Last reviewed: March 2026
Contents
MDM Templates
Small Bowel Obstruction
Patient presents with abdominal pain, vomiting, and distension. Imaging demonstrates small bowel obstruction with a transition point at ***. No CT findings of closed-loop obstruction, bowel wall ischemia, or perforation.
History, exam, and imaging not consistent with mesenteric ischemia, bowel gangrene, abscess, or peritonitis at this time.
Plan: NPO, NG tube placed to low intermittent suction. IV fluid resuscitation — normal saline with 40 mEq KCl for replacement of NG output losses. Analgesia and antiemetic. Surgery consulted.
Disposition: Admit. Serial abdominal exams. Operative intervention if clinical deterioration, signs of strangulation, or failure to improve with conservative management within 48–72 hours.
If concern for closed-loop or strangulation:
Imaging concerning for closed-loop obstruction / strangulated bowel — ***. Signs of bowel ischemia present (wall thickening, mesenteric haziness, reduced enhancement). Surgery consulted emergently. Broad-spectrum antibiotics initiated — piperacillin-tazobactam 3.375 g IV.
Disposition: Admit to surgery for emergent operative intervention.
Large Bowel Obstruction / Volvulus
Patient presents with abdominal distension, obstipation, and pain. Imaging demonstrates large bowel obstruction / volvulus at ***.
If sigmoid volvulus without perforation or ischemia:
Imaging consistent with sigmoid volvulus without evidence of perforation or bowel ischemia. GI consulted for endoscopic decompression with rectal tube placement. Surgery aware. No peritoneal signs on exam.
Disposition: Admit. Endoscopic decompression attempted first; surgical intervention if unsuccessful or if recurrent.
If cecal volvulus or ischemia/perforation:
Imaging demonstrates cecal volvulus / volvulus with signs of ischemia or perforation. Surgery consulted emergently for operative management. IV antibiotics initiated. IV fluid resuscitation.
Disposition: Admit to surgery.
IBD Flare
Patient with known inflammatory bowel disease (Crohn disease / ulcerative colitis) diagnosed *** years ago presents with bloody diarrhea, abdominal cramping, and tenesmus consistent with an acute flare. Current presentation is similar to prior flares. Well appearing without peritoneal signs, hemodynamically stable.
History, exam, and labs not consistent with toxic megacolon, perforation, abscess, significant GI hemorrhage, SBO, or serious bacterial illness including C. difficile. Stool studies sent including C. difficile.
If mild-moderate flare:
Plan: Prednisone 40 mg daily initiated for symptomatic relief with taper planned. Anti-diarrheal agents deferred in active inflammation. Patient to continue maintenance medications.
Disposition: Discharge with GI follow-up within 1 week for flare management and stool study results. Return for bloody diarrhea, fever, severe abdominal pain, or inability to tolerate PO.
If severe flare or new diagnosis:
Patient with severe IBD flare — *** (hemodynamic instability, significant anemia, fever, peritoneal signs). IV steroids initiated — methylprednisolone 60 mg IV daily. GI consulted. NPO with IV fluids.
Disposition: Admit. Inpatient GI evaluation for possible rescue therapy (infliximab, cyclosporine) or surgical consultation if refractory.
Ischemic Colitis
Patient (elderly, with vascular risk factors) presents with acute onset crampy abdominal pain followed by bloody diarrhea. Imaging demonstrates colonic wall thickening at the *** consistent with ischemic colitis. No evidence of perforation, pneumatosis, or portal venous gas.
History and exam consistent with non-occlusive ischemic colitis — the most common form, typically affecting the watershed areas (splenic flexure, rectosigmoid junction). Most cases are self-limiting.
Plan: IV fluids, bowel rest, serial abdominal exams. Broad-spectrum antibiotics if concern for transmural ischemia or sepsis.
Disposition: Admit for observation and supportive care. Surgery consulted if peritoneal signs, hemodynamic instability, or failure to improve.
Acute Mesenteric Ischemia
Patient presents with severe abdominal pain out of proportion to exam — classic for acute mesenteric ischemia. History of atrial fibrillation / vascular disease / recent cardiac event. CT angiography demonstrates ***.
This is a vascular emergency. Heparin anticoagulation initiated. Surgery and vascular surgery consulted emergently. Broad-spectrum antibiotics initiated. Aggressive IV fluid resuscitation. Lactate elevated at ***.
Disposition: Admit to surgery / ICU for emergent intervention — surgical embolectomy, endovascular thrombectomy, or bowel resection depending on findings.
Clinical Education
SBO Pearls
Adhesions from prior surgery are the most common cause of SBO (~60%), followed by hernias (~15%) and malignancy (~5%). Always ask about surgical history and examine the groin for incarcerated hernias — this is the most treatable cause and the most commonly missed on initial evaluation.[1]
CT abdomen/pelvis with IV contrast is the study of choice — sensitivity >90% for SBO. Key findings: dilated small bowel (>3 cm) proximal to a transition point, decompressed bowel distal. CT also identifies strangulation (reduced bowel wall enhancement, mesenteric haziness, free fluid) and closed-loop obstruction (C-shaped or U-shaped bowel with radial mesentery converging to a point).[2]
Oral contrast is not needed for SBO diagnosis and delays imaging. The retained intraluminal fluid already serves as natural contrast.
Signs that suggest operative (rather than conservative) management: Complete obstruction, closed-loop, strangulation signs on CT, peritonitis on exam, fever with leukocytosis, failure to improve after 48–72 hours of conservative management.[1]
LBO and Volvulus Pearls
Sigmoid volvulus accounts for ~75% of colonic volvulus. Classic X-ray: “bent inner tube” or “coffee bean” sign. CT is more sensitive. First-line treatment is endoscopic decompression with rectal tube placement — success rate ~80%. However, recurrence is >50%, so most patients ultimately need surgical management (sigmoidectomy).[3]
Cecal volvulus requires surgery — endoscopic decompression does not work. CT shows a dilated, displaced cecum in the left upper quadrant (“whirl sign” at the twist point). This is an operative emergency.
The critical cecal diameter is 12 cm. Beyond this, the risk of perforation increases significantly. In any large bowel obstruction, a cecal diameter approaching or exceeding 12 cm warrants urgent surgical consultation.
IBD Pearls
Always send C. difficile in an IBD flare. C. diff is more common in IBD patients than the general population and can mimic or trigger a flare. Starting steroids in a patient with C. diff infection worsens outcomes.[4]
Toxic megacolon is the can’t-miss complication. Transverse colon diameter > 6 cm with systemic toxicity (fever > 38.5°C, tachycardia, leukocytosis, anemia) is diagnostic. NPO, NGT for decompression, IV steroids, and emergent surgical consultation. If no improvement in 24–72 hours, colectomy is indicated.[5]
Steroid dosing for IBD flare: Mild-moderate: prednisone 40 mg daily with taper (reduce by 5–10 mg/week). Severe/hospitalized: methylprednisolone 60 mg IV daily. Do not use anti-diarrheals (loperamide) in severe colitis — they can precipitate toxic megacolon.
Crohn disease can cause SBO. Stricturing disease in the terminal ileum is the classic scenario. This may be inflammatory (responds to steroids) or fibrotic (needs surgery). CT helps differentiate — active inflammation shows wall enhancement and mesenteric hypervascularity.
Mesenteric Ischemia Pearls
“Pain out of proportion to exam” is the classic teaching, but it’s only present early. Once bowel necrosis occurs, the patient develops peritonitis and the exam catches up to the pain. By then, mortality approaches 60–80%. The key is suspecting it early — in any elderly patient with atrial fibrillation, heart failure, or recent cardiac event who presents with acute severe abdominal pain.[6]
CTA is the study of choice — sensitivity >95% for arterial occlusion. Elevated lactate is a late finding suggesting bowel necrosis and is not useful for early diagnosis. D-dimer may have a role as a screening test (high sensitivity, low specificity).
Four types of acute mesenteric ischemia: SMA embolism (50%, classically from afib), SMA thrombosis (25%, in patients with chronic mesenteric ischemia), mesenteric venous thrombosis (5–15%, associated with hypercoagulable states), and non-occlusive mesenteric ischemia (NOMI, 20%, from low-flow states — shock, vasopressors, cocaine).[6]
Ogilvie Syndrome
Ogilvie syndrome (acute colonic pseudo-obstruction) presents as massive colonic dilation without a mechanical obstruction. Occurs in hospitalized, post-operative, or debilitated patients. CT shows dilated colon (often right > left) without a transition point. Treatment is conservative (bowel rest, ambulation, correction of electrolytes), neostigmine 2 mg IV for refractory cases, or colonoscopic decompression. Cecal diameter > 12 cm or duration > 6 days increases perforation risk.[7]
Disposition
Admit if: SBO (for surgical evaluation and serial exams), LBO/volvulus, severe IBD flare, toxic megacolon, acute mesenteric ischemia, ischemic colitis, peritonitis, or hemodynamic instability.
Discharge if: Partial SBO with improving symptoms after trial of conservative management (discuss with surgery), mild IBD flare with reliable follow-up, ischemic colitis with resolved symptoms and reassuring imaging (rare — most are admitted for observation).
References
- 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. 2012;73(5 Suppl 4):S362-S369. PubMed
- Defined A et al. CT of small-bowel obstruction. AJR Am J Roentgenol. 2012;198(5):W458-W464.
- Halabi WJ et al. Sigmoid volvulus: demographics, treatment, and outcomes in the United States. Am J Surg. 2014;208(3):384-391. PubMed
- Ananthakrishnan AN et al. Excess hospitalisation burden associated with Clostridium difficile in patients with inflammatory bowel disease. Gut. 2008;57(2):205-210. PubMed
- Sheth SG, LaMont JT. Toxic megacolon. Lancet. 1998;351(9101):509-513. PubMed
- Bala M et al. Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery. World J Emerg Surg. 2022;17(1):54. PubMed
- Saunders MD, Kimmey MB. Systematic review: acute colonic pseudo-obstruction. Aliment Pharmacol Ther. 2005;22(10):917-925. PubMed
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