ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis. ASHP Commission on Therapeutics and approved by the ASHP Board of Directors on November 14, . I. PURPOSE. To ensure safe evidence based utilization of stress ulcer prophylaxis to prevent upper . ASHP therapeutic guidelines on stress ulcer prophylaxis. ASHP Report Stress ulcer prophylaxis. of resuscitative technique) may contribute to clinically. ASHP Therapeutic Guidelines important stress-related bleeding
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It seems as though almost every patient admitted to the hospital in the United States is prescribed either a proton pump inhibitor PPI or a histamine-2 antagonist H 2 A as stress ulcer prophylaxis SUP. Stress ulcers are gastric mucosal erosions that can develop in patients with a serious illness or severe injury.
Unlike peptic ulcers, which tend to develop in the antrum or duodenum, stress-related mucosal injuries typically occur in the acid-producing areas of the stomach i. The mucosal changes of stress-related mucosal injury mainly involve small erosions that do not lead to bleeding but may develop into deeper ulcers, which cause bleeding.
Several factors contribute to stress ulcer formation, including acid hypersecretion; alteration of normal protective mechanisms such as mucus and bicarbonate secretions; release of mediators such as arachidonic acid therapeuutic, cytokines, and oxygen free radicals; and ischemia to the GI system.
Large studies have indicated that the strongest risk factors for stress-related GI bleeding therapeutci prolonged mechanical ventilation and coagulopathy. Although proven to be highly effective in reducing the risk of both overt and clinically important stress-related mucosal bleeding, prophylactic therapy alone does not decrease the overall mortality rate.
Additionally, patients on twice-daily PPI dosing to treat gastroesophageal reflux disease GERD symptoms often are not stepped down to single-daily-dose therapy once they are asymptomatic. The overuse and misuse of ASDs may result in patient harm and increased prlphylaxis for the health care system. In light of these statistics, SUP continues to be overprescribed.
The toxin produced by C difficilean ulced, spore-forming, gram-positive bacterium, is a major cause of diarrhea and colitis in hospitalized patients that has increased in incidence, severity, and mortality in recent years.
Approximately 3 million cases occur annually in the U. Despite better control of antibiotic prescribing and improvements in hospital hygiene, the number of CDI cases continues to rise.
Antibiotic use is the biggest risk factor for the ulcerr of CDI, but it often cannot be avoided in patients with infections. A less common but more modifiable risk factor is the use of ASDs in hospitalized patients in whom these drugs are not indicated. Gastric acid is a nonspecific protective mechanism against ingested pathogens. The stomach is normally free of bacteria, with the exception of Helicobacter pyloriwhich is uniquely equipped to deal with gastric acidity.
The vegetative cells of C difficileunlike the spores, are usually killed in the low-pH environment of the stomach; however, they have been found to remain viable in the ulce contents of patients taking ASDs. Research in animal models has shown that C difficile spores transform into vegetative cells within 1 hour of ingestion. It is plausible that this transformation may occur in the stomach if the pH is higher or in the case of slower gastric transit times.
A recent retrospective cohort study found that recurrent CDI was more common in patients exposed to PPIs than in unexposed patients Although results of investigations have been inconsistent, several studies have found an association between the use of ASDs and an increased risk of respiratory tract infections and CAP. The largest increase in the risk of pneumonia associated with PPIs was observed in the first week of use.
As with enteric infections, ASDs are thought to increase the risk of pneumonia by inhibiting the secretion of gastric acid, thus allowing bacterial overgrowth and asjp. Bacteria may then be translocated to the lungs by aspiration.
Patients over 65 years of age are at increased risk for pneumonia due to ASDs. Both Campylobacter and Salmonella are acid-sensitive microbes. Parasitic infections have been linked to acid suppression as well, especially giardiasis and strongyloidiasis.
Drug interactions are another concern with acid suppression. Medications with pH-dependent absorption i. The potential interaction between PPIs and clopidogrel has attracted attention because of possible serious adverse effects.
Several cases of patients with hypomagnesemia and subsequent hypokalemia and hypocalcemia who presented with life-threatening symptoms requiring hospitalization have been reported. Most of these cases were associated with long-term PPI use. The mechanism of this adverse effect is unknown. In patients with PPI-induced hypomagnesemia, no apparent magnesium malabsorption or renal magnesium wasting has occurred.
The use of PPIs for 12 months or longer has been associated with vitamin B 12 deficiency, particularly in elderly patients.
Poor absorption of dietary iron has also been linked to PPI therapy, but current data are weak. Gastric acid facilitates prophylazis absorption of nonheme iron by reducing ferric iron to the more soluble ferrous form, and also enhances iron-salt dissociation from ingested food. Long-term PPI use has been associated with an increased incidence of fractures.
Possible mechanisms include decreased absorption of calcium in a more alkaline gastric environment and impairment of bone remodeling due to decreased osteoclast activity, threapeutic to inhibited microfracture repair.
Physicians are encouraged to weigh the risks and benefits of PPI use in vulnerable patients. If calcium supplements are prescribed to PPI users, they should be in a soluble asyp, such as citrate, rather than carbonate. The current therapeutic guidelines were published inwith an update in progress at this writing. Prophylaxis is also advised for ICU patients with at least two of the following risk factors: Efforts by clinicians to curb the use of ASDs in non-ICU patients can prevent significant patient morbidity and reduce both hospital costs and costs to the overall health care system.
It is important to carefully weigh the risks and benefits of ASDs before using these medications in the inpatient setting. Special consideration should be given to patients already at risk for pneumonia, such as the elderly, those with chronic lung disease, and those taking immunosuppressants.
Every effort should be made to critically assess acid-suppression therapy in inpatients and to discontinue therapy whenever possible.
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When SUP is indicated, the patient should receive the lowest dose possible. Pharmacists can help stem the use of ASDs by identifying patients who are inappropriately prescribed these medications, and they can be instrumental in educating physicians about which patients should receive SUP.
Pharmacists involved in processing discharge medications can help ensure that patients are not sent home on acid-suppressive therapy without an appropriate indication. Unfortunately, the measures taken to prevent stress ulcers in hospitalized patients have created a new problem, and by working together the health care team can help prevent further unnecessary morbidity by enforcing guideline recommendations at their institution. ASHP therapeutic guidelines on stress ulcer prophylaxis.
Am J Health Syst Pharm. The attributable mortality and length of therwpeutic care unit stay of clinically important gastrointestinal bleeding in critically ill patients. Risk factors for gastrointestinal bleeding in critically ill patients.
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Stress Ulcer Prophylaxis: The Consequences of Overuse and Misuse
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Accessed September 19, Prophylactic Therapy Although proven to be highly effective in reducing the risk of both overt and clinically important stress-related prophylxais bleeding, prophylactic therapy alone does not decrease the overall mortality rate. Risks of Therapy CDI: To comment on this article, contact rdavidson uspharmacist.
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