Muscle Relaxant Adds No Benefit to Ibuprofen for Cervical Strain
Pain relief did not differ among patients who received ibuprofen, cyclobenzaprine, or both drugs.
Muscle relaxants often are prescribed for neck and back pain, despite the lack of evidence of benefit. Researchers evaluated the effect of cyclobenzaprine in a prospective, randomized, double-blind study in a convenience sample of 61 adult patients (mean age, 34; 58% women) who presented to a level I trauma center emergency department with acute cervical strain (87% caused by motor vehicle collisions). Patients received ibuprofen (800 mg), cyclobenzaprine (5 mg), or both drugs three times daily for up to 7 days, as needed for pain. All patients received an initial dose of 800 mg of ibuprofen in the ED.
Patients rated pain severity on a 100-mm visual analog scale 30 to 60 minutes after taking the morning dose of medication. Pain scores improved significantly over 7 days in all three groups and did not differ among groups. Adverse effects were minimal and included dizziness in four patients who received cyclobenzaprine alone or with ibuprofen and nausea in one patient who received ibuprofen alone.
Comment:
A small dose of cyclobenzaprine was used in this study, perhaps to avoid the anticholinergic, antihistaminic, and sedative side effects of this drug, which is closely related chemically to tricyclic antidepressants. No convincing evidence supports the use of cyclobenzaprine in painful musculoskeletal conditions, and the drug's benefit-to-adverse effect profile therefore argues against prescribing it. Most patients with cervical strain will get better. Provide adequate analgesia as needed, and leave the cyclobenzaprine in the pharmacy.
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Kristi L. Koenig, MD, FACEP
Published in Journal Watch Emergency Medicine February 5, 2010
Citation(s): Khwaja SM et al. Comparison of ibuprofen, cyclobenzaprine or both in patients with acute cervical strain: A randomized controlled trial. CJEM 2010 Jan; 12:39.
2010年2月5日星期五
2010年2月4日星期四
Septic Shock, Insulin, and Steroids
Intensive insulin therapy did not lower in-hospital mortality in septic shock patients who received hydrocortisone.
In a study published in 2002, patients with septic shock and impaired adrenal reserve appeared to benefit from 7-day courses of hydrocortisone (50 mg every 6 hours) plus the mineralocorticoid fludrocortisone (JW Gen Med Aug 30 2002). In contrast, hydrocortisone alone was not beneficial in the 2008 CORTICUS trial (JW Gen Med Jan 9 2008). Because patients in the 2002 trial were sicker and were treated earlier than those in CORTICUS, some experts still recommend low-dose hydrocortisone for patients with severe sepsis and refractory hypotension.
That hydrocortisone invariably induces hyperglycemia raises another question: Is intensive insulin therapy appropriate for hydrocortisone-treated patients with septic shock? To answer this question, researchers in France randomized 509 such patients to receive either intensive insulin therapy (target glucose level, 80–110 mg/dL) or usual care (target glucose level, around 150 mg/dL). In addition, to examine whether mineralocorticoid therapy is beneficial, the researchers randomized the same patients to receive or not to receive fludrocortisone in a 2x2 factorial design. The outcome: Overall in-hospital mortality was 44%; neither intensive insulin nor fludrocortisone lowered mortality or any of numerous secondary endpoints.
Comment:
In this multicenter study of hydrocortisone-treated patients with septic shock, intensive insulin therapy did not improve outcomes. An editorialist notes that (1) mean glucose levels in intensively treated patients fell short of the intended target, reaching only about 120 mg/dL, which was not markedly different from the mean glucose level (about 150 mg/dL) of the control group; and (2) the trial was underpowered to identify small differences in mortality. Thus, she calls for a much larger trial. My own sense, however, is that intensive glycemic control is not the magic bullet that will improve outcomes in septic shock patients and that research should be directed toward other pathophysiologic mechanisms.
—
Allan S. Brett, MD
Published in Journal Watch General Medicine February 4, 2010
Citation(s):
The COIITSS Study Investigators. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: A randomized controlled trial. JAMA 2010 Jan 27; 303:341.
Van den Berghe G. Should glucocorticoid-induced hyperglycemia be treated in patients with septic shock? JAMA 2010 Jan 27; 303:365.
In a study published in 2002, patients with septic shock and impaired adrenal reserve appeared to benefit from 7-day courses of hydrocortisone (50 mg every 6 hours) plus the mineralocorticoid fludrocortisone (JW Gen Med Aug 30 2002). In contrast, hydrocortisone alone was not beneficial in the 2008 CORTICUS trial (JW Gen Med Jan 9 2008). Because patients in the 2002 trial were sicker and were treated earlier than those in CORTICUS, some experts still recommend low-dose hydrocortisone for patients with severe sepsis and refractory hypotension.
That hydrocortisone invariably induces hyperglycemia raises another question: Is intensive insulin therapy appropriate for hydrocortisone-treated patients with septic shock? To answer this question, researchers in France randomized 509 such patients to receive either intensive insulin therapy (target glucose level, 80–110 mg/dL) or usual care (target glucose level, around 150 mg/dL). In addition, to examine whether mineralocorticoid therapy is beneficial, the researchers randomized the same patients to receive or not to receive fludrocortisone in a 2x2 factorial design. The outcome: Overall in-hospital mortality was 44%; neither intensive insulin nor fludrocortisone lowered mortality or any of numerous secondary endpoints.
Comment:
In this multicenter study of hydrocortisone-treated patients with septic shock, intensive insulin therapy did not improve outcomes. An editorialist notes that (1) mean glucose levels in intensively treated patients fell short of the intended target, reaching only about 120 mg/dL, which was not markedly different from the mean glucose level (about 150 mg/dL) of the control group; and (2) the trial was underpowered to identify small differences in mortality. Thus, she calls for a much larger trial. My own sense, however, is that intensive glycemic control is not the magic bullet that will improve outcomes in septic shock patients and that research should be directed toward other pathophysiologic mechanisms.
—
Allan S. Brett, MD
Published in Journal Watch General Medicine February 4, 2010
Citation(s):
The COIITSS Study Investigators. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: A randomized controlled trial. JAMA 2010 Jan 27; 303:341.
Van den Berghe G. Should glucocorticoid-induced hyperglycemia be treated in patients with septic shock? JAMA 2010 Jan 27; 303:365.
2010年2月3日星期三
Jet Lag
Jet lag is a recognized sleep disorder that results from crossing time zones too rapidly for the circadian clock to keep pace. The pathophysiology involves a temporary misalignment between the circadian clock and local time.
How can the circadian rhythm be re-entrained after travel?
A traveler may be able to accelerate re-entrainment of the circadian rhythm by intentionally seeking out bright light at the optimal times of the day. A simple recommendation for travel across six to eight time zones is to seek exposure to bright light in the morning after eastward travel and in the evening after westward travel. It may also be useful to avoid light when exposure would impede adaptation; for example, it may be helpful for a traveler to stay indoors for the first few hours of daylight after long eastward flights or for a few hours before dusk after long westward flights. The timing of sleep does not, in itself, reset the clock.
How should sleep be strategically scheduled after travel?
Shifting one's sleep schedule by 1 or 2 hours towards congruence with the destination time zone before departure may shorten the duration of jet lag. Most travelers will be sleep-deprived after an overnight flight and will require extra (recovery) sleep on the first day or two after arrival. On subsequent days, short naps are effective in reducing daytime sleepiness, whereas longer daytime naps can undermine nighttime sleep, as well as reduce exposure to the re-entraining effects of light.
How should melatonin be used?
Melatonin can be considered to be a darkness signal. To promote shifting of the body clock to an earlier time after eastward travel, the author suggests that the traveler take 0.5–3 mg of melatonin at local bedtime nightly until he or she has become adapted to local time. For westbound travel, the author suggests taking 0.5 mg (low, short-acting dose) during the second half of the night until the traveler has become adapted to local time. Melatonin is not approved as a drug by the Food and Drug Administration (FDA).
Which hypnotics are most appropriate for use during flight?
Because there is limited opportunity to sleep during a flight, a hypnotic medication that has only a 2- to 3-hour duration of action (e.g., zaleplon) is preferred. A longer-acting sleeping pill (e.g., zolpidem or eszopiclone) could result in grogginess on arrival; a sleeping pill should not be taken if there is a risk of deep-vein thrombosis because the induced sleep may further increase that risk, and it should not be combined with alcohol.
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Teaching topics from the New England Journal of Medicine - Vol. 362, No. 5, February 4, 2010
How can the circadian rhythm be re-entrained after travel?
A traveler may be able to accelerate re-entrainment of the circadian rhythm by intentionally seeking out bright light at the optimal times of the day. A simple recommendation for travel across six to eight time zones is to seek exposure to bright light in the morning after eastward travel and in the evening after westward travel. It may also be useful to avoid light when exposure would impede adaptation; for example, it may be helpful for a traveler to stay indoors for the first few hours of daylight after long eastward flights or for a few hours before dusk after long westward flights. The timing of sleep does not, in itself, reset the clock.
How should sleep be strategically scheduled after travel?
Shifting one's sleep schedule by 1 or 2 hours towards congruence with the destination time zone before departure may shorten the duration of jet lag. Most travelers will be sleep-deprived after an overnight flight and will require extra (recovery) sleep on the first day or two after arrival. On subsequent days, short naps are effective in reducing daytime sleepiness, whereas longer daytime naps can undermine nighttime sleep, as well as reduce exposure to the re-entraining effects of light.
How should melatonin be used?
Melatonin can be considered to be a darkness signal. To promote shifting of the body clock to an earlier time after eastward travel, the author suggests that the traveler take 0.5–3 mg of melatonin at local bedtime nightly until he or she has become adapted to local time. For westbound travel, the author suggests taking 0.5 mg (low, short-acting dose) during the second half of the night until the traveler has become adapted to local time. Melatonin is not approved as a drug by the Food and Drug Administration (FDA).
Which hypnotics are most appropriate for use during flight?
Because there is limited opportunity to sleep during a flight, a hypnotic medication that has only a 2- to 3-hour duration of action (e.g., zaleplon) is preferred. A longer-acting sleeping pill (e.g., zolpidem or eszopiclone) could result in grogginess on arrival; a sleeping pill should not be taken if there is a risk of deep-vein thrombosis because the induced sleep may further increase that risk, and it should not be combined with alcohol.
---
Teaching topics from the New England Journal of Medicine - Vol. 362, No. 5, February 4, 2010
2010年1月29日星期五
穿刺傷病患到院前不宜浪費時間做脊椎固定術
Spine Immobilization for Penetrating Trauma Can Be Harmful
Patients who underwent immobilization were twice as likely to die as those who did not.
Despite a lack of supportive evidence for the practice, prehospital providers often apply spine immobilization to patients who have penetrating trauma to the head, neck, or torso without neurological symptoms or deficit. These authors retrospectively assessed the effect of prehospital spine immobilization on mortality in patients with penetrating trauma using data from the American College of Surgeons National Trauma Data Bank between 2001 and 2004.
Of 45,284 patients (median age, 29), 4.3% received cervical collars, spinal backboards, or both. The overall mortality rate was 8.1%. Multiple logistic regression analysis that controlled for confounders, including Injury Severity Score and Revised Trauma Score, showed that immobilized patients had significantly increased mortality (odds ratio, 2.06); this finding held true in subgroups of patients with gunshot wounds (OR, 2.12), hypotension (OR, 2.42), and gunshot wounds and hypotension (OR, 3.19). Complete data on in-hospital procedures were available for about 31,000 patients. Only 30 patients (0.1%) underwent operative spine stabilizing procedures for incomplete spinal-cord injury. The number needed to treat with spine immobilization to potentially benefit 1 patient was 1032. The number needed to harm with spine immobilization to potentially contribute to 1 death was 66.
Comment:
Increasing evidence indicates that limited intervention at the scene allows trauma patients to receive definitive care at a trauma center more rapidly. This study indicates that prehospital spine immobilization is associated with increased mortality in patients with penetrating trauma. Trying to assign cause and effect in a retrospective study is risky, but possibly increased scene time or interference with later care (e.g., intubation, radiography, examination of the patient's back) contribute to worse outcomes. Spine immobilization might be applied more wisely to patients with altered mental status, spine tenderness, or sensorimotor dysfunction.
—
John A. Marx, MD, FAAEM
Published in Journal Watch Emergency Medicine January 29, 2010
Citation(s): Haut ER et al. Spine immobilization in penetrating trauma: More harm than good? J Trauma 2010 Jan; 68:115.
Patients who underwent immobilization were twice as likely to die as those who did not.
Despite a lack of supportive evidence for the practice, prehospital providers often apply spine immobilization to patients who have penetrating trauma to the head, neck, or torso without neurological symptoms or deficit. These authors retrospectively assessed the effect of prehospital spine immobilization on mortality in patients with penetrating trauma using data from the American College of Surgeons National Trauma Data Bank between 2001 and 2004.
Of 45,284 patients (median age, 29), 4.3% received cervical collars, spinal backboards, or both. The overall mortality rate was 8.1%. Multiple logistic regression analysis that controlled for confounders, including Injury Severity Score and Revised Trauma Score, showed that immobilized patients had significantly increased mortality (odds ratio, 2.06); this finding held true in subgroups of patients with gunshot wounds (OR, 2.12), hypotension (OR, 2.42), and gunshot wounds and hypotension (OR, 3.19). Complete data on in-hospital procedures were available for about 31,000 patients. Only 30 patients (0.1%) underwent operative spine stabilizing procedures for incomplete spinal-cord injury. The number needed to treat with spine immobilization to potentially benefit 1 patient was 1032. The number needed to harm with spine immobilization to potentially contribute to 1 death was 66.
Comment:
Increasing evidence indicates that limited intervention at the scene allows trauma patients to receive definitive care at a trauma center more rapidly. This study indicates that prehospital spine immobilization is associated with increased mortality in patients with penetrating trauma. Trying to assign cause and effect in a retrospective study is risky, but possibly increased scene time or interference with later care (e.g., intubation, radiography, examination of the patient's back) contribute to worse outcomes. Spine immobilization might be applied more wisely to patients with altered mental status, spine tenderness, or sensorimotor dysfunction.
—
John A. Marx, MD, FAAEM
Published in Journal Watch Emergency Medicine January 29, 2010
Citation(s): Haut ER et al. Spine immobilization in penetrating trauma: More harm than good? J Trauma 2010 Jan; 68:115.
2010年1月22日星期五
CT Radiation Exposure and Cancer
Radiation from CT scans might cause 2% of future cancers.
An estimated 72 million computed tomography (CT) scans were performed in the U.S. in 2007. Two research groups assessed radiation dose from CT scans and future cancer risk.
Smith-Bindman and colleagues studied CT scans performed at four hospitals (private and public, large and small) in San Francisco in 2008. For each of 11 types of CT studies, the researchers estimated the effective dose of radiation, which takes into account "the amount of radiation to the exposed organs and each organ's sensitivity to developing cancer from radiation exposure."
The effective dose varied widely both within and between institutions for each type of CT study. The median effective dose was 2 millisieverts (mSv) for a noncontrast head CT scan and 31 mSv for an abdomen-pelvis study. For comparison, the effective dose is 0.065 mSv from posteroanterior and lateral chest radiography and 0.42 mSv from conventional mammography.
The authors estimated that a coronary angiogram delivers radiation to the breast equivalent to 15 mammograms and to the lung equivalent to 711 chest x-rays. The lag time between exposure and cancer development makes exposure potentially riskier for younger than older patients; the authors estimated that 1 in every 270 women who undergo coronary CT angiography at age 40 will develop cancer.
Berrington de Gonzalez and colleagues used a national database to estimate age-specific cancer risks from CT studies performed in the U.S. in 2007. CT scans performed during the last 5 years of life or after a diagnosis of cancer were excluded from the analysis. Thirty percent of CT scans were performed on patients aged 35 to 54. The authors predict that 2% (29,000) of future cancers will be caused by CT scans performed in 2007, and they estimate a cancer mortality rate of 50%.
Comment:
An editorialist terms these numbers "eye opening" and calls for dose standardization, patient education, and test ordering guidelines. A recent government report shows an eightfold difference in test ordering across states, with no detectable mortality benefit from higher rates of testing. One approach to limiting radiation exposure is to display patients' historical cumulative radiation dose in electronic order entry systems. It is time for someone to shout "stop."
—
J. Stephen Bohan, MD, MS, FACP, FACEP
Published in Journal Watch Emergency Medicine January 22, 2010
Citation(s): Smith-Bindman R et al. Radiation dose associated with common computed tomography examinations and the associated lifetime attributable risk of cancer. Arch Intern Med 2009 Dec 14/28; 169:2078.
An estimated 72 million computed tomography (CT) scans were performed in the U.S. in 2007. Two research groups assessed radiation dose from CT scans and future cancer risk.
Smith-Bindman and colleagues studied CT scans performed at four hospitals (private and public, large and small) in San Francisco in 2008. For each of 11 types of CT studies, the researchers estimated the effective dose of radiation, which takes into account "the amount of radiation to the exposed organs and each organ's sensitivity to developing cancer from radiation exposure."
The effective dose varied widely both within and between institutions for each type of CT study. The median effective dose was 2 millisieverts (mSv) for a noncontrast head CT scan and 31 mSv for an abdomen-pelvis study. For comparison, the effective dose is 0.065 mSv from posteroanterior and lateral chest radiography and 0.42 mSv from conventional mammography.
The authors estimated that a coronary angiogram delivers radiation to the breast equivalent to 15 mammograms and to the lung equivalent to 711 chest x-rays. The lag time between exposure and cancer development makes exposure potentially riskier for younger than older patients; the authors estimated that 1 in every 270 women who undergo coronary CT angiography at age 40 will develop cancer.
Berrington de Gonzalez and colleagues used a national database to estimate age-specific cancer risks from CT studies performed in the U.S. in 2007. CT scans performed during the last 5 years of life or after a diagnosis of cancer were excluded from the analysis. Thirty percent of CT scans were performed on patients aged 35 to 54. The authors predict that 2% (29,000) of future cancers will be caused by CT scans performed in 2007, and they estimate a cancer mortality rate of 50%.
Comment:
An editorialist terms these numbers "eye opening" and calls for dose standardization, patient education, and test ordering guidelines. A recent government report shows an eightfold difference in test ordering across states, with no detectable mortality benefit from higher rates of testing. One approach to limiting radiation exposure is to display patients' historical cumulative radiation dose in electronic order entry systems. It is time for someone to shout "stop."
—
J. Stephen Bohan, MD, MS, FACP, FACEP
Published in Journal Watch Emergency Medicine January 22, 2010
Citation(s): Smith-Bindman R et al. Radiation dose associated with common computed tomography examinations and the associated lifetime attributable risk of cancer. Arch Intern Med 2009 Dec 14/28; 169:2078.
2010年1月21日星期四
Heart Failure
Which patients with heart failure should be treated with angiotensin-converting–enzyme (ACE) inhibitors?
ACE inhibitors are the first-line therapy for patients with systolic heart failure; therapy should be initiated promptly after diagnosis and continued indefinitely. ACE inhibitors increase the ejection fraction modestly and reduce ventricular size, symptoms, hospitalization, and overall mortality. ACE inhibitors also reduce the risk of myocardial infarction.
When should spironolactone be used in patients with heart failure?
In a large, placebo-controlled, randomized trial in which patients received spironolactone in addition to a diuretic, digoxin, and an ACE inhibitor, a reduction in symptoms and in hospital admissions, and a 30% reduction in mortality, were seen among patients with severe systolic heart failure (NYHA class III or IV). Therefore, the addition of an aldosterone antagonist should be considered for any patient who remains in NYHA class III or IV, despite treatment with a diuretic, an ACE inhibitor (or angiotensin-receptor blocker [ARB]), and a beta-blocker.
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Teaching topics from the New England Journal of Medicine - Vol. 362, No. 3, January 21, 2010
ACE inhibitors are the first-line therapy for patients with systolic heart failure; therapy should be initiated promptly after diagnosis and continued indefinitely. ACE inhibitors increase the ejection fraction modestly and reduce ventricular size, symptoms, hospitalization, and overall mortality. ACE inhibitors also reduce the risk of myocardial infarction.
When should spironolactone be used in patients with heart failure?
In a large, placebo-controlled, randomized trial in which patients received spironolactone in addition to a diuretic, digoxin, and an ACE inhibitor, a reduction in symptoms and in hospital admissions, and a 30% reduction in mortality, were seen among patients with severe systolic heart failure (NYHA class III or IV). Therefore, the addition of an aldosterone antagonist should be considered for any patient who remains in NYHA class III or IV, despite treatment with a diuretic, an ACE inhibitor (or angiotensin-receptor blocker [ARB]), and a beta-blocker.
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Teaching topics from the New England Journal of Medicine - Vol. 362, No. 3, January 21, 2010
What is Takotsubo cardiomyopathy?
Takotsubo cardiomyopathy
Also known as transient left ventricular apical ballooning syndrome or stress cardiomyopathy. One of the hallmarks of this syndrome is that the apical ballooning is transient, typically resolving in days to weeks. Takotsubo cardiomyopathy typically arises in the context of acute emotional or physical stress. It often resembles an acute coronary syndrome. The pathognomic findings are ballooning (dilatation and akinesis) of the left ventricular apex, with compensatory hyperkinesis of the basal walls of the left ventricle. Coronary angiography reveals no obstructive coronary-artery lesions; in addition, the distribution of left ventricular dysfunction often extends beyond the distribution of a single coronary artery.
Also known as transient left ventricular apical ballooning syndrome or stress cardiomyopathy. One of the hallmarks of this syndrome is that the apical ballooning is transient, typically resolving in days to weeks. Takotsubo cardiomyopathy typically arises in the context of acute emotional or physical stress. It often resembles an acute coronary syndrome. The pathognomic findings are ballooning (dilatation and akinesis) of the left ventricular apex, with compensatory hyperkinesis of the basal walls of the left ventricle. Coronary angiography reveals no obstructive coronary-artery lesions; in addition, the distribution of left ventricular dysfunction often extends beyond the distribution of a single coronary artery.
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