Bradley Phillips
A 47-year-old female with a medical history of right nephrectomy complicated by incisional “Swiss cheese” ventral hernias with recurrent incarceration and bowel strangulation presented to the ED with acute abdominal pain localized to the ventral hernia, nausea, and vomiting.
About three years earlier, the patient had undergone an exploratory laparotomy while admitted for peritonitis, which revealed an ischemic segment of small bowel and incarcerated omentum within a ventral hernia. She then underwent omentectomy, small bowel resection with primary anastomosis, and ventral hernia repair.
Following this surgery, the patient had recurrence of the hernia and frequent admissions for small bowel obstruction (SBO), all managed nonoperatively with nasogastric tube decompression and small bowel follow-through. She was discharged from the last such admission the day before presentation, and at that time was tolerating a liquid diet, passing flatus and having bowel movements. She believed that advancing her diet at home had triggered her symptoms, which included 6-7 episodes of non-bloody, non-bilious emesis following a solid meal.
Vitals: BP 128/83 mmHg | Pulse 103 | Temp 98.7 °F (37.1 °C) | Resp 16 | SpO2 93%
On physical examination, the patient was in acute distress and tachycardic. Abdominal exam revealed distension, tenderness in the periumbilical area, and guarding without rebound, as well as a large ventral hernia adjacent to a well-healed midline scar. The right side of the hernia was firmer than the left side but was mostly reducible.
A focused bedside ultrasound exam of the bowel was performed using the curvilinear transducer.
Figure 1. A dilated loop of small bowel, shown here in long axis, measures 3.78 cm in diameter. Bowel wall distension increases the visibility of the plicae circulares.
Figure 2: A loop of small bowel shown in long axis with bidirectional intraluminal content flow, also known as to-and-fro peristalsis.
Computed tomography of the abdomen showed dilated loops of small bowel measuring up to 3.9 cm with fecalization of the internal contents and a transition point at the anastomotic site at the hernia mouth, confirming SBO. There was no radiographic evidence of ischemia or perforation. General surgery was consulted. It was thought that the obstruction was likely due to adhesions or stenosis at the prior anastomosis and unrelated to the large ventral hernia.
The patient was admitted and treated conservatively with intravenous fluids and nasogastric tube decompression. Small bowel follow-through showed delayed passage of contrast and slow return of bowel function. She was discharged on a full liquid diet with planned follow-up with minimally invasive surgery for complex hernia repair.
Discussion
SBO is a significant cause of morbidity and hospital admissions. In the United States, the annual incidence of SBO is approximately 350,000 cases [1,2]. Prolonged obstruction can cause intestinal ischemia and necrosis of the bowel wall [3]. Combined with increased intraluminal pressure from the obstruction, this can lead to bowel perforation, peritonitis, and sepsis. The overall mortality rate for SBO is approximately 10%, but it can increase to 30% in cases complicated by bowel necrosis or perforation [1].
Adhesions are the most common cause of SBO, responsible for 65-74% of cases, and typically result from previous abdominal or pelvic surgeries. Other risk factors for SBO include hernias, neoplasms, Crohn disease, radiation enteritis, volvulus and foreign bodies [1,4].
Patients with SBO typically present with abdominal pain (often colicky and centrally located), nausea and vomiting, and constipation or obstipation. On physical examination, there may be abdominal distension. Early in the course of the obstruction, bowel sounds may be high-pitched and hyperactive. Advanced SBO can present with hypoactive or absent bowel sounds as well as severe abdominal tenderness with signs of peritoneal inflammation [1,5-6]. An elevated lactate supports clinical concern for bowel ischemia [7-8]. This patient’s lactate was normal at 1.1 mmol/L, although at the time of her episode of bowel strangulation and ischemia three years earlier, it was 2.5 mmol/L (elevated).
The differential diagnosis of SBO includes the myriad non-obstructive causes of nausea, vomiting, and abdominal pain; functional small bowel obstruction (adynamic ileus, pseudo-obstruction); and large bowel obstruction.
If SBO is suspected, the American College of Radiology recommends early imaging, particularly abdominal CT, to evaluate the severity of the obstruction, identify the etiology, and detect complications such as volvulus, strangulation, closed-loop obstruction, and ischemia [5]. However, point-of-care ultrasound (POCUS) has been shown to have a sensitivity of 83% to 92% and specificity of 93% to 96% in the evaluation of SBOs, and its use can save time and reduce radiation exposure [9,10].
When performing a POCUS exam for SBO, the curvilinear probe should be used for adult patients. The exam can be started at the patient-identified point of maximum tenderness, with the examiner applying graded compression to slowly and gently displace air out of the way of the probe. Segments of small bowel should be inspected in both long and short axis for dilation (diameter greater than 2.5 cm), absent or to-and-fro peristalsis, the presence of a transition point, free fluid, and bowel wall edema. Once an area of interest is identified, examiners can switch to the linear probe to increase image resolution [11].
The presence of a transition point is highly specific for SBO, as it is not seen in ileus. On ultrasound, a transition point will appear as an area of dilated bowel adjacent to an area of decompressed bowel. In the duodenum and jejunum, bowel wall distension can increase the visibility of the plicae circulares. An edematous bowel wall appears thickened on ultrasound with decreased echogenicity [11].
Management of small bowel obstruction (SBO) involves both nonoperative and operative strategies, depending on the patient's clinical presentation and response to initial treatment. Surgical intervention is indicated in cases of generalized peritonitis or signs of bowel ischemia (e.g., fever, leukocytosis, tachycardia, metabolic acidosis, or evidence of ischemia on imaging) or if the obstruction fails to resolve after 3 days of nonoperative management [2,12].
The risk of recurrence of adhesive small bowel obstruction is higher in patients who are managed nonoperatively compared to those who undergo surgical management, with recurrence rates ranging from 13% to 29% over long-term follow-up periods. The risk of recurrence also increases with the number of prior SBO episodes [13-15].
References
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