Complications of abdominal cavity diseases

Etiology and sources of infection

In the vast majority of cases (about 85–90%), peritoneal inflammation has a bacterial nature. The infection penetrates either from the external environment in open wounds and surgical operations, or endogenously — from the lumen of hollow organs against the background of their destruction and perforation.

As a rule, mixed pyogenic microflora is detected in the abdominal cavity, but one specific pathogen often takes the leading role. Most commonly, Escherichia coli and various non-spore-forming anaerobes dominate. Staphylococci, streptococci, or Proteus predominate less frequently in cultures.

The course of the pathological process is largely determined by the type of the leading microorganism:

• Streptococcal peritonitis: is characterized by a pronounced tendency to rapid spread. The inflammatory process is diffuse in nature, the adhesion barrier is practically not formed, and the resulting pus has a liquid consistency with a small amount of fibrin.
• Colibacillary peritonitis (caused by E. coli): conversely, it tends to localization of the inflammatory focus (encapsulation). This form releases a thick exudate, abundantly saturated with fibrin, which promotes the formation of dense adhesions.

Aseptic peritoneal inflammation

Inflammation does not always start with microbial invasion. Aseptic peritonitis develops under the influence of non-infectious aggressive factors that damage the serous membrane.

The main causes of this condition include:

1. Mechanical trauma: abdominal contusions, closed injuries without rupture of hollow organs.
2. Intraoperative insults: hypothermia and drying of the peritoneal leaves during prolonged interventions or evisceration.
3. Chemical effects: contact of aggressive antiseptics (e.g., alcohol or iodine) with the sensitive serous membrane.

The clinical picture of the aseptic form has its own characteristics. Such a process itself does not cause the severe systemic intoxication typical of purulent lesions. The main clinical manifestation becomes persistent gastrointestinal paresis. However, the main danger lies in high tissue vulnerability: against the background of damaged peritoneum, even minor microorganism contamination rapidly transforms the inflammation into a severe purulent form.

Main causes of purulent peritonitis

Purulent inflammation rarely occurs spontaneously; it is usually a fatal consequence of other acute abdominal organ diseases. The absolute leader is acute appendicitis — it accounts for more than 50% of all diagnosed episodes.

Other common sources of the pathology include:

• Destructive cholecystitis and acute pancreatitis.
• Acute intestinal obstruction and strangulated hernias.
• Perforated gastric or duodenal ulcer.
• Perforation of tumor nodes due to their decay, stenosis, or bleeding.
• Inflammatory pathologies of the female reproductive system.

A separate group consists of traumatic injuries. The organ wall can be destroyed under the influence of a purulent-necrotic process (ulcer, decaying tumor) or as a result of external trauma. This includes direct wounds (gunshot, stab), blunt abdominal trauma causing subcutaneous ruptures of internal organs, and punctures by foreign objects (needles, swallowed bones). The development mechanism is always identical: polymicrobial contents spill into the abdominal cavity, instantly triggering severe inflammation.

Specific complications of typhoid fever

As a classic example of surgical complications of specific infections, it is important to consider typhoid fever. Pathological changes in the body during this disease are divided into non-specific (pneumonia, otitis, cholecystitis, thrombophlebitis, epidemic parotitis) and specific intestinal complications.

The main specific complications include:

• Intestinal hemorrhage. It occurs due to arrosion (destruction) of the walls of large blood vessels in the necrosis zone of typhoid ulcers.
• Ulcer perforation. Perforation occurs at the moment when the necrotic process penetrates through all layers of the intestine down to the serous membrane, or during the rejection of dead tissue at the stage of "clean ulcer" formation. As a result, intestinal contents spill outward, causing fulminant acute peritonitis. The main clinical marker of this event is sharp, sudden "dagger-like" abdominal pain.

Class and exam questions

What else to study on this topic

• Pathogenesis of gastrointestinal paresis in aseptic inflammation
• Mechanisms of arrosion bleeding from typhoid ulcers
• Morphological stages of typhoid fever development and the formation of "clean ulcers"
• Features of the course of inflammation caused by non-spore-forming anaerobes
• Classification and biomechanics of closed abdominal trauma with rupture of hollow organs

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.