Best management of acute ankle sprain
Source: Lamb SE, et al. Mechanical supports for acute ankle sprain. Lancet 2009;375:575-581.
A severe ankle sprain (ANK-S) might seem like a minor injury, but clinicians may be underestimating the burden of consequence. In addition to the immediate period of limited mobility, full functional restoration takes between 3-9 months for as many as 70% of affected individuals. Indeed, it is not uncommon to see long-term symptoms referable to the ankle sprain, including recurrent swelling, pain, and limitation of activity. Because ANK-S is a commonplace event, confirming the best approach to initial management merits investigation.
Lamb et al randomized participants presenting to EDs in the United Kingdom with severe ANK-S (n = 584) to 1 of 4 treatments: an Aircast® brace, Bledsoe boot, below-knee cast, or double-layer tubular compression bandage.
Participants generally used treatments short-term, i.e., 10 days, and then PRN. Tubular compression bandage was the least efficacious method at 1, 3, and 9 months and was similar in efficacy to the Bledsoe boot. The below-knee cast was the most effective treatment, but Aircast outcomes were similar for ankle functionality at 3 months. Overall, the below-knee cast showed the best early symptomatic recovery, as well as functional recovery by 3 months. Although the philosophy of early mobilization has achieved some popularity, these data would suggest that tools that limit mobilization early (i.e., cast, Aircast), should be considered preferential. (Note: There is more than one Bledsoe boot; because Bledsoe provides boots with either flexion-extension mobility or full immobilization, it is possible that other versions of the Bledsoe boot might be more efficacious).
Metabolic syndrome and salt sensitivity
Source: Chen J, et al. Metabolic syndrome and salt sensitivity of blood pressure in non-diabetic people in China. Lancet 2009;373:829-835.
Although definitions of what constitutes metabolic syndrome (MBS) vary, there is general agreement that insulin resistance (IR) is a fundamental component. By leading to sodium retention, IR may contribute to the development of hypertension (HTN).
Blood pressure effects of salt restriction are highly variable, but one would anticipate that MBS subjects might respond more intensely based upon the IR-to-sodium retention link. To investigate this, Chen et al studied 1881 nondiabetic subjects, of whom 283 had MBS. All participants were fed a low-sodium diet (= 3 g NaCl/d) for 7 days, followed by a high-sodium diet (= 18 g NaCl/d) for 7 days. At baseline, the mean BP in the MBS group was 128/81 mm Hg vs 115/72 mm Hg in those without MBS.
High-salt sensitivity was defined as a BP change of 5 mm Hg or more in response to dietary salt modulation. At the end of each diet period, MBS subjects had a threefold or greater odds ratio for high-salt sensitivity (both to a rise in BP with sodium load, as well as a reduction in BP with sodium restriction). The benefits of salt restriction in persons with MBS may be more substantial than the general population.
Oseltamivir-resistant influenza
Source: Dharan NJ, et al. Infections with oseltamivir-resistant influenza A(H1N1) virus in the United States. JAMA 2009;301:1034-1041.
Progressive resistance of influenza A virus (FLU-A) to adamantanes (i.e., amantadine, rimantadine) led to the 2006 CDC recommendation against their use. Initial resistance patterns of next-generation pharmacotherapies for FLU-A, the neuraminidase inhibitors (i.e., oseltamivir, zanamivir), were very reassuring. Recently, growing resistance patterns to oseltamivir (OSTV) are shaping revised CDC recommendations.
Volunteer clinicians around the United States, known as sentinel physicians, monitor patients who present with influenza-like illness and send samples to the CDC for confirmation of influenza virus status. Among FLU-A viruses assessed in the 2007-2008 influenza season, only 12.3% were OSTV-resistant. Comparison of the demographics of subjects with OSTV-resistant FLU-A to subjects with non-resistant profiles did not provide any insight into particular at-risk groups (or protected groups), including age, geography, symptoms, etc.
OSTV resistance profiles changed dramatically in the FLU-A samples from Sept. 28, 2008, to Feb. 19, 2009: 98.5% of H1N1 FLU-A samples (264/268) were OSTV-resistant! Experts are uncertain about the mechanism by which OSTV resistance has proliferated. Current options in an environment of high OSTV resistance include zana-mivir, or OSTV plus rimantadine.
Low back radiology: Roadmap or mirage?
Source: Chou R, et al. Imaging strategies for low-back pain. Lancet 2009;373:463-472.
Low back pain (LBP) is responsible for as much as one-third of all disability dollars spent in the United States. When patients present with acute LBP, clinicians are tempted to perform radio-graphic studies (MRI, CT, plain films) to try to identify the source of the symptomatology. Unfortunately, the preponderance of current evidence suggests that findings commonly reported on radiographic studies such as narrowed disk space, loss of lumbar lordosis, and osteoarthritic changes, are just as common in asymptomatic volunteers as in symptomatic LBP sufferers.
Chou et al performed a meta-analysis of clinical trials which enrolled patients and included immediate imaging (CT, MRI, or plain films) and compared them with trials of similar patients who did not undergo imaging (total n = 1804). In addition to reporting radiography utilization, included trials had to provide information on outcomes of pain or function, quality of life, mental health, overall improvement, and patient satisfaction.
Chou et al found that in the absence of signs of a serious underlying condition (e.g., fever, weight loss, history of cancer), immediate imaging was not associated with improved outcomes. Indicative of the need for more public education, the article also reminds us that in one study, patient preference to undergo radiography was as high as 80%.
Routine radiography for acute LBP does not improve outcomes, is associated with substantial cost, and may suggest pathology which is, in effect, unrelated to the symptomatology.
Bariatric surgery and reversal of dysglycemia
Source: Salinari S, et al. First-phase insulin secretion restoration and differential response to glucose load depending on the route of administration in type 2 diabetic subjects after bariatric surgery. Diabetes Care 2009;32:375-380.
Most type 2 diabetics (DM2) who undergo bariatric surgery enjoy a prompt reversal—or at least a substantial diminution—of their dysglycemia. These salutary effects occur both after malabsorptive surgery (diverting the digestive tract around to bypass components of the small intestine) or restrictive surgery (diminishing gastric capacity). The mechanisms by which surgery improves glucose regulation appear to go beyond simple weight loss; indeed, glucose regulation improves well before meaningful weight loss has occurred, suggesting that some change in intestinal glucose modulation factors must be involved.
Salinari et al studied glucose metabolism in 9 DM2 subjects who underwent biliopancreatic diversion bariatric surgery, comparing their glucose metabolism with healthy, normal-weight controls.
The healthy pancreas provides a bolus of preformed insulin immediately in response to mealtime increases in plasma glucose. One of earliest manifestations of DM2 is loss of first-phase insulin secretion, leading to a consistent mismanagement of glucose, since early elevations of plasma glucose are not met with a prompt matching insulin bolus. In this trial, the first-phase insulin response was restored by 1 month after surgery. Similarly, beta-cell responsiveness to glucose elevation was normalized; and lastly, insulin sensitivity was restored to essentially normal. Concordant with the concept that elimination of some intestinal component is central to these phenomena, sensitivity to oral glucose was improved to a greater degree than was intravenous glucose. Incretin levels (GLP, GIP), however, were unchanged.
Malabsorptive bariatric surgery provides prompt regression of DM2, apparently due (at least in part) to some as yet unidentified intestinal hormone, and independent of identified incretin hormones such as GLP and GIP.
Herpes zoster in TNF-treated RA patients
Source: Strangfeld A, et al. Risk of herpes zoster in patients with rheumatoid arthritis treated with anti-TNF-a agents. JAMA 2009;301:737-744.
The evolution of pharmacotherapy for rheumatoid arthritis (RA) has led to the development of agents which, at least, offer major symptomatic improvement, and at best, promise remission. Because TNF agents involve modulation of steps critical to immune integrity, vigilance for serious bacterial infections is required. Yet, whether TNF agents impact the incidence of viral infections, which is also important, has been little-studied. Population studies on patients with RA have demonstrated a doubling of risk for herpes zoster compared to a control population.
Strangfeld et al enrolled RA patients (n = 5040) receiving either TNF agents or conventional DMARDS, such as methotrexate. Herpes zoster incidence was monitored over 36 months.
Overall, TNF agents were associated with an increased zoster incidence (hazard ratio = 1.82) compared to conventional treatment. Among the TNF agents, there was a distinct difference between etanercept, which did not show a statistically significant increase in zoster risk, vs infliximab and adalimumab, which did. The authors suggest that patients treated with the latter two agents merit particular vigilance for early signs and symptoms of herpes zoster to allow prompt intervention.
Best management of acute ankle sprain; Metabolic syndrome and salt sensitivity; Oseltamivir-resistant influenza; Low back radiology: Roadmap or mirage?; Bariatric surgery and reversal of dysglycemia; Herpes zoster in TNF-treated RA patientsYou have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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