You cannot accurately diagnose gastroesophageal reflux disease or an ulcer in the ED. (JAMA 2006;295:1566.) Instead, we call it uninvestigated dyspepsia if the patient has not had an upper endoscopy and workup. This acute dyspepsia may include but is not limited to pancreatitis, viral gastroenteritis, biliary colic, ileus, irritable bowel syndrome, nonulcer dyspepsia, gastritis, peptic ulcer, or GERD. The prevalence of dyspepsia in the United States is 20-40 percent. A response to a proton-pump inhibitor does not indicate a peptic ulcer or GERD either. The uninvestigated dyspepsia diagnosis is broad, the prevalence is high, and first-line treatments should be behavioral and dietary.
Even for patients who have had a relatively recent upper endoscopy, 70 percent or more with a diagnosis of GERD have a negative endoscopy. We must take the extra time to question this diagnosis because all patients say they have GERD, and they are all on a PPI. Many will say that the doctor said he saw a little bit of inflammation (kind of like a touch of pneumonia on a chest x-ray). We should make the patient convince us that he has esophagitis to stay on a PPI.
But should we even care? Why not just use it and make everybody happy if PPIs make a few patients feel better and it is what the gastroenterologists use? First, PPIs are not the best treatment for acute dyspepsia in the ED. Antacids may take around 19 minutes to work, H2 blockers may take up to 70 minutes (Aliment Pharmacol Ther 1999;13:1605), but PPIs may take up to four days. PPIs must be taken 30 minutes to an hour before meals, and cost $100-$300 a month more than antacids or H2 blockers. Who would ever prescribe a PPI for acute dyspepsia in the ED?
PPIs also can be harmful. Their use is associated with increased mortality among the hospitalized elderly and among patients with cirrhosis. (JAMA Intern Med 2013:173:518; Aliment Pharmacol Ther 2015;41:459.) PPIs also increase Clostridium difficile colitis (JAMA Intern Med 2015;175:784), hip fractures (Arch Intern Med 2010;170:765), community-acquired pneumonia (Ann Intern Med 2008;149:391), interstitial nephritis (Clin Gastroenterol Hepatol 2006;4:597), B12 deficiency, magnesium deficiency, and iron deficiency (Am J Gastroenterol 2009;104[Suppl 2]:S5), interfere with synthroid and urease breath tests (Internal Medicine Board Review Course 2014; MedStudy, Book I, pp. I-5-6), and cause rebound hypersecretion for those trying to go off PPIs. (Gastroenterology 2009;13780.)
These harms are not just for PPIs in dyspepsia. IV PPIs are associated with increased mortality in Western studies for the undifferentiated upper GI bleed (and even for the known peptic ulcer bleed) without any benefit in mortality, need for surgery, and rebleeding in any population. (Scand J Gastroenterol 1997;32:328; stopped early because of increased mortality; Cochrane Database Syst Rev 2010;Jul 7:CD005415; Ann Emerg Med 2014;63:759.)
One could argue that the emergency physician should prescribe a PPI and something else for dyspeptic pain for the patient with known esophagitis. One could also argue that an oral PPI may not be harmful (but may not provide clinical benefit) for the Asian patient with a known bleeding peptic ulcer.
But in the age of less is more, why are PPIs among the best-selling drugs in the world? Empiric PPIs are not the right economic or professional approach. Choosing Wisely states, “Many people with heartburn don't need drugs at all. [A]nd in most cases, PPIs are not necessary.” We must all choose wisely and say no benefit is seen in prescribing or recommending a PPI in the ED for uninvestigated dyspepsia. Nor is there benefit to using IV PPI for undifferentiated upper GI bleed. PPIs may produce significant harm.
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