Also known as Wilkie syndrome is a duodenal obstruction resulting from compression of the third duodenal portion during the passage between superior mesenteric artery and the aorta, following the disappearance of perivascular fatty tissue [1]. Thus, major burns, major surguries, cancer patients, malnourished patients, surgery involving traction on the mesentery, spinal deformity correction surgery are the risk factors of predisposition to this syndrome [2],[3]. Clinical findings of duodenal obstruction are epigastric pain, vomiting, anorexia, and weight loss [1]. Surgical treatment is recommended in case of failure of medical treatment [1]. Our concern is what the best treatment is and when to undertake it.

A 64-year-old female patient widowed followed for Helicobacter pylori gastritis who was admitted in emergency room for anorexia, vomiting, abdominal pain, and weight loss evolving context of deterioration in general condition since three months. Clinical examination revealed a hypotension with blood pressure of 80/40 mmHg, heartbeat of 130 beat per minute, body mass index (BMI) of 15.08 kg/m², skin folds of dehydration, and epigastric region lapping. The biological assessment was disturbed as recorded in Table 1. An abdominal computed tomography (CT) scan requested urgently demonstrated a reduction in the aorto-mesenteric space not exceeding 5 mm with aorto-mesenteric angle measuring 19° (Figure 1). Medical management was first undertaken: urinary catheter, nasogastric tube, parenteral fluid, and electrolyte supplies within 72 hours without therapeutic success. Thus, a surgical option was undertaken with a laparotomic approach: supra-umbilical midline incision. On exploration, we found a duodenal and gastric distension upstream of the obstacle while the small intestine was collapsed downstream of the obstacle (Figure 2). The surgical procedure performed was gastro-entero-anastomosis (Figure 3A and Figure 3B), the nasogastric tube was removed two days after the surgery and oral feeding was authorized five days postoperative. The good clinical and biological evolution allowed the patient to be discharged ten days postoperative.

However, five days after discharging, the patient was readmitted to hospital for intermittent vomiting. Then, both biological and radiological investigations led to the conclusion of the diagnosis of gastroparesis (delay gastric emptying). The following arguments led to confirm this diagnosis: persistence of hydroelectrolytic disorders; disruption of the glycemic cycle; anastomotic permeability evidence on frontal abdominal X-ray performed after ingestion of product of contrast (poc) showing gastric atony and the presence of product in the small intestine (Figure 4). Thus, medical treatment based on prokinetics was instituted. The patient presented melena which led to perform a colonoscopy coupled with biopsies which highlighted at 15 cm from the anal margin an erythematous area and ulcerations mucosa at 30 cm from the anal margin (Figure 5A and Figure 5B). The histological examination of the biopsies concluded to subacute ulcerative rectosigmoiditis of non-specific appearance with foci of high-grade dysplasia, subacute mucoerosive colitis with foci of low-grade dysplasia, and other foci of high-grade.

Following the patient’s hemodynamic instability, she was transferred to the intensive care unit where she died.

In 1927, Wilkie described the first series of 75 patients and since then this syndrome bears his name [1]. While the duodenum is protected by fatty tissue perivascular, this syndrome occurs during rapid weight loss following the decompensation of a pre-existing tare [2],[4]. Our patient had clinical manifestations: vomiting, abdominal pain, while other studies reported a chronic clinical expression made up of repeated postprandial plenitudes and intermittent vomiting [1],[2]. In our patient, the angle between the superior mesenteric artery and the aorta was 19° and the aorto-mesenteric space was reduced to 5 mm while the normal values of the angle and the aorto-mesenteric space are respectively 25° and 60 at 10 mm and 28 mm [1],[5]. The goal of treatment is to break the dehydration and malnutrition caused by duodenal occlusion [4]. The effectiveness of medical treatment is estimated at 72% while recurrence is about 30% of cases [6]. However, the duration of medical treatment varies between two and twelve days even if a period of 169 days of successful treatment has been reported in child case study [1],[6]. For our patient, given her precarious nutritional state, BMI collapsed, a period of three days was granted for medical treatment. Several surgical techniques have been described, either derivation by gastro-jejunostomy or duodeno-jejunostomy or mobilization and uncrossing of the duodeno-jejunal angle by positioning the jejunum to the right of the superior mesenteric artery after sectioning the Treitz ligament according to Strong [1]. However, Strong’s procedure is not practicable in all patients due to duodenal distension with failure risk [1]. Our patient underwent a gastro-entero-anastomosis dictated by local conditions: duodenal and gastric distension.

Concerning her gastroparesis, a diet low in fat and fiber was recommended [7]. Prokinetics associated with the correction of the blood sugar, which was disturbed in our patient, by using insulin therapy allowed our patient to progress positively [8],[9].

Superior mesenteric artery syndrome is rare, sometimes unrecognized entity. Delay in diagnosis and treatment can cause dramatic consequences. The abdominal CT scan is a simple and powerful examination to make the diagnosis. Surgical treatment is only recommended in case of failure of medical treatment and a major challenge persists in the management of this syndrome. In addition, several complications can be associated with this syndrome.