Acute and stress ulcers: causes, diagnosis, treatment

Acute ulcers are superficial or deep defects in the gastric/duodenal mucosa that develop rapidly due to strong provoking factors: severe stress (shock, sepsis, burns, traumatic brain injury), major surgery, multiple organ failure, and certain medications. In intensive care units, the term stress-related mucosal disease (SRMD) is used to describe diffuse acute lesions: initially, multiple superficial erosions in the body/fundus of the stomach, then—if the course is unfavorable—true ulcers with the risk of bleeding. Classic clinical symptoms (pain) are often absent: the first symptoms are gastrointestinal bleeding or anemia. [1]

Historically, the risk of stress ulcers in critically ill patients was high, but with improvements in intensive care and early enteral nutrition, the incidence of clinically significant bleeding has decreased significantly. This has also changed the approach to prevention: today, the goal is not to "cover everyone just in case"; it is more important to recognize high-risk patients and provide targeted prevention. The latest SCCM/ASHP consensus (2024) emphasizes that the greatest risk is in patients with coagulopathy, shock, and severe liver disease, and the evidence for "ventilation for >48 hours" as the sole criterion is weaker than previously thought. Early enteral nutrition itself reduces the risk of bleeding. [2]

It is important to distinguish acute stress ulcers from chronic peptic ulcer disease ( Helicobacter pylori, NSAIDs): the mechanisms, tactics, prognosis, and coding differ. In acute bleeding, these differences are not always immediately apparent, so endoscopy becomes crucial: it will determine the type of lesion, the source of bleeding, and allow for immediate hemostasis. Current ACG/ESGE guidelines detail the route: rapid risk assessment (Glasgow-Blatchford), early endoscopy after stabilization, endoscopic hemostasis, and intensive acid inhibition in patients with high-risk ulcers. [3]

Finally, in some patients, "acute ulcers" develop outside the intensive care unit—for example, after major surgeries, due to severe burns, or high doses of glucocorticoids combined with anticoagulants. Here, too, the principle of "selective prevention" applies: we assess risk factors, improve nutrition, and prescribe short courses of antisecretory drugs only to those who truly need them. This reduces side effects (pneumonia, Clostridioides difficile ) while maintaining effectiveness. [4]

Code according to ICD-10 and ICD-11

In ICD-10, acute ulcers are coded by location and complications. For acute gastric ulcers, K25.0 (with bleeding), K25.1 (with perforation), K25.2 (with bleeding and perforation), and K25.3 (without complications) are used. For acute duodenal ulcers, K26.0-K26.3 are used according to the same logic. If bleeding occurs from erosive gastritis/duodenitis without a formed ulcer, codes for gastroduodenitis with bleeding are used (e.g., K29.6). Additional external codes are used for drug-induced causes (NSAIDs, anticoagulants). [5]

In ICD-11, peptic ulcer disease is grouped into the DA60-DA63 block: DA60 - gastric ulcer, DA63 - duodenal ulcer, DA61 - "peptic ulcer, site unspecified." Detailing of complications (bleeding, perforation), severity, and risk factors is achieved through post-coordination—by adding attributes and external codes. This approach allows for the accurate coding of, for example, "acute gastric ulcer with bleeding due to shock/coagulopathy" or "stress-induced mucosal injury with bleeding." [6]

Table 1. Examples of coding of acute/stress ulcers

Clinical situation	ICD-10 (example)	Comment	ICD-11 (example)
Acute gastric ulcer with bleeding	K25.0	Indication "acute" + complication	DA60 + "bleeding" attribute
Acute duodenal ulcer with perforation	K26.1	Urgent surgical tactics	DA63 + "perforation"
Bleeding from erosive gastritis (SRMD)	K29.6	Without formed ulcer	DA4Y (gastritis) + "bleeding"
History of peptic ulcer (for discharge)	Z87.11	History of peptic ulcer disease	Historical modifier in ICD-11 [7]

Epidemiology

Acute stress-induced mucosal injury develops rapidly—in the first 4-5 days of a severe critical condition. Clinically significant bleeding is significantly less common today than decades ago, which is attributed to improved intensive care and early enteral nutrition. However, in the presence of significant risk factors, it remains dangerous and is associated with increased mortality and length of hospital stay. [8]

The classic "major" risk factors in critically ill patients were described in Cook's landmark study: respiratory failure with mechanical ventilation and coagulopathy sharply increased the likelihood of significant bleeding. Later meta-analyses and new guidelines added nuance: coagulopathy, shock, and severe liver disease are the most compelling factors today, while "mechanical ventilation for >48 hours" is assessed more cautiously in isolation. In any case, a combination of factors increases the risk exponentially. [9]

In non-intensive care units, "acute ulcers" are more often associated with surgical stress, trauma, burns, high doses of glucocorticoids/anticoagulants, and severe sepsis. Their contribution to the pattern of non-variceal upper gastrointestinal bleeding varies across centers but is significant, especially in elderly and polypharmacy-treated patients. [10]

Non-variceal bleeding remains a common cause of emergency hospitalization in the general population, with an estimated incidence of 80-150 cases per 100,000 per year and a mortality rate of 2-10%, depending on age/comorbidity. The proportion of acute ulcers among all blood sources ranges from several to tens of percent, necessitating standardized management: rapid stabilization, early endoscopy, and proton pump therapy. [11]

Reasons

The initial "spark" for acute and stress ulcers is the mismatch between the aggressiveness of gastric contents and the protective properties of the mucosa. In critical conditions, blood flow and mucus/bicarbonate secretion are reduced, the epithelial barrier is disrupted, and ischemia-reperfusion is activated. Against this backdrop, even normal acid levels become destructive, and microerosions quickly transform into ulcers. [12]

Outside of intensive care units, acute ulcers are triggered by surgical stress, burns (classic "Curling's ulcers"), severe trauma/neurotrauma ("Cushing's ulcers"), massive blood loss, and shock. Medications play a significant role: combinations of anticoagulants/antiplatelet agents, systemic glucocorticoids (especially with NSAIDs), and high doses of sympathomimetics. [13]

Bleeding most often occurs from fundal/corpus lesions of SRMD, but can also originate from the duodenum. Multiple superficial defects are observed in critical stress, while deep, solitary ulcers are possible in drug-induced lesions (NSAIDs) and ischemia. Endoscopic examination helps differentiate these variants. [14]

The role of the absence of nutrition is worth mentioning separately: a long zero-oral pause deprives the mucosa of “trophic” stimuli, and early enteral nutrition reduces the risk of bleeding and is sometimes comparable in prophylactic effectiveness to medications in patients who tolerate it. [15]

Risk factors

Traditionally, mechanical ventilation for >48 hours and coagulopathy were considered "major" risk factors; these findings have been confirmed by numerous cohorts and reviews. However, the updated 2024 SCCM/ASHP guidelines highlight coagulopathy, shock, and chronic liver disease as the most reliable predictors, while isolated prolonged ventilation is assessed with caution. In practice, this means that prophylaxis is indicated not for "everyone on mechanical ventilation," but for those at truly high risk. [16]

Clinically significant additional factors include renal failure, multiple injuries, high severity index, large burns, spinal injury, high doses of steroids combined with anticoagulants, and lack of enteral nutrition. The more factors combined, the higher the risk of bleeding without prophylaxis. [17]

In general medical departments, attention is paid to combinations of anticoagulants/antiplatelet agents, advanced age, severe infections, and hypotension. Here, the absolute risk is lower than in intensive care, but the consequences of blood loss in vulnerable patients are serious, hence the interest in short, targeted prophylaxis courses. [18]

Table 2. Risk factors for bleeding in SRMD/acute ulcers

Factor	Comment
Coagulopathy	The most stable predictor (modern guides)
Shock/hypoperfusion	Mucosal ischemia → erosions/ulcers
Severe liver disease	Coagulopathy + portal gastropathy
Mechanical ventilation >48 h (isolated)	Evaluate with caution; more significant in combinations
Lack of enteral nutrition	Nutrition is a protective factor [19]

Pathogenesis

The key factor is visceral hypoperfusion in shock/sepsis: oxygen delivery is reduced, mucosal microcirculation is disrupted, and the production of protective mucus and bicarbonate decreases. When perfusion is restored, oxidative stress is added, further exacerbating the damage. This results in the typical "carpet" erosive lesion of the upper stomach. [20]

In non-nursed patients, a long-term "zero" diet eliminates trophic signals: gastrointestinal hormones, vagal mechanisms, and local prostaglandins. Therefore, early enteral nutrition is not only about calories but also about supporting barrier function; this is the basis for studies demonstrating a lower incidence of bleeding in fed patients. [21]

In drug-induced acute ulcers, inhibition of prostaglandin synthesis (NSAIDs) is important, while the combination of GCS and anticoagulants reduces mucosal regeneration and disrupts hemostasis. Severe liver disease can lead to coagulation and hemodynamic changes. [22]

If the ulcer is already bleeding, the leading role is played by a local vascular defect (visible vessel, active leakage) - hence the effectiveness of endoscopic hemostasis (injections, thermal/mechanical techniques) and the need for subsequent intensive acid suppression to stabilize the clot. [23]

Symptoms

In critically ill patients, specific complaints are rare: hematemesis, "coffee grounds" on the catheter, melena or sudden anemia, and hemodynamic instability are common initial manifestations. Often, the source is precisely "stress erosions/ulcers" in the stomach. Blood loss can be occult; therefore, hemoglobin is monitored and gastric aspirate is carefully examined. [24]

In general hospital settings, acute ulcers often cause black stools, bloody vomiting, weakness, dizziness, and sometimes epigastric pain. It's important to remember that in older patients, the pain may "dissipate," while hemodynamics suffer quickly, especially when anticoagulants are used. [25]

When combined with duodenitis/erosive gastritis, bleeding may be self-limiting, but it is impossible to assess the risk of recurrence without endoscopy. Warning signs include tachycardia, hypotension, a drop in hemoglobin to >20 g/L, and comorbidity. [26]

A rare but dangerous onset is perforation with acute "dagger-like" pain syndrome and signs of peritonitis—this is more common with a single deep ulcer (NSAIDs, ischemia) than with diffuse SRMD. Urgent surgical intervention is required. [27]

Forms and stages

In practice, the following are distinguished: (1) stress-induced mucosal lesions (diffuse erosions, sometimes “fresh” small ulcers) in critically ill patients; (2) acute solitary ulcers (medicinal, ischemic, postoperative); (3) acute bleeding ulcers as a subtype of non-varicose bleeding. The division is important for prevention and treatment tactics. [28]

Bleeding stigmas are assessed endoscopically: active blood flow, visible vessel, clot, and a "clear" base. These factors determine the extent of hemostasis and the intensity of subsequent proton pump inhibitor therapy. Current guidelines also allow intermittent PPI regimens as an alternative to continuous infusion for high-risk ulcers. [29]

In intensive care, it is advisable to stratify patients by risk profile: high-risk patients (coagulopathy, shock, severe liver disease, etc.) receive prophylaxis, while low-risk patients do not; tolerance of enteral feeding is considered as a risk-reducing factor. This "triage" reduces hyperprescription of PPI/H2 blockers. [30]

Table 3. Endoscopic stigmas and management (ACG/ESGE simplified)

Stigma	Action in endoscopy	After endoscopy
Active bleeding/visible vessel	Combined hemostasis (injection + clip/heat)	High-dose PPI 72 h (continuous or intermittent)
A firmly attached clot	Attempt to remove → as above; if not possible - intensive PPI	Observation, PPI
"Clean" bottom/flat spot	Hemostasis is not needed	Standard doses of PPI, early diet/discharge [31]

Complications and consequences

The main complications are massive bleeding, recurrent bleeding, and perforation. In critically ill patients, even moderate blood loss impairs oxygenation and increases the burden of blood transfusions. The risk of recurrence is high in cases of severe stigmata (active blood flow/visible vessel), requiring enhanced PPI regimens and observation. [32]

If endoscopy fails, the next step is transcatheter arterial embolization (TAE): in recent years, it has established itself as an effective and relatively safe alternative to emergency surgery. Recent reviews and meta-analyses demonstrate good technical and clinical success of TAE for non-variceal bleeding. [33]

Widespread use of prophylaxis also carries its risks: associations with hospital-acquired pneumonia and Clostridioides difficile are inconclusive and depend on the population and study design. Modern network meta-analyses generally confirm a reduction in "major" bleeding with PPI/H2 blockers compared to no prophylaxis, but side effects require targeted use and early discontinuation when the risk has decreased. [34]

Outside of intensive care, complications are different: even a "small" ulcer can lead to significant blood loss when treated with anticoagulants. Early endoscopy, adjustment of anticoagulation, and reintroduction of antithrombotics within a safe time after hemostasis are essential. [35]

When to see a doctor

Immediately - if vomiting blood, passing tarry stools, experiencing sudden weakness/dizziness, or fainting. These are signs of potentially dangerous bleeding, requiring emergency care with access to an endoscope. Even if the episode has stopped, the risk of recurrence remains without treatment. [36]

For hospitalized patients, the following are warning signs: blood/"coffee grounds" in the gastric aspirate, a drop in hemoglobin, and unstable blood pressure. Urgent evaluation by a physician, adjustment of anticoagulation according to protocol, and preparation for endoscopy are required. [37]

After discharge, contact your doctor if you experience recurrence of black stools/bloody vomit, increased weakness, or abdominal pain with muscle tension (suspected perforation). For patients on anticoagulants, any blood loss requires immediate medical attention. [38]

If you are at risk (severe liver disease, history of shock, recent hospitalization, major surgery), discuss short-term prophylaxis and an early drug withdrawal strategy once you are no longer at “high risk.” [39]

Diagnostics

Diagnosis begins with an assessment of severity: pulse, blood pressure, volume of blood loss, and the need for transfusion. ACG guidelines suggest targeted management: red blood cell transfusions for Hb <7 g/dL, early administration of erythromycin before endoscopy (improves visualization), and use of the Glasgow-Blatchford classification system to identify very low risk. [40]

Endoscopy is the "gold standard": it allows one to visualize the source, assess stigmas, and immediately perform hemostasis (injections, thermocoagulation, clipping; in case of recurrence, a "drip-clip"). Maintenance acid suppression stabilizes the clot and reduces recurrence. If endoscopy fails, angiography with embolization is performed. [41]

Laboratory minimum: complete blood count, coagulogram, biochemistry, blood type/Rhesus factor. If drug-induced blood loss is suspected, medications are specified; in sepsis, inflammatory markers are tested. In the intensive care unit, tolerance to enteral nutrition is assessed simultaneously; this influences the preventive strategy. [42]

Differential diagnosis includes variceal bleeding (due to portal hypertension), erosive esophagitis, Mallory-Weiss syndrome, and tumors. Endoscopic examination and medical history help differentiate these. If the source is in doubt, especially with ongoing bleeding, CT angiography is performed. [43]

Table 4. Diagnostic route for suspected acute ulcerative bleeding

Step	What are we doing?	For what
Stabilization	Veins, fluids, correction of coagulopathy	Safety before endoscopy
Risk assessment	GBS, Hb-trigger 7 g/dl, erythromycin	Stratification and preparation
Endoscopy	Verification + immediate hemostasis	We treat and determine the risk of relapse.
In case of failure	CT angio → TAE	Rescue strategy [44]

Differential diagnosis

Stress erosions/ulcers should be distinguished from chronic peptic ulcers ( H. pylori, NSAIDs): chronic ulcers often have solitary duodenal ulcers with "scarred" edges; SRMDs have superficial multiple defects in the body/fundus of the stomach. However, in the case of active bleeding, the decision is made not by morphology, but by stigmata and available hemostasis tactics. [45]

Stress ulcers are differentiated from variceal bleeding (cirrhosis) by endoscopy and medical history; treatment and medications (vasopressors, ligation) are different. With erosive esophagitis, bleeding is usually less, but is possible in patients on mechanical ventilation and nasogastric tubes. [46]

In the first hours, it is important not to miss ischemic/drug-induced ulcers (single, "deep," with risk of perforation), Mallory-Weiss syndrome (after vomiting), and, in cancer patients, bleeding tumors. The key here is endoscopy with targeted hemostasis and biopsy if necessary. [47]

Table 5. “Hints” for differentiation

Sign	More likely
Multiple superficial lesions on the body/bottom	SRMD/stress erosions
Single deep ulcer + NSAIDs/ischemia	Acute drug/ischemic ulcer
Esophageal/gastric varices, cirrhosis	Varicose bleeding
Linear rupture of the cardia after vomiting	Mallory-Weiss [48]

Treatment

1) Acute bleeding episode. ACG/ESGE standard: early endoscopy after stabilization, if necessary - intravenous erythromycin before the procedure, endoscopic hemostasis using combined methods for high-risk stigmas, then high-dose proton pump inhibitor therapy for 72 hours (continuous infusion of 80 mg bolus → 8 mg/h or intermittent doses of 40 mg 2-4 times a day). Then - transition to standard doses of PPI. In case of failure/relapse: repeat endoscopy → TAE as a salvage option. [49]

2) Prophylaxis in the critically ill (CPI). The modern approach is selective: prophylaxis is indicated for high-risk patients (coagulopathy, shock, severe liver disease, etc.), and not for everyone. Enteral nutrition, if tolerated, itself reduces the risk of bleeding and can reduce the need for drugs; RCTs and meta-analyses show a very low incidence of bleeding with early feeding and no additional benefit from "routine" PPI in such patients. If pharmacoprophylaxis is necessary, PPI or H2 blockers are used in standard doses, assessing the risk of pneumonia/ C. difficile and discontinuing it as soon as possible if the risk decreases. [50]

3) Drug selection and safety. Network meta-analyses confirm that both PPIs and H2 blockers reduce clinically important bleeding compared with no prophylaxis; PPIs are likely more effective than H2 blockers, but may be associated with a higher risk of pneumonia compared with sucralfate (data are heterogeneous). Recent reviews from 2024-2025 indicate minimal or no effect on C. difficile and overall mortality, but emphasize the importance of adequate patient selection. Conclusion: drug selection should be individualized, with the lowest effective dose and duration. [51]

4) Postoperative/medication-induced acute ulcers. A short course of PPI (e.g., 4-8 weeks) is standard; it is essential to review the trigger medications (NSAIDs, GCS in combination with anticoagulants) and optimize pain control with alternatives. If it is necessary to continue antithrombotics, discuss the gastroprotective properties of PPI and the timing of resumption after hemostasis. [52]

5) Interventional technologies. In endoscopy, the role of cap-clips has increased for recurrent ulcer bleeding; in the X-ray endovascular service, embolization with NBCA/coils is a reliable option in case of endoscopy failure. Prophylactic embolization "just in case" is discussed, but according to recent data, it does not improve outcomes compared to the standard in high-risk lesions; it is reserved for clear indications. [53]

Table 6. Prevention in the Critically Ill (2024 SCCM/ASHP Summary)

Situation	Tactics
High risk (coagulopathy, shock, severe liver disease, etc.)	SUP needs: PPI or H2 blocker + early enteral feeding
No high risk, tolerates feeding	Enteral nutrition without pharmaco-SUP
Any scenario	Regularly reassess and discontinue SUP early when risk decreases [54]

Prevention

In intensive care, prevention is built on two pillars: early enteral nutrition and targeted pharmacoprophylaxis for high-risk patients only. This approach simultaneously reduces bleeding and minimizes the side effects of unnecessary PPI/H2 blockers. Maintaining perfusion (treating shock), monitoring coagulation, and gentle sedation are important non-pharmacological measures. [55]

In surgical/burn units, the extent of the injury and hemodynamic stability are the primary consideration. Short courses of PPI (or H2) are used where the risk is high and are immediately discontinued when nutrition and stabilization are initiated. Standardized departmental protocols help avoid hyperprescription. [56]

In the outpatient setting, prevention primarily involves managing drug risks: minimizing NSAID use, avoiding dangerous combinations (NSAIDs + GCS + anticoagulant/antiplatelet agent), and selecting gastroprotective measures when anticoagulation is unavoidable. It is important for patients to recognize the "red flags" and not delay seeking medical attention at the first episode of black stool or bloody vomiting. [57]

Table 7. Do's and Don'ts for SUP Practice

Can	It is forbidden
Feed as early as possible if tolerated.	Assign SUP to everyone "just in case"
Give PPI/H2 only if risk is high	Keep SUP after risk reduction/switching to nutrition
Review the need for SUP daily	Ignore the risk of pneumonia/intestinal infections
In case of bleeding: endoscopy + intensive PPI	Delaying endoscopy without reason [58]

Forecast

Thanks to standardized treatment, the prognosis for acute/stress ulcers has improved: with proper routing, most bleeding can be controlled endoscopically with a low risk of recurrence when PPI protocols are followed. Mortality is now determined primarily by the severity of the underlying condition, not the ulcer itself. [59]

In critically ill patients, the greatest benefit is achieved by targeted prophylaxis and early enteral feeding, which reduces the incidence of bleeding without excessive side effects. Where endoscopy is unsuccessful or unavailable, TAE offers a high chance of controlling bleeding with less invasiveness than emergency surgery. [60]

In drug-induced acute ulcers, the prognosis is good with prompt discontinuation of triggers and a short course of PPI. Recurrent episodes are usually associated with reintroduction of risky drug combinations—a drug interaction checklist is helpful here. [61]

It's important to remember: even successfully treated bleeding requires secondary prevention—from adjusting medications to educating the patient about red flags. This reduces rehospitalizations and improves quality of life. [62]

FAQ

Is this the same as a "regular" ulcer due to H. pylori?
No. Stress ulcers and SRMD are acute lesions in severe conditions, often multiple and superficial; a "regular" ulcer is a chronic condition (often H. pylori /NSAID). Approaches to prevention and treatment differ. [63]

Do all patients in intensive care require prophylaxis?
No. Current guidelines recommend prophylaxis only for high-risk patients (coagulopathy, shock, severe liver disease, etc.) and to begin enteral nutrition as early as possible. [64]

Which is better for prophylaxis: PPIs or H2 blockers?
Both classes reduce clinically important bleeding compared with no prophylaxis; PPIs are probably more effective, but safety issues (pneumonia) require individual choice and early discontinuation. [65]

How is acute ulcer bleeding treated?
Stabilization → early endoscopy with hemostasis → intensive PPI for 72 hours → transition to standard doses. If unsuccessful, embolization. This algorithm improves outcomes and reduces recurrence. [66]

What diagnosis codes should be used?
ICD-10: K25.0-K25.3 (acute gastric ulcer), K26.0-K26.3 (acute duodenal ulcer); for erosive gastritis with bleeding - K29.6. ICD-11: DA60/DA63 with post-coordination complications. [67]