Mechanical blockage of small bowel; adhesions are the most common cause in adults with prior surgery.
Also known as: SBO, small bowel obstruction, small intestinal obstruction
Overview
Mechanical obstruction of the small intestine causing impaired passage of luminal contents. Classified as partial (some flow continues) or complete; simple (no vascular compromise) or strangulated (compromised blood supply — surgical emergency).
Epidemiology
Accounts for ~15% of acute abdominal admissions. ~300,000 hospitalizations annually in the US. Recurrence rates 5-30% after adhesive SBO management.
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Question 1GastrointestinalMedium
A 70-year-old man with prior abdominal surgeries has colicky abdominal pain, bilious vomiting, distention, and obstipation. Which of the following is the most appropriate initial diagnostic study?
AAbdominal ultrasound of the dilated bowel loops
BCT of the abdomen and pelvis with IV contrast
CUpright and supine abdominal radiographs
DWater-soluble oral small bowel follow-through
Reveal answer & full explanation
Correct answer: B — CT of the abdomen and pelvis with IV contrast
AAbdominal ultrasound of the dilated bowel loops
BCT of the abdomen and pelvis with IV contrast✓
CUpright and supine abdominal radiographs
DWater-soluble oral small bowel follow-through
Why CT of the abdomen and pelvis with IV contrast is correct
The picture is small bowel obstruction (colicky pain, bilious vomiting, distention, obstipation) with adhesions from prior surgery as the likely cause.
CT is the test of choice: it localizes the transition point, grades severity, and identifies closed-loop or ischemic obstruction that mandates surgery.
It also excludes alternative causes such as hernia, tumor, or volvulus.
Why the others are wrong
Upright and supine abdominal radiographs — Plain films may show air-fluid levels but miss the transition point and ischemia; they are a screening adjunct, not the definitive initial study (premature closure on a quick film).
Abdominal ultrasound of the dilated bowel loops — Overlying bowel gas limits ultrasound for obstruction; it is reserved for specific questions like intussusception in children (right-test-wrong-patient).
Water-soluble oral small bowel follow-through — A Gastrografin challenge is used to predict resolution of partial adhesive obstruction after CT, not as the first diagnostic step (right-step-wrong-time).
Question 2GastrointestinalMedium
A 64-year-old man with a prior open appendectomy presents with 2 days of crampy abdominal pain, bilious vomiting, and obstipation. Vitals: HR 108, BP 102/64. Exam shows a distended, tympanitic abdomen with high-pitched bowel sounds. Labs reveal Na 138, K 2.9, Cl 91, HCO3 34, and pH 7.50. CT confirms adhesive small bowel obstruction without ischemia. Which of the following best explains his acid-base and electrolyte abnormalities?
ARenal bicarbonate wasting from proximal tubular dysfunction
BRenal potassium and acid loss from an aldosterone-secreting adenoma
CRetention of carbon dioxide from hypoventilation and splinting
DLoss of gastric hydrogen and chloride from recurrent vomiting
Reveal answer & full explanation
Correct answer: D — Loss of gastric hydrogen and chloride from recurrent vomiting
ARenal bicarbonate wasting from proximal tubular dysfunction
BRenal potassium and acid loss from an aldosterone-secreting adenoma
CRetention of carbon dioxide from hypoventilation and splinting
DLoss of gastric hydrogen and chloride from recurrent vomiting✓
Why Loss of gastric hydrogen and chloride from recurrent vomiting is correct
In SBO, proximal dilation and emesis lead to loss of upper GI fluid rich in H+ and Cl-, producing the classic hypokalemic, hypochloremic metabolic alkalosis.
Volume depletion drives renal Na+/H2O retention; the kidney exchanges Na+ for K+ and H+, worsening hypokalemia and perpetuating the alkalosis (contraction alkalosis).
This patient's K 2.9, Cl 91, HCO3 34, and pH 7.50 fit a primary metabolic alkalosis from vomiting, the expected derangement in obstruction.
Why the others are wrong
Renal potassium and acid loss from an aldosterone-secreting adenoma — primary aldosteronism also produces a hypokalemic metabolic alkalosis, but it presents with hypertension and volume expansion rather than the tachycardia and BP of 102/64 seen here after 2 days of vomiting and obstipation.
Renal bicarbonate wasting from proximal tubular dysfunction — proximal (type 2) RTA causes a normal-anion-gap metabolic acidosis with bicarbonate loss, not an alkalosis, and is not a feature of SBO.
Retention of carbon dioxide from hypoventilation and splinting — respiratory acidosis would show a high PCO2 with low pH; here the pH is elevated, indicating a metabolic, not respiratory, process.
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Mechanical obstruction causes proximal dilation with accumulation of fluid, gas, and swallowed air. Initial increase in peristalsis (high-pitched bowel sounds) gives way to ileus and quiet abdomen. Bowel wall edema and increased intraluminal pressure compromise venous outflow first, then arterial supply → ischemia, necrosis, perforation. Third-spacing causes hypovolemia and electrolyte derangement (hypokalemic, hypochloremic metabolic alkalosis from emesis).
Clinical presentation
Symptoms
Crampy, intermittent abdominal pain (initially every 4-5 min in proximal SBO; longer intervals in distal)
Nausea and vomiting (early and bilious in proximal; feculent in distal SBO)
Abdominal distension (more pronounced in distal obstruction)
Obstipation — no flatus or stool (complete obstruction)
Diarrhea early in partial obstruction (paradoxical)
Severe constant pain suggests strangulation/ischemia
Signs / physical exam
Abdominal distension, tympany
High-pitched, hyperactive bowel sounds with rushes (early); diminished/absent in late or ileus
Tenderness — diffuse and mild in simple SBO; focal/peritoneal signs suggest strangulation
Look for hernias — exam ALL hernia orifices
Surgical scars (adhesive risk)
Rectal exam — empty vault, mass, blood
Signs of hypovolemia: tachycardia, hypotension, decreased skin turgor
Crampy abdominal pain + vomiting + distension + obstipation in a patient with prior abdominal surgery.
Differential diagnosis
Paralytic ileus (post-operative, post-laparotomy, opioids, electrolytes) — No mechanical obstruction; diffuse gas distribution including colon; treat underlying cause; supportive
Large bowel obstruction (volvulus, mass, fecal impaction) — Distension dominant; haustral markings; coffee-bean sign in sigmoid volvulus
Acute mesenteric ischemia — Pain out of proportion, atrial fibrillation, elevated lactate; CT angiography
Acute pancreatitis — Lipase >3× ULN; epigastric pain to back
Clinical features + imaging findings. CT signs of strangulation: bowel wall thickening, mesenteric edema, ascites, lack of contrast enhancement, pneumatosis intestinalis, portal venous gas.
Labs
CBC — leukocytosis suggests strangulation
BMP — hypokalemia, hypochloremia, metabolic alkalosis from vomiting
Lactate — elevated in strangulation/ischemia
Lipase
Type and screen / crossmatch if surgery anticipated
Coagulation studies
Imaging
Upright and supine abdominal radiograph — historically first; air-fluid levels, dilated small bowel loops (>3 cm), 'string of pearls,' paucity of colonic gas (but limited sensitivity)
CT abdomen/pelvis with IV contrast — MODALITY OF CHOICE; identifies transition point, cause (hernia, mass, intussusception, volvulus), closed loop, signs of ischemia (bowel wall thickening, pneumatosis, lack of bowel wall enhancement, mesenteric edema, free fluid)
Water-soluble contrast (Gastrografin) challenge — both diagnostic and therapeutic; contrast reaching colon by 24 h predicts non-operative success in adhesive SBO and may help resolve obstruction
MRI — alternative in pregnancy or contrast allergy
Diagnostic algorithm
flowchart TD
A[Suspected SBO<br/>crampy pain, vomiting,<br/>distension, obstipation] --> B[Resuscitate: NPO, NG tube,<br/>IV fluids, correct K+/electrolytes]
B --> C[CT abdomen/pelvis<br/>with IV contrast]
C --> D{Signs of strangulation<br/>or closed loop?<br/>peritonitis, lactate, ischemic CT}
D -->|Yes| E[Emergent surgery]
D -->|No| F{Complete vs partial?}
F -->|Complete or<br/>virgin abdomen| G[Surgical exploration]
F -->|Partial / adhesive| H[Gastrografin challenge<br/>+ non-operative management<br/>up to 48-72h]
H --> I{Resolved?}
I -->|Yes| J[Diet advancement<br/>+ discharge]
I -->|No| G
Small bowel obstruction management pathway.
Treatment
First-line
NPO, nasogastric tube decompression for symptomatic relief
IV fluid resuscitation (lactated Ringer's preferred)
Correct electrolyte and acid-base derangements
Analgesia, antiemetics
Foley catheter for accurate I/O monitoring
Broad-spectrum IV antibiotics if signs of infection, strangulation, or perforation suspected
Surgical consultation
Identify and address reversible cause (reduce hernia, treat ileus)
Partial / adhesive SBO without strangulation or peritonitis
Non-operative management with NG decompression and IV fluids
Water-soluble contrast (Gastrografin) — 100 mL via NG tube; if contrast reaches colon within 24 h, 80% resolve without surgery
Serial abdominal exams and lab monitoring
Failure of non-operative management at 48-72 h → surgical exploration
Complete SBO, strangulation, closed loop, peritonitis, or failed non-op management
Urgent or emergent surgical exploration (laparoscopic or open)
Adhesiolysis, hernia reduction and repair, resection of non-viable bowel, treatment of underlying cause
SBO due to incarcerated hernia
Attempt manual reduction in absence of strangulation
Urgent operative reduction and repair if reduction fails or strangulation suspected
SBO due to malignancy / carcinomatosis
Multidisciplinary discussion (palliative care, oncology, surgery)
Palliative interventions: venting gastrostomy, octreotide for symptom relief, palliative surgery (bypass, ostomy) if appropriate
Avoid surgery in patients with diffuse carcinomatosis and short life expectancy
Complications
Strangulation, ischemia, perforation
Sepsis, septic shock
Bowel necrosis requiring resection
Short bowel syndrome (extensive resection)
Aspiration pneumonia (from vomiting)
Volume depletion, electrolyte derangement, AKI
Recurrent SBO
Postoperative ileus, adhesions
Mortality: 2-10% simple obstruction; up to 30% with strangulation/delayed surgery
PANCE pearls
Always examine ALL hernia orifices in a patient with SBO — incarcerated hernia is the 2nd most common cause and the most easily missed.
Hypokalemic, hypochloremic metabolic alkalosis is the classic acid-base disturbance from upper GI fluid losses.
CT is the modality of choice — identifies transition point, cause, closed loop, and signs of ischemia.
Gastrografin (water-soluble contrast) challenge is both diagnostic and therapeutic — passage to colon within 24 h predicts successful non-operative management of adhesive SBO.
Closed-loop obstruction (bowel obstructed at two adjacent points) → high risk of strangulation; surgical emergency.
Virgin abdomen (no prior surgery) with SBO — strongly consider alternative cause (hernia, malignancy, Crohn, intussusception); proceed earlier to operation.
Adhesive SBO: 65-80% resolve without surgery; failure to resolve by 48-72 h warrants operation.
Gallstone ileus (Rigler triad): pneumobilia + SBO + ectopic gallstone — treat with enterolithotomy; cholecystectomy ± fistula repair often staged.
Bezoars (phytobezoars from fiber, trichobezoars from hair) — endoscopic disruption ± enzymatic dissolution (Coca-Cola for phytobezoar).
References
EAST 2019 — Maung AA et al. Evaluation and Management of Small-Bowel Obstruction: An Eastern Association for the Surgery of Trauma Practice Management Guideline. J Trauma Acute Care Surg 2019
WSES 2017 — Ten Broek RPG et al. Bologna guidelines for diagnosis and management of adhesive small bowel obstruction (ASBO). World J Emerg Surg 2018;13:24
Gastrografin Trial — Branco BC et al. Systematic review and meta-analysis of the diagnostic and therapeutic role of water-soluble contrast agent in adhesive SBO. Br J Surg 2010;97:470-478
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