Intestinal Obstruction, Ileus & Mesenteric Ischemia
When the bowel is blocked, stalled, or starved of blood
Mechanical obstruction
Small vs large bowel. Mechanical obstruction is a physical block to transit. In adults, postoperative adhesions cause most small-bowel obstructions (SBO), followed by incarcerated hernias, which lead in patients without prior surgery. Tumors, Crohn strictures, intussusception, and gallstone ileus (a stone that enters the bowel through a cholecystoenteric fistula and lodges at the ileocecal valve) are less common. Large-bowel obstruction (LBO) is most often due to colorectal carcinoma, followed by volvulus and diverticular stricture.
| Feature | Small bowel | Large bowel |
|---|---|---|
| Top causes | Adhesions, hernias, tumors | Colorectal cancer, volvulus, diverticular stricture |
| Vomiting | Early and bilious (proximal) | Late, may become feculent |
| Distension | Mild if proximal, marked if distal | Marked |
| Imaging | Dilated central loops, air-fluid levels, little colonic gas | Dilated peripheral colon with haustra; cecum at risk |
Pathophysiology. Swallowed air and unabsorbed secretions distend the bowel above the block. Rising wall tension impairs venous return, so the wall becomes edematous and secretes fluid into the lumen instead of absorbing it. Liters are sequestered in the lumen, wall, and peritoneal cavity (third spacing), producing hypovolemia, hemoconcentration, and prerenal azotemia, while stasis allows bacterial overgrowth and translocation. Early on, colicky pain comes with high-pitched, tinkling bowel sounds; obstipation follows.
Acid-base effects. Vomiting gastric contents removes HCl and produces a hypochloremic metabolic alkalosis. Volume depletion stimulates aldosterone, so the kidney reabsorbs sodium at the cost of K+ and H+, adding hypokalemia and a paradoxically acidic urine; saline and KCl correct the disturbance. Hypokalemia itself slows motility. Once the bowel becomes ischemic, lactic acid produces an anion-gap metabolic acidosis.
Closed loop and strangulation. A segment occluded at two points (volvulus, a hernia with a narrow neck, an adhesive band) cannot decompress, so its pressure rises quickly. Venous outflow fails first, then arterial inflow: this is strangulation, which leads to gangrene and perforation. Warning signs are pain that becomes constant, fever, tachycardia, peritoneal signs, leukocytosis, and rising lactate. An incarcerated hernia is irreducible; a strangulated one has lost its blood supply, and femoral hernias are the most prone to strangulate. An LBO with a competent ileocecal valve is also a closed loop: the cecum, as the widest segment, has the highest wall tension for a given pressure (Laplace law) and is the usual site of perforation.
Colonic volvulus. Sigmoid volvulus occurs when a redundant sigmoid on a long, narrow mesentery twists, typically in elderly, institutionalized, or neuropsychiatric patients with chronic constipation. Radiographs show a giant inverted-U coffee-bean loop pointing to the right upper quadrant, and contrast enema shows a bird's beak taper. Flexible endoscopic detorsion is first-line, followed by elective sigmoid resection because recurrence is common; gangrene or perforation requires emergency surgery. Cecal volvulus affects younger adults with a congenitally mobile, poorly fixed cecum; the dilated cecum points to the left upper quadrant, often with dilated small bowel, and because endoscopic detorsion rarely succeeds it is treated with right hemicolectomy.
Functional obstruction: ileus and Ogilvie syndrome
Paralytic ileus. Ileus is hypomotility without a mechanical block. It follows abdominal surgery (the small bowel recovers first and the colon last) and is promoted by opioids, anticholinergics, hypokalemia, hypercalcemia, hypothyroidism, sepsis, peritonitis, pancreatitis, and retroperitoneal hemorrhage. The abdomen is distended and quiet, pain is less colicky, and films show gas throughout small bowel and colon without a transition point. Treatment corrects electrolytes and limits opioids; alvimopan, a peripherally restricted μ-opioid antagonist, shortens postoperative ileus after bowel resection.
Ogilvie syndrome. Acute colonic pseudo-obstruction is massive dilation of the cecum and right colon without obstruction, seen in hospitalized patients after orthopedic surgery, cesarean delivery, or cardiac surgery, and with sepsis, electrolyte disturbance, or opioids. It reflects autonomic imbalance, with reduced sacral parasympathetic drive to the distal colon.
- Supportive careBowel rest, decompression tubes, correct K+ and Mg2+, stop opioids and anticholinergics
- NeostigmineAcetylcholinesterase inhibitor; monitor for bradycardia with atropine at hand
- Colonoscopic decompressionIf neostigmine fails or is contraindicated
- SurgeryFor perforation or ischemia
A cecum dilated beyond about 12 cm, or distension that persists for days, carries a real risk of perforation.
Acute mesenteric ischemia
Presentation. Sudden, severe periumbilical pain that is out of proportion to a soft, minimally tender abdomen is the classic early picture, because ischemia begins in the mucosa and spares the peritoneum. Gut emptying (vomiting, diarrhea), leukocytosis, elevated lactate, and metabolic acidosis follow; peritoneal signs, bloody stools, and shock mean transmural infarction. CT angiography is the key diagnostic test.
| Type | Cause | Clues |
|---|---|---|
| SMA embolus (about half) | Atrial fibrillation, LV mural thrombus after MI, endocarditis | Abrupt onset; embolus lodges beyond the middle colic origin, sparing proximal jejunum |
| SMA thrombosis | Atherosclerosis at the SMA origin | Prior intestinal angina; extensive infarction from jejunum to transverse colon |
| Nonocclusive (NOMI) | Low flow plus splanchnic vasoconstriction | Shock, heart failure, sepsis, dialysis, vasopressors, digoxin, cocaine |
| Mesenteric venous thrombosis | Hypercoagulable state, portal hypertension, pancreatitis | Gradual onset; edematous, hemorrhagic bowel |
Why the SMA. Its large caliber and oblique aortic takeoff make it the usual target of cardiac emboli. Venous thrombosis instead reflects hypercoagulability: factor V Leiden, protein C or S deficiency, antiphospholipid syndrome, JAK2-positive myeloproliferative neoplasms, oral contraceptives, and malignancy.
Pathology. The villus tips are the most vulnerable tissue because countercurrent exchange in the villus leaves them relatively hypoxic, so injury progresses from mucosal sloughing to mural to transmural infarction. Intestinal infarcts are hemorrhagic (red) even with arterial occlusion because of collateral and venous backflow. Transmural necrosis perforates, causing peritonitis and sepsis. Late imaging signs include thumbprinting from submucosal edema, pneumatosis intestinalis, and portal venous gas.
Treatment principles. Resuscitation, broad-spectrum antibiotics, and heparin; restoration of flow by embolectomy, thrombectomy, or stenting; resection of dead bowel with a planned second look. NOMI is treated by correcting the low-flow state, sometimes with intra-arterial papaverine, and venous thrombosis mainly with anticoagulation.
Chronic mesenteric ischemia and neonatal NEC
Intestinal angina. Atherosclerotic narrowing of the mesenteric arteries in an older smoker with vascular disease causes dull periumbilical pain 15–60 minutes after eating, fear of food (sitophobia), and weight loss, sometimes with an abdominal bruit. Because collaterals are rich, symptoms usually require significant stenosis of at least two of the three vessels (celiac trunk, SMA, IMA). Revascularization prevents progression to acute thrombosis. Contrast ischemic colitis: a usually nonocclusive, self-limited injury of the colonic watershed (splenic flexure, rectosigmoid) with crampy pain and bloody diarrhea.
Necrotizing enterocolitis. NEC is the most common GI emergency of preterm infants. Risk rises with prematurity and very low birth weight, formula feeding (human milk is protective), and hypoxic-ischemic stress; an immature mucosal barrier and immune response combined with abnormal bacterial colonization lead to inflammation and necrosis, most often of the terminal ileum and proximal colon. Infants develop feeding intolerance, distension, bilious residuals, and bloody stools. Pneumatosis intestinalis is the radiographic hallmark, while portal venous gas and pneumoperitoneum mark advanced disease. Treatment is bowel rest, gastric decompression, and broad-spectrum antibiotics, with surgery for perforation; survivors can develop strictures or short bowel syndrome.