Signature ✍️
Uncomplicated
- Acute: abrupt-onset nausea/vomiting, paroxysmal abdominal cramping, distension (progressive dilation of proximal bowel, bowel edema → ↓ absorption → air-fluid levels ⊕/⊖ transudative ascites), obstipation (i.e. inability to pass flatus or stool)
- Chronic Partial: same as above (acute), but with postprandial > constitutive tempo allowing chronic symptoms. (Notably, symptoms never resolve.)
- Recurrent Intermittent: same as above (acute), but with complete resolution of symptoms between episodes
↔︎ The frequency & severity of SBO symptoms is variable & depends upon the location of obstruction (i.e. more proximal = less bowel for compensatory dilatation = more symptomatic), as well as the degree of obstruction (i.e. complete obstructions = more symptomatic) ↔︎
Complicated
- Ischemia*: transition of colicky abdominal pain → static, severe abdominal pain
*Mechanisms of ischemia include twisting of bowel and/or its mesentery around a fixed structure (”strangulation;” more common), or massive bowel dilation resulting in intramural vessel compression (less common), with ischemia being particularly common in closed-loop obstructions
🚨 While an elevated lactate is expected in the late stages of bowel ischemia, lactate may be ⊖ in cases of ischemia due to hernia strangulation with a closed-loop obstruction, which can be accounted for by lack of venous return to the portal vein
DDx 🏳️🌈
Constitutive ⏳
- Foreign body (e.g. bezoar)
- Gallstone (i.e. chronic cholecystitis)
- Intussusception
- Tumors (see Principles)
- Stricture (e.g. IBD, ischemic colitis)
- Gastric outlet edema (e.g. PUD, tumor)
- Intramural hematoma (warfarin)
- Adhesions
- SMA syndrome
Intermittent ⏱️
- Intusussception
- Volvulus
- Internal hernia
Functional 🦀
- Peritoneal carcinomatosis
Principles❗️
Epidemiology 🌎
- ~55-80% = Adhesions. ~80% of patients with adhesive SBO have a history of prior abdominal surgery, with open surgery carrying a much higher risk than laparoscopic surgery. Even in patients without a history of surgery, adhesive SBO is the most common culprit of SBO (~55%), which can be accounted for by prior abdominal inflammation (e.g. diverticulitis, undiagnosed Crohn’s) or serosal inflammation (e.g. PID, Fitz-Hugh-Curtis). However, some guidelines recommend a strict search for a non-adhesive endpoint diagnosis should your patient with SBO not have a surgical history
- ~20% = Malignancy-related. Metastatic malignancy is the most frequent neoplastic cause & often heralded by a period of chronic partial SBO, but acute SBO can also result from volvulus around a tumor deposit as well as intraluminal seeding resulting in endoluminal blockage. Primary small bowel tumors include GIST tumors (~35%), lymphomas (~25%), & GI adenocarcinomas (~20%); most of these arise in the ileum (~65%), & mechanisms of obstruction include endoluminal blockage vs. intussusception, both of which can present cryptically (see “False ⊖ CT” below)
- ~10% = Hernias. When abdominal wall hernias remains reducible, patients usually present with intermittent symptoms followed by acute SBO when hernia becomes incarcerated. However, internal hernias are not diagnosable via physical examination & rely instead on cross-sectional imaging.
Diagnostic Arc 🗻
- Confirm Dx ✅ : abdominal X-ray is recommended up-front to …
- Quickly confirm the diagnosis
- Assess for findings that require immediate decompression (e.g. volvulus)
- Avoid repeated radiation exposure
Confirmatory findings include dilated loops of bowel with air-fluid levels, proximal bowel dilation with distal bowel collapse, or a “gasless” abdomen:

- Stratify Dx 🤔 : while abdominal X-ray may confirm the Dx, the sensitivity is only ~80%, the site or cause of obstruction is usually not apparent, & partial SBO can be confused for ileus. For these reasons, the best next step is the CT scan w/ IV contrast, which can identify the site of obstruction (”transition point”), severity of obstruction (partial vs. complete), presence of secondary ischemia (↓ intraluminal enhancement, delayed hyperenhancement, bowel wall thickening), & evidence of the endpoint Dx (e.g. “target sign” of intussusception, “whirl sign” of internal hernia or volvulus, “venous cut-off sign” of volvulus with associated thrombosis)*
*Note: the absence of IV contrast has numerous diagnostic implications, including ↓ sensitivity for bowel perfusion (i.e. ischemia) & contrast-enhancing endpoint diagnoses (e.g. tumor, infection)
- ⊖ CT 😯 : there are a few mechanisms by which abdominal CT may not apparently reveal the site of obstruction & underlying diagnosis, despite there being CT evidence of the downstream consequences of obstruction (e.g. air-fluid levels):
“False ⊖” CT
- ‘Constitutive’ (Low-grade, partial): the sensitivity of CT for low-grade partial SBOs is substantially lower than for high-grade partial SBOs (63% versus greater than 95%). Primary mural neoplasms* & strictures are two examples
- ‘Intermittent’ process: implies a dynamic process & that the obstruction may not be captured if the obstructive episode has spontaneously resolved prior to image acquisition. Examples include intussusception, volvulus, & internal hernias
“True ⊖” CT
- ‘Functional’ obstruction: implies a pathophysiology that ultimately results in impaired GI motility, such as neuromuscular diseases resulting in myenteric plexus dysfunction, infiltrative diseases resulting in ↓ bowel compliance, or simply the ileus DDx
*GI adenocarcinomas with signet-ring cell features classically cause progressive infiltrate bowel wall without a discrete mass formation until late in disease: infiltrative, mural spread of early disease can even be missed on colonoscopy!
- Final Steps❓: the diagnostic armamentarium includes ex- lap- for the patient with acute SBO that is failing to progress with nonoperative management or accompanied by concern for secondary ischemia, as well as colonoscopy for the patient with resolution of intermittent SBO who may have an endoluminal or mural disease
Treatment 🙃
- Non-operative Management = NG Suction 🤮 : while nonoperative management of SBO is successful in up to ~85% of adhesive SBOs, patients must be stable, have resolving leukocytosis & acidosis, & not have a need for immediate surgical management. Indications for early surgical management include closed-loop obstruction, irreducable hernias, & suspected primary neoplasm, which are all unlikely to resolve without surgical intervention, & which also carry a higher risk of strangulation

- Gastrografin Challenge ✨ : administration of radiopaque gastrografin followed by abdominal X-rays taken at 0, 4, 8, 12, & 24 hours hours can demonstrate the location of contrast over time. If the contrast doesn’t reach the colon by 24 hours, nonoperative management has failed. The presence of contrast in the colon within 24 hours predicts SBO resolution with a sensitivity of 92%

References 📚