Critically ill patients often experience gastrointestinal organ involvement due to the massive release of inflammatory mediators, capillary leakage, significant fluid exudation, and vascular dysregulation. When gastrointestinal function is impaired, it affects the digestion and absorption of nutrients and water, disrupts the absorption and regulation of gut microbiota and its products, and subsequently impacts the gastrointestinal endocrine and immune functions.
Acute gastrointestinal injury (AGI) frequently occurs during critical illness and is a component of multiple organ dysfunction syndrome (MODS). The more organs involved, the higher the incidence and mortality rate. With the advancement of critical care medicine, our understanding and research of gastrointestinal dysfunction is gradually deepening.
In 2012, the European Society of Intensive Care Medicine (ESICM) formally proposed the concept of acute gastrointestinal injury (AGI), defining it as “gastrointestinal dysfunction caused by the acute disease itself in critically ill patients.” The definition and classification standards of AGI are based on objective indicators such as visible bleeding in stool or gastric contents, the frequency of diarrhea, lower gastrointestinal paralysis, feeding intolerance, nausea, vomiting, bowel movement frequency, bowel sounds, gastric retention, and intra-abdominal pressure.
AGI is classified into four levels of severity: Level 1 indicates the risk of gastrointestinal dysfunction and failure; Level 2 indicates gastrointestinal dysfunction; Level 3 indicates gastrointestinal failure; and Level 4 indicates gastrointestinal failure accompanied by distant organ dysfunction. This classification is elaborated from the perspectives of definitional criteria, basic pathology, symptom examples, and treatment recommendations, providing clear and detailed guidance for clinical practice and academia.
Definition of AGI Classification
Level 1: The so-called risk of gastrointestinal dysfunction and failure is defined as having a clear cause with partial impairment of gastrointestinal function. Common symptoms include early postoperative nausea and vomiting; disappearance of bowel sounds in early shock; and reduced intestinal motility. The pathophysiology is characterized by a temporary and self-limiting response following a significant insult to the patient, such as surgery or shock.
Treatment recommendations include early enteral nutrition within 24-48 hours following gastrointestinal injury and minimizing the use of medications that impair gastrointestinal motility. For nausea and vomiting symptoms, antiemetics should be initiated as soon as possible if prevention has not been effective, with commonly used medications including dexamethasone, ondansetron, dolasetron, haloperidol, and ephedrine. For symptoms of absent bowel sounds or reduced intestinal motility, the use of medications that impair gastrointestinal motility (such as catecholamines and opioids) should be minimized.
Level 2: Gastrointestinal dysfunction is defined as the inability of the intestine to maintain complete digestion and absorption functions, failing to meet the body’s needs for nutrients and water. Common symptoms include gastroparesis with significant gastric retention or reflux; lower gastrointestinal paralysis; diarrhea; visible bleeding in gastric contents or stool; and feeding intolerance (enteral nutrition not reaching the target of 20 kcal/kg BW/day within 72 hours). At this level, the concept of intra-abdominal hypertension (IAH) is introduced, with Level I (IAP= 12-15 mmHg) representing severe gastrointestinal complications without specific interventions for the gastrointestinal tract (or due to abdominal surgery).
Treatment recommendations include addressing IAH; restoring gastrointestinal function, such as using prokinetic agents; and starting or maintaining enteral nutrition. If significant gastric retention or reflux occurs, or if feeding intolerance is present, a trial of small amounts of enteral nutrition may be considered. For patients with gastroparesis, if prokinetic agents are ineffective, post-pyloric feeding should be considered.
For gastric retention symptoms, routine use of prokinetic agents is not recommended; opioids should be avoided or minimized to reduce sedation depth; and routine post-pyloric feeding is not advocated. For diarrhea symptoms, active investigation and correction of the underlying causes should be pursued; the feeding speed should be slowed, the feeding tube repositioned, or the nutritional formula diluted, potentially adding soluble dietary fiber to extend transit time.
For feeding intolerance symptoms, limit the use of medications that impair intestinal motility, and consider using prokinetic agents and/or laxatives (1C), controlling IAP; routinely consider trying small amounts of enteral nutrition. Patients intolerant to enteral nutrition should receive supplemental parenteral nutrition (PN) (2D).
For IAH symptoms, dynamic monitoring of fluid resuscitation should be performed to avoid over-resuscitation (1C); for patients with primary IAH post-surgery, continuous thoracic epidural analgesia may reduce IAP (2B); the use of nasogastric tubes/colonic decompression methods to evacuate gastrointestinal contents is recommended (2D); for patients with abdominal effusion, percutaneous drainage is recommended (1C); muscle relaxants can lower IAP, but due to excessive side effects, they should only be used in specific patients (2C).
Level 3: Gastrointestinal failure is defined as the inability to restore gastrointestinal function despite intervention, with no improvement in overall condition. The pathophysiology is characterized by persistent intolerance to enteral nutrition, with no improvement even after treatment (e.g., erythromycin, placement of post-pyloric tubes), leading to the persistence or worsening of MODS. Clinically, this is manifested as persistent intolerance to enteral nutrition after treatment, significant gastric retention, and persistent gastrointestinal paralysis, with intestinal dilation appearing or worsening IAH progressing to Level II (IAP 15-20 mmHg) and decreased abdominal perfusion pressure (APP <60 mmHg, APP = MAP-IAP). Treatment should include stopping medications that cause gastrointestinal paralysis as soon as possible (1C), and if EN is insufficient, avoid early initiation of PN (within 7 days before ICU admission) to reduce the incidence of hospital-acquired infections (2B).
Level 4: Gastrointestinal failure accompanied by distant organ dysfunction is defined as the progressive deterioration of AGI, with worsening MODS and shock, posing an imminent life threat. The pathophysiology is characterized by a dramatic deterioration in the patient’s general condition, accompanied by distant organ dysfunction. Clinical manifestations include intestinal ischemia and necrosis, gastrointestinal bleeding leading to hemorrhagic shock, Ogilvie’s syndrome, and abdominal compartment syndrome (ACS) requiring active decompression. Conservative treatment is ineffective, necessitating emergency laparotomy or other urgent interventions (e.g., colonoscopic decompression) (1D).
Treatment Principles for AGI
Due to the severe adverse impact of IAH/ACS on the prognosis of critically ill patients, the clinical management principles are as follows:
1. Actively and effectively manage the primary disease, enhancing early treatment of shock, trauma, and infection to eliminate conditions that produce excessive inflammatory responses.
2. Correct shock and improve gastrointestinal mucosal blood perfusion, with particular attention to correcting hidden compensatory shock. Monitoring of gastric mucosal pH (pHi) may be necessary.
3. Selective decontamination of the digestive tract (SDD) antibiotic ecological therapy: targeting pathogenic and opportunistic bacteria, SDD falls within this category. Microecological agent ecological therapy: used for commensal and neutral bacteria.
4. Scavenging of oxygen free radicals: Oxygen free radicals play a significant role in ischemia-reperfusion injury, hence prevention is key. Vitamin E and Vitamin C are low-molecular-weight scavengers of oxygen free radicals, primarily acting by providing hydrogen to convert oxygen free radicals into inert molecules, thus losing their harmful effects. Allopurinol reduces the production of free radicals by inhibiting xanthine oxidase activity. Glucose and mannitol also help scavenge free radicals, mainly reacting with hydroxyl radicals (-OH).
5. Traditional Chinese medicine treatment: Utilizing the theories of “activating blood circulation and removing stasis,” “clearing heat and detoxifying,” and “supporting the body and nourishing yin,” treatments centered on rhubarb for catharsis and mirabilite external application have achieved good clinical efficacy. The protective effects of rhubarb on the intestinal mucosa include promoting intestinal motility, relieving intestinal paralysis, protecting tight junctions between cells, maintaining structural integrity, preserving intestinal microecological balance, activating blood circulation and removing stasis, improving microcirculation, and increasing tissue perfusion.
6. Nutritional support: Its significance lies in improving the structure of the digestive tract; reducing the catabolic response to injury; promoting wound healing; lowering complication rates, shortening hospital stays, reducing associated costs, and improving clinical outcomes. Nutritional support can be administered via parenteral nutrition, either through peripheral or central venous routes, or enteral nutrition via feeding tubes through the gastrointestinal tract.
According to AGI guidelines, early enteral nutrition for patients with gastrointestinal dysfunction can effectively improve nutritional status, reduce gastrointestinal injury, and lower the risk of mortality.
It significantly aids in restoring gastrointestinal function, increasing protein intake, synthesizing enzymes, and other substances, with the timing of administration being within 24-48 hours of ICU admission; the conditions for implementation are hemodynamic stability and absence of contraindications to enteral nutrition.
If shock or high-dose vasopressors are present in the acute resuscitation early stage, initiation may be postponed; on the first day: monitor gastric retention for 4-6 hours, if gastric retention fluid is <200ml, and there is no significant abdominal distension or contraindications to enteral nutrition, enteral nutrition may be administered. Bowel sounds: it is common for critically ill patients not to have bowel sounds, which does not imply that the small intestine lacks absorptive capacity. Do not stop EN or reduce the speed due to the absence of bowel sounds.
In cases of intestinal obstruction and intestinal ischemia leading to excessive intestinal dilation, worsening intestinal blood flow, or even intestinal necrosis and perforation, enteral nutrition should not be administered. Severe abdominal distension or abdominal compartment syndrome increases intra-abdominal pressure, raising the incidence of reflux and aspiration pneumonia, further worsening respiratory and circulatory function. Enteral nutrition should also be stopped in cases of severe abdominal distension and diarrhea not improving with general treatment.
The key to treating gastrointestinal dysfunction in critically ill patients lies in actively addressing the primary disease during the early stages of critical illness and emphasizing the maintenance of gastrointestinal barrier function and early enteral nutrition to prevent gastrointestinal function from progressing from dysfunction to failure. This is beneficial for reducing the occurrence of MODS and improving the success rate of clinical rescue.