Classification and Etiology
Based on the mechanism of occurrence, there are two fundamental forms of obstruction: mechanical and paralytic.
Mechanical (obstructive) obstruction occurs due to a physical blockade of the lumen. The main causes include:
- Hernias (inguinal, femoral, umbilical), in which a loop of bowel becomes entrapped in a hernial ring.
- Intussusception — the telescoping of one segment of the intestine into the lumen of an adjacent (typically distal) segment.
- Obstruction and luminal narrowing due to tumors, fibrous adhesions, foreign bodies, or strictures (e.g., in inflammatory bowel disease).
- Volvulus — twisting of a bowel loop along the axis of its mesentery.
Paralytic (dynamic) obstruction is associated with impaired peristalsis of neurogenic or myogenic origin. Most commonly, it results from intra-abdominal pathologies, primarily mesenteric vascular thrombosis or embolism.
Tumors as a Factor of Obstruction
Malignant neoplasms are a leading cause of mechanical obstruction. Epidemiological trends over recent decades show a steady worldwide increase in incidence. In the US and Europe, this pathology ranks second among cancer-related deaths.
Tumors can affect any segment: the cecum, appendix, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, rectum, and anorectal zone.
Key predisposing factors:
- Dietary factors: a diet high in protein and fat combined with a fiber deficiency. This leads to the formation of polycyclic hydrocarbons, altered microflora, and secondary bile acids. Coprostasis occurs, increasing the contact time between carcinogens and the intestinal epithelium.
- Obesity: a direct correlation has been proven between excess body weight and the risk of tumor development.
A high-fiber diet serves as a protective factor. It ensures timely evacuation, lowers carcinogen concentration, and inhibits the proliferation of bacteria that produce toxic metabolites.
Pathogenesis and Morphological Changes
In mechanical obstruction, the pathological process develops in stages. Initially, there is a sharp spasm proximal to the obstruction site (and later in the distal segment as well), driven by damage to intramural nerve plexuses. This spasm is soon replaced by paralytic luminal dilation. Venous outflow is impaired while arterial dilation occurs.
Morphological consequences include blood stasis and microcirculatory thrombosis. Ischemic necrosis develops, originating in the mucosa and gradually involving all layers of the wall, culminating in perforation. If the obstruction presents as a strangulated type, blood supply is compromised from the outset, multiplying the risk of necrosis.
In paralytic obstruction secondary to vascular catastrophes, bowel infarction (typically hemorrhagic) develops. Affected loops and segments abruptly change color, acquiring a characteristic cherry-blue hue. Surgeons rely on this exact color to visually determine the resection margins of necrotic fragments during surgery.
Systemic Manifestations and Complications
Regardless of etiology, ileus leads to severe local and systemic complications. Locally, peritonitis develops, characterized by the accumulation of fibrinous-purulent or putrid exudate in the abdominal cavity.
Progressive endotoxemia triggers a systemic cascade of pathological reactions:
- Generalized microcirculatory disturbances.
- Multiple diapedetic hemorrhages.
- Pronounced tissue edema.
- Fatty degeneration of vital organs (myocardium, liver, kidneys).