Etiology and routes of infection
The purulent-inflammatory process in the abdominal cavity after delivery is initiated by various microbial associations. A leading role in the development of the disease is played by Gram-negative flora. These include bacteria of the family Enterobacteriaceae (in particular, Escherichia coli, Proteus spp., Klebsiella spp., Enterobacter spp.), as well as microorganisms of the genus Pseudomonas. Non-spore-forming anaerobes are of particular importance, among which bacteroids dominate. Gram-positive microflora acts as a pathogen somewhat less frequently—it is detected in approximately one-third of female patients.
Infection enters the abdominal cavity via two main routes:
- Through suture defects: in case of uterine suture dehiscence, the infectious agent along with necrotic detritus enters directly from the uterine cavity.
- Ascending route: against the background of pronounced endometritis, the infection spreads through the Fallopian tubes.
Pathogenesis: from local inflammation to shock
How exactly inflammation will develop directly depends on two factors: the virulence of the penetrated microorganisms and the initial state of the woman's immune defense.
The further scenario may follow the path of limitation (resolution) or progress to diffuse peritonitis. Limitation of the process is possible with an adequate defense reaction: immunity is activated, the release of pro-inflammatory cytokines decreases, and the expression of anti-inflammatory interleukins increases. If this barrier fails, inflammatory mediators massively accumulate in the bloodstream. This leads to an increase in the manifestations of the disease, an increase in exotoxemia, and the unfolding of the picture of diffuse peritonitis.
The main pathogenetic links of obstetric peritonitis are recognized to be severe intoxication and intestinal paresis.
Mechanism of intestinal paresis development
Intestinal paresis is a complex pathological cascade that repeatedly increases the severity of the patient's condition:
- Inflammation of the visceral and parietal peritoneum causes reflex suppression of normal peristalsis.
- Intestinal loops become paretically dilated and overfilled.
- Mechanical overdistension provokes ischemia and hypoxic damage to the intramural nervous apparatus of the intestinal wall.
- Under conditions of stasis, the intestinal microflora is activated, which begins to actively release endo- and exotoxins.
- The process of active reabsorption is disrupted, and the intestinal lumen fills with liquid contents.
- The intestinal wall loses its barrier function: it becomes permeable to microorganisms, their toxins, as well as autolysis products, kinins, and lysosomal enzymes.
This breakthrough leads to a sharp, avalanche-like increase in endogenous intoxication. In addition, pronounced abdominal distension forces the dome of the diaphragm to rise high, which inevitably entails the development of pulmonary failure.
Hemodynamics and clinical presentation
In parallel with intoxication, critical hemodynamic disorders develop. The body loses large volumes of fluid, which is further aggravated by fever and vomiting. This leads to a drop in circulating blood volume (CBV) and a decrease in cardiac output, paving the way for the development of endotoxic shock.
The clinical presentation of obstetric peritonitis, especially after cesarean section (CS), has its own specifics. Unlike classical surgical peritonitis, the postpartum variant manifests early—as early as the 2nd–3rd day after surgery. However, its symptoms are often mild or masked, which requires special attention from the physician.
Key clinical manifestations include:
- Signs of increasing intoxication: pronounced weakness, thirst, and dry mouth.
- Abdominal distension (a consequence of paresis).
- Persistent tachycardia.
- Increase in body temperature up to 37.5–38 °C, often accompanied by chills.
Briefly: answers to topical questions
What laboratory blood changes are typical for postpartum pelvioperitonitis?
Postpartum pelvioperitonitis is characterized by pronounced changes in clinical and biochemical blood tests.
- Leukocytosis with a left shift in the leukocyte formula (increase in the number of band neutrophils)
- Elevated procalcitonin level
- Hypoproteinemia — decrease in total protein, primarily due to albumin
- Electrolyte disorders — decrease in K⁺ levels
- In the reactive stage of peritonitis, moderate leukocytosis with a left shift in the formula is noted; in the toxic stage, leukocytosis increases, accompanied by water-electrolyte balance disorders, acid-base balance disorders, hypo- and dysproteinemia.
What principles of surgical treatment are used for postpartum pelvioperitonitis?
Surgical treatment is performed when conservative therapy is ineffective and depends on the intraoperative picture.
- Indications for surgery — lack of effect from conservative therapy within 12–24 hours, increase in inflammatory symptoms, inability to rule out rupture of a purulent formation
- Organ-sparing tactics — sanitation and drainage of the abdominal cavity with an intact uterus and serous-fibrous exudate
- Organ-sparing surgery on the uterus — in case of suture dehiscence after CS with symptoms of peritonitis: laparotomy, nasogastric decompression, excision of uterine wound edges, suturing, drainage
- Radical surgery (extirpation of the uterus with tubes) — in the absence of conditions for organ preservation
Any intervention for peritonitis must be completed with drainage of the abdominal cavity.
A logical chain will help remember the consequences of intestinal paresis: Peritonitis → Cessation of peristalsis → Wall ischemia → Release of toxins and enzymes → Endogenous intoxication.
Class and exam questions
How does obstetric peritonitis differ from surgical peritonitis?
When it develops after a cesarean section, it starts early (already on the 2nd–3rd day), but its clinical manifestations are often masked, which can complicate timely diagnosis.
How does infection enter the abdominal cavity after childbirth?
The main pathways are uterine suture dehiscence (release of the infectious agent and detritus) and the spread of pathogens through the Fallopian tubes against the background of pronounced endometritis.
Why is the respiratory system affected in peritonitis?
Intestinal distension due to paresis leads to a high standing of the diaphragmatic dome. This mechanically limits the excursion of the lungs and causes pulmonary failure.
What else to study on this topic
- The role of anti-inflammatory interleukins in the resolution of peritonitis
- Mechanisms of hypoxic damage to the intramural nervous apparatus
- The effect of lysosomal enzymes and kinins on endogenous intoxication
- Differential diagnosis of mild/masked forms of obstetric peritonitis
Master the entire topic in the "Obstetrics and Gynecology" course
This is a summary. The course covers everything tested in classes and exams.
- Full study guide on the topic "Postpartum pelvioperitonitis" and another 973 pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 21 video lessons on the subject
Other topics in the "Obstetrics" section
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.