Stress ulcer prophylaxis in critically ill patients
Stress ulcer prophylaxis is the prevention of stomach ulcers and bleeding in at-risk critically ill patients, and the first-line drug is a proton pump inhibitor, which suppresses acid.
Remember
In at-risk critically ill patients, give a proton pump inhibitor before any bleeding starts, and stop it once the risk has gone.
Very sick patients in intensive care can develop stress-related mucosal disease: shallow ulcers in the lining of the stomach (the mucosa) that can bleed. The disease arises mainly from poor blood flow to the gut, followed by injury when flow returns (reperfusion injury), which weakens the lining's defences against stomach acid. Recognised risk settings include mechanical ventilation, a clotting abnormality (coagulopathy), sepsis and burns. Guidelines also highlight shock and chronic liver disease as likely risk factors.
The first-line drug is a proton pump inhibitor (PPI), such as omeprazole or pantoprazole. It binds the H+/K+ ATPase, the "proton pump", which is the enzyme in the stomach's acid-making parietal cells that pushes acid out, and it irreversibly inactivates each working pump. Acid output then stays low until new pumps are built over 24 to 48 hours. A PPI can be given into a vein, which suits a sedated, ventilated patient.
A 2020 international BMJ guideline suggested a PPI rather than an H2 receptor antagonist (a drug that blocks one of the three signals that stimulate acid secretion), because PPIs probably reduce bleeding more. The same guideline recommended against sucralfate, which coats the stomach lining with a sticky protective barrier but does not lower acid. An H2 receptor antagonist remains a reasonable alternative, but not first choice.
Prophylaxis means acting before the complication occurs, so in a high-risk patient a PPI is started before any bleeding. It is for the period of risk only, so it should be stopped when the critical illness or risk factor has resolved. Prophylaxis is not for everyone: lower-risk patients may not need it.
Key facts
- Who is at risk
- for example patients in shock, with coagulopathy or severe burns, or who are mechanically ventilated and septic; chronic liver disease is also highlighted as a likely risk factor.
- Cause
- mainly poor blood flow to the gut, then injury when flow returns, which weakens the lining's defences against stomach acid.
- First-line drug
- a PPI, which can be given into a vein in a sedated, ventilated patient.
- How a PPI works
- it irreversibly inactivates each working proton pump, so acid output stays low until new pumps are built over 24 to 48 hours.
- Not first choice
- an H2 receptor antagonist is a reasonable alternative, while a 2020 international BMJ guideline recommended against sucralfate.
- Stopping
- prophylaxis should end once the critical illness or risk factor has resolved.
Exam traps
- An H2 receptor antagonist is a reasonable alternative in intensive care, but it is not first-line, because a 2020 BMJ guideline suggested a proton pump inhibitor rather than an H2 blocker since PPIs probably reduce bleeding more.
- Sucralfate coats the stomach lining with a sticky protective barrier, which makes it tempting, but it does not lower acid and a 2020 international BMJ guideline recommended against it for stress ulcer prophylaxis.
- Misoprostol replaces protective prostaglandins (the chemicals that keep the stomach lining protected) and is mainly used to prevent ulcers caused by NSAIDs, which are anti-inflammatory painkillers such as ibuprofen. It causes diarrhoea and uterine contractions and is not standard prophylaxis for stress ulcers in critical illness.
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