Pseudo-obstruction of the intestine

　　It is generally believed that chronic pseudo-obstruction of the intestine is caused by lesions in the intestinal muscle or nerve. It can be divided into the following two types.

　　Primary chronic pseudo-obstruction of the intestine:Also known as chronic idiopathic pseudo-obstruction, it was officially named by Maldonado in 1970. The etiology is unclear and may be related to dominant chromosomal inheritance, as many patients have a family history and can affect some organs outside the gastrointestinal tract (such as the bladder), so it is sometimes called familial visceral myopathy or hereditary jejuno-visceral myopathy. It can be divided into the following three types according to the condition of the intestinal wall lesions.

　　1. Myopathic pseudo-obstruction (visceral myopathy): The lesions are mainly in the intestinal wall smooth muscle, which can be familial or sporadic. The main pathological changes are degenerative changes in the annular or longitudinal muscles of the intestinal wall, with the latter being more severe. Sometimes the muscles are completely atrophic and replaced by collagen.

　　2. Neuropathic pseudo-obstruction (visceral neuropathy): The lesions are mainly in the neural plexus between the intestinal wall muscles, which can be sporadic or familial. In 1969, Dyer et al. reported that the pathological changes mainly occur in the neural plexus between the intestinal wall muscles, characterized by degenerative changes and swelling of neurons and neuronal processes, and some cases also have involvement of other parts of the nervous system.

　　3. Acetylcholine receptor dysfunction pseudo-obstruction: No organic abnormalities of muscle or nerve are found, but physiological tests show abnormalities in intestinal motility. In 1981, Bannister et al. reported a case of pseudo-obstruction where no histological changes of muscle or nerve disease were found in the tissue sections, suggesting that the occurrence of the case may be related to the defect in the muscarinic acetylcholine receptor function of the intestinal smooth muscle.

　　Secondary chronic pseudo-obstruction of the intestine:Most cases are secondary to other diseases or due to drug abuse. Diseases and drugs related to chronic pseudo-obstruction of the intestine include:

　　1. Diseases of the small intestinal smooth muscle: ① Collagen vascular diseases: systemic sclerosis, progressive systemic sclerosis, dermatomyositis, polymyositis, systemic lupus erythematosus; ② Invasive muscle diseases: amyloidosis; ③ Primary muscle diseases: dystrophic myotonia, progressive muscular dystrophy; ④ Other:蜡样色素沉着症、non-tropical stomatitis diarrhea.

　　2. Endocrine diseases: ① Hypothyroidism; ② Diabetes; ③ Pheochromocytoma.

　　3. Neurological diseases: Parkinson's disease, familial dysautonomia, Hirschsprung's disease, Chang disease, mental illness, enteric ganglionopathy.

　　4. Drug-related causes: ① Toxic drugs: lead poisoning, mushroom poisoning; ② Side effects of drugs: phenothiazines, tricyclic antidepressants, antiparkinsonian drugs, ganglion blockers, chloropressin.

　　5. Electrolyte disorders: hypocalcemia, hypomagnesemia, uremia.

　　6. Other: bypass of the jejunum and ileum, jejunal diverticulum, spinal cord injury, malignant tumors.

　　Systemic sclerosis leading to chronic pseudo-obstruction of the intestine is common, with the main pathological changes being atrophy and fibrosis of the intestinal wall smooth muscle, especially in the annular muscle; amyloidosis is characterized by large amounts of amyloid deposits in the muscular layer of the intestinal wall; mucinous edema involves mucinous edematous substances in the muscular layer of the intestinal wall; diabetes usually does not show obvious changes in the intestinal wall muscle and intermuscular plexus.

　　When pseudo-obstruction involves the esophagus, it can cause difficulty swallowing; when the bladder is involved, it can cause urinary retention; when the extraocular muscles are involved, it can cause extraocular muscle paralysis and ptosis of the upper eyelid. Chronic pseudo-obstruction, due to malabsorption, can cause anemia, hypoproteinemia, and other malnutrition manifestations.

　　1, Intestinal obstruction:Due to the weight of the tumor, it can cause mesenteric torsion and intestinal intussusception, leading to acute intestinal obstruction; large cysts squeezing the intestine can cause chronic intestinal obstruction.

　　2, Urinary tract obstruction:Large cysts pressing on the ureter can cause symptomatic or asymptomatic urinary tract obstruction. A few patients may have symptoms such as anemia and intestinal obstruction. Hematochezia can be caused by acute mesenteric torsion or the intestinal wall being invaded by a cyst. Mesenteric cysts can cause ureteral obstruction, symptoms may be present or absent, occasionally found in laparotomy. Abdominal mass is the most common abdominal sign. Benign tumors are usually smooth on the surface, with texture ranging from cystic to tough and hard, with mild tenderness, except for those located at the root of the mesentery or adherent to surrounding tissues, generally have a large degree of mobility, with obvious movement from右上 to 左下.

　　Pseudo-obstruction can occur at any age, with more females than males, having a family history, mainly manifested as chronic or recurrent nausea, vomiting, abdominal pain, abdominal distension, abdominal pain often located in the upper abdomen or around the umbilicus, persistent or paroxysmal, often accompanied by varying degrees of diarrhea or constipation, some diarrhea and constipation alternate, or there may be difficulty swallowing, urinary retention, incomplete bladder emptying, and recurrent urinary tract infection, dysfunction of thermoregulation, dilated pupils, etc., physical examination has abdominal distension, tenderness, but no muscle tension, can hear the splash sound, decreased or absent bowel sounds, weight loss, malnutrition is common.

　　Actively and effectively treat neurological diseases (such as Parkinson's disease, intestinal plexus inflammation, etc.), connective tissue diseases (such as systemic lupus erythematosus, dermatomyositis, and polymyositis, etc.), endocrine diseases (such as diabetes, pheochromocytoma, etc.), and pay attention to the use of certain drugs (such as: phenothiazines, ganglion blockers, morphine, etc.) that may cause chronic pseudo-obstruction, to prevent the occurrence of pseudo-obstruction.

　　The abdominal X-ray imaging of pseudo-obstruction does not show intestinal distension and liquid-air interface that appear in mechanical intestinal obstruction; gastrointestinal manometry shows esophageal and gastrointestinal function abnormalities; histological examination of small intestinal tissue with Smith silver staining is positive, which can make a definite diagnosis.

　　For patients with pseudo-obstruction who undergo surgery, they can have semi-liquid food after one week, such as noodles, wontons, millet dates porridge, buns, bread, soda crackers, braised tofu, steamed fish, and braised fresh vegetables.

　　Eat easily digestible foods that promote defecation. For example, vegetables: kelp, pork blood, carrots, and fruits such as hawthorn, pineapple, papaya, etc.; eating more fiber-rich foods such as various vegetables, fruits, brown rice, whole grains, and beans can help defecate, prevent constipation, stabilize blood sugar, and lower blood cholesterol.

　　It is recommended to eat light and nutritious liquid foods, such as rice soup, vegetable soup, lotus root powder, egg flower soup, noodles, etc.

　　At present, there is no specific treatment for this disease, and comprehensive treatment can be adopted, such as reducing small intestinal dilation, using antibiotics, restoring normal gastrointestinal motility, and total parenteral nutrition.

　　1. Diet therapy:A low-fat, low-lactose, and low-fiber diet is required. Because the symptoms and signs of the patient are closely related to the degree of small intestinal dilation, and the degree of dilation is related to the volume and type of food intake. Malabsorbed fat can be decomposed into fatty acids by bacteria in the small intestine, which stimulate the large secretion of the small intestine, causing dilation. This disease often accompanied by varying degrees of small intestinal mucosal damage, affecting the decomposition and metabolism of lactose, resulting in increased gas and fluid secretion in the intestinal lumen, aggravating small intestinal dilation. In addition, long-term food accumulation in the intestines with disordered peristalsis, especially foods rich in fiber, can form fecal stones, which can cause mechanical intestinal obstruction on the basis of pseudo-obstruction. Therefore, the fat provided each day should not exceed 40g, and it is best to be long-chain fat; lactose should not exceed 0.5g/100cal, and fiber should not exceed 1.5g/100cal. In addition, it is necessary to supplement vitamins B12, D, K, and trace elements in moderation. During an acute attack, fasting and continuous gastrointestinal decompression should be prohibited.

　　2. Antibiotic therapy:Overgrowth of bacteria in the small intestine can cause malabsorption of fat, leading to steatorrhea. Antibiotic treatment can alleviate symptoms. The choice of antibiotics should be based on the results of small intestinal fluid culture.

　　3. Drug therapy:The purpose is to stimulate small intestinal contraction and restore the normal peristaltic function of the small intestine. Many drugs have been tried, such as acetylcholine, pentagastrin, urethane, metoclopramide, corticosteroids, carbamylcholine, amphetamine, propranolol, and others, but none have significantly improved the symptoms. Luder et al. treated a patient with elevated prostaglandin E levels with indomethacin, and when prostaglandin E levels returned to normal, the obstructive symptoms disappeared. Boige et al. treated four pediatric patients with intravenous trimebutine, a peripheral morphine agonist, which induced stage III intestinal electrical activity, enhanced intestinal peristalsis, and alleviated the symptoms of the children. Some believe that excessive endorphin release in patients with pseudo-obstruction inhibits intestinal peristalsis, and the use of morphine antagonists can effectively block this action. Schang treated a patient with naloxone for 15 days, and the symptoms disappeared, and the gastrointestinal transit time returned to normal. Larustesen reported that simultaneous intravenous administration of neostigmine and cholecystokinin can significantly improve the symptoms of patients, and shorten the small intestinal transit time. Cisapride is a new non-cholinergic stimulant that selectively acts on the gastrointestinal tract, causing the myenteric plexus to release acetylcholine, thereby increasing muscle contraction activity and avoiding systemic side effects, with good clinical application effects. Erythromycin has a motilin-like effect and can effectively promote gastrointestinal motility, showing certain efficacy in the treatment of pseudo-obstructive ileus.

　　4. Total Parenteral Nutrition (TPN):Due to varying degrees of absorption disorders, malnutrition, and poor effects of diet and drug treatment, surgical treatment is only effective for a small part of patients, so most patients need TPN treatment, especially severe patients, where long-term TPN treatment is the only method to maintain life. Schufflen reported that 9 patients received TPN at home for 2 to 42 months, with 1 patient dying of a cerebral vascular accident after 2 months, and the other 8 patients all gained weight and had significant improvement in symptoms. Pitt et al. reported that 22 patients were hospitalized an average of 1.2 times per year due to acute attacks of pseudo-obstruction before receiving TPN treatment, but after receiving treatment at home, they were hospitalized only 0.2 times. However, TPN is expensive, has many complications, and has a high mortality rate. There are reports that over a 10-year period, 10 children died due to TPN treatment, including 4 deaths from sepsis and 2 from liver failure. Another 10 adult patients had 3 cases of catheter infection and sepsis, 1 case of immune complex glomerulonephritis, and 1 case of superior vena cava thrombosis.

　　Once the disease is diagnosed, surgery is generally not performed. However, when symptoms persist and it cannot be completely ruled out that there is mechanical intestinal obstruction, laparotomy is necessary. If no cause of mechanical intestinal obstruction is found during surgery, the full thickness of the diseased intestinal segment should be resected, and a histological examination should be performed to determine the nature. Different surgical methods are used for lesions in different locations. When esophageal symptoms are predominant, balloon dilatation can be performed; when gastric symptoms are predominant, vagotomy and gastric antrum resection, along with gastric jejunum Roux-en-Y anastomosis, can be performed; if duodenal dilation is predominant, small intestinal suspension fistula decompression surgery can be performed, and the combination of TPN is more effective. There are reports that the combination of small intestinal fistula and enterostimulatory agents can restore the contraction ability of the smooth muscle of the intestinal tract in patients with myopathic pseudo-obstruction. If the lesion is limited to a segment of small intestine, a short-circuit operation can be performed. The radical resection of the diseased intestinal segment is a more ideal treatment. If the small intestinal lesions are extensive, after the near-total resection of the small intestine, combined long-term TPN treatment is required, which is actually difficult to achieve. For severe patients, small intestinal transplantation may be a promising treatment method, but currently there are only animal experiments, and there are no clinical application reports.