I. Definition of early postoperative inflammatory intestinal obstruction There are various types of intestinal obstruction complicating abdominal surgery, and the causes of intestinal obstruction occurring in different postoperative periods are different. Early postoperative inflammatory ileus (EPII) occurs in the early postoperative period after abdominal surgery and refers to a mechanical and dynamic adhesive intestinal obstruction caused by abdominal surgical trauma or intra-abdominal inflammation, which leads to edema and exudation of the intestinal wall. The abdominal surgical trauma refers to extensive separation of intestinal adhesions, prolonged intestinal exposure and other intestinal injuries caused by surgical operations. Intra-abdominal inflammation refers to aseptic inflammation, such as accumulation of blood, fluid or other residual material capable of causing sterile inflammation in the abdominal cavity. Mechanical obstruction and paralytic obstruction secondary to intraperitoneal or retroperitoneal infection, electrolyte disturbance, and other causes must be excluded before diagnosing EPII.
Second, the medical history characteristics of early postoperative inflammatory bowel obstruction EPII patients must have a history of recent abdominal surgery, and according to statistics, the majority of cases start within 1 to 2 weeks after surgery. The surgical procedure has a greater impact on the recovery of gastrointestinal function, especially gastrointestinal surgery, repeated surgery within a short period of time, extensive separation of intestinal adhesions, peritonitis, intestinal alignment, residual foreign body or necrotic tissue, and other factors causing extensive damage to the plasma surface of the intestine. Due to the lack of knowledge of this disease among the treating physicians, they are indolent in the treatment process, and also due to the lack of necessary means of nutritional support, they are unable to maintain the nutritional status of the patient under long-term fasting, thus putting all their hopes on surgery, resulting in repeated surgical operations in a short period of time, trying to release the obstruction by separating the adhesions, not knowing that at this time the intestinal canal is widely and severely adhered, highly congested Repeated surgery not only fails to relieve the obstruction, but also leads to the aggravation of the symptoms of inflammatory bowel obstruction due to repeated damage to the intestinal canal, resulting in a longer recovery period of intestinal function and even the formation of intestinal fistula. Therefore, a proper understanding of EPII can help determine the treatment plan and avoid unnecessary surgical trauma and complications.
Clinical symptoms and diagnosis of early postoperative inflammatory bowel obstruction The clinical manifestations of EPII are the same as other intestinal obstructions, which are manifested as abdominal distension, vomiting, and cessation of gas and defecation, but EPII has its obvious peculiarities. has recovered and is ready to eat, as symptoms of obstruction appear immediately once food is consumed. It is often described that the patient passes gas very early after surgery, or passes a little dry stool, and then starts to eat, but the obstruction appears soon after eating. This is a typical symptom of EPII. abdominal pain in EPII is not significant, but if the patient has severe abdominal pain, the possibility of mechanical or strangulated intestinal obstruction should be alerted. EPII may be diffuse or confined to one part of the abdomen, depending on the abdominal surgery and the site and extent of intestinal involvement, with the most common site of confined lesions being below the incision.
EPII patients do not have high fever, abdominal distension is usually symmetrical, abdominal distension, but the degree is not as severe as mechanical or paralytic intestinal obstruction, and no bowel pattern or peristaltic waves can be seen. With the gradual relief of the obstruction, the bowel sounds gradually recovered. CT examination of the whole abdomen has an important reference value for the diagnosis of EPII. CT examination can show edema, thickening and adhesions of the intestinal wall as well as fluid and gas accumulation in the intestinal cavity, uniform dilatation of the intestinal canal and intra-abdominal exudation, and help to exclude other abdominal pathologies (such as abdominal infection and mechanical intestinal obstruction). By dynamically observing the patient’s abdominal symptoms, signs and changes in CT images, the progress of lesions can be understood.
IV. Treatment of early postoperative inflammatory bowel obstruction The basic principles of treatment of intestinal obstruction are the same, including fasting, gastrointestinal decompression and correction of internal homeostasis. In addition, the treatment of EPII has its obvious special features. The duration of EPII is generally long, and the statistical results show that the average healing time of patients is about 1 month, therefore, long-term planning should be made. Total parenteral nutrition support. Nutritional support is not only a means of support to condition the patient to wait for remission, but also an important therapeutic measure. Malnutrition causes hypoproteinemia, which leads to edema of the intestinal wall, affects the recovery of intestinal peristaltic function, increases the loss of body fluids from the digestive tract, and even causes narrowing or obstruction of the intestinal lumen. Nutritional support is necessary to improve the patient’s nutritional status, and even plasma albumin should be infused along with nutritional support, and intravenous diuretics should be given after the infusion to help excess water drainage. Without nutritional support, the therapeutic effect of EPII can hardly be guaranteed. Total parenteral nutrition also helps to reduce malnutrition due to high catabolism after surgery, promote wound healing, and correct water-electrolyte disturbances. Nutritional support has to be maintained until the patient is able to eat normally before it is gradually discontinued. Recognizing EPII as an inflammatory response in the intestinal wall, adrenocorticosteroids, such as dexamethasone, should be started after the diagnosis of EPII is established to promote the reduction of intestinal inflammation and edema. The dosage of the hormone depends on the severity of the disease and the general condition of the patient. The usual dose is dexamethasone 5 mg intravenously every 8 hours, which is gradually discontinued after about 1 week of application.
After the start of the treatment, the changes of the disease should be closely observed, especially the changes of the abdominal signs. In order to stimulate the peristalsis of the gastrointestinal tract, protect the gastric mucosa and help remove the accumulated stool in the intestinal cavity, warm saline gastric lavage and enema can be used. For patients whose abdominal signs have been significantly relieved but with poor motility, neostigmine can be applied to promote intestinal peristalsis. After the gastrointestinal tract has regained patency, Prevacid is started to help empty the gastrointestinal tract and maintained until normal feeding can be achieved.
The following criteria should be followed to determine whether EPII is in remission: the patient’s abdominal distension disappears and he passes gas and stools because the symptoms of intestinal obstruction are relieved. Since a large amount of intestinal fluid accumulated in the intestine is discharged after the intestine is restored, most patients resolve watery stools after the relief of obstruction, which is an important indicator to judge the relief of intestinal obstruction. Physical examination shows that gastric juice is significantly reduced, becomes clear and free of bile (but make sure that the gastric tube does not enter the duodenum), intestinal sounds turn active from sparse, and the abdomen changes from initially firm to soft.
It is unlikely that EPII causes strangulated intestinal obstruction, and should be treated mainly with medication (or conservative treatment), and there is no urgency to release the obstruction by surgical means. Since the intestinal canal is highly edematous and densely adherent at this time, even in the shape of cerebral gyrus, the plasma membrane surface of the intestinal canal is extensively damaged and oozing blood during stripping. Since EPII is not a mechanical obstruction of the intestinal canal and cannot be removed surgically, extensive peeling of the adhesions to find the site of obstruction, in addition to causing more serious intestinal wall damage and bleeding, is very likely to cause intestinal fistula due to factors such as intestinal wall edema, poor healing ability, and failure to recover intestinal peristaltic function within a short period of time, which is a painful lesson. Among them, 22 cases underwent multiple operations to relieve the obstruction, and 90 cases (29.4%) died. The number of cured cases reached 56, 7 cases were treated with elective surgery for coexisting disease after EPII cure, and 1 case died suddenly due to pulmonary artery embolism. The mean time to cure was (27.6±10.0)d, with a maximum of 58 d. In 1989, Pickleman also summarized 101 cases of EPII, 78 of which were treated non-operatively, with only 3 deaths. The mean duration of treatment was 6.3 d, with a maximum of 17 d. The continuation of pharmacological treatment is contingent on the condition not continuing to deteriorate or progressing for the better. Although it is highly unlikely that EPII will lead to strangulated intestinal obstruction, it is important to closely monitor the condition and once the signs and symptoms of intestinal obstruction worsen or even signs of strangulation appear, the diagnosis of EPII is wrong and the treatment plan should be adjusted immediately until surgical treatment is performed. We should especially beware of misdiagnosing mechanical intestinal obstruction as EPII, which leads to strangulation of mechanical intestinal obstruction.
V. Prevention of early postoperative inflammatory bowel obstruction In many cases, EPII can be prevented, and the key to prevention is to raise awareness of this disease. Any foreign body in the peritoneal cavity (including autologous blood and tissue debris, etc.) can stimulate the peritoneal mononuclear macrophage system and produce a large number of cytokines and inflammatory mediators, resulting in sterile inflammation and intestinal adhesions, which can lead to EPII. Therefore, a large amount of saline should be used to flush the peritoneal cavity at the end of the procedure to remove cytokines, inflammatory mediators, foreign bodies and necrotic tissue from it. In patients who had undergone secondary surgery, it was found that patients with clean abdominal cavity flushing had minimal or no abdominal adhesions, indicating that massive saline flushing can prevent not only EPII but also adhesive bowel obstruction. Among the various methods known to prevent intestinal adhesions, the most effective methods are to reduce intestinal tube injury and to flush the abdominal cavity with large amounts of saline, while all other methods have shortcomings. During the surgical operation, special attention should be paid to protect the intestinal canal, avoid blunt dissection, use sharp dissection, and try to eliminate the rough surface of the intestinal canal and make it plasma membrane. Reducing the exposure time and exposure area of the intestinal canal in the air and protecting the canal with wet saline gauze pads can help to protect the plasma membrane surface of the intestinal canal and reduce the unobtrusive water loss. There are external and internal intestinal alignment. The disadvantages of external alignment are now recognized and gradually eliminated, but internal alignment also has an impact on the recovery of intestinal function and should not be abused. In case EPII is unavoidable, the severity of abdominal harassment should be fully estimated beforehand. If serious contamination of the abdominal cavity is found during surgery, or if extensive intraoperative adhesion separation and other reasons are estimated to lead to extensive postoperative intestinal adhesions, the possibility of EPII should be alerted, and exhaust symptoms appearing very early after surgery should be treated with caution and fasting time should be extended to avoid aggravating EPII with premature feeding. At the same time, the nutritional status of the patient should be actively improved to enable the patient to recover as soon as possible.