Defensive Medicine
It is the practice of diagnostic or therapeutic measures conducted primarily not to ensure the health of the patient, but as a safeguard against possible malpractice liability. Defensive medicine takes two main forms: assurance behavior and avoidance behavior. Assurance behavior involves the charging of additional, unnecessary services in order to a) reduce adverse outcomes, b) deter patients from filing medical malpractice claims, or c) provide documented evidence that the practitioner is practicing according to the standard of care, so that if, in the future, legal action is initiated, liability can be pre-empted. Avoidance behavior occurs when providers refuse to participate in high risk procedures or circumstances. [Wikipedia]
While the direct costs of defensive medical practices is being debated, it is clear that the indirect costs are large and insidious. For example, a study-- Investigation of Defensive Medicine in Massachusetts shows the fear of being sued is a serious burden on health care and it dramatically increases health care costs:
The results showed that 83% of the physicians surveyed reported practicing defensive medicine and that an average of 18 to 28% of tests, procedures, referrals and consultations and 13% of hospitalizations were ordered for defensive reasons.
A discussion on this topic typically begins with knee-jerk over-testing from xrays for a simple sprain, to sinus films, to the overuse of uterine sonograms in normal pregnancies, to CT and MRI scans for early, minimally symptomatic trauma.
In a discussion elsewhere, I offered an unexpected example - the easy prescribing of PPIs. I was asked, "Is this really an example of DM? I responded it was related to defensive practices in that PPI's are prescribed with reckless abandon. It's almost as if not prescribing isn't an option. And what about having to deal with long-term adverse effects? There's 7 degrees of separation and the risk of messing with calcium metabolism and subsequent osteoporosis and/or fractures; pneumonia and C. Difficile? Well, that's someone else's problem. Here are cautionary notes:
Note: the following information was requested from GlaxoSmithKline's Consumer Healthcare division:
Millions of patients use PPIs on a continuous or long-term basis to control symptoms of heartburn and GERD.1,2Empirical PPI therapy has become commonplace. In a survey of primary care physicians, 83% reported willingness to prescribe PPIs without first trying an H2RA; 87% reported being "very comfortable" with prescribing long-term PPI therapy.3
Long-term PPI therapy is supported by clinical guidelines,4,5 with a recommendation that, "Long-term therapy should be titrated down to the lowest effective dose based on symptom control."4 But despite widespread utilization of PPI therapies, problems remain in the management of heartburn and GERD symptoms:Many patients continue to experience symptoms despite PPI therapy.
A survey reported that among patients taking low-dose PPIs (n=260), 29% continued to experience heartburn or acid reflux at least twice weekly, as did 53% of those on high-dose PPIs (n=40).2 Nocturnal symptoms are especially common—a survey reported that 74% of patients with symptomatic GERD experienced nocturnal symptoms.6 Gastric acid secretion typically peaks during the night, so that not even high-dose or twice-daily PPI therapy may be sufficient to control nocturnal acid breakthrough.6,7
Nearly all the efficacy data for PPIs came from once-daily dosing studies.4 Still, many physicians are willing to increase the PPI dose or dose frequency in the attempt to manage heartburn or GERD symptoms. A survey of primary care physicians asked about management of a hypothetical patient with evening and nocturnal heartburn despite once-daily PPI therapy. The option chosen most often was to increase the PPI dose to twice daily.3
Extending or increasing PPI dosing may cause other problems. Both the average daily PPI dose1 and the duration of PPI use1,8 have been linked to higher risk of certain adverse events:• Fracture risk: A study conducted in 192,028 PPI users to test whether long-term PPI therapy (>1 year duration), particularly at higher doses, was associated with increased risk of hip fracture, reported the risk of hip fracture was markedly higher among long-term users of high-dose PPI therapy vs non-users (AOR, 1.44; 95% CI, 1.30-1.59; P<.001).– A significant dose response was noted in long-term users of PPIs, with an AOR of 2.65 (1.80-3.90;P<.001) for high-dose vs 1.40 (1.26-1.54; P<.001) for lower-dose, long-term users of PPIs.1• Pneumonia risk: A study of persons with community-acquired pneumonia in a Netherlands database (n=5551) found that with PPIs taken for extended periods (mean duration of 5 months), the adjusted relative risk for pneumonia among PPI users vs non-users was 1.89 (95% CI, 1.36-2.62).8– A significant dose response was noted in PPI users. Those who used more than 1 defined daily dose of PPI medication had a 2.3-fold increase in risk of pneumonia compared to those who had used PPIs in the past, but were not taking them currently.8• Clostridium difficile-associated diarrhea (CDAD) risk: A 2005 study evaluated the effect of PPIs and other acid-suppressing therapies on community-acquired CDAD. In 1233 patients identified with community-acquired CDAD, the adjusted relative risk of current PPI exposure was 2.9 (95% CI, 2.4-3.4). The authors concluded that PPI exposure was associated with increased risk of CDAD.9– A 2006 study re-examined these data using a stricter definition of CDAD—that patients received a prescription for vancomycin, the sole indication for which was the treatment of CDAD.10,11,12 This study also observed a strong correlation between treated CDAD and current PPI exposure (OR 3.5, 95% CI, 2.3–5.2).10
What do these risks mean in clinical practice?
The potential benefit of chronic PPI therapy in patients with chronic or complicated GERD would seem to outweigh risks associated with chronic PPI use. Nonetheless, indefinite maintenance therapy with PPIs is not supported for patients with nonerosive disease. In such cases, guidelines support "on-demand" therapy4 with other acid-suppressing therapies such as H2RAs or antacids. Even for patients suffering from chronic GERD, on demand adjunctive therapy may help manage nocturnal symptoms, which may not be well managed with PPIs at any dose.7In some cases, on demand therapies may even help clinicians avoid increasing PPI dosing.
Choosing an adjunctive therapy
Antacids such as TUMS have been proposed as adjunctive therapy, both independently and in combination with other acid suppressive therapies, because they can provide fast relief from heartburn symptoms.13 H2RAs have been shown to significantly relieve overnight heartburn symptoms in patients who experienced nocturnal heartburn symptoms despite PPI therapy.14 Therefore, clinicians could confidently recommend a combination product consisting of an H2RA plus an antacid as PPI adjunct therapy, especially for patients who experience heartburn in the late evening or during the night.
Adjunctive therapy with OTC antacids and H2RAs may also be a less expensive treatment strategy than increasing the PPI dosage to control breakthrough heartburn, particularly when the prescribed PPI is not a generic.
Rather than change their PPI or increase PPI dosing for these patients, consider recommending either TUMS Ultra 1000—the strongest TUMS available for fast relief—or new TUMS Dual Action, which adds an H2RA for hours of extended relief.
REFERENCES
1. Yang YX, Lewis JD, Epstein S, Metz DC. Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006;296:2947–2953.
2. Jacobson BC, Ferris TG, Shea TL, et al. Who is using chronic acid suppression therapy and why? Am J Gastroenterol. 2003 Jan;98(1):51–58.
3. Chey WD, Inadomi JM, Booher AM, et al. Primary-care physicians' perceptions and practices on the management of GERD: results of a national survey. Am J Gastroenterol. 2005;100:1237–1242.
4. Kahrilas PJ, Shaheen NJ, Vaezi MF, et al.; American Gastroenterological Association. American Gastroenterological Association Medical Position Statement on the management of gastroesophageal reflux disease.Gastroenterology. 2008;135:1383–1391.
5. DeVault KR, Castell DO; American College of Gastroenterology. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. 2005;100:190–200.
6. Farup C, Kleinman L, Sloan S, Ganoczy D, et al. The impact of nocturnal symptoms associated with gastroesophageal reflux disease on health-related quality of life. Arch Intern Med. 2001;161(1):45–52.
7. Peghini PL, Katz PO, Bracy NA, Castell DO. Nocturnal recovery of gastric acid secretion with twice-daily dosing of proton pump inhibitors. Am J Gastroenterol. 1998;93:763–767.
8. Laheij RJ, Sturkenboom MC, Hassing RJ, et al. Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs. JAMA. 2004;292:1955–1960.
9. Dial S, Delaney JA, Barkun AN, Suissa S. Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated disease. JAMA. 2005;294:2989–2995.
10. Dial S, Delaney JA, Schneider V, Suissa S. Proton pump inhibitor use and risk of community-acquired Clostridium difficile-associated disease defined by prescription for oral vancomycin therapy. CMAJ. 2006;175:745–748.
11. Poutanen SM, Simor AE. Clostridium difficile-associated diarrhea in adults. CMAJ. 20046;171:51–58.
12. Bouza E, Muñoz P, Alonso R. Clinical manifestations, treatment and control of infections caused by Clostridium difficile. Clin Microbiol Infect. 2005;11 Suppl 4:57–64.
13. Tytgat GN, McColl K, Tack J, et al. New algorithm for the treatment of gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2008;27:249–256.
14. Rackoff A, Agrawal A, Hila A, et al. Histamine-2 receptor antagonists at night improve gastroesophageal reflux disease symptoms for patients on proton pump inhibitor therapy. Dis Esophagus. 2005;18:370–373.
Fredrick (MD, PhS, JD) responded:
"Defensive Medicine" is not a general pejorative that includes "prescribing with reckless abandon." What it specifically means is: "Prescribing to protect oneself from a possible lawsuit." Anyway, what lawsuit is prescribing PPIs is a protection from?
Certainly there are plenty of other alternatives for GERD, such as H2RAs, but ANYTHING that reduces stomach acidity will have those same side effects.
If you're just upset that PPIs are too expensive, why not just say so?
From: jgk 4/27/10
I am concerned about the abuse of anti-reflux medications and the long-term untoward effect they may have. Speaking as a Pediatrician, here's something from the British Medical Journal Group that we all can relate to:
Refluxing babies
Are you uneasy about the medicalisation of babies who have reflux but are otherwise thriving? This article says
- Functional reflux in babies is common and the prognosis is benign
- Management includes positioning, avoidance of overfeeding, and consideration of thickening feeds
- Consider a period of excluding cow's milk if symptoms are severe
- Try these strategies before embarking on investigation or drug treatment
Source: Archives of Disease in Childhood 2010;95:243-244
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Another area where we tend to over-diagnose and/or over-treat is rheumatic fever prevention as it relates to Strep. Rheumatic fever (RF), a systemic illness, may occur as an autoimmune reaction following group A beta hemolytic streptococcal (GABHS) pharyngitis in children; its most serious complication rheumatic heart disease (RHD).
"Studies in the 1950s during an epidemic on a military base demonstrated 3% incidence of rheumatic fever in adults with streptococcal pharyngitis not treated with antibiotics.1 Studies in children during the same period demonstrated an incidence of only 0.3%. The current incidence of rheumatic fever after GABHS infection is now thought to have decreased to less than 1%. Cardiac involvement is reported to occur in 30-70% of patients with their first attack of rheumatic fever and in 73-90% of patients when all attacks are counted."
"After an incubation period of 2-4 days, the invading organisms elicit an acute inflammatory response, with 3-5 days of sore throat, fever, malaise, headache, and elevated leukocyte count. In a small percent of patients, infection leads to rheumatic fever several weeks after the sore throat has resolved. Only infections of the pharynx initiate or reactivate rheumatic fever.
Direct contact with oral (PO) or respiratory secretions transmits the organism, and crowding enhances transmission. Patients remain infected for weeks after symptomatic resolution of pharyngitis and may serve as a reservoir for infecting others. Penicillin treatment shortens the clinical course of streptococcal pharyngitis and more importantly prevents the major sequelae."
Clearly, common practice does not follow the above highlighted observations.
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