Puerperal fever

Puerperal fever

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Puerperal fever

Streptococcus pyogenes (red-stained spheres) is responsible for most cases of severe puerperal fever. It is commonly found in the throat and nasopharynx of otherwise healthy carriers, particularly during winter. Details: A pus specimen, viewed using Pappenheim's stain @ 900x magnification

Puerperal fever (from the Latin puer, child), also called childbed fever, can develop into puerperal sepsis, which is a serious form of septicaemia contracted by a woman during or shortly after childbirth, miscarriage or abortion. If untreated, it is life-threatening.

The most common infection causing puerperal fever is genital tract sepsis. Other types of infection that can lead to sepsis after childbirth include urinary tract infection, breast infection (mastitis) and respiratory tract infection (more common after anaesthesia due to lesions in the windpipe).

Puerperal fever is now rare in the West due to improved hygiene during delivery, and deaths have been reduced by antibiotics.

Terminology
Causal organisms
Definition of puerperal fever
Incidence
History
Prevention via hygienic measures
See also
References

Terminology

Puerperal fever is no longer favored as a diagnostic category. Instead, contemporary terminology specifies:^[1]

the specific target of infection: endometritis (inflammation of the inner lining of the uterus), metrophlebitis (inflammation of the veins of the uterus), and peritonitis (inflammation of the membrane lining of the abdomen)
the severity of the infection: (relatively) uncomplicated infection (excessive multiplication of microbes), and possibly life-threatening sepsis (destruction of tissue by microbes)

Causal organisms

The most causative agents in inflammation of the inner lining of the uterus (endometritis) are Staphylococcus aureus and Streptococcus.^[2]

Group A Streptococcus (abbreviated to GAS, or more specifically the Streptococcus pyogenes) is a form of Streptococcus bacteria responsible for most cases of severe hemolytic streptococcal illness. Other types (B, C, D, and G) may also cause infection.^[3] Group B Streptococcus (abbreviated to GBS, or more specifically Streptococcus agalactiae usually causes less severe maternal disease^[4].

Other causal organisms, in order of prevalence, include staphylococci, coliform bacteria, anaerobe bacteria, chlamydia bacteria, mycoplasma and very rarely, Clostridium welchii.

There are several strains of GAS (Group A Streptococcus). Some strains usually cause skin infections, they are more common in warm climates, and they usually cause local rather than systemic effects. Other strains, in particular Streptococcus pyogenes attack the throat and cause severe infections. The human nasopharynx is the main reservoir of Streptococcus pyogenes and infection is more common during winter and it is rarely found in the normal vaginal flora. It is likely that most puerperal hemolytic infections arise from this reservoir in the patient or attendants.^[5]

Group B Streptococcus (Streptococcus agalactiae) causes pneumonia and meningitis in neonates and the elderly, with occasional systemic bacteremia. They can also colonize the intestines and the female reproductive tract, increasing the risk for transmission to the infant. The American College of Obstetricians and Gynecologists, American Academy of Pediatrics and the Centers for Disease Control recommend all pregnant women between 35 and 37 weeks gestation should be tested for GBS.^[6]

Definition of puerperal fever

A temperature rise above 38.0 °C maintained over 24 hours or recurring during the period from the end of the 1st to the end of the 10th day after childbirth or abortion. (ICD-10)
Oral temperature of 38.0 °C or more on any two of the first ten days postpartum. (USJCMW)^[7]

Incidence

The incidence of puerperal sepsis shows wide variations among published literature ? this may be related to different definition, recording etc.^[8]

Today in USA, puerperal infection is believed to occur in between 1 and 8 percent of all deliveries. About 3 die from puerperal sepsis for every 100,000 deliveries. The single most important risk factor is Caesarean section.^[9]

In the United Kingdom 1985-2005, the number of direct deaths associated with genital tract sepsis per 100,000 maternities was 0.40-0.85.^[10]

The incidence of maternal deaths in the United States is 13 in 100,000.

Puerperal fever or childbed fever in the 18th and 19th centuries affected, on average, 6 to 9 women in every 1000 deliveries, killing 2 to 3 of them with peritonitis or septicemia. It was the single most common cause of maternal mortality, accounting for about half of all deaths related to childbirth, and was second only to tuberculosis in killing women of childbearing age. A rough estimate is that about 250,000-500,000 died from puerperal fever in the 1700s and 1800s in England and Wales alone.^[11]

The Confidential Enquiry into Maternal and Child Health (UK) reported that, in 2003-2005, genital tract sepsis accounted for 14% of direct causes of maternal death^[12] still making puerperal fever a significant factor in maternal death.

History

In his 1861 book, Ignaz Semmelweis presented evidence to demonstrate that the advent of pathological anatomy in Vienna in 1823 (vertical line) was correlated to the incidence of fatal childbed fever there. Onset of chlorine handwash in 1847 marked by vertical line. Rates for Dublin maternity hospital, which had no pathological anatomy, is shown for comparison (view rates). His efforts were futile, however.

Hospitals for childbirth became common in the 17th century in many European cities. These "lying-in" hospitals were established at a time when there was no knowledge of antisepsis or epidemiology, and patients were subjected to crowding, frequent vaginal examinations, and the use of contaminated instruments, dressings, and bedding. It was common for a doctor to deliver one baby after another, without washing his hands or changing clothes in between.

The first recorded epidemic of puerperal fever occurred at the Hôtel-Dieu de Paris in 1646. Hospitals throughout Europe and America consistently reported death rates between 20% to 25% of all women giving birth, punctuated by intermittent epidemics with up to 100% fatalities of women giving birth, in childbirth wards.^[13]

A number of physicians began to suspect contagion and hygiene as causal factors in spreading puerperal fever. In 1795, Alexander Gordon of Aberdeen, Scotland suggested that the fevers were infectious processes, that physicians were the carrier, and that "I myself was the means of carrying the infection to a great number of women.?^[14] Thomas Watson, Professor of Medicine at King's College Hospital, London, wrote in 1842: "Wherever puerperal fever is rife, or when a practitioner has attended any one instance of it, he should use most diligent ablution." Watson recommended handwashing with chlorine solution and changes of clothing for obstetric attendants "to prevent the practitioner becoming a vehicle of contagion and death between one patient and another." ^[15]

Prevention via hygienic measures

In 1843, Oliver Wendell Holmes published The Contagiousness of Puerperal Fever and controversially concluded that puerperal fever was frequently carried from patient to patient by physicians and nurses and suggesting that hand-washing, clean clothing, and avoidance of autopsies by those aiding birth would prevent the spread of puerperal fever.^[16] Holmes stated that ". . . in my own family, I had rather that those I esteemed the most should be delivered unaided, in a stable, by the mangerside, than that they should receive the best help, in the fairest apartment, but exposed to the vapors of this pitiless disease."^[17]

Holmes' conclusions were ridiculed by many contemporaries, including Charles Delucena Meigs, a well-known obstetrician, who stated "Doctors are gentlemen, and gentlemen's hands are clean."^[18]

In 1844, Ignaz Semmelweis was appointed assistant lecturer in the First Obstetric Division of the Vienna General Hospital (Allgemeines Krankenhaus), where medical students received their training. Working without knowledge of Holmes' essay, Ignaz Semmelweis noticed his ward?s 16% mortality rate from fever was substantially higher than the 2% mortality rate in the Second Division, where midwifery students were trained. Ignaz Semmelweis also noticed that puerperal fever was rare in women who gave birth before arriving at the hospital. Semmelweis noted that doctors in First Division performed autopsies each morning on women who had died the previous day but the midwives were not required or allowed to perform such autopsies. He made the connection between the autopsies and puerperal fever after a colleague, Jakob Kolletschka, died of septicaemia after accidentally cutting his hand while performing an autopsy.

Semmelweis began experimenting with various cleansing agents and, from May 1847, ordered that all doctors and students working in the First Division wash their hands in chlorinated lime solution before starting ward work, and later before each vaginal examination. The mortality rate from puerperal fever in the division fell from 18% in May 1847 to less than 3% in June?November of the same year.^[19] While his results were extraordinary, he too was treated with skepticism and ridicule (see Rejection of Semmelweis).

The true mechanism of puerperal fever was not generally understood until the start of the 20th century. In 1879 Louis Pasteur showed that streptococcus was present in the blood of women with puerperal fever. By the turn of the century, the need for antiseptic techniques was widely accepted, and their practice along with the mid-century introduction of new antibiotics greatly diminished the rate of death during childbirth.