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Duodenal vascular compression syndrome

  Duodenal vascular compression syndrome refers to intestinal lumen obstruction caused by compression of the third part of the duodenum (i.e., the transverse part) by the superior mesenteric artery, hence also known as superior mesenteric artery compression syndrome, Wilke syndrome, and duodenal stasis syndrome, etc.

Table of Contents

1. What are the causes of duodenal vascular compression syndrome?
2. What complications can duodenal vascular compression syndrome easily lead to?
3. What are the typical symptoms of duodenal vascular compression syndrome?
4. How to prevent duodenal vascular compression syndrome?
5. What laboratory tests are needed for duodenal vascular compression syndrome?
6. Diet taboos for patients with duodenal vascular compression syndrome
7. Conventional methods of Western medicine for the treatment of duodenal vascular compression syndrome

1. What are the causes of the onset of duodenal vascular compression syndrome?

  The transverse part of the duodenum is located retroperitoneally and is the most fixed part of the digestive tract. It runs from right to left across the third lumbar vertebra and the abdominal aorta. The distal part of the duodenum is fixed by the duodenal suspensory ligament (Trietz ligament). Behind it are the inferior vena cava, vertebral bodies, and abdominal aorta. In front, it is crossed by the superior mesenteric vascular nerve bundle within the root of the mesentery. The superior mesenteric artery usually branches at the level of the first lumbar vertebra, forming an angle of 30-42° with the aorta. If the angle between the superior mesenteric artery and the abdominal aorta becomes smaller, the superior mesenteric artery can compress the transverse part of the duodenum onto the vertebral body or abdominal aorta, causing intestinal stenosis and obstruction.

  The mechanical obstruction mentioned above is often a comprehensive result of various factors, such as the origin of the superior mesenteric artery at a narrow angle, the short duodenal suspensory ligament fixing the distal part of the duodenum at a higher position, the origin of the superior mesenteric artery being too low from the abdominal aorta, the abnormal course of the superior mesenteric artery in front of the vertebral body where the duodenum crosses, etc. In addition, lumbar anterior convex deformity, inflammatory swelling of the duodenal suspensory ligament and paraaortic lymph nodes, reduced mesenteric and retroperitoneal fat due to emaciation, and visceral prolapse can all reduce the space between the vertebral column and the proximal part of the superior mesenteric artery, making it easy for the duodenum to be compressed.

2. What complications can duodenal vascular compression syndrome easily lead to?

  Long-term repeated vomiting can lead to symptoms such as emaciation, dehydration, and malnutrition of the whole body.

  1. Dehydration:Sodium salts (NaCl, NaHCO3) are the main inorganic salts that determine the osmotic pressure of extracellular fluid, therefore, the serum sodium concentration is the main factor that determines the high and low of plasma osmotic pressure. Due to the different proportions of water and sodium loss, different changes in plasma sodium concentration and osmotic pressure occur. In cases of dehydration, clinical practice often divides dehydration into three types according to the level of serum sodium concentration: isotonic dehydration, hypotonic dehydration, and hypertonic dehydration.

  2, Malnutrition:It is due to insufficient intake of energy and (or) protein, leading to poor nutritional status or inability to maintain normal growth and development, mainly seen in infants and young children under 3 years old. Clinical common types include: energy supply deficiency, manifested as significant weight loss and decreased subcutaneous fat, known as the emaciated type; protein supply deficiency, manifested as edema, known as the edematous type; and an intermediate type between the two, known as the emaciated-edematous type.

3. What are the typical symptoms of duodenal vascular compression syndrome

  Duodenal obstruction caused by superior mesenteric artery compression can be divided into acute and chronic types. Acute obstruction usually has no gastrointestinal prodromal symptoms and often occurs after trunk plaster fixation, traction, or lying on an excessively extended brace. The main manifestations are acute gastric dilatation signs.

  Chronic obstruction is the most common type in clinical practice, with main symptoms such as vomiting, which often occurs after meals, containing bile and food intake. The symptoms are intermittent and recurrent, with a relief period that can be long or short. The symptoms can be alleviated by changing body positions, such as lying on the side, prone, or in the chest-knee position. This is a characteristic of the disease. Vomiting is often not accompanied by abdominal pain, or only with discomfort in the upper abdomen. During the relief period, there may be fullness after eating, fatigue, weakness, nervousness, anorexia, and emotional instability. Prolonged and repeated vomiting can lead to weight loss, dehydration, and malnutrition throughout the body.

4. How to prevent duodenal vascular compression syndrome

  Duodenal vascular compression syndrome refers to intestinal cavity obstruction caused by compression of the third part of the duodenum (i.e., the transverse segment) by the superior mesenteric artery. There are no particularly effective preventive measures for this disease, and early detection and treatment are the key to its prevention and treatment.

5. What laboratory tests are needed for duodenal vascular compression syndrome

  Gastrointestinal barium meal examination shows the first and second parts of the duodenum are dilated, with repeated strong retrograde peristalsis, and barium can reflux into the stomach. There is a regular oblique pressure mark and a phenomenon of obstruction of barium through the transverse segment of the duodenum. If the barium meal swallowed cannot be emptied from the duodenum within 2 to 4 hours, it indicates the presence of obstruction. If the patient assumes a prone or left lateral position, the duodenal retention disappears, which is very helpful for the diagnosis of this syndrome.

  Simultaneous aortography and barium enema can show the relationship between duodenal compression and superior mesenteric artery, the narrowing angle between the superior mesenteric artery and the abdominal aorta, and the abnormal course of the superior mesenteric artery, but this method is rarely needed in clinical practice.

6. Dietary taboos for patients with duodenal vascular compression syndrome

  Fluid diet such as milk and congee, with small amounts and frequent meals, should gradually be changed to soft food and semi-liquid food.

  1, It is recommended to eat more clam, kelp, nori, tortoise shell, turtle, sea cucumber, water snake, Job's tears, water chestnut, walnut, goat kidney, pork kidney, soybean sprouts, sand worm, sea bream, and mackerel.

  2, Suitable for eating kelp, wakame, nori, and green crab.

  3. It is recommended to eat yellowfish bladder, shark fin, water snake, pigeon, jellyfish, lotus root powder, buckwheat, malan head, earth ear, turnip, olive, eggplant, fig, mung bean sprouts, soy milk, amaranth, mulberry, conger eel.

  4. It is recommended to eat celery, chrysanthemum, leek, winter melon, black plum, dried persimmon, sesame, lotus seeds, sea cucumber.

7. Conventional methods of Western medicine for treating duodenal vascular compression syndrome

  Patients diagnosed with duodenal vascular compression syndrome should first adopt non-surgical treatment, especially during the acute attack period, providing intravenous nutrition, fasting, nasogastric decompression, and antispasmodic drugs. After the symptoms are relieved, they can start with liquid diet, eating small and frequent meals, and gradually change to soft food. After meals, they should take a prone or left lateral position, and the above methods have been reported to cure the disease more and more. Improved nutrition and weight gain can cause fat deposition in the retroperitoneal space, which may improve the symptoms.

  After the above treatments fail, surgical treatment is adopted. The methods of surgery are mainly the following three: ① Freeing the duodenal suspensory ligament; ② Duodenal jejunal anastomosis; ③ Duodenal reduction surgery.

  The first method is not very effective and is only suitable for cases where the duodenal suspensory ligament is too short, causing compression of the duodenum. However, it is rarely used in clinical practice.

  Although the second method is widely used, the results are often not satisfactory. After flipping the transverse colon upwards and cutting the transverse mesocolon, the dilated third part of the duodenum can be exposed. A segment of jejunum about 10-15 cm away from the duodenal jejunum flexure is then used for a side-to-side anastomosis. Finally, the edges of the incision of the transverse mesocolon are sutured to the duodenal wall to prevent the anastomotic site of the duodenum and jejunum from retracting and forming an internal hernia.

  Gastric jejunal anastomosis should not be used because it cannot effectively relieve duodenal stasis.

  In recent years, the duodenal reduction surgery has been promoted, and it is often applied to children. The surgical method involves freeing the right half of the colon and the entire 'C' shaped duodenal loop, including the third and fourth parts behind the peritoneum, directly to the compression site of the mesenteric blood vessels, and then releasing the duodenal suspensory ligament. The duodenum and jejunum are then placed behind the mesenteric blood vessels on the right side of the median line (see Figure 25-20). The advantage of this method is that it does not cut the intestinal wall, but only returns the proximal small intestine and colon to their original position before the transposition in the embryonic stage. It is necessary to cut the blood vessels when freeing the duodenum, and attention must be paid to the viability of the duodenum.

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