use of aseptic techniques will be paramount in combating severe puerperal sepsis. However, the risk of sepsis is higher following Caesarean section, particularly when performed after onset of labour. There is now overwhelming evidence that prophylactic antibiotics during emergency Caesarean section decreases the risk of post-operative infection, namely wound infection, metritis, pelvic abscess, pelvic thrombophlebitis and septic shock. A single intraoperative dose of antibiotics (amoxiclav or cephalosporin plus metronidazole) should be given after clamping of the umbilical cord to avoid unnecessary exposure of the baby to antibiotics. The benefit of prophylaxis for elective Caesarean section is of greater significance in units where the background infectious morbidity is high.