Obstetrics and Gynecology - A. M. Gromova 2000

Postpartum septic conditions

Postpartum infection typically develops As a result of pathogens penetrating through the birth canal. The incidence of Postpartum Septic Conditions ranges from 10.4% to 30.7%, according to various authors. These conditions are characterized by polyetiology, a wide spectrum of clinical manifestations, including atypical clinical forms.

There is no single specific pathogen responsible for postpartum septic conditions, though they are most frequently caused by pyogenic organisms (staphylococci, streptococci, Escherichia coli, and in recent years, opportunistic and non-spore-forming anaerobes, Chlamydia, Mycoplasma, etc.). In recent years, a continuous shift in the primary bacterial causative agents has been observed.

The primary focus of infection, which can be localized in various PARTS OF THE body, plays a crucial role in The Development of the infectious process. Postpartum infections are most commonly triggered by a suppression or dysregulation of immune responses resulting from Pregnancy or childbirth. Contributing factors are also significant, such as anemia, gestosis, Hemorrhage, operative delivery—particularly Cesarean Section—and placental abnormalities, all of which must be properly evaluated in terms of the likelihood of infectious complications during labor and the postpartum period.

The factors contributing to the high incidence and mortality rates of purulent-septic complications in this pathology include the following:

1) constant shifts in bacterial species and their biological properties driven by antibacterial therapy;

2) irrational antibiotic regimens, regarding both drug Selection and dosage;

3) suppression of the body's immune reactivity amid deteriorating environmental conditions and adverse social factors.

Infections are classified into exogenous and endogenous:

- exogenous infection is introduced into the genital tract directly via instruments and medical staff or via airborne transmission;

- endogenous infection spreads from adjacent parts of the Reproductive System, neighboring Organs (such as the intestines and bladder), or distant foci of infection (Kidneys, nasopharynx, Oral Cavity, etc.).

Since the female body develops local and systemic defense mechanisms (Immunity) during phylogenesis to prevent infection, the mere entry of microbes onto the wounded surface of the genital organs is not enough to trigger a postpartum infection. The virulence of the pathogen, the condition of the Tissues at the entry site, and the extent of tissue trauma are all critical factors. Typically, the primary infectious focus coincides with the entry portal. Portals of entry for postpartum infection may include Premature Rupture of membranes, as well as tears of the Perineum, Vagina, cervix, and uterine body. In postpartum septic conditions, the infection predominantly spreads via an ascending (intracanalicular) pathway, though hematogenous and lymphogenous routes cannot be ruled out.

The most appropriate clinical Classification of postpartum infectious diseases is the one proposed by S. V. Sazonov (1935) and A. V. Bartels (1973), which outlines the stages of infection spread:

Stage One — the infection is confined to the birth trauma site (postpartum ulcer on the perineum, vaginal walls, or cervix; Postpartum Endometritis).

Stage Two — the infection extends beyond the birth wound but remains localized (metritis, parametritis, localized thrombophlebitis such as metrotrombophlebitis, pelvic thrombophlebitis, leg vein thrombophlebitis, salpingo-oophoritis, Pelvioperitonitis).

Stage Three — the infection approaches a generalized state in severity (diffuse Peritonitis, septic Shock, progressive thrombophlebitis).

Stage Four — generalized infection (Sepsis with or without metastasis).

Extragenital postpartum conditions include mastitis.