Prompt and appropriate treatment is required when intestinal necrosis occurs in patients with AMI. Surgical delays often lead to death due to disease complications such as acute intestinal failure, sepsis, multiple organ failure[14–16], peritonitis, and short bowel syndrome in advanced or unresected intestinal necrosis[5, 17]. The extent of the small intestine resection is independently associated with initial mortality[18–20]. Thus, intestinal necrosis should be identified and tissue should be removed before clinical symptoms of peritonitis and organ failure appear in order to reduce morbidity and mortality and to improve intestinal function. In addition, accurate preoperative screening can avoid unnecessary laparotomy and resection in some patients with non-transmural intestinal necrosis[21, 22]. This research may help identify the criteria for emergency surgery based on clinical presentation.
We identified BUN level, LnD-dimer level and WBC count as the parameters predictive of intestinal necrosis in AMI patients. Urea nitrogen is the primary end-product of human protein metabolism and is predominantly excreted by the kidney. When the glomerular filtration rate drops below 50% of the standard value, BUN rises rapidly. Accordingly, elevated BUN is one of the leading indicators for renal function testing. After ischemic necrosis of the small intestine, intestinal cells become hypoxic. As a result, anaerobic glycolysis is enhanced and lactic acid production increases, leading to hypoxia-associated changes in renal cells that subsequently cause inflammation. As necrosis of the small intestine progresses, blood volume, cardiac output, and renal blood flow decrease leading to increased levels of renally toxic substances in the blood; in turn, this process affects renal function and leads to increased BUN levels. Wei Q et al. found that the BUN levels significantly increase when necrosis of the small intestine occurs, including in patients with AMI. However, there are currently few studies on this association; thus, further investigation of the relationship between BUN level and ischemic necrosis of the small intestine is required.
D-dimer is the end-product of fibrin degradation and is often used for diagnosis- by-exclusion of venous thrombosis[25, 26]. There are few studies on the dynamic level of D-dimer in AMI. Intestinal necrosis causes microcirculation, blood coagulation, and blood circulation disturbances in the intestine, while tissue ischemia and hypoxia can cause coagulation disorders and microthrombosis. Therefore, coagulation function markers such as D-dimer and fibrinogen can indirectly reflect the blood circulation to the diseased abdominal organs[27–29]. We found that the D-dimer levels were significantly different between patients in the intestinal necrosis group and the non-intestinal necrosis group. This also indicates that an increase in the level of plasma D-dimer suggests intestinal necrosis.
When a patient develops ischemic necrosis of the intestines, the permeability of the intestinal wall decreases, and bacteria in the intestine can migrate into the abdominal cavity. This causes abdominal cavity infection, leading to an increase in WBC count. In the context of AMI, elevated WBC count therefore indicates that intestinal strangulation or necrosis should be considered[31, 32]. Kassahun found that an increase in WBC counts can be used as an indicator of ischemic necrosis of the small intestine through analysis of clinical manifestations, laboratory examinations, and imaging of 60 cases of ischemic necrosis of the small intestine, which can support the decision to perform surgery for intestinal necrosis. Consistent with this result, we identified a statistically significant difference in WBC counts between patients in the intestinal necrosis group and the non-intestinal necrosis group.
The predictive model of intestinal necrosis based on serum BUN and plasma D-dimer levels as well as WBC counts offers a useful tool to guide clinical decision making for AMI patients. Most previous studies on this topic have focused on inflammatory or imaging indicators to predict the need for bowel resection, but biochemical indicators have rarely been included. Our model integrates inflammatory, thrombus-related, and biochemical indicators. Based on the accuracy of our model, the CPMIN can effectively predict intestinal necrosis and guide precise early intervention. Patients with high-risk AMI (CPMIN score≥-0.1992) should be promptly treated with surgery to avoid the various potential complications of delayed operation, whereas Patients in the low-risk AMI group (CPMIN score < -0.1992) can receive non-surgical treatment (Fig. 5). Thus, using the CPMIN may help to reduce the overall mortality of intestinal necrosis.
This study was somewhat limited by its small sample size, which may have resulted in some bias. In the subsequent research, we will expand the sample size and/or conduct a multi-center study to further validate the CPMIN. Furthermore, imaging data were not included in this study, but will be examined in follow-up studies. Professional radiologists will be invited to guide data collection and analysis. Finally, it was found in this study that some patients in the low-risk AMI group still had intestinal necrosis; further research is needed to reliably identify these patients. Nonetheless, the CPMIN presented here based on BUN level, WBC count, and D-dimer level is a simple and effective predictive model of intestinal necrosis in the context of AMI.