Recognizing and Challenging Dogma

Patients and other health care professionals often ask sport medicine physicians to comment on the value of a diagnostic test or treatment. In controversial areas, most of us would respond cautiously. When there is no apparent controversy, we often repeat current recommendations without hesitation or reservations. This simple practice may perpetuate inaccurate dogma (“a point of view or tenet put forth as authoritative without adequate grounds”1) in clinical practice. Dogma unchallenged over the last 30 years dictated that stretching before exercise improves performance. In reality, there are no studies showing this practice is beneficial and 22 studies showing that it either has no effect or is in fact detrimental.2 The effect of stretching is only one example of many. Three other areas of contemporary clinical practice in which clinicians may not realize that our decisions are based on dogma rather than evidence are described here. Clinicians often counsel patients with edematous limbs to avoid exercise because it is believed that exercise increases swelling. New research suggests that exercise has no effect on swelling and actually improves quality if life in patients with lymphedema secondary to breast cancer treatment.3 In addition, our own group has shown that exercise 1 month after a deep venous thrombosis is associated with a reduction in symptoms and reduced swelling.4 Nonsteroidal antiinflammatory drugs (NSAIDs) are believed to reduce swelling after a traumatic injury. However, NSAIDs had no effect on acute posttraumatic swelling in the 4 studies retrieved that used water displacement to measure volume changes (considered the most objective and reliable measure of volume).5–8 Theoretically, medications would not be expected to reduce swelling resulting from bleeding. Reconstruction of the anterior cruciate ligament (ACL) is often promoted as necessary to reduce the risk of osteoarthritis (OA). Daniel et al9 found no difference in the severity of OA between individuals with unstable knees who opted for early surgery and those who did not. Although this study contradicts current opinion and has limitations (eg, certain subjects excluded, length of follow-up not reported), it is supported by another investigation demonstrating that anterior–posterior instability after ACL reconstruction did not predict the development of OA.10 There are several possible theoretical paradigms that merit consideration in assessing these findings. Current surgical techniques that restore anterior–posterior stability may increase the risk of irreducible tibial subluxation,11 do not restore tibial rotation,12 do not restore proprioception, and, if OA is a result of cartilage damage at the time of injury, reconstruction is after the fact and would have no effect. These examples represent strongly held and entrenched beliefs that many clinicians likely believe were based on solid evidence. In reality, much of clinical practice is based on dogma rather than evidence. The first step toward improving the care we provide to our patients is recognizing which treatments are based on evidence. This requires improvements by both producers and consumers of knowledge. First, producers of knowledge should never cite other work without reading the original research. This would reduce the risk of one person's misinterpretation being continually referenced as fact. Second, consumers of knowledge should challenge current theories as strongly as they challenge new ones. Most of us immediately look for reasons to ignore results that are not in accord with our personal paradigm. Challenging new theories is essential, but we must at the same time apply the same standard to the old theory. In the case of the relationship between ACL repair and the development of OA, we are unlikely to question the long-held view that ligaments provide stability to a joint, and that without ligamentous stability, there is increased articular and meniscal cartilage wear. Is this paradigm true? When a Lachman or anterior drawer test is performed, anterior–posterior movement of the tibiofemoral joint can always be produced with minimal amounts of force. This same movement does not occur when one walks, runs, or jumps. Therefore, it is impossible that the ligaments are the sole source of stability during movement, and coordinated muscle activity is the likely source of “dynamic stability.”14 In this paradigm, ligaments contribute proprioceptive information essential to appropriate muscle activity and coordination,15 and primarily act as a secondary restraint when muscles fail (ie, to prevent excessive damage to major blood vessels and nerves). There is some evidence that muscle dysfunction is an important cause of primary OA,16,17 and loss of proprioception after injury could be an important mechanism leading to muscle dysfunction. If so, ACL reconstruction would only prevent OA if it restored the proprioceptive feedback loops that were lost with the original injury, but it does not.18 Finally, in this paradigm, ACL reconstruction would increase OA if the surgery further damages surrounding muscles and these were not properly rehabilitated. In considering these examples, it is clear that we do not yet know which theory best describes clinical reality. It should be equally clear that any proposed new paradigms may be completely false. It is most important that we are constantly aware of the existence and quality of evidence that support or refute any approach to clinical management. We must refrain from propagating theory as fact, and challenge our mentors and ourselves with the same vigor with which we challenge our students.

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