Teaching topics from the New England Journal of Medicine - Vol. 358, No. 5, January 31, 2008
Abdominal Aortic Aneurysm
Abdominal aortic aneurysm is frequently asymptomatic and often detected incidentally on abdominal imaging (computed tomography, ultrasonography, or magnetic resonance imaging). Although some aneurysms may become symptomatic (manifesting with abdominal or back pain), the first clinical manifestation in many cases is rupture. The risk of rupture is low for aneurysms 5.5 cm or less in diameter, but above this threshold the risk increases markedly. In patients without symptoms, interventional management is generally recommended when the aneurysm exceeds 5.5 cm in diameter, becomes tender, or grows more than 1 centimeter in diameter per year.
Surgical versus Endovascular Repair
Open surgical repair has been the established treatment option for abdominal aortic aneurysm. This form of therapy is associated with a greater use of intensive or critical care, a longer hospital stay, and more postoperative pain than endovascular repair. Open repair requires general anesthesia. Endovascular repair, which may involve either general or local anesthesia, is associated with a lower early mortality but with a higher risk of subsequent need for reintervention and a less certain long-term outcome as compared to open repair. Endovascular repair is feasible only in patients who satisfy certain specific anatomical requirements regarding the aorta, the aneurysm, and the iliac arteries — which are usually assessed by means of CT.
Morning Report Questions
Q: What is a major risk factor for abdominal aortic aneurysm?
A: A major risk factor for the development of abdominal aortic aneurysm is smoking, and more than 90% of patients with such aneurysms have a history of smoking.
Q: What are two genetic disorders that increase the risk for developing abdominal aortic aneurysms?
A: Two rare monogenic disorders associated with an increased risk of abdominal aortic aneurysm are Marfan's syndrome (caused by a fibrillin-1 defect) and Ehlers–Danlos syndrome type IV (caused by a defect in the gene for type III collagen [COL3A1] in the majority of cases).
See OMIM: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=130050
2008年1月30日 星期三
2008年1月29日 星期二
2008年1月27日 星期日
2008年1月23日 星期三
2008年1月16日 星期三
H5N1 新知 from NEJM
Q1: Among the 340 cases of avian influenza (H5N1) virus infection in the world to date, which age group has the highest case fatality rate?
A: The overall case fatality rate is highest among persons 10 to 19 years of age and lowest among persons 50 years of age or older. Whether preexisting immunity, differences in exposure, or other factors might contribute to the apparently lower frequency of infection (90% of patients are 40 years of age or younger) and lethal illness among older adults is uncertain.
Q2: What is the best method for diagnosing avian influenza A (H5N1) virus infection?
A: Detection of viral RNA by means of conventional or real-time reverse-transcriptase polymerase chain reaction remains the best method for the initial diagnosis of influenza A (H5N1). These assays can provide results within 4 to 6 hours and can be performed under biosafety level 2 conditions. Diagnostic yields are higher with throat specimens than with nasal swabs because of higher viral loads of influenza A (H5N1) in the throat. However, nasal swabs are also useful for detecting human influenza viruses, so collection of both specimens is recommended.
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 3, January 17, 2008
A: The overall case fatality rate is highest among persons 10 to 19 years of age and lowest among persons 50 years of age or older. Whether preexisting immunity, differences in exposure, or other factors might contribute to the apparently lower frequency of infection (90% of patients are 40 years of age or younger) and lethal illness among older adults is uncertain.
Q2: What is the best method for diagnosing avian influenza A (H5N1) virus infection?
A: Detection of viral RNA by means of conventional or real-time reverse-transcriptase polymerase chain reaction remains the best method for the initial diagnosis of influenza A (H5N1). These assays can provide results within 4 to 6 hours and can be performed under biosafety level 2 conditions. Diagnostic yields are higher with throat specimens than with nasal swabs because of higher viral loads of influenza A (H5N1) in the throat. However, nasal swabs are also useful for detecting human influenza viruses, so collection of both specimens is recommended.
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 3, January 17, 2008
HbA1c 多少算正常？
What is the recommended glycated hemoglobin level?
A: The International Diabetes Foundation guidelines recommend glycated hemoglobin levels be below 6.5% in order to minimize the risk of future complications from diabetes. Ideally, glycemic control should be handled in a proactive manner, according to the joint consensus algorithm for the management of hyperglycemia from the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD), which suggests that a glycated hemoglobin value of 7% or more should serve as “a call to action to initiate or change therapy, with the goal of achieving a glycated hemoglobin level as close to the nondiabetic range as possible.”
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 3, January 17, 2008
A: The International Diabetes Foundation guidelines recommend glycated hemoglobin levels be below 6.5% in order to minimize the risk of future complications from diabetes. Ideally, glycemic control should be handled in a proactive manner, according to the joint consensus algorithm for the management of hyperglycemia from the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD), which suggests that a glycated hemoglobin value of 7% or more should serve as “a call to action to initiate or change therapy, with the goal of achieving a glycated hemoglobin level as close to the nondiabetic range as possible.”
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 3, January 17, 2008
What is preeclampsia
Preeclampsia is a multisystem disorder characterized by hypertension and proteinuria and occurs after 20 weeks of pregnancy. Preeclampsia is associated with substantial risks for the mother and the fetus. The fetus is at risk for intrauterine growth restriction, death and prematurity, whereas the mother is at risk for seizures (eclampsia), renal failure, pulmonary edema, stroke, and death. (Solomon, NEJM, 2004). However, the clinical findings in patients with preeclampsia are relatively nonspecific, and while a renal biopsy might clarify whether changes are due to preeclampsia or some other renal disease, there is understandable reluctance to perform a renal biopsy during pregnancy. As a result, there is a tendency to ascribe all new-onset renal disease during pregnancy to preeclampsia.
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 3, January 17, 2008
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 3, January 17, 2008
2008年1月12日 星期六
大量輸血會引起何種電解質問題？
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 2, January 10, 2008
Q: Why is it important to measure electrolyte levels and monitor the electrocardiogram of a patient who is receiving massive transfusions?
Q: Why is it important to measure electrolyte levels and monitor the electrocardiogram of a patient who is receiving massive transfusions?
- Citrate in the red blood cell units may cause hypocalcemia.
- Extracellular potassium levels may become too high (because of red-cell lysis) or too low (when transfused red blood cells become active) in patients receiving blood transfusions.
插管後血壓掉的原因
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 2, January 10, 2008
Q: How could intubating a patient exacerbate a circulatory shock state?
Q: How could intubating a patient exacerbate a circulatory shock state?
- Positive-pressure ventilation reduces the pressure gradient for venous return.
- Many anesthesia-induction agents may exacerbate shock by means of either centrally medicated sympatholysis or direct vasodilatation.
- PEEP use.
何謂 Permissive Hypotension？
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 2, January 10, 2008
Permissive Hypotension
The optimal systolic blood pressure in patients with uncontrolled hemorrhage is not known. Normal blood pressures may theoretically disrupt recently formed thrombi at the site of bleeding and drive additional hemorrhage. Some animal models suggest a survival benefit with permissive hypotension, defined as delayed resuscitation, leading to lower blood pressure, during uncontrolled hemorrhage. Data on clinical outcomes are mixed, with one study after penetrating trauma showing a benefit and another after penetrating and blunt trauma showing no benefit with prolonged permissive hypotension. Some clinicians used a target of 90 mm Hg for systolic blood pressure.
Permissive Hypotension
The optimal systolic blood pressure in patients with uncontrolled hemorrhage is not known. Normal blood pressures may theoretically disrupt recently formed thrombi at the site of bleeding and drive additional hemorrhage. Some animal models suggest a survival benefit with permissive hypotension, defined as delayed resuscitation, leading to lower blood pressure, during uncontrolled hemorrhage. Data on clinical outcomes are mixed, with one study after penetrating trauma showing a benefit and another after penetrating and blunt trauma showing no benefit with prolonged permissive hypotension. Some clinicians used a target of 90 mm Hg for systolic blood pressure.
腹痛合併休克之可能原因
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 2, January 10, 2008
Differential Diagnosis of Abdominal Pain and Circulatory Shock
The differential diagnosis of shock in a patient with abdominal pain includes hemorrhage, which can result from perforated viscus, a ruptured abdominal aortic aneurysm, or, in female patients, a ruptured ovarian cyst. Other processes that cause hypovolemia because of interstitial fluid sequestration could include pancreatitis or relative hypovolemia due to sepsis caused by bacterial peritonitis. Cardiogenic shock, anaphylaxis, adrenal insufficiency, arterial dissection, and pulmonary embolism are also possible causes.
Differential Diagnosis of Abdominal Pain and Circulatory Shock
The differential diagnosis of shock in a patient with abdominal pain includes hemorrhage, which can result from perforated viscus, a ruptured abdominal aortic aneurysm, or, in female patients, a ruptured ovarian cyst. Other processes that cause hypovolemia because of interstitial fluid sequestration could include pancreatitis or relative hypovolemia due to sepsis caused by bacterial peritonitis. Cardiogenic shock, anaphylaxis, adrenal insufficiency, arterial dissection, and pulmonary embolism are also possible causes.
Long-QT Syndrome
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 2, January 10, 2008
Long-QT Syndrome
The most common cause of sudden death in a young person is the long-QT syndrome characterized by abnormal QT prolongation and increased risk of ventricular fibrillation. Common presentations of the long-QT syndrome are palpitations, presyncope, syncope, and cardiac arrest. The differential diagnosis of syncope in a young patient ranges from benign conditions such as vasovagal syncope to serious genetic conditions such as hypertrophic cardiomyopathy and catecholaminergic polymorphic ventricular tachycardia.
Long-QT Syndrome Genetic Testing and Treatment
Genetic testing for the long-QT syndrome is most useful in two settings. First, when a clinical diagnosis is relatively certain, knowing the specific gene (or the site of the mutation within the gene) may clarify the prognosis and guide therapeutic choices. Second, in a family with an affected proband and a known genetic defect, the genotyping can help rule out the diagnosis in some family members. The major therapeutic options for the long-QT syndrome are beta-blockers and implantable cardioverter defibrillators (ICDs).
Morning Report Questions
Q: What would the physical examination and echocardiography reveal in a patient with long-QT syndrome?
A: The physical examination and echocardiography (or magnetic resonance imaging, if performed) generally show no abnormalities in patients with this syndrome; thus, they are helpful only in ruling out other diagnoses such as hypertrophic cardiomyopathy.
Q: What can cause acquired QT prolongation?
A: Acquired causes of QT prolongation include hypocalcemia and hypothyroidism, as well as drugs such as sotalol, dofetilide, haloperidol, methadone, and pentamidine. The QT interval, the surface ECG representation of ventricular repolarization, is affected by the patient's heart rate and sex; the upper limits of the QT interval corrected for heart rate (the QTc) are below 460 msec for women and below 440 msec for men.
Long-QT Syndrome
The most common cause of sudden death in a young person is the long-QT syndrome characterized by abnormal QT prolongation and increased risk of ventricular fibrillation. Common presentations of the long-QT syndrome are palpitations, presyncope, syncope, and cardiac arrest. The differential diagnosis of syncope in a young patient ranges from benign conditions such as vasovagal syncope to serious genetic conditions such as hypertrophic cardiomyopathy and catecholaminergic polymorphic ventricular tachycardia.
Long-QT Syndrome Genetic Testing and Treatment
Genetic testing for the long-QT syndrome is most useful in two settings. First, when a clinical diagnosis is relatively certain, knowing the specific gene (or the site of the mutation within the gene) may clarify the prognosis and guide therapeutic choices. Second, in a family with an affected proband and a known genetic defect, the genotyping can help rule out the diagnosis in some family members. The major therapeutic options for the long-QT syndrome are beta-blockers and implantable cardioverter defibrillators (ICDs).
Morning Report Questions
Q: What would the physical examination and echocardiography reveal in a patient with long-QT syndrome?
A: The physical examination and echocardiography (or magnetic resonance imaging, if performed) generally show no abnormalities in patients with this syndrome; thus, they are helpful only in ruling out other diagnoses such as hypertrophic cardiomyopathy.
Q: What can cause acquired QT prolongation?
A: Acquired causes of QT prolongation include hypocalcemia and hypothyroidism, as well as drugs such as sotalol, dofetilide, haloperidol, methadone, and pentamidine. The QT interval, the surface ECG representation of ventricular repolarization, is affected by the patient's heart rate and sex; the upper limits of the QT interval corrected for heart rate (the QTc) are below 460 msec for women and below 440 msec for men.
2008年1月9日 星期三
Intensive insulin 及 Pentastarch 對 septic shock 有害！
Adjunctive Therapy in Septic Shock and Severe Sepsis
In two prospective, multicenter trials, researchers examined the roles of adjunctive hydrocortisone, intensive insulin therapy, and colloid resuscitation in patients with sepsis.
Despite the use of antimicrobials, mortality rates remain very high in patients with severe forms of sepsis. The role of adjunctive therapies is uncertain. In two recent multicenter, randomized trials, researchers investigated the use of such therapies.
Sprung and colleagues compared hydrocortisone with placebo in a multinational, double-blind trial involving 499 adults with septic shock. The primary outcome measure was 28-day mortality among patients who did not have a response to a corticotropin test. Mortality also was evaluated in two other cohorts: patients who did respond to a corticotropin test and the overall group. In all three study cohorts, mortality rates were similar between treatment groups.
In an open-label, two-by-two factorial trial conducted with partial industry support, Brunkhorst and colleagues compared insulin therapies (intensive vs. conventional) and resuscitation fluids (colloid [pentastarch] vs. crystalloid [Ringer’s lactate]) among 537 adults in Germany with severe sepsis or septic shock. Hypoglycemia was more common in the intensive-insulin group than in the conventional-insulin group (12.1% vs. 2.1%; P<0.001). Moreover, life-threatening hypoglycemic episodes were more common in the intensive-insulin group than in the conventional-insulin group (5.3% vs. 2.1%; P=0.05). Intensive insulin therapy was terminated after the first safety analysis; all participants received conventional insulin therapy until the next planned interim analysis. Acute renal failure was more common in the pentastarch group than in the Ringer’s lactate group (34.9% vs. 22.8%; P=0.002). The proportion of days during which renal-replacement therapy was required was higher in the pentastarch group than in the Ringer’s lactate group (18.3% vs. 9.2%).
Comment: Sprung and colleagues acknowledged that their study was underpowered because of various factors, including low enrollment. An editorialist calculated that its power was <35% to detect a 20% reduction in the relative risk for death. Nonetheless, the likelihood of seeing differences in outcomes between the study groups was deemed low.
These two trials provide critical data on the role of adjunctive therapies in patients with severe sepsis or septic shock. Based on findings from these and other investigations, the current message is that corticosteroids are probably not effective and that both intensive insulin therapy and pentastarch resuscitation are harmful.
— Larry M. Baddour, MD
Published in Journal Watch Infectious Diseases January 9, 2008
Citation(s):
Sprung CL et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008 Jan 10; 358:111.
In two prospective, multicenter trials, researchers examined the roles of adjunctive hydrocortisone, intensive insulin therapy, and colloid resuscitation in patients with sepsis.
Despite the use of antimicrobials, mortality rates remain very high in patients with severe forms of sepsis. The role of adjunctive therapies is uncertain. In two recent multicenter, randomized trials, researchers investigated the use of such therapies.
Sprung and colleagues compared hydrocortisone with placebo in a multinational, double-blind trial involving 499 adults with septic shock. The primary outcome measure was 28-day mortality among patients who did not have a response to a corticotropin test. Mortality also was evaluated in two other cohorts: patients who did respond to a corticotropin test and the overall group. In all three study cohorts, mortality rates were similar between treatment groups.
In an open-label, two-by-two factorial trial conducted with partial industry support, Brunkhorst and colleagues compared insulin therapies (intensive vs. conventional) and resuscitation fluids (colloid [pentastarch] vs. crystalloid [Ringer’s lactate]) among 537 adults in Germany with severe sepsis or septic shock. Hypoglycemia was more common in the intensive-insulin group than in the conventional-insulin group (12.1% vs. 2.1%; P<0.001). Moreover, life-threatening hypoglycemic episodes were more common in the intensive-insulin group than in the conventional-insulin group (5.3% vs. 2.1%; P=0.05). Intensive insulin therapy was terminated after the first safety analysis; all participants received conventional insulin therapy until the next planned interim analysis. Acute renal failure was more common in the pentastarch group than in the Ringer’s lactate group (34.9% vs. 22.8%; P=0.002). The proportion of days during which renal-replacement therapy was required was higher in the pentastarch group than in the Ringer’s lactate group (18.3% vs. 9.2%).
Comment: Sprung and colleagues acknowledged that their study was underpowered because of various factors, including low enrollment. An editorialist calculated that its power was <35% to detect a 20% reduction in the relative risk for death. Nonetheless, the likelihood of seeing differences in outcomes between the study groups was deemed low.
These two trials provide critical data on the role of adjunctive therapies in patients with severe sepsis or septic shock. Based on findings from these and other investigations, the current message is that corticosteroids are probably not effective and that both intensive insulin therapy and pentastarch resuscitation are harmful.
— Larry M. Baddour, MD
Published in Journal Watch Infectious Diseases January 9, 2008
Citation(s):
Sprung CL et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008 Jan 10; 358:111.
2008 NEJM: Steroid 治 septic shock 沒效
Steroids in Septic Shock: Not Looking Good
Mortality rates at 28 days did not differ between steroid and placebo groups, regardless of response to corticotropin testing.
Guidelines for septic shock therapy recommend the use of hydrocortisone largely on the basis of one well-conducted study in which benefit was seen only in patients who did not respond to a corticotropin test (Journal Watch Emergency Medicine Nov 13 2002). In the current multicenter, randomized, controlled, double-blind study, researchers included a broad population of 499 patients with sepsis who had evidence of shock that persisted for more than 1 hour during the 72 hours before enrollment, despite adequate fluid replacement. Patients received either 50 mg of intravenous hydrocortisone or placebo every 6 hours for 5 days, followed by dose tapering over 6 days.
Rates of death at 28 days (the primary outcome) did not differ between treatment groups overall, or for patients who did not have a response to a short corticotropin test, or for patients who did have a response. This finding also held true for those patients who were enrolled within 12 hours after an episode of shock. A second episode of infection (superinfection) was more common in the steroid group, as was hyperglycemia. Reversal of shock was more rapid in the steroid group, but earlier reversal had no effect on outcome. Post hoc analysis revealed significantly higher death rates among patients who received etomidate before randomization than among those who did not (45.1% vs. 31.5% in the steroid group and 40.0% vs. 29.6% in the placebo group).
An editorialist notes that the study was underpowered to allow a definitive statement on the role of steroids in septic shock and recommends a trial involving at least 2600 patients.
Comment: The story of steroids in septic shock is long, and the final chapter remains to be written. Presently, there is insufficient evidence to support steroid administration for sepsis with shock, regardless of a patient’s response to corticotropin testing. The authors cite "an absolute reduction in mortality of 11.2% in the hydrocortisone group" for patients with persistent systolic blood pressure <90 mm Hg 1 day after fluid and vasopressor resuscitation, but their own statistical analysis demonstrates that there was not a significant difference in mortality between the hydrocortisone and placebo groups. Although a post hoc analysis identified a higher mortality rate in patients who were given etomidate as an induction agent, the authors correctly did not make any cause-and-effect statement, likely because of selection bias (clinicians may use etomidate more often in more-unstable patients), conflicting findings from prior studies, and the inability of the study to determine whether etomidate had any real effect (Journal Watch Emergency Medicine Sep 21 2007). This study also delivers a serious blow to the present fascination with corticotropin testing as a guide to treatment for such patients.
— J. Stephen Bohan, MD, MS, FACP, FACEP
Published in Journal Watch Emergency Medicine January 9, 2008
Citation(s):
Sprung CL et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008 Jan 10; 358:111.
Mortality rates at 28 days did not differ between steroid and placebo groups, regardless of response to corticotropin testing.
Guidelines for septic shock therapy recommend the use of hydrocortisone largely on the basis of one well-conducted study in which benefit was seen only in patients who did not respond to a corticotropin test (Journal Watch Emergency Medicine Nov 13 2002). In the current multicenter, randomized, controlled, double-blind study, researchers included a broad population of 499 patients with sepsis who had evidence of shock that persisted for more than 1 hour during the 72 hours before enrollment, despite adequate fluid replacement. Patients received either 50 mg of intravenous hydrocortisone or placebo every 6 hours for 5 days, followed by dose tapering over 6 days.
Rates of death at 28 days (the primary outcome) did not differ between treatment groups overall, or for patients who did not have a response to a short corticotropin test, or for patients who did have a response. This finding also held true for those patients who were enrolled within 12 hours after an episode of shock. A second episode of infection (superinfection) was more common in the steroid group, as was hyperglycemia. Reversal of shock was more rapid in the steroid group, but earlier reversal had no effect on outcome. Post hoc analysis revealed significantly higher death rates among patients who received etomidate before randomization than among those who did not (45.1% vs. 31.5% in the steroid group and 40.0% vs. 29.6% in the placebo group).
An editorialist notes that the study was underpowered to allow a definitive statement on the role of steroids in septic shock and recommends a trial involving at least 2600 patients.
Comment: The story of steroids in septic shock is long, and the final chapter remains to be written. Presently, there is insufficient evidence to support steroid administration for sepsis with shock, regardless of a patient’s response to corticotropin testing. The authors cite "an absolute reduction in mortality of 11.2% in the hydrocortisone group" for patients with persistent systolic blood pressure <90 mm Hg 1 day after fluid and vasopressor resuscitation, but their own statistical analysis demonstrates that there was not a significant difference in mortality between the hydrocortisone and placebo groups. Although a post hoc analysis identified a higher mortality rate in patients who were given etomidate as an induction agent, the authors correctly did not make any cause-and-effect statement, likely because of selection bias (clinicians may use etomidate more often in more-unstable patients), conflicting findings from prior studies, and the inability of the study to determine whether etomidate had any real effect (Journal Watch Emergency Medicine Sep 21 2007). This study also delivers a serious blow to the present fascination with corticotropin testing as a guide to treatment for such patients.
— J. Stephen Bohan, MD, MS, FACP, FACEP
Published in Journal Watch Emergency Medicine January 9, 2008
Citation(s):
Sprung CL et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008 Jan 10; 358:111.
2002 JAMA: Steroid 治 septic shock 有效
Low-Dose Steroid Therapy Reduces Mortality from Septic Shock
In patients with septic shock and relative adrenal insufficiency, low-dose corticosteroid therapy reduced mortality without increasing adverse events.
Because septic shock may be associated with relative adrenal insufficiency, corticosteroid replacement has been advocated. Trials of short-course, high-dose corticosteroid therapy have not been successful, however. These authors evaluated treatment with low-dose corticosteroids in a controlled, randomized, double-blind study conducted at 19 intensive care units in France.
Three hundred adults who met each of 6 clinical or laboratory criteria for septic shock (including systolic arterial blood pressure <90 mm Hg for at least 1 hour despite adequate fluid replacement and treatment with dopamine, epinephrine, or norepinephrine) received placebo or hydrocortisone (50-mg IV bolus every 6 hours) and fludrocortisone (50-µg oral dose once daily) for 7 days. Patients were classified as nonresponders (i.e., having adrenal insufficiency) or responders (i.e., having normal adrenal function) according to corticotropin stimulation test (CST) results. Among the 229 patients in the nonresponder cohort, the placebo recipients had a higher incidence of death at 28 days (the primary outcome) than did corticosteroid recipients (63% vs. 53%; P=0.02) and a lower incidence of withdrawal from vasopressor support (40% vs. 57%; P=0.001). Among patients in the responder cohort, there were no significant differences in these measures between the groups. The incidence of adverse events was similar in the corticosteroid and placebo groups.
Comment: Severe sepsis accounts for nearly 10% of all deaths in the U.S. The dramatic results of this study indicate that for every 7 patients with septic shock and relative adrenal insufficiency, 1 life would be saved at day 28 by using this corticosteroid regimen. The authors advocate instituting this regimen empirically for patients who present with septic shock but continuing the regimen only in patients whose CST results demonstrate nonresponsiveness (i.e., adrenal insufficiency).
— John A. Marx, MD, FACEP
Published in Journal Watch Emergency Medicine November 13, 2002
Citation(s):
Annane D et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002 Aug 21; 288:862-71.
In patients with septic shock and relative adrenal insufficiency, low-dose corticosteroid therapy reduced mortality without increasing adverse events.
Because septic shock may be associated with relative adrenal insufficiency, corticosteroid replacement has been advocated. Trials of short-course, high-dose corticosteroid therapy have not been successful, however. These authors evaluated treatment with low-dose corticosteroids in a controlled, randomized, double-blind study conducted at 19 intensive care units in France.
Three hundred adults who met each of 6 clinical or laboratory criteria for septic shock (including systolic arterial blood pressure <90 mm Hg for at least 1 hour despite adequate fluid replacement and treatment with dopamine, epinephrine, or norepinephrine) received placebo or hydrocortisone (50-mg IV bolus every 6 hours) and fludrocortisone (50-µg oral dose once daily) for 7 days. Patients were classified as nonresponders (i.e., having adrenal insufficiency) or responders (i.e., having normal adrenal function) according to corticotropin stimulation test (CST) results. Among the 229 patients in the nonresponder cohort, the placebo recipients had a higher incidence of death at 28 days (the primary outcome) than did corticosteroid recipients (63% vs. 53%; P=0.02) and a lower incidence of withdrawal from vasopressor support (40% vs. 57%; P=0.001). Among patients in the responder cohort, there were no significant differences in these measures between the groups. The incidence of adverse events was similar in the corticosteroid and placebo groups.
Comment: Severe sepsis accounts for nearly 10% of all deaths in the U.S. The dramatic results of this study indicate that for every 7 patients with septic shock and relative adrenal insufficiency, 1 life would be saved at day 28 by using this corticosteroid regimen. The authors advocate instituting this regimen empirically for patients who present with septic shock but continuing the regimen only in patients whose CST results demonstrate nonresponsiveness (i.e., adrenal insufficiency).
— John A. Marx, MD, FACEP
Published in Journal Watch Emergency Medicine November 13, 2002
Citation(s):
Annane D et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002 Aug 21; 288:862-71.
2008年1月7日 星期一
2008年1月6日 星期日
2008年1月4日 星期五
2008年1月3日 星期四
用 metformin 治療 PCOS
Teaching topics from the New England Journal of Medicine - Vol. 358, No. 1, January 3, 2008
Polycystic Ovary Syndrome
The polycystic ovary syndrome is a clinical diagnosis characterized by the presence of two or more of the following features: chronic oligo-ovulation or anovulation, androgen excess, and polycystic ovaries. It affects 5 to 10% of women of childbearing age, and is the most common cause of anovulatory infertility in developed countries. Common clinical manifestations include menstrual irregularities and signs of androgen excess such as hirsutism, acne, and alopecia. The presence of type 2 diabetes in the United States is 10 times as high among young women with the polycystic ovary syndrome as among normal women, and impaired glucose tolerance or overt type 2 diabetes develops by the age of 30 years in 30 to 50% of obese women with PCOS.
Metformin: Mechanism of Action
Metformin, a biguanide, is the most widely used drug for the treatment of type 2 diabetes worldwide. Its primary action is to inhibit hepatic glucose production, but it also increases the sensitivity of peripheral tissues to insulin. Metformin can also lower fasting serum insulin and androgen levels in women with the polycystic ovary syndrome — and may improve ovulation and menstrual cycling. (Hyperinsulinemia inhibits the hepatic production of sex hormone-binding globulin — increasing the circulating free testosterone levels.) Although metformin is not approved by the F.D.A. for the treatment of polycystic ovary syndrome, it is often used for this purpose.
Morning Report Questions
Q: What are the absolute contraindications for the use of metformin?
A: Metformin should not be used in patients with renal impairment (a serum creatinine level greater than 1.4 mg per deciliter [124 µmol per liter]), hepatic dysfunction, severe congestive heart failure, or a history of alcohol abuse. Repeat testing during metformin treatment is not indicated unless the patient develops another illness or condition (e.g., dehydration) that might affect renal or hepatic function.
Q: What are risk factors for type 2 diabetes?
A: Obesity, family history of diabetes, and polycystic ovary syndrome are all risk factors for type 2 diabetes. In fact all women with the polycystic ovary syndrome, regardless of weight, should be screened for glucose intolerance with the use of a glucose-tolerance test at the initial presentation and every 2 years thereafter. (J Clin Endocrinol Metab, 2007.)
Polycystic Ovary Syndrome
The polycystic ovary syndrome is a clinical diagnosis characterized by the presence of two or more of the following features: chronic oligo-ovulation or anovulation, androgen excess, and polycystic ovaries. It affects 5 to 10% of women of childbearing age, and is the most common cause of anovulatory infertility in developed countries. Common clinical manifestations include menstrual irregularities and signs of androgen excess such as hirsutism, acne, and alopecia. The presence of type 2 diabetes in the United States is 10 times as high among young women with the polycystic ovary syndrome as among normal women, and impaired glucose tolerance or overt type 2 diabetes develops by the age of 30 years in 30 to 50% of obese women with PCOS.
Metformin: Mechanism of Action
Metformin, a biguanide, is the most widely used drug for the treatment of type 2 diabetes worldwide. Its primary action is to inhibit hepatic glucose production, but it also increases the sensitivity of peripheral tissues to insulin. Metformin can also lower fasting serum insulin and androgen levels in women with the polycystic ovary syndrome — and may improve ovulation and menstrual cycling. (Hyperinsulinemia inhibits the hepatic production of sex hormone-binding globulin — increasing the circulating free testosterone levels.) Although metformin is not approved by the F.D.A. for the treatment of polycystic ovary syndrome, it is often used for this purpose.
Morning Report Questions
Q: What are the absolute contraindications for the use of metformin?
A: Metformin should not be used in patients with renal impairment (a serum creatinine level greater than 1.4 mg per deciliter [124 µmol per liter]), hepatic dysfunction, severe congestive heart failure, or a history of alcohol abuse. Repeat testing during metformin treatment is not indicated unless the patient develops another illness or condition (e.g., dehydration) that might affect renal or hepatic function.
Q: What are risk factors for type 2 diabetes?
A: Obesity, family history of diabetes, and polycystic ovary syndrome are all risk factors for type 2 diabetes. In fact all women with the polycystic ovary syndrome, regardless of weight, should be screened for glucose intolerance with the use of a glucose-tolerance test at the initial presentation and every 2 years thereafter. (J Clin Endocrinol Metab, 2007.)
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