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What interventions reduce the risk of contrast nephropathy for high-risk patients?
Several interventions may reduce the risk of contrast nephropathy for high-risk patients; however, most evidence uses surrogate markers for clinically relevant outcomes. Because dehydration is a risk factor for developing contrast nephropathy, periprocedural hydration is routinely recommended (strength of recommendation [SOR]: C, expert opinion). Single studies have suggested that isotonic saline is associated with less risk than half-normal saline, and hydration with fluids containing sodium bicarbonate is more efficacious than those containing isotonic saline (SOR: B, single randomized controlled trial [RCT]).
Oral acetylcysteine lowers the risk of post-contrast elevations in creatinine if taken more than 24 hours before contrast administration (SOR: A, RCTs). Acetylcysteine’s low cost and favorable side effect profile make it an appealing option. Hypoosmolar contrast media are less likely to induce contrast nephropathy than hyper-osmolar media (SOR: A, RCTs). Finally, hemofiltration might be considered for patients with extremely high risk of developing contrast nephropathy (SOR: B, single RCT).
Evidence summary
Intravascular administration of radiocontrast is frequently associated with acute reductions in renal function, particularly for patients with risk factors (TABLE 1). Most studies have used operational definitions of contrast nephropathy based on predefined elevations in serum creatinine from baseline, the great majority of which are transient and clinically insignificant. It is unclear if interventions that reduce the rate of mild creatinine elevations (TABLE 2) also reduce the risk of clinically relevant adverse outcomes.
A single RCT showed decreased risk of contrast nephropathy for patients pretreated with intravenous fluids containing sodium bicarbonate compared with those pretreated with a sodium chloride solution (number needed to treat [NNT]=8.4).2 Another RCT showed that periprocedural hydration with isotonic saline is superior to half-normal saline in preventing contrast nephropathy (NNT=77).3 Several studies have demonstrated decreased risk of contrast nephropathy for high-risk patients when low-osmolality contrast media are used rather than high-osmolality contrast media (NNT=27).4 A single study suggested that iso-osmolar contrast media generate less contrast induced nephropathy than low-osmolar contrast media.5 Because the primary outcome in these studies was a change in serum creatinine, the NNTs listed above may not predict clinical outcomes.
Periprocedural administration of acetylcysteine reduces the risk of contrast nephropathy in high-risk patients (odds ratio=0.56; 95% confidence interval, 0.37–0.84). Oral acetylcysteine is effective if intervention is begun 24 hours before contrast administration.6 Preliminary evidence shows that intravenous administration of acetylcysteine immediately before contrast administration lowers the risk of contrast nephropathy.7 Oral acetylcysteine is low in cost and has no known side effects.
A single RCT suggests that hemofiltration initiated 4 to 6 hours before contrast administration reduces the incidence of contrast nephropathy among high-risk patients.8 The study was unusual in that patients in the intervention group experienced statistically significant reductions in several clinically relevant outcomes, including in-hospital mortality and cumulative 1-year mortality (in-hospital mortality, NNT=8.3; cumulative 1-year mortality, NNT=5). Hemofiltration is expensive and is not available in many institutions.
TABLE 1
Risk factors for the development of contrast nephropathy
| Advanced age |
| Diabetes mellitus |
| Chronic renal insufficiency |
| Congestive heart failure |
| Acute myocardial infarction |
| Cardiogenic shock |
| Renal transplant |
| Hemodynamic instability |
| Dehydration |
| Low serum albumin |
| Angiotensin-converting enzyme use |
| Nonsteroidal anti-inflammatory drug use |
| Furosemide use |
| Higher volume of contrast media |
| Source: Nikolsky et al, Rev Cardiovasc Med 2003.1 |
TABLE 2
Interventions to reduce risk of contrast nephropathy
| INTERVENTION | SOR | PROTOCOLS |
|---|---|---|
| Acetylcysteine (oral) | A | Acetylcysteine 600 mg PO twice daily is generally given for 2 days beginning on the day prior to the procedure.6 |
| Hypo-osmolar contrast media | A | A variety of protocols have been demonstrated to be effective.4 |
| Acetylcysteine (IV) | B | 150 mg/kg of acetylcysteine was given in 500 mL of normal saline over 30 min immediately before contrast followed by 50 mg/kg of acetylcysteine in 500 mL of normal saline over 4 h. 7 |
| Iso-osmolar contast media | B | Varying volumes of iodixanol, an iso-osmolar contrast medium, were used rather than iohexol, a low osmolar contrast medium.5 |
| Sodium bicarbonate | B | Patients were given 4.23% dextrose in H20 with 154 mEq of sodium bicarbonate added per liter. Fluids were begun 1 hour prior to contrast administration running at 3 mL/kg/hr for 1 hour and then at 1 mL/kg/hr until 6 hours after contrast administration.2 |
| Isotonic saline | B | 0.9% sodium chloride was run at 1 mL/kg/hr beginning at 8 a.m. on the morning of the procedure or as early as possible prior to emergency procedures. The infusion was discontinued at 8 a.m. on the morning following the procedure.3 |
| Hemofiltration | B | Hemofiltration was started 4 to 6 hours before the procedure. It was resumed after the procedure was completed and continued for 18 to 24 hours.8 |
| SOR, strength of recommendation. (For more on evidence ratings, see “Evidence-based medicine terms” on page 381. | ||
Recommendations from others
The American College of Radiology recommends using low-osmolality contrast media for patients with renal insufficiency, particularly those with diabetes.9 Clinical Evidence found support for the use of low-osmolality contrast media, periprocedural hydration, and acetylcysteine as interventions to reduce the risk of contrast nephropathy.10
Avoid radiocontrast agents when possible; consider hydration and acetylcysteine
Richard A. Guthmann, MD
Illinois Masonic Family Practice Residency, University of Illinois at Chicago
The best prevention of contrast nephropathy is to avoid radiocontrast agents whenever possible. Ultrasound, MRI, or CT scanning without radiocontrast can often provide adequate information. However, when contrast agents must be used for high-risk patients, lower doses and iso-osmolal nonionic agents should be considered, and serial studies should be spaced out.
Adequate hydration and avoidance of drugs with renal effects, including nonsteroidal anti-inflammatory drugs, diuretics, and angiotensin-converting enzyme inhibitors, can decrease the risk of contrast nephropathy for patients requiring a contrast study. Patients can be hydrated and their medicines held starting the day before the procedure. For patients with any risk factors for contrast nephropathy, acetylcysteine should also be administered. Sodium bicarbonate can also lower the risk of nephropathy by administering it at the time of the procedure.
Contrast nephropathy has often been defined as an immediate increase in creatinine greater than 25%. The clinical significance of small transient elevations in creatinine is unclear. Furthermore, the wide variability reported in the incidence of contrast nephropathy results from differences in the presence of risk factors. Therefore, it is important to assess each patient’s risk individually and undertake additional preventive measures accordingly.
1. Nikolsky E, Aymong ED, Dangas G, Mehran R. Radiocontrast nephropathy: identifying the high-risk patient and the implications of exacerbating renal function. Rev Cardiovasc Med 2003;4 Suppl 1:S7-S14.
2. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 2004;291:2328-2334.
3. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002;162:329-336.
4. Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology 1993;188:171-178.
5. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003;348:491-499.
6. Birck R, Krzossok S, Markowetz F, Schnulle P, van der Woude FJ, Braun C. Acetylcysteine for prevention of contrast nephropathy: meta-analysis. Lancet 2003;362:598-603.
7. Baker CS, Wragg A, Kumar S, De Palma R, Baker LR, Knight CJ. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study. J Am Coll Cardiol 2003;41:2114-2118.
8. Marenzi G, Marana I, Lauri G, et al. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med 2003;349:1333-1340.
9. Hauser JB, Segal A, et al. ACR Practice Guideline for the Use of Intravascular Contrast Media. American College of Radiology Practice Guidelines. 2001 (effective 1/1/2002).
10. Kellum JA, Leblanc M, Venkataraman R. Acute renal failure. Clinical Evidence. Available at: www.clinicalevidence.org. Accessed April 2004.
Several interventions may reduce the risk of contrast nephropathy for high-risk patients; however, most evidence uses surrogate markers for clinically relevant outcomes. Because dehydration is a risk factor for developing contrast nephropathy, periprocedural hydration is routinely recommended (strength of recommendation [SOR]: C, expert opinion). Single studies have suggested that isotonic saline is associated with less risk than half-normal saline, and hydration with fluids containing sodium bicarbonate is more efficacious than those containing isotonic saline (SOR: B, single randomized controlled trial [RCT]).
Oral acetylcysteine lowers the risk of post-contrast elevations in creatinine if taken more than 24 hours before contrast administration (SOR: A, RCTs). Acetylcysteine’s low cost and favorable side effect profile make it an appealing option. Hypoosmolar contrast media are less likely to induce contrast nephropathy than hyper-osmolar media (SOR: A, RCTs). Finally, hemofiltration might be considered for patients with extremely high risk of developing contrast nephropathy (SOR: B, single RCT).
Evidence summary
Intravascular administration of radiocontrast is frequently associated with acute reductions in renal function, particularly for patients with risk factors (TABLE 1). Most studies have used operational definitions of contrast nephropathy based on predefined elevations in serum creatinine from baseline, the great majority of which are transient and clinically insignificant. It is unclear if interventions that reduce the rate of mild creatinine elevations (TABLE 2) also reduce the risk of clinically relevant adverse outcomes.
A single RCT showed decreased risk of contrast nephropathy for patients pretreated with intravenous fluids containing sodium bicarbonate compared with those pretreated with a sodium chloride solution (number needed to treat [NNT]=8.4).2 Another RCT showed that periprocedural hydration with isotonic saline is superior to half-normal saline in preventing contrast nephropathy (NNT=77).3 Several studies have demonstrated decreased risk of contrast nephropathy for high-risk patients when low-osmolality contrast media are used rather than high-osmolality contrast media (NNT=27).4 A single study suggested that iso-osmolar contrast media generate less contrast induced nephropathy than low-osmolar contrast media.5 Because the primary outcome in these studies was a change in serum creatinine, the NNTs listed above may not predict clinical outcomes.
Periprocedural administration of acetylcysteine reduces the risk of contrast nephropathy in high-risk patients (odds ratio=0.56; 95% confidence interval, 0.37–0.84). Oral acetylcysteine is effective if intervention is begun 24 hours before contrast administration.6 Preliminary evidence shows that intravenous administration of acetylcysteine immediately before contrast administration lowers the risk of contrast nephropathy.7 Oral acetylcysteine is low in cost and has no known side effects.
A single RCT suggests that hemofiltration initiated 4 to 6 hours before contrast administration reduces the incidence of contrast nephropathy among high-risk patients.8 The study was unusual in that patients in the intervention group experienced statistically significant reductions in several clinically relevant outcomes, including in-hospital mortality and cumulative 1-year mortality (in-hospital mortality, NNT=8.3; cumulative 1-year mortality, NNT=5). Hemofiltration is expensive and is not available in many institutions.
TABLE 1
Risk factors for the development of contrast nephropathy
| Advanced age |
| Diabetes mellitus |
| Chronic renal insufficiency |
| Congestive heart failure |
| Acute myocardial infarction |
| Cardiogenic shock |
| Renal transplant |
| Hemodynamic instability |
| Dehydration |
| Low serum albumin |
| Angiotensin-converting enzyme use |
| Nonsteroidal anti-inflammatory drug use |
| Furosemide use |
| Higher volume of contrast media |
| Source: Nikolsky et al, Rev Cardiovasc Med 2003.1 |
TABLE 2
Interventions to reduce risk of contrast nephropathy
| INTERVENTION | SOR | PROTOCOLS |
|---|---|---|
| Acetylcysteine (oral) | A | Acetylcysteine 600 mg PO twice daily is generally given for 2 days beginning on the day prior to the procedure.6 |
| Hypo-osmolar contrast media | A | A variety of protocols have been demonstrated to be effective.4 |
| Acetylcysteine (IV) | B | 150 mg/kg of acetylcysteine was given in 500 mL of normal saline over 30 min immediately before contrast followed by 50 mg/kg of acetylcysteine in 500 mL of normal saline over 4 h. 7 |
| Iso-osmolar contast media | B | Varying volumes of iodixanol, an iso-osmolar contrast medium, were used rather than iohexol, a low osmolar contrast medium.5 |
| Sodium bicarbonate | B | Patients were given 4.23% dextrose in H20 with 154 mEq of sodium bicarbonate added per liter. Fluids were begun 1 hour prior to contrast administration running at 3 mL/kg/hr for 1 hour and then at 1 mL/kg/hr until 6 hours after contrast administration.2 |
| Isotonic saline | B | 0.9% sodium chloride was run at 1 mL/kg/hr beginning at 8 a.m. on the morning of the procedure or as early as possible prior to emergency procedures. The infusion was discontinued at 8 a.m. on the morning following the procedure.3 |
| Hemofiltration | B | Hemofiltration was started 4 to 6 hours before the procedure. It was resumed after the procedure was completed and continued for 18 to 24 hours.8 |
| SOR, strength of recommendation. (For more on evidence ratings, see “Evidence-based medicine terms” on page 381. | ||
Recommendations from others
The American College of Radiology recommends using low-osmolality contrast media for patients with renal insufficiency, particularly those with diabetes.9 Clinical Evidence found support for the use of low-osmolality contrast media, periprocedural hydration, and acetylcysteine as interventions to reduce the risk of contrast nephropathy.10
Avoid radiocontrast agents when possible; consider hydration and acetylcysteine
Richard A. Guthmann, MD
Illinois Masonic Family Practice Residency, University of Illinois at Chicago
The best prevention of contrast nephropathy is to avoid radiocontrast agents whenever possible. Ultrasound, MRI, or CT scanning without radiocontrast can often provide adequate information. However, when contrast agents must be used for high-risk patients, lower doses and iso-osmolal nonionic agents should be considered, and serial studies should be spaced out.
Adequate hydration and avoidance of drugs with renal effects, including nonsteroidal anti-inflammatory drugs, diuretics, and angiotensin-converting enzyme inhibitors, can decrease the risk of contrast nephropathy for patients requiring a contrast study. Patients can be hydrated and their medicines held starting the day before the procedure. For patients with any risk factors for contrast nephropathy, acetylcysteine should also be administered. Sodium bicarbonate can also lower the risk of nephropathy by administering it at the time of the procedure.
Contrast nephropathy has often been defined as an immediate increase in creatinine greater than 25%. The clinical significance of small transient elevations in creatinine is unclear. Furthermore, the wide variability reported in the incidence of contrast nephropathy results from differences in the presence of risk factors. Therefore, it is important to assess each patient’s risk individually and undertake additional preventive measures accordingly.
Several interventions may reduce the risk of contrast nephropathy for high-risk patients; however, most evidence uses surrogate markers for clinically relevant outcomes. Because dehydration is a risk factor for developing contrast nephropathy, periprocedural hydration is routinely recommended (strength of recommendation [SOR]: C, expert opinion). Single studies have suggested that isotonic saline is associated with less risk than half-normal saline, and hydration with fluids containing sodium bicarbonate is more efficacious than those containing isotonic saline (SOR: B, single randomized controlled trial [RCT]).
Oral acetylcysteine lowers the risk of post-contrast elevations in creatinine if taken more than 24 hours before contrast administration (SOR: A, RCTs). Acetylcysteine’s low cost and favorable side effect profile make it an appealing option. Hypoosmolar contrast media are less likely to induce contrast nephropathy than hyper-osmolar media (SOR: A, RCTs). Finally, hemofiltration might be considered for patients with extremely high risk of developing contrast nephropathy (SOR: B, single RCT).
Evidence summary
Intravascular administration of radiocontrast is frequently associated with acute reductions in renal function, particularly for patients with risk factors (TABLE 1). Most studies have used operational definitions of contrast nephropathy based on predefined elevations in serum creatinine from baseline, the great majority of which are transient and clinically insignificant. It is unclear if interventions that reduce the rate of mild creatinine elevations (TABLE 2) also reduce the risk of clinically relevant adverse outcomes.
A single RCT showed decreased risk of contrast nephropathy for patients pretreated with intravenous fluids containing sodium bicarbonate compared with those pretreated with a sodium chloride solution (number needed to treat [NNT]=8.4).2 Another RCT showed that periprocedural hydration with isotonic saline is superior to half-normal saline in preventing contrast nephropathy (NNT=77).3 Several studies have demonstrated decreased risk of contrast nephropathy for high-risk patients when low-osmolality contrast media are used rather than high-osmolality contrast media (NNT=27).4 A single study suggested that iso-osmolar contrast media generate less contrast induced nephropathy than low-osmolar contrast media.5 Because the primary outcome in these studies was a change in serum creatinine, the NNTs listed above may not predict clinical outcomes.
Periprocedural administration of acetylcysteine reduces the risk of contrast nephropathy in high-risk patients (odds ratio=0.56; 95% confidence interval, 0.37–0.84). Oral acetylcysteine is effective if intervention is begun 24 hours before contrast administration.6 Preliminary evidence shows that intravenous administration of acetylcysteine immediately before contrast administration lowers the risk of contrast nephropathy.7 Oral acetylcysteine is low in cost and has no known side effects.
A single RCT suggests that hemofiltration initiated 4 to 6 hours before contrast administration reduces the incidence of contrast nephropathy among high-risk patients.8 The study was unusual in that patients in the intervention group experienced statistically significant reductions in several clinically relevant outcomes, including in-hospital mortality and cumulative 1-year mortality (in-hospital mortality, NNT=8.3; cumulative 1-year mortality, NNT=5). Hemofiltration is expensive and is not available in many institutions.
TABLE 1
Risk factors for the development of contrast nephropathy
| Advanced age |
| Diabetes mellitus |
| Chronic renal insufficiency |
| Congestive heart failure |
| Acute myocardial infarction |
| Cardiogenic shock |
| Renal transplant |
| Hemodynamic instability |
| Dehydration |
| Low serum albumin |
| Angiotensin-converting enzyme use |
| Nonsteroidal anti-inflammatory drug use |
| Furosemide use |
| Higher volume of contrast media |
| Source: Nikolsky et al, Rev Cardiovasc Med 2003.1 |
TABLE 2
Interventions to reduce risk of contrast nephropathy
| INTERVENTION | SOR | PROTOCOLS |
|---|---|---|
| Acetylcysteine (oral) | A | Acetylcysteine 600 mg PO twice daily is generally given for 2 days beginning on the day prior to the procedure.6 |
| Hypo-osmolar contrast media | A | A variety of protocols have been demonstrated to be effective.4 |
| Acetylcysteine (IV) | B | 150 mg/kg of acetylcysteine was given in 500 mL of normal saline over 30 min immediately before contrast followed by 50 mg/kg of acetylcysteine in 500 mL of normal saline over 4 h. 7 |
| Iso-osmolar contast media | B | Varying volumes of iodixanol, an iso-osmolar contrast medium, were used rather than iohexol, a low osmolar contrast medium.5 |
| Sodium bicarbonate | B | Patients were given 4.23% dextrose in H20 with 154 mEq of sodium bicarbonate added per liter. Fluids were begun 1 hour prior to contrast administration running at 3 mL/kg/hr for 1 hour and then at 1 mL/kg/hr until 6 hours after contrast administration.2 |
| Isotonic saline | B | 0.9% sodium chloride was run at 1 mL/kg/hr beginning at 8 a.m. on the morning of the procedure or as early as possible prior to emergency procedures. The infusion was discontinued at 8 a.m. on the morning following the procedure.3 |
| Hemofiltration | B | Hemofiltration was started 4 to 6 hours before the procedure. It was resumed after the procedure was completed and continued for 18 to 24 hours.8 |
| SOR, strength of recommendation. (For more on evidence ratings, see “Evidence-based medicine terms” on page 381. | ||
Recommendations from others
The American College of Radiology recommends using low-osmolality contrast media for patients with renal insufficiency, particularly those with diabetes.9 Clinical Evidence found support for the use of low-osmolality contrast media, periprocedural hydration, and acetylcysteine as interventions to reduce the risk of contrast nephropathy.10
Avoid radiocontrast agents when possible; consider hydration and acetylcysteine
Richard A. Guthmann, MD
Illinois Masonic Family Practice Residency, University of Illinois at Chicago
The best prevention of contrast nephropathy is to avoid radiocontrast agents whenever possible. Ultrasound, MRI, or CT scanning without radiocontrast can often provide adequate information. However, when contrast agents must be used for high-risk patients, lower doses and iso-osmolal nonionic agents should be considered, and serial studies should be spaced out.
Adequate hydration and avoidance of drugs with renal effects, including nonsteroidal anti-inflammatory drugs, diuretics, and angiotensin-converting enzyme inhibitors, can decrease the risk of contrast nephropathy for patients requiring a contrast study. Patients can be hydrated and their medicines held starting the day before the procedure. For patients with any risk factors for contrast nephropathy, acetylcysteine should also be administered. Sodium bicarbonate can also lower the risk of nephropathy by administering it at the time of the procedure.
Contrast nephropathy has often been defined as an immediate increase in creatinine greater than 25%. The clinical significance of small transient elevations in creatinine is unclear. Furthermore, the wide variability reported in the incidence of contrast nephropathy results from differences in the presence of risk factors. Therefore, it is important to assess each patient’s risk individually and undertake additional preventive measures accordingly.
1. Nikolsky E, Aymong ED, Dangas G, Mehran R. Radiocontrast nephropathy: identifying the high-risk patient and the implications of exacerbating renal function. Rev Cardiovasc Med 2003;4 Suppl 1:S7-S14.
2. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 2004;291:2328-2334.
3. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002;162:329-336.
4. Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology 1993;188:171-178.
5. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003;348:491-499.
6. Birck R, Krzossok S, Markowetz F, Schnulle P, van der Woude FJ, Braun C. Acetylcysteine for prevention of contrast nephropathy: meta-analysis. Lancet 2003;362:598-603.
7. Baker CS, Wragg A, Kumar S, De Palma R, Baker LR, Knight CJ. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study. J Am Coll Cardiol 2003;41:2114-2118.
8. Marenzi G, Marana I, Lauri G, et al. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med 2003;349:1333-1340.
9. Hauser JB, Segal A, et al. ACR Practice Guideline for the Use of Intravascular Contrast Media. American College of Radiology Practice Guidelines. 2001 (effective 1/1/2002).
10. Kellum JA, Leblanc M, Venkataraman R. Acute renal failure. Clinical Evidence. Available at: www.clinicalevidence.org. Accessed April 2004.
1. Nikolsky E, Aymong ED, Dangas G, Mehran R. Radiocontrast nephropathy: identifying the high-risk patient and the implications of exacerbating renal function. Rev Cardiovasc Med 2003;4 Suppl 1:S7-S14.
2. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 2004;291:2328-2334.
3. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002;162:329-336.
4. Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology 1993;188:171-178.
5. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003;348:491-499.
6. Birck R, Krzossok S, Markowetz F, Schnulle P, van der Woude FJ, Braun C. Acetylcysteine for prevention of contrast nephropathy: meta-analysis. Lancet 2003;362:598-603.
7. Baker CS, Wragg A, Kumar S, De Palma R, Baker LR, Knight CJ. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study. J Am Coll Cardiol 2003;41:2114-2118.
8. Marenzi G, Marana I, Lauri G, et al. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med 2003;349:1333-1340.
9. Hauser JB, Segal A, et al. ACR Practice Guideline for the Use of Intravascular Contrast Media. American College of Radiology Practice Guidelines. 2001 (effective 1/1/2002).
10. Kellum JA, Leblanc M, Venkataraman R. Acute renal failure. Clinical Evidence. Available at: www.clinicalevidence.org. Accessed April 2004.
Evidence-based answers from the Family Physicians Inquiries Network
What effect do inhaled steroids have on delaying the progression of COPD?
The annual rate of decline in forced expiratory volume for 1 second (FEV1) has been researchers’ gold standard as an objective measure for progression of chronic obstructive pulmonary disease (COPD). Inhaled corticosteroids (ICS) do not consistently have a statistically significant impact on FEV1 decline, and thus on the progression of COPD (strength of recommendation [SOR]: B, 2 conflicting meta-analyses and numerous conflicting randomized controlled trials). In those studies that did show improvements in FEV1 decline, the change does not appear to be clinically significant (7.7 to 9.0 mL/year).
These findings do not take into account the potential impact of ICS on such patient oriented outcomes as exacerbation rates, quality of life, outpatient visits, hospitalization, and mortality.
Evidence summary
No therapies are known to improve long-term lung function in COPD; the goal of disease-moderating therapy is therefore to slow the rate of decline compared with the expected rate. All of the studies reviewed used FEV1 as an objective measure of whether ICS reduce this rate of decline in lung function.
Two recent meta-analyses evaluating medium- to high-dose ICS effects on FEV1 decline provided conflicting results. One meta-analysis evaluated 8 controlled clinical trials lasting at least 2 years (n=3715) and found that, when compared with placebo, ICS significantly reduced the rate of FEV1 decline by 7.7 mL/year (P=.02) and that high-dose ICS had a greater effect of 9.9 mL/year (P=.01).1 Another meta-analysis of 6 randomized, placebo-controlled trials with a duration of at least 2 years (n=3571) found a nonsignificant trend in favor of ICS, with a difference in FEV1 decline of 5.31 mL/year (P=.08) between the ICS and placebo groups.2
The differences observed in these 2 meta-analyses may be explained by the authors using slightly different approximations to the standard error, applying slightly different statistical analytical methods, and using different inclusion criteria for trials. However, 5 of the trials in these reviews were the same. Both meta-analyses determined only rate of lung function decline and did not evaluate clinical outcomes.
A trial not included in the previously mentioned meta-analyses evaluated post-bronchodilator FEV1 decline in 48 patients with early signs and symptoms of COPD for 2 years.3 Subjects were assigned to medium-dose fluticasone propionate or placebo. Early initiation of ICS treatment did not affect the progressive deterioration of lung function as no modifying effect on annual FEV1 decline was observed, however, the study only had power to detect a 60-mL annual drop in FEV1.
Meta-analyses and trials evaluating COPD progression have focused on a disease-oriented outcome (the rate of FEV1 decline). However, patient-oriented outcomes such as exacerbation frequency, hospitalization, health-related quality of life, and mortality might be more important measures of successful therapy. Although such patient-oriented outcomes are not the focus of this review or the included meta-analyses, a few of the small randomized controlled trials included in these meta-analyses suggest that ICS may improve such patient-oriented outcomes. Notably, exacerbation rates significantly decreased by 25% (P=.026), and health status improved (P=.0043) among patients with moderate to severe COPD who were taking fluticasone compared with those taking placebo.4 In mild to moderate COPD, patients treated with triamcinolone had fewer respiratory symptoms (P=.005), fewer visits to a physician because of respiratory illness (P=.003), and improved airway reactivity (P=.02).5 Some systematic reviews and other randomized trials suggest that ICS have significant benefit on these patient outcomes.6
Recommendations from others
Scientists from the National Heart, Lung, and Blood Institute and the World Health Organization provided an update of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) in 2003.7 They reported that regular treatment with ICS does not modify the long-term decline of FEV1 in patients with COPD. However, they recommended treatment with ICS for symptomatic COPD patients with an FEV1 less than 50% of predicted (stage III: severe COPD and stage IV: very severe COPD) and repeated exacerbations (ie, 3 in the last 3 years). Guidelines from other countries also suggest that ICS do not affect the progression of COPD, but support the use of ICS for patients with severe COPD and repeated exacerbations.8-10
Smoking cessation a huge benefit to all COPD patients
Vincent Lo, MD
St. Elizabeth Family Medicine Residency Program, Utica, NY; SUNY Upstate Medical University, Syracuse
In adults aged more than 30 years old with COPD, the physiological abnormality is primarily an accelerated decline in the FEV1 from the normal rate of about 30 mL per year to nearly 60 mL per year. In patients with COPD, smoking cessation is the only proven means to slow down the progression of the disease, with up to a sustained 50% reduction in the rate of lung-function decline.
Therefore, it is imperative for family physicians to underscore the magnitude of the benefit of smoking cessation to all COPD patients and to emphasize the current evidence that inhaled corticosteroid has a limited impact in delaying the progression of the disease.
1. Sutherland ER, Allmers H, Ayas NT, Venn AJ, Martin RJ. Inhaled corticosteroids reduce the progression of airflow limitation in chronic obstructive pulmonary disease: a meta-analysis. Thorax 2003;58:937-941.
2. Highland KB, Strange C, Heffner JE. Long-term effects of inhaled corticosteroids on FEV1 in patients with chronic obstructive pulmonary disease. A meta-analysis. Ann Intern Med 2003;138:969-973.
3. van Grunsven P, Schermer T, Akkermans R, et al. Short-and long-term efficacy of fluticasone propionate in subjects with early signs and symptoms of chronic obstructive pulmonary disease. Results of the DIMCA study. Respir Med 2003;97:1303-1312.
4. Burge PS, Calverley PM, Jones PW, Spencer S, Anderson JA, Maslen TK. Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ 2000;320:1297-1303.
5. The Lung Health Study Research Group. Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med 2000;343:1902-1909.
6. Sin DD, McAlister FA, Man SF, Anthonisen NR. Contemporary management of chronic obstructive pulmonary disease: scientific review. JAMA 2003;290:2301-2312.
7. Global initiative for chronic obstructive lung disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease. NHLBI/WHO workshop report. Bethesda, National Heart, Lung and Blood Institute, April 2001; update of the management sections, GOLD website (www.goldcopd.com). Accessed April 3, 2004.
8. Chronic Obstructive Pulmonary Disease. National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care. Thorax 2004;59 Suppl 1:1-232.
9. McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;178 Suppl:S7-S39.
10. O’Donnell DE, Aaron S, Bourbeau J, et al. Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease—2003. Can Respir J 2003;10 Suppl A:11A-65A.
The annual rate of decline in forced expiratory volume for 1 second (FEV1) has been researchers’ gold standard as an objective measure for progression of chronic obstructive pulmonary disease (COPD). Inhaled corticosteroids (ICS) do not consistently have a statistically significant impact on FEV1 decline, and thus on the progression of COPD (strength of recommendation [SOR]: B, 2 conflicting meta-analyses and numerous conflicting randomized controlled trials). In those studies that did show improvements in FEV1 decline, the change does not appear to be clinically significant (7.7 to 9.0 mL/year).
These findings do not take into account the potential impact of ICS on such patient oriented outcomes as exacerbation rates, quality of life, outpatient visits, hospitalization, and mortality.
Evidence summary
No therapies are known to improve long-term lung function in COPD; the goal of disease-moderating therapy is therefore to slow the rate of decline compared with the expected rate. All of the studies reviewed used FEV1 as an objective measure of whether ICS reduce this rate of decline in lung function.
Two recent meta-analyses evaluating medium- to high-dose ICS effects on FEV1 decline provided conflicting results. One meta-analysis evaluated 8 controlled clinical trials lasting at least 2 years (n=3715) and found that, when compared with placebo, ICS significantly reduced the rate of FEV1 decline by 7.7 mL/year (P=.02) and that high-dose ICS had a greater effect of 9.9 mL/year (P=.01).1 Another meta-analysis of 6 randomized, placebo-controlled trials with a duration of at least 2 years (n=3571) found a nonsignificant trend in favor of ICS, with a difference in FEV1 decline of 5.31 mL/year (P=.08) between the ICS and placebo groups.2
The differences observed in these 2 meta-analyses may be explained by the authors using slightly different approximations to the standard error, applying slightly different statistical analytical methods, and using different inclusion criteria for trials. However, 5 of the trials in these reviews were the same. Both meta-analyses determined only rate of lung function decline and did not evaluate clinical outcomes.
A trial not included in the previously mentioned meta-analyses evaluated post-bronchodilator FEV1 decline in 48 patients with early signs and symptoms of COPD for 2 years.3 Subjects were assigned to medium-dose fluticasone propionate or placebo. Early initiation of ICS treatment did not affect the progressive deterioration of lung function as no modifying effect on annual FEV1 decline was observed, however, the study only had power to detect a 60-mL annual drop in FEV1.
Meta-analyses and trials evaluating COPD progression have focused on a disease-oriented outcome (the rate of FEV1 decline). However, patient-oriented outcomes such as exacerbation frequency, hospitalization, health-related quality of life, and mortality might be more important measures of successful therapy. Although such patient-oriented outcomes are not the focus of this review or the included meta-analyses, a few of the small randomized controlled trials included in these meta-analyses suggest that ICS may improve such patient-oriented outcomes. Notably, exacerbation rates significantly decreased by 25% (P=.026), and health status improved (P=.0043) among patients with moderate to severe COPD who were taking fluticasone compared with those taking placebo.4 In mild to moderate COPD, patients treated with triamcinolone had fewer respiratory symptoms (P=.005), fewer visits to a physician because of respiratory illness (P=.003), and improved airway reactivity (P=.02).5 Some systematic reviews and other randomized trials suggest that ICS have significant benefit on these patient outcomes.6
Recommendations from others
Scientists from the National Heart, Lung, and Blood Institute and the World Health Organization provided an update of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) in 2003.7 They reported that regular treatment with ICS does not modify the long-term decline of FEV1 in patients with COPD. However, they recommended treatment with ICS for symptomatic COPD patients with an FEV1 less than 50% of predicted (stage III: severe COPD and stage IV: very severe COPD) and repeated exacerbations (ie, 3 in the last 3 years). Guidelines from other countries also suggest that ICS do not affect the progression of COPD, but support the use of ICS for patients with severe COPD and repeated exacerbations.8-10
Smoking cessation a huge benefit to all COPD patients
Vincent Lo, MD
St. Elizabeth Family Medicine Residency Program, Utica, NY; SUNY Upstate Medical University, Syracuse
In adults aged more than 30 years old with COPD, the physiological abnormality is primarily an accelerated decline in the FEV1 from the normal rate of about 30 mL per year to nearly 60 mL per year. In patients with COPD, smoking cessation is the only proven means to slow down the progression of the disease, with up to a sustained 50% reduction in the rate of lung-function decline.
Therefore, it is imperative for family physicians to underscore the magnitude of the benefit of smoking cessation to all COPD patients and to emphasize the current evidence that inhaled corticosteroid has a limited impact in delaying the progression of the disease.
The annual rate of decline in forced expiratory volume for 1 second (FEV1) has been researchers’ gold standard as an objective measure for progression of chronic obstructive pulmonary disease (COPD). Inhaled corticosteroids (ICS) do not consistently have a statistically significant impact on FEV1 decline, and thus on the progression of COPD (strength of recommendation [SOR]: B, 2 conflicting meta-analyses and numerous conflicting randomized controlled trials). In those studies that did show improvements in FEV1 decline, the change does not appear to be clinically significant (7.7 to 9.0 mL/year).
These findings do not take into account the potential impact of ICS on such patient oriented outcomes as exacerbation rates, quality of life, outpatient visits, hospitalization, and mortality.
Evidence summary
No therapies are known to improve long-term lung function in COPD; the goal of disease-moderating therapy is therefore to slow the rate of decline compared with the expected rate. All of the studies reviewed used FEV1 as an objective measure of whether ICS reduce this rate of decline in lung function.
Two recent meta-analyses evaluating medium- to high-dose ICS effects on FEV1 decline provided conflicting results. One meta-analysis evaluated 8 controlled clinical trials lasting at least 2 years (n=3715) and found that, when compared with placebo, ICS significantly reduced the rate of FEV1 decline by 7.7 mL/year (P=.02) and that high-dose ICS had a greater effect of 9.9 mL/year (P=.01).1 Another meta-analysis of 6 randomized, placebo-controlled trials with a duration of at least 2 years (n=3571) found a nonsignificant trend in favor of ICS, with a difference in FEV1 decline of 5.31 mL/year (P=.08) between the ICS and placebo groups.2
The differences observed in these 2 meta-analyses may be explained by the authors using slightly different approximations to the standard error, applying slightly different statistical analytical methods, and using different inclusion criteria for trials. However, 5 of the trials in these reviews were the same. Both meta-analyses determined only rate of lung function decline and did not evaluate clinical outcomes.
A trial not included in the previously mentioned meta-analyses evaluated post-bronchodilator FEV1 decline in 48 patients with early signs and symptoms of COPD for 2 years.3 Subjects were assigned to medium-dose fluticasone propionate or placebo. Early initiation of ICS treatment did not affect the progressive deterioration of lung function as no modifying effect on annual FEV1 decline was observed, however, the study only had power to detect a 60-mL annual drop in FEV1.
Meta-analyses and trials evaluating COPD progression have focused on a disease-oriented outcome (the rate of FEV1 decline). However, patient-oriented outcomes such as exacerbation frequency, hospitalization, health-related quality of life, and mortality might be more important measures of successful therapy. Although such patient-oriented outcomes are not the focus of this review or the included meta-analyses, a few of the small randomized controlled trials included in these meta-analyses suggest that ICS may improve such patient-oriented outcomes. Notably, exacerbation rates significantly decreased by 25% (P=.026), and health status improved (P=.0043) among patients with moderate to severe COPD who were taking fluticasone compared with those taking placebo.4 In mild to moderate COPD, patients treated with triamcinolone had fewer respiratory symptoms (P=.005), fewer visits to a physician because of respiratory illness (P=.003), and improved airway reactivity (P=.02).5 Some systematic reviews and other randomized trials suggest that ICS have significant benefit on these patient outcomes.6
Recommendations from others
Scientists from the National Heart, Lung, and Blood Institute and the World Health Organization provided an update of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) in 2003.7 They reported that regular treatment with ICS does not modify the long-term decline of FEV1 in patients with COPD. However, they recommended treatment with ICS for symptomatic COPD patients with an FEV1 less than 50% of predicted (stage III: severe COPD and stage IV: very severe COPD) and repeated exacerbations (ie, 3 in the last 3 years). Guidelines from other countries also suggest that ICS do not affect the progression of COPD, but support the use of ICS for patients with severe COPD and repeated exacerbations.8-10
Smoking cessation a huge benefit to all COPD patients
Vincent Lo, MD
St. Elizabeth Family Medicine Residency Program, Utica, NY; SUNY Upstate Medical University, Syracuse
In adults aged more than 30 years old with COPD, the physiological abnormality is primarily an accelerated decline in the FEV1 from the normal rate of about 30 mL per year to nearly 60 mL per year. In patients with COPD, smoking cessation is the only proven means to slow down the progression of the disease, with up to a sustained 50% reduction in the rate of lung-function decline.
Therefore, it is imperative for family physicians to underscore the magnitude of the benefit of smoking cessation to all COPD patients and to emphasize the current evidence that inhaled corticosteroid has a limited impact in delaying the progression of the disease.
1. Sutherland ER, Allmers H, Ayas NT, Venn AJ, Martin RJ. Inhaled corticosteroids reduce the progression of airflow limitation in chronic obstructive pulmonary disease: a meta-analysis. Thorax 2003;58:937-941.
2. Highland KB, Strange C, Heffner JE. Long-term effects of inhaled corticosteroids on FEV1 in patients with chronic obstructive pulmonary disease. A meta-analysis. Ann Intern Med 2003;138:969-973.
3. van Grunsven P, Schermer T, Akkermans R, et al. Short-and long-term efficacy of fluticasone propionate in subjects with early signs and symptoms of chronic obstructive pulmonary disease. Results of the DIMCA study. Respir Med 2003;97:1303-1312.
4. Burge PS, Calverley PM, Jones PW, Spencer S, Anderson JA, Maslen TK. Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ 2000;320:1297-1303.
5. The Lung Health Study Research Group. Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med 2000;343:1902-1909.
6. Sin DD, McAlister FA, Man SF, Anthonisen NR. Contemporary management of chronic obstructive pulmonary disease: scientific review. JAMA 2003;290:2301-2312.
7. Global initiative for chronic obstructive lung disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease. NHLBI/WHO workshop report. Bethesda, National Heart, Lung and Blood Institute, April 2001; update of the management sections, GOLD website (www.goldcopd.com). Accessed April 3, 2004.
8. Chronic Obstructive Pulmonary Disease. National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care. Thorax 2004;59 Suppl 1:1-232.
9. McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;178 Suppl:S7-S39.
10. O’Donnell DE, Aaron S, Bourbeau J, et al. Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease—2003. Can Respir J 2003;10 Suppl A:11A-65A.
1. Sutherland ER, Allmers H, Ayas NT, Venn AJ, Martin RJ. Inhaled corticosteroids reduce the progression of airflow limitation in chronic obstructive pulmonary disease: a meta-analysis. Thorax 2003;58:937-941.
2. Highland KB, Strange C, Heffner JE. Long-term effects of inhaled corticosteroids on FEV1 in patients with chronic obstructive pulmonary disease. A meta-analysis. Ann Intern Med 2003;138:969-973.
3. van Grunsven P, Schermer T, Akkermans R, et al. Short-and long-term efficacy of fluticasone propionate in subjects with early signs and symptoms of chronic obstructive pulmonary disease. Results of the DIMCA study. Respir Med 2003;97:1303-1312.
4. Burge PS, Calverley PM, Jones PW, Spencer S, Anderson JA, Maslen TK. Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ 2000;320:1297-1303.
5. The Lung Health Study Research Group. Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med 2000;343:1902-1909.
6. Sin DD, McAlister FA, Man SF, Anthonisen NR. Contemporary management of chronic obstructive pulmonary disease: scientific review. JAMA 2003;290:2301-2312.
7. Global initiative for chronic obstructive lung disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease. NHLBI/WHO workshop report. Bethesda, National Heart, Lung and Blood Institute, April 2001; update of the management sections, GOLD website (www.goldcopd.com). Accessed April 3, 2004.
8. Chronic Obstructive Pulmonary Disease. National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care. Thorax 2004;59 Suppl 1:1-232.
9. McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;178 Suppl:S7-S39.
10. O’Donnell DE, Aaron S, Bourbeau J, et al. Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease—2003. Can Respir J 2003;10 Suppl A:11A-65A.
Evidence-based answers from the Family Physicians Inquiries Network
Does injection of steroids and lidocaine in the shoulder relieve bursitis?
Subacromial steroid injection may provide a small, short-term benefit compared with placebo. The short-term effectiveness of steroid injection compared with nonsteroidal anti-inflammatory agents (NSAIDs) remains unclear.
Steroid injections are better than physiotherapy alone in the short term. However, injection does not appear to provide any meaningful long-term benefit compared with other therapies (strength of recommendation: B). Data are insufficient to make recommendations regarding the proper timing of injection in the sequence of other treatments. Side effects of steroid injection, such as steroid flare and infection, are rare.
Evidence summary
A Cochrane Review of corticosteroid injections for shoulder pain found 7 randomized controlled trials comparing subacromial steroid injections with placebo.1 The placebos were either injectable anesthetics alone or injectable anesthetics combined with oral placebo tablets. Six of the 7 studies used the anterolateral approach to inject under the acromion.
All studies used a clinical exam for diagnosis that showed pain with range of motion (especially abduction) or pain that was consistent with impingement syndrome. Most of the follow-up times were short, typically 4 to 12 weeks, and the longest study was 33 weeks. Meta-analyses often report the effect size using standard mean difference (SMD). A rule of thumb for interpretation of SMD is a value of 0.2 indicates a small effect, a value of 0.5 indicates a medium effect, and a value of 0.8 or larger indicates a large effect. If the 95% confidence interval [CI] does not include zero, then the SMD is statistically significant at the 5% level (P<.05).2
Two of the studies comparing steroid injection with placebo were methodologically suitable for meta-analysis; these studies showed thatsteroids provided a mild, short-term (4-week)benefit with respect to pain (SMD=0.83; 95% CI,0.39–1.26), function (SMD=0.63; 95% CI,0.20–1.06), and abductive range of motion(SMD=0.82; 95% CI, 0.39–1.25).3,4
Results of the remaining, less rigorous trialswere conflicting and inconclusive. The reviewersalso found 3 randomized controlled trials comparing subacromial steroid injection with oralNSAIDs. The pooled results of these trials,encompassing 120 patients, found no differences in these 3 outcomes at 4 or 6 weeks. The review of an additional trial of 50 patients comparing subacromial steroid injection plus simultaneous oral NSAIDs with oral NSAIDs alone found no differences at 4 weeks. All 11 studies had small sample sizes, and suffered from variable methodological quality and heterogeneous results.
The reviewers concluded that steroids are probably better than placebo but provide little or no benefit in addition to NSAIDs, and that evidence is insufficient to guide treatment. Likewise, a Cochrane Review of multiple interventions for shoulder pain also found “little evidence to support or refute the efficacy of common interventions” and highlighted the need for new, well-designed trials.5
Another Cochrane Review examined 4 randomized controlled trials comparing physiotherapy interventions for shoulder pain.6 They found that steroid injections may be superior to physiotherapy for rotator cuff disease, but the type of physiotherapy and injection sites were not consistent across the studies, making creation of summary estimates inappropriate. The individual studies showed significant short-term benefits (3–7 weeks) of steroid injection over physiotherapy; however, long-term (6–52 weeks) benefits ranged from some benefit to no difference. These studies were consistent regarding age (mean age=53–55 years, SD ± 13–14 years) and complications reported, with the only side effect being postinjection soreness.
Hay et al7 conducted a multicenter, primary care–based randomized controlled trial with more than 200 patients, which was published too recently for inclusion in the Cochrane Review. They found no statistical difference in improvement between steroid injection without physiotherapy and physiotherapy alone at 6 weeks.
In 1996, van der Heijden et al8 systematically reviewed randomized clinical trials of steroid injections for shoulder disorders, including rota-tor cuff disease, adhesive capsulitis, rheumatoid conditions, and periarthritis. They screened more than 200 articles from searches in Medline (1966–1995) and EMBASE (1984–1995) and found 16 articles that met qualifying conditions for further review. Of these, 3 were methodologically adequate for final review. None of these 3 studies provided evidence showing the efficacy of steroid injections. The results of the major trials reviewed can be found in the Table .
TABLE
Major placebo-controlled trials of injectable steroids for shoulder pain
| Steroid (n) | Comparison | Follow-up arms (n) | Reported results | Conclusions |
|---|---|---|---|---|
| Methylprednisolone 1% lignocaine (28) | 1% lignocaine (28) | 12wks | 2 wks:insignificant improvement in steroid arm 2, 4, 6, 12 wks:no difference in pain, range of motion;all P>.05 | No significant advantage of subacromial methyl prednisolone over lignocaine10 |
| Triamcinolone, 0.5% lignocaine, placebo tabs (20) | C1:diclofenac, lignocaine (20) C2:placebo tabs, lignocaine (20) | 4 wks | 4 wks:steroid and C1 showed significant benefit over C2 for pain and range of motion (P<.05) Steroid vs C1:no difference (P=.0268) | Triamcinolone and diclofenac are equivalent, and superior to placebo3 |
| S1:triamcinolone, 1% lidocaine, naproxen (25) S2:triamcinolone, 1% lidocaine, placebo (25) | C1:1% lidocaine, naproxen (25) C2:1% lidocaine, placebo (25) | 4 wks | S1 superior to S2, C1, C2 S2 superior to C1, C2 For pain and clinical index at 2 and 4 wks, P<.05 | Triamcinolone and naproxen superior to placebo.More severe cases see most benefit4 |
| Triamcinolone, placebo tabs (15); reinjection at 3 wks if not better | Saline injection, indomethacin (15); reinjection at 3 wks if not | 6 wks | Pain and global scores improved in both groups (P<0.05), but no difference between them (P>.05) | No difference between indomethacin andtriamcinolone better injection11 |
| S1:methylprednisolone, lidocaine, placebo tabs (12) S2:methylprednisolone, NSAID (12) | C1:acupuncture (12) C2:ultrasound (12) C3:placebo tab, placebo U/S (12) | 4 wks | All patients improved. No differences in pain scores or abduction measurements at 2 or 4 wks (P=n/a) | Painful stiff shoulder may be self-limiting condition and bene- ficial effect may be natural recovery12 |
| Methylprednisolone, 1% lidocaine (104) | Physiotherapy (103) | 6 mos, option of other therapies given at 6 weeks | No differences in disability scores 6 wks:mean difference= –.05 (95% CI, –.02 to 3.0) 6 mos:mean difference= 1.4 (95% CI, –0.2 to 3.0) (7) episodes of unilateral | Physiotherapy and steroid injection were of similar short- and long-term effectiveness for treating new shoulder pain |
| Triamcinolone, 1% lidocaine (19) | 1% lidocaine (21) | Mean:33 wk; range:12–52 wk | Steroid:significant improvements of pain (P<.005) and range of motion (P<.005) vs control.No difference in activities of daily living seen (13) | Subacromial injection of steroids is effective for short-term therapy of impingement syndrome |
Recommendations from others
The American Academy of Orthopaedic Surgeons’ clinical guideline for shoulder pain9 recommends the following for rotator cuff disease: avoidance of irritating activity; anti-inflammatory medications if tolerated; exercises to recover and maintain passive range of motion; exercises to strengthen the rotator cuff once acute symptoms abated. If these are unsuccessful over several weeks, they recommend considering subacromial injection of local anesthetic and a short-acting corticosteroid. They gave their recommendation a “B” rating (some evidence exists to suggest benefit).
Consider injection with anesthetic and steroid for rotator cuff impingement
Sourav Poddar, MD
Team Physician, University of Colorado Buffaloes, University of Colorado Health Sciences Center, Denver
Subacromial injection is an integral component of the treatment armamentarium for certain types of shoulder pathology. Diagnostically, injection of a local anesthetic such as lidocaine can help differentiate true weakness caused by a full-thickness rotator cuff tear from inhibition due to inflammation and impingement pain. Strongly consider subacromial injection with both a local anesthetic and corticosteroid for patients with true rotator cuff impingement as diagnosed by positive Neer and Hawkins signs on examination.
If injection is appropriately administered, the patient should have near-immediate and significant reduction of impingement symptoms. They may regain motion sooner and advance quicker through their initial therapy program.
1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
2. Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, NJ: Lawrence Erlbaum; 1988.
3. Adebajo AO, Nash P, Hazleman BL. A prospective double blind dummy placebo controlled study comparing triamcinolone hexacetonide injection with oral diclofenac 50 mg TDS in patients with rotator cuff tendinitis. J Rheumatol 1990;17:1207-1210.
4. Petri M, Dobrow R, Neiman R, Whiting-O’Keefe O, Seaman WE. Randomized, double-blind, placebo-controlled study of the treatment of the painful shoulder. Arthritis Rheum 1987;30:1040-1045.
5. Green S, Buchbinder R, Glazier R, Forbes A. Interventions for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
6. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
7. Hay EM, Thomas E, Paterson SM, Dziedzic K, Croft PR. A pragmatic randomised controlled trial of local corticosteroid injection and physiotherapy for the treatment of new episodes of unilateral shoulder pain in primary care. Ann Rheum Dis 2003;62:394-399.
8. van der Heijden GJ, van der Windt DA, Kleijnen J, Koes BW, Bouter LM. Steroid injections for shoulder disorders: a systematic review of randomized clinical trials. Br J Gen Pract 1996;46:309-316.
9. American. Academy of Orthopedic Surgeons. AAOS clinical guideline on shoulder pain: support document. Rosemont, IL: AAOS, 2001. Available at: www.guideline.gov/summary/summary.aspx?doc_id=2998. Accessed on May 5, 2004.
10. Vecchio PC, Hazleman BL, King RH. A double-blind trial comparing subacromial methylprednisolone and ligno-caine in acute rotator cuff tendinitis. Br J Rheumatol 1993;32:743-745.
11. White RH, Paull DM, Fleming KW. Rotator cuff tendinitis: comparison of subacromial injection of a long acting corticosteroid versus indomethacin therapy. J Rheumatol 1986;13:608-613.
12. Berry H, Fernandes L, Bloom B, Clarke R, Hamilton EB. Clinical study comparing acupuncture, physiotherapy, injection and oral anti-inflammatory therapy in shoulder cuff lesions. Curr Med Res Opin 1980;7:121-126.
13. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am 1996;78:1685-1689.
Subacromial steroid injection may provide a small, short-term benefit compared with placebo. The short-term effectiveness of steroid injection compared with nonsteroidal anti-inflammatory agents (NSAIDs) remains unclear.
Steroid injections are better than physiotherapy alone in the short term. However, injection does not appear to provide any meaningful long-term benefit compared with other therapies (strength of recommendation: B). Data are insufficient to make recommendations regarding the proper timing of injection in the sequence of other treatments. Side effects of steroid injection, such as steroid flare and infection, are rare.
Evidence summary
A Cochrane Review of corticosteroid injections for shoulder pain found 7 randomized controlled trials comparing subacromial steroid injections with placebo.1 The placebos were either injectable anesthetics alone or injectable anesthetics combined with oral placebo tablets. Six of the 7 studies used the anterolateral approach to inject under the acromion.
All studies used a clinical exam for diagnosis that showed pain with range of motion (especially abduction) or pain that was consistent with impingement syndrome. Most of the follow-up times were short, typically 4 to 12 weeks, and the longest study was 33 weeks. Meta-analyses often report the effect size using standard mean difference (SMD). A rule of thumb for interpretation of SMD is a value of 0.2 indicates a small effect, a value of 0.5 indicates a medium effect, and a value of 0.8 or larger indicates a large effect. If the 95% confidence interval [CI] does not include zero, then the SMD is statistically significant at the 5% level (P<.05).2
Two of the studies comparing steroid injection with placebo were methodologically suitable for meta-analysis; these studies showed thatsteroids provided a mild, short-term (4-week)benefit with respect to pain (SMD=0.83; 95% CI,0.39–1.26), function (SMD=0.63; 95% CI,0.20–1.06), and abductive range of motion(SMD=0.82; 95% CI, 0.39–1.25).3,4
Results of the remaining, less rigorous trialswere conflicting and inconclusive. The reviewersalso found 3 randomized controlled trials comparing subacromial steroid injection with oralNSAIDs. The pooled results of these trials,encompassing 120 patients, found no differences in these 3 outcomes at 4 or 6 weeks. The review of an additional trial of 50 patients comparing subacromial steroid injection plus simultaneous oral NSAIDs with oral NSAIDs alone found no differences at 4 weeks. All 11 studies had small sample sizes, and suffered from variable methodological quality and heterogeneous results.
The reviewers concluded that steroids are probably better than placebo but provide little or no benefit in addition to NSAIDs, and that evidence is insufficient to guide treatment. Likewise, a Cochrane Review of multiple interventions for shoulder pain also found “little evidence to support or refute the efficacy of common interventions” and highlighted the need for new, well-designed trials.5
Another Cochrane Review examined 4 randomized controlled trials comparing physiotherapy interventions for shoulder pain.6 They found that steroid injections may be superior to physiotherapy for rotator cuff disease, but the type of physiotherapy and injection sites were not consistent across the studies, making creation of summary estimates inappropriate. The individual studies showed significant short-term benefits (3–7 weeks) of steroid injection over physiotherapy; however, long-term (6–52 weeks) benefits ranged from some benefit to no difference. These studies were consistent regarding age (mean age=53–55 years, SD ± 13–14 years) and complications reported, with the only side effect being postinjection soreness.
Hay et al7 conducted a multicenter, primary care–based randomized controlled trial with more than 200 patients, which was published too recently for inclusion in the Cochrane Review. They found no statistical difference in improvement between steroid injection without physiotherapy and physiotherapy alone at 6 weeks.
In 1996, van der Heijden et al8 systematically reviewed randomized clinical trials of steroid injections for shoulder disorders, including rota-tor cuff disease, adhesive capsulitis, rheumatoid conditions, and periarthritis. They screened more than 200 articles from searches in Medline (1966–1995) and EMBASE (1984–1995) and found 16 articles that met qualifying conditions for further review. Of these, 3 were methodologically adequate for final review. None of these 3 studies provided evidence showing the efficacy of steroid injections. The results of the major trials reviewed can be found in the Table .
TABLE
Major placebo-controlled trials of injectable steroids for shoulder pain
| Steroid (n) | Comparison | Follow-up arms (n) | Reported results | Conclusions |
|---|---|---|---|---|
| Methylprednisolone 1% lignocaine (28) | 1% lignocaine (28) | 12wks | 2 wks:insignificant improvement in steroid arm 2, 4, 6, 12 wks:no difference in pain, range of motion;all P>.05 | No significant advantage of subacromial methyl prednisolone over lignocaine10 |
| Triamcinolone, 0.5% lignocaine, placebo tabs (20) | C1:diclofenac, lignocaine (20) C2:placebo tabs, lignocaine (20) | 4 wks | 4 wks:steroid and C1 showed significant benefit over C2 for pain and range of motion (P<.05) Steroid vs C1:no difference (P=.0268) | Triamcinolone and diclofenac are equivalent, and superior to placebo3 |
| S1:triamcinolone, 1% lidocaine, naproxen (25) S2:triamcinolone, 1% lidocaine, placebo (25) | C1:1% lidocaine, naproxen (25) C2:1% lidocaine, placebo (25) | 4 wks | S1 superior to S2, C1, C2 S2 superior to C1, C2 For pain and clinical index at 2 and 4 wks, P<.05 | Triamcinolone and naproxen superior to placebo.More severe cases see most benefit4 |
| Triamcinolone, placebo tabs (15); reinjection at 3 wks if not better | Saline injection, indomethacin (15); reinjection at 3 wks if not | 6 wks | Pain and global scores improved in both groups (P<0.05), but no difference between them (P>.05) | No difference between indomethacin andtriamcinolone better injection11 |
| S1:methylprednisolone, lidocaine, placebo tabs (12) S2:methylprednisolone, NSAID (12) | C1:acupuncture (12) C2:ultrasound (12) C3:placebo tab, placebo U/S (12) | 4 wks | All patients improved. No differences in pain scores or abduction measurements at 2 or 4 wks (P=n/a) | Painful stiff shoulder may be self-limiting condition and bene- ficial effect may be natural recovery12 |
| Methylprednisolone, 1% lidocaine (104) | Physiotherapy (103) | 6 mos, option of other therapies given at 6 weeks | No differences in disability scores 6 wks:mean difference= –.05 (95% CI, –.02 to 3.0) 6 mos:mean difference= 1.4 (95% CI, –0.2 to 3.0) (7) episodes of unilateral | Physiotherapy and steroid injection were of similar short- and long-term effectiveness for treating new shoulder pain |
| Triamcinolone, 1% lidocaine (19) | 1% lidocaine (21) | Mean:33 wk; range:12–52 wk | Steroid:significant improvements of pain (P<.005) and range of motion (P<.005) vs control.No difference in activities of daily living seen (13) | Subacromial injection of steroids is effective for short-term therapy of impingement syndrome |
Recommendations from others
The American Academy of Orthopaedic Surgeons’ clinical guideline for shoulder pain9 recommends the following for rotator cuff disease: avoidance of irritating activity; anti-inflammatory medications if tolerated; exercises to recover and maintain passive range of motion; exercises to strengthen the rotator cuff once acute symptoms abated. If these are unsuccessful over several weeks, they recommend considering subacromial injection of local anesthetic and a short-acting corticosteroid. They gave their recommendation a “B” rating (some evidence exists to suggest benefit).
Consider injection with anesthetic and steroid for rotator cuff impingement
Sourav Poddar, MD
Team Physician, University of Colorado Buffaloes, University of Colorado Health Sciences Center, Denver
Subacromial injection is an integral component of the treatment armamentarium for certain types of shoulder pathology. Diagnostically, injection of a local anesthetic such as lidocaine can help differentiate true weakness caused by a full-thickness rotator cuff tear from inhibition due to inflammation and impingement pain. Strongly consider subacromial injection with both a local anesthetic and corticosteroid for patients with true rotator cuff impingement as diagnosed by positive Neer and Hawkins signs on examination.
If injection is appropriately administered, the patient should have near-immediate and significant reduction of impingement symptoms. They may regain motion sooner and advance quicker through their initial therapy program.
Subacromial steroid injection may provide a small, short-term benefit compared with placebo. The short-term effectiveness of steroid injection compared with nonsteroidal anti-inflammatory agents (NSAIDs) remains unclear.
Steroid injections are better than physiotherapy alone in the short term. However, injection does not appear to provide any meaningful long-term benefit compared with other therapies (strength of recommendation: B). Data are insufficient to make recommendations regarding the proper timing of injection in the sequence of other treatments. Side effects of steroid injection, such as steroid flare and infection, are rare.
Evidence summary
A Cochrane Review of corticosteroid injections for shoulder pain found 7 randomized controlled trials comparing subacromial steroid injections with placebo.1 The placebos were either injectable anesthetics alone or injectable anesthetics combined with oral placebo tablets. Six of the 7 studies used the anterolateral approach to inject under the acromion.
All studies used a clinical exam for diagnosis that showed pain with range of motion (especially abduction) or pain that was consistent with impingement syndrome. Most of the follow-up times were short, typically 4 to 12 weeks, and the longest study was 33 weeks. Meta-analyses often report the effect size using standard mean difference (SMD). A rule of thumb for interpretation of SMD is a value of 0.2 indicates a small effect, a value of 0.5 indicates a medium effect, and a value of 0.8 or larger indicates a large effect. If the 95% confidence interval [CI] does not include zero, then the SMD is statistically significant at the 5% level (P<.05).2
Two of the studies comparing steroid injection with placebo were methodologically suitable for meta-analysis; these studies showed thatsteroids provided a mild, short-term (4-week)benefit with respect to pain (SMD=0.83; 95% CI,0.39–1.26), function (SMD=0.63; 95% CI,0.20–1.06), and abductive range of motion(SMD=0.82; 95% CI, 0.39–1.25).3,4
Results of the remaining, less rigorous trialswere conflicting and inconclusive. The reviewersalso found 3 randomized controlled trials comparing subacromial steroid injection with oralNSAIDs. The pooled results of these trials,encompassing 120 patients, found no differences in these 3 outcomes at 4 or 6 weeks. The review of an additional trial of 50 patients comparing subacromial steroid injection plus simultaneous oral NSAIDs with oral NSAIDs alone found no differences at 4 weeks. All 11 studies had small sample sizes, and suffered from variable methodological quality and heterogeneous results.
The reviewers concluded that steroids are probably better than placebo but provide little or no benefit in addition to NSAIDs, and that evidence is insufficient to guide treatment. Likewise, a Cochrane Review of multiple interventions for shoulder pain also found “little evidence to support or refute the efficacy of common interventions” and highlighted the need for new, well-designed trials.5
Another Cochrane Review examined 4 randomized controlled trials comparing physiotherapy interventions for shoulder pain.6 They found that steroid injections may be superior to physiotherapy for rotator cuff disease, but the type of physiotherapy and injection sites were not consistent across the studies, making creation of summary estimates inappropriate. The individual studies showed significant short-term benefits (3–7 weeks) of steroid injection over physiotherapy; however, long-term (6–52 weeks) benefits ranged from some benefit to no difference. These studies were consistent regarding age (mean age=53–55 years, SD ± 13–14 years) and complications reported, with the only side effect being postinjection soreness.
Hay et al7 conducted a multicenter, primary care–based randomized controlled trial with more than 200 patients, which was published too recently for inclusion in the Cochrane Review. They found no statistical difference in improvement between steroid injection without physiotherapy and physiotherapy alone at 6 weeks.
In 1996, van der Heijden et al8 systematically reviewed randomized clinical trials of steroid injections for shoulder disorders, including rota-tor cuff disease, adhesive capsulitis, rheumatoid conditions, and periarthritis. They screened more than 200 articles from searches in Medline (1966–1995) and EMBASE (1984–1995) and found 16 articles that met qualifying conditions for further review. Of these, 3 were methodologically adequate for final review. None of these 3 studies provided evidence showing the efficacy of steroid injections. The results of the major trials reviewed can be found in the Table .
TABLE
Major placebo-controlled trials of injectable steroids for shoulder pain
| Steroid (n) | Comparison | Follow-up arms (n) | Reported results | Conclusions |
|---|---|---|---|---|
| Methylprednisolone 1% lignocaine (28) | 1% lignocaine (28) | 12wks | 2 wks:insignificant improvement in steroid arm 2, 4, 6, 12 wks:no difference in pain, range of motion;all P>.05 | No significant advantage of subacromial methyl prednisolone over lignocaine10 |
| Triamcinolone, 0.5% lignocaine, placebo tabs (20) | C1:diclofenac, lignocaine (20) C2:placebo tabs, lignocaine (20) | 4 wks | 4 wks:steroid and C1 showed significant benefit over C2 for pain and range of motion (P<.05) Steroid vs C1:no difference (P=.0268) | Triamcinolone and diclofenac are equivalent, and superior to placebo3 |
| S1:triamcinolone, 1% lidocaine, naproxen (25) S2:triamcinolone, 1% lidocaine, placebo (25) | C1:1% lidocaine, naproxen (25) C2:1% lidocaine, placebo (25) | 4 wks | S1 superior to S2, C1, C2 S2 superior to C1, C2 For pain and clinical index at 2 and 4 wks, P<.05 | Triamcinolone and naproxen superior to placebo.More severe cases see most benefit4 |
| Triamcinolone, placebo tabs (15); reinjection at 3 wks if not better | Saline injection, indomethacin (15); reinjection at 3 wks if not | 6 wks | Pain and global scores improved in both groups (P<0.05), but no difference between them (P>.05) | No difference between indomethacin andtriamcinolone better injection11 |
| S1:methylprednisolone, lidocaine, placebo tabs (12) S2:methylprednisolone, NSAID (12) | C1:acupuncture (12) C2:ultrasound (12) C3:placebo tab, placebo U/S (12) | 4 wks | All patients improved. No differences in pain scores or abduction measurements at 2 or 4 wks (P=n/a) | Painful stiff shoulder may be self-limiting condition and bene- ficial effect may be natural recovery12 |
| Methylprednisolone, 1% lidocaine (104) | Physiotherapy (103) | 6 mos, option of other therapies given at 6 weeks | No differences in disability scores 6 wks:mean difference= –.05 (95% CI, –.02 to 3.0) 6 mos:mean difference= 1.4 (95% CI, –0.2 to 3.0) (7) episodes of unilateral | Physiotherapy and steroid injection were of similar short- and long-term effectiveness for treating new shoulder pain |
| Triamcinolone, 1% lidocaine (19) | 1% lidocaine (21) | Mean:33 wk; range:12–52 wk | Steroid:significant improvements of pain (P<.005) and range of motion (P<.005) vs control.No difference in activities of daily living seen (13) | Subacromial injection of steroids is effective for short-term therapy of impingement syndrome |
Recommendations from others
The American Academy of Orthopaedic Surgeons’ clinical guideline for shoulder pain9 recommends the following for rotator cuff disease: avoidance of irritating activity; anti-inflammatory medications if tolerated; exercises to recover and maintain passive range of motion; exercises to strengthen the rotator cuff once acute symptoms abated. If these are unsuccessful over several weeks, they recommend considering subacromial injection of local anesthetic and a short-acting corticosteroid. They gave their recommendation a “B” rating (some evidence exists to suggest benefit).
Consider injection with anesthetic and steroid for rotator cuff impingement
Sourav Poddar, MD
Team Physician, University of Colorado Buffaloes, University of Colorado Health Sciences Center, Denver
Subacromial injection is an integral component of the treatment armamentarium for certain types of shoulder pathology. Diagnostically, injection of a local anesthetic such as lidocaine can help differentiate true weakness caused by a full-thickness rotator cuff tear from inhibition due to inflammation and impingement pain. Strongly consider subacromial injection with both a local anesthetic and corticosteroid for patients with true rotator cuff impingement as diagnosed by positive Neer and Hawkins signs on examination.
If injection is appropriately administered, the patient should have near-immediate and significant reduction of impingement symptoms. They may regain motion sooner and advance quicker through their initial therapy program.
1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
2. Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, NJ: Lawrence Erlbaum; 1988.
3. Adebajo AO, Nash P, Hazleman BL. A prospective double blind dummy placebo controlled study comparing triamcinolone hexacetonide injection with oral diclofenac 50 mg TDS in patients with rotator cuff tendinitis. J Rheumatol 1990;17:1207-1210.
4. Petri M, Dobrow R, Neiman R, Whiting-O’Keefe O, Seaman WE. Randomized, double-blind, placebo-controlled study of the treatment of the painful shoulder. Arthritis Rheum 1987;30:1040-1045.
5. Green S, Buchbinder R, Glazier R, Forbes A. Interventions for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
6. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
7. Hay EM, Thomas E, Paterson SM, Dziedzic K, Croft PR. A pragmatic randomised controlled trial of local corticosteroid injection and physiotherapy for the treatment of new episodes of unilateral shoulder pain in primary care. Ann Rheum Dis 2003;62:394-399.
8. van der Heijden GJ, van der Windt DA, Kleijnen J, Koes BW, Bouter LM. Steroid injections for shoulder disorders: a systematic review of randomized clinical trials. Br J Gen Pract 1996;46:309-316.
9. American. Academy of Orthopedic Surgeons. AAOS clinical guideline on shoulder pain: support document. Rosemont, IL: AAOS, 2001. Available at: www.guideline.gov/summary/summary.aspx?doc_id=2998. Accessed on May 5, 2004.
10. Vecchio PC, Hazleman BL, King RH. A double-blind trial comparing subacromial methylprednisolone and ligno-caine in acute rotator cuff tendinitis. Br J Rheumatol 1993;32:743-745.
11. White RH, Paull DM, Fleming KW. Rotator cuff tendinitis: comparison of subacromial injection of a long acting corticosteroid versus indomethacin therapy. J Rheumatol 1986;13:608-613.
12. Berry H, Fernandes L, Bloom B, Clarke R, Hamilton EB. Clinical study comparing acupuncture, physiotherapy, injection and oral anti-inflammatory therapy in shoulder cuff lesions. Curr Med Res Opin 1980;7:121-126.
13. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am 1996;78:1685-1689.
1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
2. Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, NJ: Lawrence Erlbaum; 1988.
3. Adebajo AO, Nash P, Hazleman BL. A prospective double blind dummy placebo controlled study comparing triamcinolone hexacetonide injection with oral diclofenac 50 mg TDS in patients with rotator cuff tendinitis. J Rheumatol 1990;17:1207-1210.
4. Petri M, Dobrow R, Neiman R, Whiting-O’Keefe O, Seaman WE. Randomized, double-blind, placebo-controlled study of the treatment of the painful shoulder. Arthritis Rheum 1987;30:1040-1045.
5. Green S, Buchbinder R, Glazier R, Forbes A. Interventions for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
6. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for shoulder pain (Cochrane Review). In: The Cochrane Library,Issue 2, 2004. Chichester, UK: John Wiley & Sons.
7. Hay EM, Thomas E, Paterson SM, Dziedzic K, Croft PR. A pragmatic randomised controlled trial of local corticosteroid injection and physiotherapy for the treatment of new episodes of unilateral shoulder pain in primary care. Ann Rheum Dis 2003;62:394-399.
8. van der Heijden GJ, van der Windt DA, Kleijnen J, Koes BW, Bouter LM. Steroid injections for shoulder disorders: a systematic review of randomized clinical trials. Br J Gen Pract 1996;46:309-316.
9. American. Academy of Orthopedic Surgeons. AAOS clinical guideline on shoulder pain: support document. Rosemont, IL: AAOS, 2001. Available at: www.guideline.gov/summary/summary.aspx?doc_id=2998. Accessed on May 5, 2004.
10. Vecchio PC, Hazleman BL, King RH. A double-blind trial comparing subacromial methylprednisolone and ligno-caine in acute rotator cuff tendinitis. Br J Rheumatol 1993;32:743-745.
11. White RH, Paull DM, Fleming KW. Rotator cuff tendinitis: comparison of subacromial injection of a long acting corticosteroid versus indomethacin therapy. J Rheumatol 1986;13:608-613.
12. Berry H, Fernandes L, Bloom B, Clarke R, Hamilton EB. Clinical study comparing acupuncture, physiotherapy, injection and oral anti-inflammatory therapy in shoulder cuff lesions. Curr Med Res Opin 1980;7:121-126.
13. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am 1996;78:1685-1689.
Evidence-based answers from the Family Physicians Inquiries Network