Prenatal manifestation of superior mesenteric artery syndrome

Abstract

Intestinal obstruction is not a rarity in the newborn. Its etiology is diverse. Superior mesenteric artery syndrome (SMAS) is a phenomenon in which the duodenum is obstructed by the SMA. This causes bowel obstruction accompanied by duodenal dilatation. It has previously been described in adults and children but rarely in infants. We report for the first time on an intrauterine manifestation of SMAS.

Superior mesenteric artery syndrome: a rare cause of complete intestinal obstruction in neonates

“…Few cases have been documented in infancy [3,[6][7][8] and only 2 in the newborn period; both were girls who presented with bilious vomiting and incomplete intestinal obstruction shortly after birth [3,7]. To our knowledge, SMAS with complete intestinal obstruction preceded by symptoms of a gastroenteritis-like illness and features of sepsis has never been previously reported.…”

Superior Mesenteric Artery Syndrome Diagnosed with Linear Endoscopic Ultrasound (with Video) in a Patient with Normal Body Mass Index

“…The development of SMA syndrome may also be related to variation or distortion of the normal anatomy, such as short ligament of Treitz,5 low origin of the SMA,4 or esophagectomy 16. A case report of identical twins17 with SMA syndrome and another case in utero 18 suggest a genetic predisposition in some patients. Therefore, anatomical variation or genetic susceptibility might have contributed to the SMA syndrome in our case.…”

Robotic duodenojejunostomy for superior mesenteric artery syndrome in a teenager

“…They suggested that weight loss is not a requirement for development of SMAS. It has been hypothesized that rapid weight loss results in loss of the fat pad between the SMA and the duodenum, thus causing duodenal compression [14,15]. In our patient, however, she had managed to gain some weight but still suffered from significant post-prandial pain.…”

“…Causes of SMAS may be congenital or acquired. Congenital causes include 1. high insertion of the duodenojejunal flexure to the ligament of Treitz; 2. a low SMA origin; and 3. compression of the duodenum by peritoneal adhesions because of intestinal malrotation [1,14,15].…”