Anemia of Prematurity - Portal Neonatal

PROXIMAL BOWEL OBSTRUCTION Section 5 of 11
Most babies with a proximal bowel obstruction present with vomiting. Depending on the level of
obstruction, abdominal distention may also be a feature. If the obstruction is distal to the drainage of
the common bile duct at the ampulla of Vater in the second portion of the duodenum, the vomitus is
likely to be bilious. The differential diagnosis for proximal bowel obstruction includes atresias, both
duodenal and jejunoileal, as well as malrotation with volvulus. Responsibility rests with the clinician to
expeditiously exclude the diagnosis of volvulus. Plain radiography of proximal bowel obstruction may
demonstrate little gas beyond the proximal duodenum. Placement of a nasogastric tube may be both
diagnostic and therapeutic. An upper GI contrast study through the nasogastric tube may be helpful.
Malrotation and volvulus
Because of the potential for midgut volvulus and loss of the entire small bowel, malrotation represents
perhaps the most feared cause for proximal small-bowel obstruction. Midgut volvulus from malrotation
is a life-threatening surgical emergency in the newborn. Remember that malrotation is not
synonymous with volvulus. Malrotation occurs in approximately 1 in 6000 newborns; rotational
abnormalities may be present in as many as 1% of the population. Volvulus represents the acute
twisting of the intestines upon their mesentery and can occur in a patient with malrotation due to the
lack of normal fixation of the bowel to the retroperitoneum. Patients who develop obstructive
symptoms of malrotation usually present in the first month of life. Of those who are eventually
symptomatic, 90% present in the first year of life. Associated anomalies include duodenal or jejunoileal
atresia, Hirschsprung disease, and, rarely, mesenteric cysts.
Malrotation results from a failure of the GI tract to complete its normal rotation as it returns to the
abdominal cavity at 8-10 weeks' gestation. The bowel develops outside of the abdominal cavity as a
single long loop of bowel based on the pedicle of the superior mesenteric vessels. As the bowel
returns to the abdomen, the proximal small bowel returns first and the duodenum rotates underneath
the superior mesenteric vessels to assume a retroperitoneal position. Rotation continues as the large
bowel returns to the peritoneal cavity, rotating over the vascular pedicle to place the ileocecal valve in
the right lower quadrant and establishing the hepatic and splenic flexures.
Fixation points develop in the peritoneum at the duodenum, ligament of Treitz, ileocecal valve, and
right and left paracolic gutters. This arrangement results in a broad fixed base of the small-bowel
mesentery by 10 weeks' gestation. If the rotation of the bowel is incomplete or does not occur, normal
mesenteric attachments are absent and abnormal peritoneal bands may develop. These bands may
obstruct the duodenum and are known as Ladd bands. Most worrisome in malrotation is the lack of
peritoneal attachments of the bowel. The unfixed bowel may twist around itself and compromise the
blood supply of the superior mesenteric pedicle.
The initial presentation of a newborn with volvulus of the midgut may be bilious vomiting. The
abdomen is initially soft and scaphoid and may or may not be tender on physical examination. As the
obstruction progresses, the volvulus compromises flow in the superior mesenteric pedicle and the
ischemic bowel becomes dilated, distended, and firm. The child may become hypotensive from
sequestration of fluid within the obstructed bowel; peritonitis and shock may develop. Metabolic
acidosis on laboratory evaluation may indicate bowel compromise. Prompt surgical intervention is
required.
Some patients with malrotation present with a more indolent course of long-standing partial obstructive
symptoms, constipation, and associated intestinal dysmotility. A history of chronic intermittent
abdominal pain may also be associated with malrotation, presumably from intermittent partial volvulus.
Radiographic imaging that exhibits a characteristic pattern can confirm a diagnosis of malrotation in a
stable patient. An upper GI series usually shows incomplete obstruction with extrinsic compression of
the duodenum and torsion of the small bowel. The ligament of Treitz may be found in an abnormal
position to the right of the midline or below the level of the pylorus. Obstructive bands may partially
block the duodenum. The position of the splenic and hepatic flexure as well as the cecum may not