A 66-year-old man with a history of benign prostatic hyperplasia and obstructive sleep apnea presented to the emergency department (ED) with subacute abdominal pain that had become much worse the previous evening. He reported relatively mild abdominal pain for the past 2–3 weeks, which was described as in his "mid-abdomen and crampy." The previous night, soon after eating dinner, he developed severe mid-abdominal pain that did not radiate and did not remit. He had never experienced abdominal pain of this severity. He reported no nausea, vomiting, diarrhea, fevers, chills, weight loss, or night sweats. He did report occasional constipation but had a normal bowel movement the day prior to presentation. The patient had never had a colonoscopy. On initial evaluation, the patient had stable vital signs, a tender abdomen without rebound or guarding, and unremarkable laboratory test results. A CT of his abdomen/pelvis noted mild dilation of the ascending, transverse, and proximal descending colon with associated air-fluid levels in the ileum and a possible "transition point concerning for stricture/mass or physiologic peristalsis."
Because the patient appeared well, he was admitted to the medicine (instead of surgery) service for observation, pain control, and serial abdominal exams. Surgical consultation was not requested at time of admission. Approximately 48 hours into the hospitalization, the patient's abdomen became more distended, with increased abdominal pain and tenderness with rebound on exam. A surgical consultation was requested. After the surgeons reviewed the imaging and performed a physical examination, they took the patient urgently to the operating room, where an obstructive mass with associated perforation was noted. The patient had a prolonged postoperative course with intra-abdominal infection before ultimately dying. The institution formally reviewed the case because of concerns regarding a possible delay in treatment and surgical consultation.
by Jonathan Carter, MD
This case illustrates the difficulty in diagnosing a strangulating bowel obstruction on the basis of clinical features and modern imaging. This comes as no surprise. For more than 50 years, there have been numerous attempts to identify predictors of strangulating obstruction on the basis of symptoms, signs, laboratory tests, and imaging characteristics.(1-3) Sadly, such attempts have failed. There is simply no good predictor, or combination of predictors, that allows accurate identification of a strangulating bowel obstruction. Even experienced intestinal surgeons can miss the diagnosis.
This fact is disheartening, given that intestinal obstruction is one of the most common surgical emergencies in the United States, resulting in more than 300,000 intestinal operations per year.(4,5) About 75% of intestinal obstructions in the US are caused from adhesions from prior operations.(6) The remaining obstructions are caused by Crohn disease, neoplasia, hernia (internal or abdominal wall), radiation, congenital adhesions, or other causes.(6) Patients with intestinal obstruction present with abdominal pain, nausea, vomiting, bloating, distension, and obstipation. Early in the illness, hyperperistalsis may produce loose stools, as the bowel downstream evacuates itself. By the time the patient presents to the physician, however, diarrhea is rarely a prominent symptom. Signs are abdominal distension, tenderness, oliguria, tachycardia, dry mucous membranes, and in some cases, peritonitis. Bowel auscultation provides no useful information—hyperactive, normal, and quiet bowel sounds are all compatible with obstruction. As the disease progresses, the obstructed bowel becomes edematous, dilated, and overgrown with bacteria. Luminal pressure exceeds capillary perfusion pressure, resulting in ischemia of the intestinal wall. Peritonitis ensues, followed by perforation and sepsis. Ultimately, if the process goes uninterrupted, death may result, from either septic or hypovolemic shock.
Initial evaluation should include assessment of cell blood counts, electrolytes, creatinine, urine output, and vital signs. Both metabolic alkalosis (from vomiting) and metabolic acidosis can be seen. Although serum lactate is frequently measured, it has no predictive value for strangulating obstruction.(1-3) Initial management is bowel rest, resuscitation with an isotonic crystalloid solution, serial abdominal exams, and nasogastric tube suction. The nasogastric tube is really just for patient comfort and may be omitted if the patient is not retching.
The best imaging study for intestinal obstruction is a CT of the abdomen and pelvis, with IV contrast and without oral contrast.(1,7-11) Plain films of the abdomen add little; they are useful to confirm the diagnosis of bowel obstruction in lieu of a CT scan for patients with recurrent obstructions who present with typical symptoms. The classic findings for intestinal obstruction are proximally dilated bowel (less than 3 cm), with air-fluid levels, terminating in a transition point, followed by decompressed bowel and colon. Findings that raise concern for strangulation are ascites, thick-walled bowel, segmental mesenteric fluid, free air, mesenteric stranding, decreased mucosal enhancement, pneumatosis, and a closed loop (i.e., dilated bowel, pinched on both ends). Of these, one multivariate analysis showed that decreased mucosal enhancement was the only independent predictor of strangulating obstruction.(1) The identification of a so-called transition point does not help the clinician know if a strangulating obstruction is present. Rather, it can help differentiate mechanical bowel obstruction from adynamic ileus, or alternatively, suggest that a neoplastic process is the cause of the obstruction.
Once the diagnosis of intestinal obstruction had been established, the first question is whether any features of strangulation are present. Fever, tachycardia, leukocytosis, constant pain (as opposed to colicky pain), and peritonitis are still taught to be the five cardinal signs of strangulation. Unfortunately, even these classic signs have poor positive and negative predictive value. Decreased mucosal enhancement on CT is a powerful predictor of strangulating obstruction, and when accompanied by leukocytosis, peritonitis, or other worrisome CT findings noted above, it is an indication for surgical exploration.
In this case, several features of the obstruction warranted early surgical evaluation. First, no prior abdominal operation had been performed, making adhesions unlikely to be the culprit (congenital adhesions do exist, but they are rare). Of the remaining causes of obstruction, most require an operation. Second, a strong argument can be made for early laparoscopic evaluation in this setting, both to confirm the diagnosis and to treat the offending lesion that may be found at laparoscopy.(12) Third, the radiographic reporting deserves scrutiny—was the transition point in the small bowel or colon? Were any concerning features of strangulation present? Is neoplasia suspected? Commonly, in-person review of the CT scan with the radiologist can clue the treatment team into subtle signs of strangulation, which in turn raises index of suspicion and prompts earlier surgical evaluation. In this case, it is unlikely that the patient progressed to perforation in 48 hours without subtle warning signs on the index CT; these signs may not have appeared in the dictated report.
As this case illustrates, a patient can have strangulated bowel with no clinical or radiographic predictors at the time of presentation—a surgeon would not have necessarily found the diagnosis early on. So we must add time as one of our diagnostic tests. With close observation and serial examinations, a physician comes to understand the trajectory of the patient's illness. Here's a practice pearl: "Obstructions destined to resolve nonoperatively generally do so within 72 hours. A patient who is getting sicker needs urgent surgical evaluation."
Finally, this case begs the question: "Is a patient with intestinal obstruction better served on a medicine or surgical service?" The University of Michigan developed and validated a triage protocol to address this issue.(13) Patients were admitted to medicine when obstruction was from intra-abdominal metastases, active inflammatory bowel disease, or when the patient had acute, severe medical conditions requiring stabilization (such as acute myocardial infarction and severe chronic obstructive pulmonary disease exacerbation). Additionally, patients with known dilated bowel secondary to chronic narcotic-induced obstipation, chronic psychotropic medication usage, cystic fibrosis, collagen vascular diseases, or other motility disorders were admitted to medicine. The remaining patients—largely those with classic small bowel obstructions due to adhesions without significant medical comorbidities—were admitted by surgeons. The protocol shortened the time to operation and length of stay for those operated upon, while reducing time to surgical consultation.(13) Unfortunately, many hospitals now lack adequate surgical coverage, so in the future we may see increasing number of patients with intestinal obstruction managed, at least initially, by nonsurgeons.
- Strangulating intestinal obstruction remains challenging to diagnose. No clinical signs, symptoms, laboratory values, or radiographic findings reliably identify patients with strangulating obstruction. Often, time and observation are the best diagnostic tools.
- Obstructions in patients without a history of abdominal surgery are uncommon and warrant early surgical evaluation.
- The test of time is one of the most important in intestinal obstruction. Those obstructions destined to resolve without surgery generally do so within 72 hours.
- Most intestinal obstructions are best managed by surgeons; protocol-driven triage may improve patient outcomes.
Jonathan Carter, MD Associate Professor of Surgery Division of General Surgery University of California, San Francisco San Francisco, CA
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