Complications of non-specific inflammatory diseases
Crohn's disease (Crohn's disease) and ulcerative colitis are organic pathological processes that currently cannot be completely cured. Their consequences are associated with profound structural remodeling of the intestinal tissues.
In Crohn's disease, inflammation is transmural in nature (the infiltrate with clusters of lymphocytes and epithelioid cell granulomas involves all layers of the wall). This predetermines the specifics of local complications. Deep slit-like ulcers penetrating down to the serosa are prone to perforation.
- Fistulas: form when ulcers rupture. They can be external (opening onto the abdominal wall or perianal region) and internal (communicating with other bowel loops or hollow organs). A characteristic feature is the absence of generalized peritonitis. This is explained by pronounced serositis, in which adhesive processes reliably isolate the fistulous tracts.
- Stenoses: macroscopically manifest as the "handlebar" phenomenon (segmental narrowing of the hollow organ lumen). The formation of abscesses is also characteristic.
In ulcerative colitis, the process begins in the rectum and spreads in a proximal direction, causing ulceronecrotic changes. The disease proceeds with a wide range of local and systemic (extraintestinal) complications.
Consequences of dysenteric colitis
The severity of complications in shigellosis directly depends on the species of the pathogen. While S. flexneri and S. sonnei usually cause milder catarrhal gastroenterocolitis, S. dysenteriae provokes the classical stage-by-stage development of colitis with deep necrosis.
- Damage to the nervous apparatus. Develops at the stage of fibrinous (diphtheritic) inflammation. Dystrophic and necrotic changes in neurons, up to vacuolization and karyolysis, are observed in the intramural nerve plexuses of the intestine.
- Cicatricial stenoses. Formed during the reparative stage. Deep and extensive defects left after the rejection of fibrinous membranes and necrotic masses are replaced by granulation tissue. Its subsequent epithelization and maturation lead to narrowing of the intestinal lumen.
- Post-dysenteric colitis. Most infectious disease specialists view chronic changes (mucosal atrophy, inflammatory polyps) not as the persistence of shigellae, but as the consequences of a past infection.
In young children, the lymphoid apparatus of the intestine is primarily affected. With progression, necrosis and ulceration of the centers of hyperplastic solitary follicles occur, leading to a specific complication — follicular-ulcerative colitis with the formation of crater-like ulcers with overhanging edges.
Complications of specific lesions (viruses and protozoa)
Viral and parasitic infections cause severe complications predominantly against the background of reduced immune reactivity of the body (for example, in HIV infection or oncological diseases).
| Etiology | Pathological process | Characteristic complications |
|---|---|---|
| Cytomegalovirus | Generalized form (occurs with hematogenous dissemination) with the development of ulcerative colitis. | Addition of secondary infection, severe cachexia. Fatal outcome from the underlying disease is possible. |
| Cryptosporidiosis | Chronic catarrhal or serous-hemorrhagic gastroenteritis (pathogen — Cryptosporidium parvum). | Atrophy of the intestinal mucosal villi, formation of pronounced malabsorption syndrome. |
"In Crohn's disease, fistulas drain, but do not cause peritonitis." This is due to pronounced inflammation of the serosa: adhesions tightly wall off the process, keeping it out of the free abdominal cavity.
Class and exam questions
Why doesn't generalized peritonitis occur during the perforation of deep ulcers in Crohn's disease?
Due to concomitant pronounced serositis, an active adhesive process develops. Adhesions reliably isolate the forming fistulous tracts, separating the destruction focus from the free abdominal cavity.
What complication does the chronic course of cryptosporidiosis lead to?
Prolonged persistence of coccidia in the intestine causes atrophy of the mucosal villi. This naturally leads to the development of malabsorption syndrome (severe impairment of nutrient absorption).
What is the morphological cause of scar strictures in dysentery?
Stenoses arise as the outcome of the ulcer stage (from the 10th–12th day). Deep and extensive ulcers formed after the rejection of dense fibrinous membranes heal through the formation of coarse granulation and connective tissue.
What does the term "post-dysenteric colitis" mean?
These are residual morphological changes in the large intestine, such as mucosal atrophy and the formation of inflammatory polyps. They are interpreted as consequences of past shigellosis, rather than as an ongoing chronic infection.
What else to study on this topic
- Macroscopic and microscopic picture of the intestine in Crohn's disease ("cobblestone" appearance, epithelioid cell granulomas).
- Stages of development of classical dysenteric colitis upon infection with Shigella dysenteriae.
- Morphological differences between Crohn's disease and ulcerative colitis (localization, depth of wall lesion).
- Features of the course of dysentery in childhood (follicular and follicular-ulcerative colitis).
- Pathogenesis and pathways of generalization of cytomegalovirus infection in immunodeficient states.
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