41. ICU stress ulceration

Question 1

Can you tell me something about the pathophysiology of stress ulcers in
intensive care patients.

Answer 1

Stress ulceration in intensive care patients is relatively common (approaching
90% by day 3 with no prophylaxis), although the incidence of clinically
important gastrointestinal bleeding is less than 2%.

Question 2

There are six major risk factors:

Answer 2

Respiratory failure requiring ventilation for >48 hours
Coagulopathy
Sepsis
Hypotension
Hepatic failure
Renal failure

Question 3

Pathophys

Answer 3

The normal mechanisms that aim to ensure an intact mucosal barrier to
protect the gastric epithelium come under attack in the critically ill patient.

Mucus production is reduced from surface mucous cells.

Mucosal blood flow is impaired.

Mucosal prostaglandin production is reduced and these (especially PGE2)
are involved in the regulation of gastric acid secretion by parietal cells.

Other factors may include increased gastrin production, acid-base
abnormalities and reflux of bile.

Question 4

Two types of ulcer are classically eponymised:

Answer 4

Curling’s ulcers associated with extensive burns

Cushing’s ulcers associated with intracranial pathology
and gastric acid hypersecretion.

Question 5

Agents Rx

Answer 5

Ranitidine and sucralfate are the most effective agents. Ranitidine is
associated with a lower incidence of clinically significant bleeding,
sucralfate with a lower incidence of pneumonia.
Nosocomial pneumonia is the main complication of ulcer prophylaxis
treatment.

Question 6

What measures have been employed to try and reduce the incidence of
stress ulcers?

Answer 6

Adequate resuscitation is the main priority with maximal oxygen transport to the gastric mucosa.

Attention should be paid to optimising cardiovascular
variables and ensuring adequate gas exchange.

Enteral feeding

Sulcralfate

Antacids and
H2-antagonists

Question 7

Antacids + H2RA

Answer 7

These are the more traditional drugs used for stress
ulcer prophylaxis and may effectively reduce the risk
of bleeding. There is, however, some concern that, by
increasing the pH of gastric contents, there is an
increased risk of bacterial colonisation and subsequent
nosocomial pneumonia.

Question 8

COMPLICATIONS OF STRESS ULCER PROPHYLAXIS

Answer 8

General

drug allergy, drug side-effects and drug interactions (esp cimetidine)
pneumonia (HAP and CAP)
PPIs

interstitial nephritis (rare — but PPIs are a major drug causes)
Clostridium difficile enterocolitis (PPIs have dose-dependent relationship)
GI upset and headaches
long-term use associated with fractures, hypomagnesemia, hypocalcemia
H2 blockers

CNS side-effects (esp in the elderly)
tolerance after 72h

Question 9

AN APPROACH TO STRESS ULCER PROPHYLAXIS

Answer 9

feed early unless contraindicated
don’t use prophylaxis if feeding established
if unable to establish enteral feed, risk assess for GIH: if high risk -> use prophylaxis (some would use prohylaxis in this group regardless of whether they are enterally fed)
PPIs are generally preferred, but ranitidine is an acceptable alternative
if stress ulcers develop treat appropriately
be vigilant for hospital acquired pneumonia and C. difficile enterocolitis if stress ulcer prophylaxis given
reassess daily and de-escalate stress ulcer prophylaxis when no longer needed

Question 10

Evidence

Answer 10

Barkun Proton pump inhibitors vs. histamine 2 receptor antagonists for stress-related mucosal bleeding prophylaxis in critically ill patients: a meta-analysi

Cook DJ,