Causes and routes of infection spread
Purulent inflammation of the peritoneum most often becomes a formidable complication of other surgical pathologies. In more than 50% of cases, acute appendicitis is the culprit. Inflammation is also triggered by cholecystitis, strangulated hernias, pancreatitis, perforated ulcers, and gastrointestinal tumor perforation.
Infection can enter the abdominal cavity through several pathways:
- Direct spread: contact propagation from an inflamed organ.
- Rupture of a hollow organ: in trauma (e.g., blunt impact or stab wound) or wall necrosis, contents rich in polymicrobial flora are spilled.
- Bacterial translocation: penetration of microbes through the intestinal wall without macroperforation. This occurs when blood circulation is impaired (thrombosis, intestinal obstruction).
- Aseptic inflammation: chemical impact (bile, iodine, alcohol) or desiccation of the peritoneum during prolonged surgery. However, without appropriate intervention, bacterial flora quickly joins in, causing a purulent process.
Stages of the clinical course
The clinical picture changes rapidly as endotoxicosis progresses and the body's compensatory mechanisms become depleted.
- Reactive stage (12–24 hours). The body actively fights. The patient experiences intense pain, which is initially localized at the source, but gradually covers the entire abdomen. The pulse quickens to 120 bpm, blood pressure is elevated. Locally: the abdomen is retracted or does not participate in breathing, marked tenderness, Blumberg's sign, and pronounced muscle guarding are determined.
- Toxic stage (24–48 hours). Severe intoxication comes to the forefront. Gastrointestinal paresis develops: the abdomen is distended (meteorism), peristaltic sounds disappear. Pain and muscle tension paradoxically subside. The patient is lethargic, pulse is weak, blood pressure drops, and frequent vomiting of intestinal contents begins.
- Terminal stage (more than 48–72 hours). Multiple organ dysfunction syndrome develops. Toxic psychosis is possible. Facies Hippocratica is observed: sunken eyes, earthy-gray skin color, cold sweat. The abdomen is sharply distended, auscultation reveals a "grave-like silence." Body temperature drops, pulse is thready, urine output decreases (oliguria).
Nature of the effusion and flora specifics
The exudate can be serous, purulent, fibrinous, hemorrhagic, or ichorous. Its properties heavily depend on the microflora:
- Escherichia coli (*E. coli*) stimulates fibrin deposition, which promotes the adhesion of peritoneal leaves and the isolation of the focus.
- Streptococcus causes the production of liquid pus with a small amount of fibrin, the process rapidly becomes diffuse without the formation of adhesions.
- Putrefactive microflora (in organ gangrene) yields an ichorous exudate of a dirty-gray color with fibrin flakes and a sharp putrid odor.
Pathophysiology and surgical tactics
Intestinal paresis leads to content stasis, fermentation, and putrefaction. Pyloric gaping occurs: toxic intestinal contents are regurgitated into the stomach, provoking profuse vomiting. Metabolism shifts toward catabolism, severe hypoproteinemia and electrolyte deficiency form. Cellular dehydration and a critical mismatch between the vascular bed volume and circulating blood volume develop.
Radical surgical treatment includes peritoneal lavage and drainage. One of the methods is programmed relaparotomy with the formation of a laparostomy (zipper suturing). This "open abdomen" method allows regular opening of the wound, removal of pus, and washing the cavity with antiseptics. Peritoneal dialysis is also used, placing the patient in Fowler's position (semi-sitting) so that pus flows down into the lesser pelvis for adequate drainage.
For stages of peritonitis, remember the triad "guarding — distension — silence": in the reactive stage, muscles are tense (guarding), in the toxic stage the abdomen is distended due to paresis, and in the terminal stage a "grave-like silence" sets in.
Class and exam questions
What is Blumberg's sign and how is it tested?
This is a sign of peritoneal irritation. The physician smoothly and carefully presses a hand onto the abdominal wall, and then sharply pulls the hand away. If pain sharply increases upon withdrawal, the sign is considered positive.
Why might abdominal pain decrease in the toxic stage?
Pain and muscle guarding temporarily subside due to increasing severe intoxication and the development of deep intestinal paresis, while the patient's general condition critically deteriorates.
Why is a patient with peritonitis placed in Fowler's position?
The semi-sitting position with the head of the bed elevated is necessary so that the inflammatory exudate flows by gravity into the lower parts of the abdominal cavity, from where it is easier to evacuate via drains.
What else to study on this topic
- Mechanisms of inflammation isolation and the role of fibrin in adhesion formation
- Features of the pain syndrome and phrenic nerve sign in various localizations
- Instrumental diagnostics: Klauber's air-fluid levels and free gas on radiographs
- Depth of tissue damage and risk of secondary organ perforation
- Systemic changes in internal organs against the background of severe toxemia
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Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"
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