Page 538 - ACCCN's Critical Care Nursing

Gastrointestinal, Liver and Nutritional Alterations 515

TABLE 19.8 Factors contributing to stress-related mucosal disease 204

Factors Mechanism Action
Protective Mucosal prostaglandins Protect the mucosa by stimulating blood flow, mucus and bicarbonate production 205
mechanisms Stimulate epithelial cell growth and repair
Mucosal bicarbonate barrier Forms a physical barrier to acid and pepsin, preventing injury to the epithelium 206
Epithelial restitution and Epithelial cells rapidly regenerate but the process is highly metabolic and may be impaired
regeneration by physiological stress 206
Mucosal blood flow Mucosal blood flow helps remove acid from the mucosa, supplies bicarbonate and oxygen
to the mucosal epithelial cells 207
Cell membrane and tight Tight junctions between mucosal epithelial cells prevents the back diffusion of hydrogen
junctions ions 208
Factors Acid Acid is a key issue in the pathogenesis of stress-related mucosal injury however not all
promoting critically ill patients hypersecrete acid. 14,208 However small amounts of acid may still cause
injury injury and the prevention of acid secretion has led to a reduction in injury 209
Pepsin May cause direct injury to the mucosa 210
Facilitates the lysis of clots 211
Mucosal hypoperfusion Reduced mucosal blood flow results in reduced oxygen and nutrient delivery, making
epithelial cells susceptible to injury. 208
Contributes to mucosal acid-base imbalances
Results in the formation of free radicals
Reperfusion injury Nitric oxide, which causes vasodilation and hyperaemia, is released during hypoperfusion
and results in an increase in cell-damaging cytokines
Intramucosal acid–base The mucus layer protects the epithelium and traps bicarbonate ions that neutralise acid thus
balance a decrease in bicarbonate secretion results in intramucosal acidosis and local injury 206
Systemic acidosis Results in increased intramucosal acidity 207
Free oxygen radicals Generated as a result of tissue hypoxia, free oxygen radicals cause oxidative injury to the
mucosa 212
Bile salts Bile salts reflux from the duodenum into the stomach and may have a role in stress-related
damage although the exact mechanism is uncertain 213
Heliobacter pylori Conflicting results about the role of H. pylori as a cause of stress-induced mucosal disease in
the critically ill 214

Factors influencing the development of stress-related higher than for those who do not develop this complica-
200
200
mucosal disease include splanchnic hypoperfusion tion. Consequently, there is a strong imperative to
which may influence mucosal ischaemia and reperfusion implement stress-ulcer prophylaxis, particularly in those
201
injury, maintenance of the gastric mucosa by sufficient patients who are considered at risk.
202
microcirculation and the mucus-bicarbonate gel layer,
decreased prostaglandin levels which impairs mucus PREVENTING STRESS-RELATED
replenishment and increased nitric oxide synthase which MUCOSAL DISEASE
203
contributes to reperfusion injury and cell death. The Prophylaxis for stress-related mucosal disease is often
protective mechanisms and factors which promote injury part of the care of the critically ill although evidence
are detailed in Table 19.8. demonstrating an added benefit when this therapy is
applied to those patients who are not identified as at risk
RISK FACTORS FOR STRESS-RELATED for developing stress-related mucosal disease, is limited.
201
MUCOSAL DISEASE Nevertheless, it is common for the majority of critically
A number of risk factors are associated with the develop- ill patients to receive some form of stress-ulcer prophy-
ment of stress-related mucosal disease, including respira- laxis during their episode of critical illness. There are a
tory failure requiring at least 48 hours of mechanical variety of pharmacological strategies that can be used to
215
ventilation and coagulopathy, acute hepatic failure, prevent stress ulcers from developing. These include ant-
hypotension, chronic renal failure, prolonged nasogastric acids, sucralfate, histamine-2-receptor antagonists and
201
tube placement, alcohol abuse, sepsis and an increased proton pump inhibitors (PPIs).
serum concentration of anti-Helicobacter pylori (H. pylori) Antacids
immunoglobulin A. 216
Antacids directly neutralise gastric acid and have been
Mortality rates for critically ill patients who develop shown to be effective in reducing significant stress-related
stress-related mucosal disease approximate 50–77% and bleeding. One of the disadvantages of this therapy is
217