Stress ulcer

Short description: Tissue defect caused by physiological stress

Stress ulcer

Specialty| Intensive care medicine, gastroenterology, digestive system surgery (upper gastrointestinal surgery)

A stress ulcer is a single or multiple mucosal defect usually caused by physiological (not psychological) stress which can become complicated by upper gastrointestinal bleeding. These ulcers can be caused by shock, sepsis, trauma or other conditions and are found in patients with chronic illnesses. These ulcers are a significant issue in patients in critical and intensive care.

It was previously thought that peptic ulcers (a different type of ulcer) could be caused by psychological stress but this was proven false with the discovery of Helicobacter pylori and its role in the formation of this ulcer. Stress ulcers are a different condition and are formed by different mechanisms. The term stress ulcer is a proper medical term and should not be misinterpreted as indicating that these ulcers are caused by emotional stress. Epigastric pain correlated with emotional or psychological stress may be due to functional dyspepsia.[1] Here the term stress refers to extreme physiological changes in the body.

Another distinction between peptic and stress ulcers is their location in the upper gastrointestinal tract. Whereas ordinary peptic ulcers are found commonly in the gastric antrum and the duodenum, stress ulcers are usually found in the fundic mucosa and can be located anywhere within the stomach and proximal duodenum. Stress ulcers tend to present with multiple lesions whereas in peptic ulcers this is much more uncommon.

## Contents

* 1 Signs and symptoms
* 2 Risk factors
* 3 Mechanisms
* 3.1 Location
* 3.2 Lesions
* 3.3 Formation
* 4 Diagnosis
* 5 Prevention
* 6 Treatment
* 7 Epidemiology
* 8 References

## Signs and symptoms

Stress ulcers, as defined by overt bleeding and hemodynamic instability, decreased hemoglobin, and/or need for transfusion, were seen in 1.5% of patients in the 2252 patients in the Canadian Critical Care Trials group study.[2] People with stress ulcers have a longer ICU length of stay (up to eight days) and a higher mortality (up to four-fold) than patients who do not have stress ulceration and bleeding.[3] While the bleeding and transfusions associated with the stress ulcerations contribute to the increased mortality, the contribution of factors like low blood pressure, sepsis, and respiratory failure to the mortality independently of the stress ulceration cannot be ignored.

## Risk factors

Risk factors for stress ulcer formation that have been identified are numerous and varied. However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:

* Non-critically ill medical patients with two or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, kidney failure, stroke, hypertension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin.
* In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy.[2]
* The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients.

## Mechanisms

### Location

The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage.[4]

### Lesions

The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive gastroduodenitis. Occasionally, there may be a large acute ulcer in the duodenum (Curling's ulcer).[5]

Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration).[6]

### Formation

The pathogenic mechanisms are similar to those of erosive gastritis.[6]

The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastroduodenal mucosa.[7]

## Diagnosis

## Prevention

The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor.[8] It is unclear which agent is best or if prevention is needed at all.[9] Benefit may only occur in those who are not being fed.[10] Possible agents include antacids, H2-receptor blockers, sucralfate, and proton pump inhibitors (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers.[11]

Concerns with the use of stress ulcer prophylaxis agents include increased rates of pneumonia and  Clostridioides difficile colitis.[10]

## Treatment

The principles of management are the same as for the chronic ulcer.[12] The steps of management are similar as in erosive gastritis.[5]

Endoscopic means of treating stress ulceration may be ineffective and operation required.[12] It is believed that shunting blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury.[5]

Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid-base balance, and treatment of other illnesses help prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk.[13]

In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent bleeding from happening again. In selected patients, either endoscopic therapy or selective infusion of vasopressin into the left gastric artery may help control the hemorrhage.[14]

## Epidemiology

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.[10]

## References

1. ↑ Ford, Alexander C; Mahadeva, Sanjiv; Carbone, M Florencia; Lacy, Brian E; Talley, Nicholas J (2020). "Functional dyspepsia". The Lancet (Elsevier BV) 396 (10263): 1689–1702. doi:10.1016/s0140-6736(20)30469-4. ISSN 0140-6736. https://eprints.whiterose.ac.uk/166986/3/THELANCET-D-19-08082R1 CLEAN.pdf.
2. ↑ 2.0 2.1 "Risk factors for gastrointestinal bleeding in critically ill patients". N Engl J Med 330 (6): 377–81. 1994. doi:10.1056/NEJM199402103300601. PMID 8284001.
3. ↑ "The attributable mortality and length of intensive care unit stay of clinically important gastrointestinal bleeding in critically ill patients". Critical Care 5 (6): 368–75. Dec 2001. doi:10.1186/cc1071. PMID 11737927.
4. ↑ Manual of Gastroenterology by Gregory L. Eastwood, M.D. & Canan Avunduk, M.D., Ph.D. (1994)
5. ↑ 5.0 5.1 5.2 Hai, A.A. & Shrivastava, R.B. (2003). Textbook of Surgery. Tata/McGraw-Hill. ISBN 0074621491, p. 409
6. ↑ 6.0 6.1 Robbins Pathological Basis of Disease 6th Edition ISBN 8178670526 p. 796
7. ↑ Manual of Gastroenterology. Gregory L. Eastwood, M.D.& Canan Avunduk, M.D., Ph.D. (1994)
8. ↑ Krag, M; Perner, A; Wetterslev, J; Wise, MP; Hylander Møller, M (Jan 2014). "Stress ulcer prophylaxis versus placebo or no prophylaxis in critically ill patients. A systematic review of randomised clinical trials with meta-analysis and trial sequential analysis.". Intensive Care Medicine 40 (1): 11–22. doi:10.1007/s00134-013-3125-3. PMID 24141808.
9. ↑ Krag, M; Perner, A; Wetterslev, J; Møller, MH (Aug 2013). "Stress ulcer prophylaxis in the intensive care unit: is it indicated? A topical systematic review.". Acta Anaesthesiologica Scandinavica 57 (7): 835–47. doi:10.1111/aas.12099. PMID 23495933.
10. ↑ 10.0 10.1 10.2 Marik, PE; Vasu, T; Hirani, A; Pachinburavan, M (Nov 2010). "Stress ulcer prophylaxis in the new millennium: a systematic review and meta-analysis.". Critical Care Medicine 38 (11): 2222–8. doi:10.1097/CCM.0b013e3181f17adf. PMID 20711074.
11. ↑ Alhazzani, W; Alenezi, F; Jaeschke, RZ; Moayyedi, P; Cook, DJ (Mar 2013). "Proton pump inhibitors versus histamine 2 receptor antagonists for stress ulcer prophylaxis in critically ill patients: a systematic review and meta-analysis.". Critical Care Medicine 41 (3): 693–705. doi:10.1097/CCM.0b013e3182758734. PMID 23318494.
12. ↑ 12.0 12.1 Bailey & Love’s SHORT PRACTICE OF SURGERY 23rd Edition ISBN 0-340-75949-6 page 916
13. ↑ Manual of Gastroenterology priyank sinha Gregory L. Eastwood, M.D. & Canan Avunduk, M.D., Ph.D. (1994)
14. ↑ A Practical Approach to Emergency Medicine by Robert J. Stine, M.D., Carl R. Chudnofsky, M.D., Cynthia K. Aaron, M.D. (1994)

* v
* t
* e

Intensive care medicine

* Health science
* Medicine
* Medical specialities
* Respiratory therapy

General terms|

* Intensive care unit (ICU)
* Neonatal intensive care unit (NICU)
* Pediatric intensive care unit (PICU)
* Coronary care unit (CCU)
* Critical illness insurance

Conditions|

| Organ system failure|

Shock sequence
SIRS
Sepsis
Severe sepsis
Septic shock
Multiple organ dysfunction syndrome

Other shock
Cardiogenic shock
Distributive shock
Anaphylaxis
Obstructive shock
Neurogenic shock
Spinal shock
Vasodilatory shock

Organ failure
Acute renal failure
Acute respiratory distress syndrome
Acute liver failure
Respiratory failure
Multiple organ dysfunction syndrome

* Neonatal infection
* Polytrauma
* Coma

|

Complications|

* Critical illness polyneuropathy / myopathy
* Critical illness–related corticosteroid insufficiency
* Decubitus ulcers
* Fungemia
* Stress hyperglycemia
* Stress ulcer

Iatrogenesis|

* Methicillin-resistant Staphylococcus aureus
* Oxygen toxicity
* Refeeding syndrome
* Ventilator-associated lung injury
* Ventilator-associated pneumonia
* Dialytrauma

Diagnosis|

* Arterial blood gas
* Catheter
* Arterial line
* Central venous catheter
* Pulmonary artery catheter
* Blood cultures
* Screening cultures

Life-supporting treatments|

* Airway management
* Chest tube
* Dialysis
* Enteral feeding
* Goal-directed therapy
* Induced coma
* Mechanical ventilation
* Therapeutic hypothermia
* Total parenteral nutrition
* Tracheal intubation

Drugs|

* Analgesics
* Antibiotics
* Antithrombotics
* Inotropes
* Intravenous fluids
* Neuromuscular-blocking drugs
* Recombinant activated protein C
* Sedatives
* Stress ulcer prevention drugs
* Vasopressors

ICU scoring systems|

* APACHE II
* Glasgow Coma Scale
* PIM2
* SAPS II
* SAPS III
* SOFA

Physiology|

* Hemodynamics
* Hypotension
* Level of consciousness
* Acid–base imbalance
* Water-electrolyte imbalance

Organisations|

* Society of Critical Care Medicine
* Surviving Sepsis Campaign
* European Society of Paediatric and Neonatal Intensive Care

Related specialties|

* Anesthesiology
* Cardiology
* Internal medicine
* Neurology
* Pediatrics
* Pulmonology
* Surgery
* Traumatology

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