Alimentary Prophylaxis
This chapter describes the following preventive practices in the alimentary tract (which extends from the mouth to the rectum):
Gastric acid suppression to prevent bleeding from stress ulcers.
Decontamination of the oral cavity to prevent nosocomial pneumonia.
Decontamination of the gastrointestinal tract to prevent systemic spread of enteric pathogens.
I. Stress-Related Mucosal Injury
A. Introduction
Erosions on the surface of the gastric mucosa are visible in 75–100% of patients within 24 hours of ICU admission (1). These erosions (called stress ulcers) are usually confined to the gastric mucosa, and are clinically silent. However, erosions can extend into the submucosa and produce visible bleeding.
Clinically apparent bleeding from stress ulcers is reported in up to 15% of ICU patients (2), but clinically significant bleeding (i.e., requires a blood transfusion) occurs in only 3–4% of patients (3).
All of the preventive measures described next have been shown to reduce the incidence of stress ulcer bleeding
(2), but much of this effect is for clinically apparent bleeding, which usually has no adverse consequences.
B. Risk Factors
Surveys indicate that about 90% of ICU patients receive prophylaxis for stress ulcer bleeding (4), but this is excessive. Preventive measures are indicated only for patients with proven risk factors for stress ulcer bleeding.
The risk factors for stress ulcer bleeding are listed in Table 3.1 (5,6). Note that the only independent risk factors (i.e., require no other risk factors to promote bleeding) are mechanical ventilation for longer than 48 hours, significant coagulopathies, and extensive burn injury.
Prophylaxis is indicated for any of the independent risk factors, and for patients with 2 or more of the other risk factors in Table 3.1.
Table 3.1 Risk Factors for Stress Ulcer Bleeding | ||||
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C. Gastric Acid Suppression
The principal preventive measure for stress ulcer bleeding is inhibition of gastric acid secretion with histamine type-2 receptor antagonists or proton pump inhibitors. The goal is a pH >4 in gastric secretions, but this is rarely monitored.
1. Histamine H2-Receptor Antagonists
Histamine H2-receptor antagonists (H2RAs) are the most frequently used drugs for stress ulcer prophylaxis (4).
Ranitidine and famotidine are the H2RAs used most often for stress ulcer prophylaxis. Both can be given intravenously using the dosing regimens shown in Table 3.2 (7,8). Famotidine has a longer duration of action than ranitidine, and is given less frequently. Both drugs are considered equally effective in preventing stress ulcer bleeding.
H2RAs are less effective in reducing gastric acidity with continued use, but this does not reduce their effectiveness in preventing stress ulcer bleeding (9).
H2RAs can accumulate in renal insufficiency and produce a neurotoxic syndrome characterized by confusion, agitation and seizures (10). Dose reduction is therefore required in renal failure. This can be accomplished by increasing the dosing interval (to 24 hours for ranitidine, and 36–48 hours for famotidine) (10).
2 Proton Pump Inhibitors
Proton pump inhibitors (PPIs) are replacing H2RAs for stress ulcer prophylaxis because they produce a more complete inhibition of gastric acid secretion, and there is no response attenuation with continued use (11).
Despite their pharmacological advantages, PPIs are not more effective than H2RAs for preventing stress ulcer bleeding (2,12).
The prophylactic dosing regimens for two PPIs are shown in Table 3.2. Both drugs are given intravenously, which is the recommended route for stress ulcer prophylaxis (11). One of the drugs (lansoprazole) requires an in-line filter to trap particulate matter, and must be given slowly (over 30 min) (11). The
other drug (pantoprazole) does not have these restrictions, and thus is the favored PPI for stress ulcer prophylaxis.
Adverse effects of PPIs are primarily related to the reduced gastric acidity (see next section). One drug interaction deserves mention: PPIs impede the activation of clopidogrel (a popular antiplatelet agent) in the liver (13). Although the significance of this interaction is unclear, current opinion favors avoiding PPIs, if possible, during antiplatelet therapy with clopidogrel.
Table 3.2 Drug Regimens for Prophylaxis of Stress Ulcer Bleeding | |||||||||||||||||||||
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3. Infectious Risks
The stomach is a relatively sterile environment, thanks to the bactericidal actions of gastric acid, as demonstrated in Figure 3.1 (14). In this case, pathogenic salmonella organisms were completely eradicated
in one hour when the gastric pH was reduced from 4 to 2.
FIGURE 3.1 The influence of gastric pH on the growth of Salmonella typhimurium, a common cause of infectious enteritis. From Reference 14.
Observations like the one in Figure 3.1 have led to the notion that gastric acid is an antimicrobial defense system that eradicates pathogens swallowed in food or transmitted via the fecal-oral route.
Three infections have been linked to gastric acid suppression: pneumonia (from aspiration of microbe-laden gastric secretions into the airways) (8,15,16), spontaneous bacterial peritonitis (10), and Clostridium difficile enterocolitis (17,18,19,20). PPIs create a much higher risk of these infections than H2RAs (16,18).Related posts:
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