Introduction
Superior mesenteric artery syndrome (SMAS), also known as Wilkie or cast syndrome, is a rare condition caused by compression of the duodenal third portion between the superior mesenteric artery (SMA) and abdominal aorta, leading to duodenal obstruction. Its incidence in the general population ranges from 0.013% to 0.3%, with pediatric cases being particularly uncommon. SMAS may occur idiopathically or secondary to predisposing factors such as rapid weight loss, anatomical variations, or abdominal trauma (1,2).
The primary pathophysiological mechanism involves a reduction in aorto-mesenteric angle (AMA), most often due to loss of mesenteric and retroperitoneal fat following extensive weight loss (3). A key diagnostic feature is a decreased AMA, typically <30°, compared with normal values ranging between 38° and 65° (4). This narrowing results in compression of the duodenal third portion between the SMA and abdominal aorta, producing upper gastrointestinal obstruction. Despite growing knowledge of the anatomical alterations involved, diagnosis is frequently delayed because of its insidious and nonspecific presentation (5). Typical symptoms include postprandial epigastric pain, nausea, vomiting, early satiety, and weight loss, reflecting duodenal compression (6).
Posttraumatic SMAS in pediatric patients is rarely reported and represents a diagnostic challenge due to overlap with other trauma-related complications, such as retroperitoneal hematoma, bowel ischemia, or postoperative ileus. We report an 8-year-old boy who developed SMAS after a high-speed motor vehicle collision resulting in a Chance fracture requiring spinal fixation, successfully managed with conservative treatment. Informed consent for publication was obtained from the patient’s parents, with assent from the patient.
Case
An 8-year-old boy was a restrained passenger in a car involved in a high-speed head-on motor vehicle collision. Two other occupants of the vehicle died at the scene or during transport to the hospital. The patient was initially evaluated in a regional hospital trauma bay where he was alert with a Glasgow Coma Scale score of 15. The initial vital signs were as follows: blood pressure, 124/83 mmHg; heart rate, 109 beats/minute; respiratory rate, 16 breaths/minute; and oxygen saturation, 100% on a 35% fraction of inspired oxygen via Venturi mask. He weighed 35 kg. Initial whole-body computed tomography (CT) showed a traumatic left diaphragmatic hernia with herniation of the stomach, spleen, colon, and small bowel into the thoracic cavity, resulting in near-complete collapse of the left lung. Additional injuries included lacerations of the liver (American Association for the Surgery of Trauma Organ Injury Scale grade IV) and spleen (grade III), left renal artery thrombosis, mesenteric root injury with suspected vascular compromise of the splenic flexure, and an L1–L2 Chance fracture-dislocation with posterior ligamentous complex disruption.
Due to respiratory distress and hemodynamic instability on day 1, the patient was intubated, resuscitated with intravenous fluids (up to 45 mL/kg), and started on a continuous infusion of epinephrine at 0.1 µg/kg/minute during transport to our pediatric trauma center. Following transient stabilization, exploratory laparotomy was performed. The diaphragmatic defect was repaired primarily. Liver and spleen injuries were managed with topical hemostatic agents. A jejunal perforation approximately 15 cm distal to the ligament of Treitz and colonic ischemia of the splenic flexure required segmental jejunal resection with primary anastomosis and segmental colonic resection with primary anastomosis. A large retroperitoneal hematoma limited visualization of the left kidney; given complete thrombosis and infarction on preoperative imaging, no renal intervention was undertaken.
Postoperatively, the patient was hospitalized to the intensive care unit and extubated on day 4, with gradual reintroduction of oral intake. Percutaneous L1–L2 transpedicular fixation was performed on day 6. On day 12, he developed bilious vomiting, abdominal distension, and feeding intolerance without prior weight loss. CT performed on the same day demonstrated marked gastric and duodenal dilation with abrupt narrowing at the third portion of the duodenum and a reduced AMA (Figure 1). Upper gastrointestinal series confirmed complete duodenal obstruction without other mechanical causes, consistent with SMAS (Figure 2).
A conservative approach was adopted, consisting of nasogastric decompression followed by fluoroscopy-guided placement of a nasojejunal feeding tube on day 13. The patient showed progressive clinical improvement, achieving full oral intake without parenteral nutrition. The nasojejunal tube was removed on day 19. Antihypertensive therapy was required due to renal ischemia. He was discharged on day 21, asymptomatic, tolerating a full oral diet, mobilizing independently, with stable renal function, controlled blood pressure, resolution of cranial nerve palsy, and a functional solitary kidney.
Discussion
SMAS secondary to abdominal trauma is rare, and its association with Chance fracture has only been documented exceptionally. To our knowledge, the only case explicitly linking SMAS to Chance fracture is that reported by Singla et al. in the context of seatbelt syndrome (7). Direct or indirect injury to the mesenteric root, together with peri-visceral edema, hematoma, or inflammatory changes, may contribute to transient narrowing of AMA and subsequent duodenal compression (3).
In the patient, SMAS manifested 5 days after posterior spinal fixation for the L1–L2 Chance fracture and approximately 11 days after the initial trauma. Prior to the symptom onset, he tolerated oral intake without evidence of weight loss or nutritional compromise. The close anatomical relationship between the L1–L2 vertebral level and the duodenal third portion suggests that perioperative factors, such as surgical manipulation, retroperitoneal edema, or hematoma, likely precipitated localized inflammation and transient functional narrowing of AMA, rather than weight loss.
No evidence of the duodenal third portion was seen on the sagittal reconstruction of the initial CT scan performed at the regional hospital. At that time, the patient had a large traumatic diaphragmatic hernia with cranial displacement of the stomach and proximal bowel, likely preventing the typical compression of the duodenum between the SMA and aorta. Therefore, SMAS developed later during the postoperative course rather than being present at initial evaluation.
Although SMAS can occur across a broad demographic spectrum, it is most frequently observed in adolescents or young adults, and diagnosis is often delayed due to the nonspecific presentation (8). In pediatric trauma patients, SMAS is particularly rare and may be overlooked, potentially leading to complications such as malnutrition, electrolyte imbalance, or gastric perforation (6,9). Diagnosis relies on imaging, with contrast-enhanced CT and upper gastrointestinal series considered the imaging modality of choice, demonstrating duodenal dilatation, abrupt obstruction at the duodenal third portion, and a narrowed AMA (8,10-13).
Initial management is conservative and aimed at relieving vascular compression and restoring nutritional status. Enteral feeding via a nasojejunal tube is preferred, while total parenteral nutrition may be required if enteral intake is not tolerated. Postural measures may provide additional symptomatic relief (13-15). Surgical intervention, most commonly duodenojejunostomy, is reserved for refractory cases (11,12). In the patient, early recognition and nasojejunal enteral feeding led to progressive symptom resolution without the need for parenteral nutrition or surgical bypass.
This case adds to the limited literature on posttraumatic SMAS in pediatric patients, particularly following spinal trauma, and highlights that the condition may develop in the postoperative period even when it is absent on initial imaging. For emergency physicians and trauma surgeons, SMAS should be considered in pediatric patients presenting with persistent bilious vomiting and gastric dilatation after spinal or abdominal trauma. Prompt imaging and early conservative management can lead to favorable outcomes while avoiding unnecessary surgical intervention.
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