Purpose of review: This study aimed to systematically review small bowel obstruction (SBO), focusing on recent changes in diagnosis/therapy.

Recent findings: SBO incidence is about 350,000/annum in the USA. Etiologies include adhesions (65%), hernias (10%), neoplasms (5%), Crohn's disease (5%), and other (15%). Bowel dilatation occurs proximal to obstruction primarily from swallowed air and secondarily from intraluminal fluid accumulation. Dilatation increases mural tension, decreases mucosal perfusion, causes bacterial proliferation, and decreases mural tensile strength that increases bowel perforation risks. Classical clinical tetrad is abdominal pain, nausea and emesis, abdominal distention, and constipation-to-obstipation. Physical exam may reveal restlessness, acute illness, and signs of dehydration and sepsis, including tachycardia, pyrexia, dry mucous membranes, hypotension/orthostasis, abdominal distention, and hypoactive bowel sounds. Severe direct tenderness, involuntary guarding, abdominal rigidity, and rebound tenderness suggest advanced SBO, as do marked leukocytosis, neutrophilia, bandemia, and lactic acidosis. Differential diagnosis includes postoperative ileus, narcotic bowel, colonic pseudo-obstruction, mesenteric ischemia, and large bowel obstruction. Medical resuscitation includes intravenous hydration, correcting electrolyte abnormalities, intravenous antibiotics, nil per os, and nasoenteral suction. Abdominal CT with oral and intravenous gastrografin contrast is highly sensitive and specific in detecting/characterizing SBO. SBO usually resolves with medical therapy but requires surgery, preferentially by laparoscopy, for unremitting total obstruction, bowel perforation, severe ischemia, or clinical deterioration with medical therapy. Overall mortality is 10% but increases to 30% with bowel necrosis/perforation. Key point in SBO is early diagnosis, emphasizing abdominal CT; aggressive medical therapy including rehydration, antibiotics, and nil per os; and surgery for failed medical therapy.