Duodenal stasis

  Duodenal stasis is mainly due to short Treitz ligament, high position of duodenum, enlarged lymph nodes at the root of superior mesenteric artery, or hypertrophic adhesions of mesenteric fibrous tissue, or compression of the transverse duodenum by the superior mesenteric artery caused by visceral prolapse pulling the mesentery, so it is also called superior mesenteric artery compression syndrome. It mostly occurs in middle-aged and young women with long and lean body types.
  Causes.
  The anatomical characteristics of the duodenum, superior mesenteric artery and abdominal aorta are closely related to the occurrence of this disease. Under normal circumstances, the duodenum is located in the angle between the abdominal aorta and its forward branches – the superior mesenteric artery, and the duodenum is preceded by the oblique superior mesenteric artery, followed by the celiac artery and the spine, and the angle is 47 to 60° in normal people by angiography.
  When the mesentery is pulled downward, the angle of entrapment becomes smaller, often <6~25° and compresses the horizontal part of the duodenum, forming a narrowing of the intestinal canal, and the symptoms of duodenal obstruction appear.
  There are many causes of this disease, but the superior mesenteric artery compresses the duodenum and forms congestion in the majority of cases (50%), which is also called superior mesenteric artery syndrome.
  Other causes include
  ① congenital anomalies: such as congenital peritoneal girdle compression and pulling and blocking the duodenum; congenital stenosis or occlusion of the distal duodenum, compression of the descending duodenum by the annular pancreas; giant duodenum produced by duodenal dysplasia, and severe prolapse of the duodenum due to congenital mutations, which can fold the duodenojejunal angle and close it, thus producing congestion.
  ②Tumors: benign and malignant duodenal tumors; retroperitoneal tumors such as renal tumors, pancreatic cancer, lymphoma; metastatic cancer of the duodenum, adjacent enlarged lymph nodes (cancer metastasis), mesenteric cysts or abdominal aortic aneurysm compressing the duodenum.
  ③Infiltrative disease and inflammation of the distal or proximal jejunum of the duodenum; such as progressive systemic sclerosis, Crohn’s disease, and inflammatory adhesions or compression of diverticula causing constriction.
  ④Adhesions occurring after gallbladder and gastric surgery pulling the duodenum; adhesions, ulcers, strictures or input collaterals syndrome after gastrojejunostomy.
  ⑤ Other congenital anomalies: duodenal inversion, duodenal obstruction due to gallbladder duodenal cords; anterior duodenal portal vein; abnormal position of Fate’s jugular (common bile duct opening in the third part of the duodenum).
  Clinical presentation.
  The diagnosis can generally be made based on intermittent post-feeding abdominal distension, nausea and vomiting, symptoms related to position, aggravated in supine position and alleviated in prone and lateral positions, and X-ray imaging showing signs of compression in the horizontal segment of the duodenum, and B-type ultrasound or angiography showing narrowing of the angle between the superior mesenteric artery and the abdominal aorta.
  Signs and symptoms.
  It can occur at any age, but is more common in wasted young and middle-aged women or those who are bedridden for long periods of time. It has a chronic intermittent onset and may resolve on its own after a few days, or occasionally in acute cases. The main clinical manifestation is the manifestation of duodenal obstruction, with epigastric fullness and pain after eating, followed by nausea and vomiting, with a large amount of vomiting, similar to pyloric obstruction, and the prominent feature of the disease is that the symptoms are related to the position, and the symptoms are aggravated by backward pressure in the supine position, while the symptoms can be relieved in the prone, knee-chest, and left-sided positions.
  Severe obstruction may be associated with dehydration and electrolyte imbalance. Patients with recurrent attacks may show malnutrition such as wasting and anemia. There is also a proportion of neurological manifestations.
  Diagnosis and differential diagnosis.
  1.Intestinal X-ray imaging: In the remission period, there are mostly no abnormal findings, and in the attack period, signs of duodenal compression can be seen, with a longitudinal knife-like block or waterfall-like descent at the center of the (horizontal end) of the third segment, slow passage of barium, which can stay in the duodenum for more than 6 hours, with dilatation of the intestinal canal proximally, and related to the change of body position, and 20% can be accompanied by gastric dilatation.
  2.B-type ultrasonography: Some people believe that timed ultrasound imaging has a high diagnostic value and propose the following diagnostic criteria for this disease.
  The maximum width of the transverse duodenal intestinal canal during peristalsis is 30 mm within the angle between the superior mesenteric artery and the aorta after drinking water.
  B-mode ultrasound shows a “bucket” or “gourd” image.
  The angle between the aorta and the superior mesenteric artery is <13°.
  Diagnostic basis
  1. Long duration of disease, periodic recurrent episodes, clinical manifestations similar to pyloric obstruction, but the vomit contains bile.
  2.Changing the position (prone, chest and knee position) can reduce or relieve the symptoms, and sometimes the dilated duodenum can be palpated.
  3.Barium X-ray examination shows that the first and second segments of the stomach and duodenum are dilated and the barium wanders in the duodenum, changing the position, the barium can enter the jejunum.
  Disease treatment.
  Those with mild symptoms should control diet, bed rest, preferably in prone or lateral position, and intravenous supplementation of fluids and electrolytes for those with obvious nausea and vomiting, and most patients can gradually relieve symptoms with symptomatic treatment. Most patients can be relieved gradually with symptomatic treatment. Lateral duodenojejunostomy or Treitz ligament release is feasible when medical treatment is ineffective and has satisfactory results.
  It is easy to complicate intestinal stricture, intestinal obstruction, duodenal obstruction, malnutrition, etc.