González JD, Mejía BS, Cruz FM

Language: Spanish
References: 15
Page: 1-12
PDF size: 230.60 Kb.

ABSTRACT

Stress ulcers are defined as erosions of the gastric mucosa, caused by physiological imbalances that are triggered by severe symptoms. Pathophysiology of stress ulcers originate from endothelin-1 excess production, nitric oxide deficiency, systemic hypoperfusion, hyperstimulation of gastrin production and therefore production of hydrochloric acid, prostaglandin deficiency and sphincter dysfunction. This pathophysiology occurs in seriously ill patients, which is why it can be found in patients admitted to an Intensive Care Unit. The use of oral anticoagulants and non-steroidal anti-inflammatory drugs, assisted mechanical ventilation, severe trauma, sepsis, and chronic kidney or liver disease are some of the most common risk factors to the development of this disease. Stress ulcers are superficial and are defined by a visible border. Patients can be asymptomatic or display a variety of symptoms as far as profuse bleeding and hemodynamic instability. Patients are classified into four categories according to the severity of risk factors; low, moderate, high, and very high risk of stress ulcers. Depending on the category of risk that the patient presents, it is recommended to start prophylactic therapy with drugs that inhibit the production of hydrochloric acid such as Proton Pump Inhibitors and Histamine Receptor Blockers. This medications have shown their benefits by reducing the mobility and mortality rates of stress ulcers patients.

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