The impact of therapeutic hypothermia on neurological function and quality of life after cardiac arrest
Aims
To assess the impact of therapeutic hypothermia on cognitive function and quality of life in comatose survivors of out of Hospital Cardiac arrest (OHCA).
Methods
We prospectively studied comatose survivors of OHCA consecutively admitted in a 4-year period. Therapeutic hypothermia was implemented in the last 2-year period, intervention period (n = 79), and this group was compared to patients admitted the 2 previous years, control period (n = 77). We assessed Cerebral Performance Category (CPC), survival, Mini Mental State Examination (MMSE) and self-rated quality of life (SF-36) 6 months after OHCA in the subgroup with VF/VT as initial rhythm.
Results
CPC in patients alive at hospital discharge was significantly better in the intervention period with a CPC of 1–2 in 97% vs. 71% in the control period, p = 0.003, corresponding to an adjusted odds ratio of a favourable cerebral outcome of 17, p = 0.01. No significant differences were found in long-term survival (57% vs. 56% alive at 30 months), MMSE, or SF-36. Therapeutic hypothermia (hazard ratio: 0.15, p = 0.007) and bystander CPR (hazard ratio 0.19, p = 0.002) were significantly related to survival in the intervention period.
Conclusion
CPC at discharge from hospital was significantly improved following implementation of therapeutic hypothermia in comatose patients resuscitated from OCHA with VF/VT. However, significant improvement in survival, cognitive status or quality of life could not be detected at long-term follow-up.
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Resuscitation, Volume 80, Issue 2, February 2009, Pages 171-176
2009年1月21日 星期三
2009年1月20日 星期二
GBS scores for UGI bleeding
Identifying Low-Risk Upper GI Bleeds for Safe Outpatient Management
A simple scale can identify patients who do not require hospitalization or early endoscopy.
Most patients with upper gastrointestinal bleeding (UGIB) are hospitalized, although most do not die; rebleed; or require urgent endoscopic therapy, transfusion, or surgery. Researchers in Scotland investigated whether the previously published Glasgow-Blatchford bleeding score (GBS) was useful for prospectively identifying patients with UGIB (hematemesis, coffee-ground vomitus, or melena) who could be discharged home safely. Patients score "0" on the GBS if they have the following characteristics:
Comment:
When clinicians used GBS scores for guidance, the admission rate for patients with UGIB was reduced from 96% to 71%, with no adverse patient outcomes. If the GBS system is validated in other settings, it could prevent many unnecessary hospitalizations, which could improve patient safety and conserve resources.
—
Bruce Soloway, MD
Published in Journal Watch General Medicine January 20, 2009.
Citation(s): Stanley AJ et al. Outpatient management of patients with low-risk upper-gastrointestinal haemorrhage: Multicentre validation and prospective evaluation. Lancet 2009 Jan 3; 373:42.
A simple scale can identify patients who do not require hospitalization or early endoscopy.
Most patients with upper gastrointestinal bleeding (UGIB) are hospitalized, although most do not die; rebleed; or require urgent endoscopic therapy, transfusion, or surgery. Researchers in Scotland investigated whether the previously published Glasgow-Blatchford bleeding score (GBS) was useful for prospectively identifying patients with UGIB (hematemesis, coffee-ground vomitus, or melena) who could be discharged home safely. Patients score "0" on the GBS if they have the following characteristics:
- Hemoglobin level >12.9 g/dL (men) or >11.9 g/dL (women)
- Systolic blood pressure >109 mm Hg
- Pulse <100/minute>
- Blood urea nitrogen level <18.2>
- No melena or syncope
- No past or present liver disease or heart failure
Comment:
When clinicians used GBS scores for guidance, the admission rate for patients with UGIB was reduced from 96% to 71%, with no adverse patient outcomes. If the GBS system is validated in other settings, it could prevent many unnecessary hospitalizations, which could improve patient safety and conserve resources.
—
Bruce Soloway, MD
Published in Journal Watch General Medicine January 20, 2009.
Citation(s): Stanley AJ et al. Outpatient management of patients with low-risk upper-gastrointestinal haemorrhage: Multicentre validation and prospective evaluation. Lancet 2009 Jan 3; 373:42.
Don't worry, be happy
The WHO wants us to be happy: it's good for our health. This study derived from the Framingham study, finds that
Source: BMJ 2008;337:a2338
---
Dr Ann Robinson, BMJ Group
- Happy people tend to be at the centre of large groups of other happy people
- Your happiness is related to the happiness of people you may not even know who are up to three degrees removed from you (such as your friend's friend's friend)
- Happiness ripples through social networks, spreading like a contagious disease
- You don't have to be friends with people just like you.
Source: BMJ 2008;337:a2338
---
Dr Ann Robinson, BMJ Group
Take the pills
A 42 year old, fit, slim, non smoking patient of mine had a heart attack recently and made a full recovery. He's got normal blood cholesterol levels and blood pressure, but his cardiologist has put him on a statin, ACE inhibitor, beta blocker, and aspirin and told him the regimen is for life. He doesn't want to take the pills and asked me if they're really necessary.
This New Zealand study shows why he should keep taking them. A low risk person like him who has had a heart attack has a similar chance of a further episode as the highest risk individual who has never had cardiovascular disease (CVD). Over the next five years, he is five times more likely to have a CVD event than those without prior CVD.
The authors suggest that if resources are limited we should concentrate our efforts on people like my patient, rather than the general population. And he should keep taking the tablets.
Source: Heart 2009;95:125-129
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Dr Ann Robinson, BMJ Group
This New Zealand study shows why he should keep taking them. A low risk person like him who has had a heart attack has a similar chance of a further episode as the highest risk individual who has never had cardiovascular disease (CVD). Over the next five years, he is five times more likely to have a CVD event than those without prior CVD.
The authors suggest that if resources are limited we should concentrate our efforts on people like my patient, rather than the general population. And he should keep taking the tablets.
Source: Heart 2009;95:125-129
---
Dr Ann Robinson, BMJ Group
Peripheral matters
Everything that you ever wanted to know, and more, about peripheral nerve diseases in this useful run through the topic. It reminds us that
Source: Practical Neurology 2008;8:396-405
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Dr Ann Robinson, BMJ Group
- Carpal tunnel syndrome is common (5% of women. 0.5% of men), it resolves in 20% of cases without treatment, in 50% with steroid injection, and in 75% with surgery
- Treat severe Bell's palsy with oral prednisolone
- The commonest causes of symmetrical axonal polyneuropathy are diabetes and alcohol consumption.
Source: Practical Neurology 2008;8:396-405
---
Dr Ann Robinson, BMJ Group
2009年1月16日 星期五
Ketamine相關之嘔吐和劑量無關？？
Ketamine-Associated Vomiting: Is it Dose-Related?
Objective: Vomiting is a common adverse event after emergency department ketamine sedation in children. We sought to determine if the rate of vomiting is dose related to intravenous ketamine.
Methods: Treating physicians administered intravenous ketamine to children requiring sedation for a procedure in a pediatric emergency department using doses of their discretion in this prospective observational study. We compared initial and total ketamine doses between children with and without vomiting directly and after controlling for age and coadministered drugs using multiple logistic regression analysis.
Results: A wide range of initial (0.2 to 2.4 mg/kg) and total (0.3 to 23.8 mg/kg) ketamine doses were administered in the 1039 sedations studied. Vomiting occurred in 74 (7%) overall. Initial and total ketamine dose distributions were similar in children with and without vomiting (medians 1.6 vs 1.6 mg/kg and 2.2 vs 2.1 mg/kg, respectively). Our multivariate analysis found no significant association between emesis and initial dose; however, it did reveal an association with total dose that was explained by a minority (3.5%) of children who received high cumulative doses (>7 mg/kg). The rate of emesis was 7.0% when the total ketamine dose was 7 mg/kg or less and 11.1% when greater than 7 mg/kg.
Conclusions: Within a wide range of intravenous doses, ketamine-associated vomiting is not related to either the initial loading dose or the total dose, except for a modest increase for those receiving high cumulative doses (>7 mg/kg).
---
Pediatric Emergency Care. 25(1):15-18, January 2009.
Objective: Vomiting is a common adverse event after emergency department ketamine sedation in children. We sought to determine if the rate of vomiting is dose related to intravenous ketamine.
Methods: Treating physicians administered intravenous ketamine to children requiring sedation for a procedure in a pediatric emergency department using doses of their discretion in this prospective observational study. We compared initial and total ketamine doses between children with and without vomiting directly and after controlling for age and coadministered drugs using multiple logistic regression analysis.
Results: A wide range of initial (0.2 to 2.4 mg/kg) and total (0.3 to 23.8 mg/kg) ketamine doses were administered in the 1039 sedations studied. Vomiting occurred in 74 (7%) overall. Initial and total ketamine dose distributions were similar in children with and without vomiting (medians 1.6 vs 1.6 mg/kg and 2.2 vs 2.1 mg/kg, respectively). Our multivariate analysis found no significant association between emesis and initial dose; however, it did reveal an association with total dose that was explained by a minority (3.5%) of children who received high cumulative doses (>7 mg/kg). The rate of emesis was 7.0% when the total ketamine dose was 7 mg/kg or less and 11.1% when greater than 7 mg/kg.
Conclusions: Within a wide range of intravenous doses, ketamine-associated vomiting is not related to either the initial loading dose or the total dose, except for a modest increase for those receiving high cumulative doses (>7 mg/kg).
---
Pediatric Emergency Care. 25(1):15-18, January 2009.
新的主動脈剝離新術
主動脈剝離新術 用「套」的有救！
氣溫驟降，醫院急診室最近因為主動脈剝離患者已增加2成，以往碰到這類病患，醫師必須進行縫合手術，不但患者可能流血過多，死亡率還高達3成，最近振興醫院自行研發了「人工血管接環」，植入心血管之後，可以降低手術時間和出血量，一年來已經讓19名患者重獲新生，而這項發明，還獲得美國FDA核准上市，患者自費需要4到8萬元。
一根手指大小，圓形的銀色金屬環，它可不是五金行的小零件，反而是主動脈剝離患者的新救星。
振興心臟醫學中心主任魏崢：「用傳統縫合的方式，我們遭遇到最大的困難，就是組織已經裂了，裂開了縫不起來，環的話就是用外面綁起來，它的受力點是很平均的，而且它受力的界面是比縫線的界面大很多。」
入冬以來，各大醫院收治的主動脈剝離患者，比其他季節還增加兩成，而主動脈每天運送相當於7公噸流量的血液到全身，一旦剝離引起破裂，出血的速度很快，數分鐘內就會死亡，但傳統的治療手術死亡率約3成。
縫合血管還得花上半小時，出血量大約3000c.c.，但人工血管接環，縫合只要2分鐘，出血量也降到500c.c.。魏崢：「兩個東西要連在一起，大家都可以想到很簡單的道理，兩個東西在一起一定要用縫的，那不要用縫的話，就用套的套在裡面，一邊固定到人工血管，一邊固定到主動脈就這麼簡單。」
除了典型主動脈剝離患者會出現胸痛現象外，醫生還提醒，下肢癱瘓、腰痛都是主動脈剝離的徵兆，民眾要是出現這些症狀要盡早就醫。
一根手指大小，圓形的銀色金屬環，它可不是五金行的小零件，反而是主動脈剝離患者的新救星。
振興心臟醫學中心主任魏崢：「用傳統縫合的方式，我們遭遇到最大的困難，就是組織已經裂了，裂開了縫不起來，環的話就是用外面綁起來，它的受力點是很平均的，而且它受力的界面是比縫線的界面大很多。」
入冬以來，各大醫院收治的主動脈剝離患者，比其他季節還增加兩成，而主動脈每天運送相當於7公噸流量的血液到全身，一旦剝離引起破裂，出血的速度很快，數分鐘內就會死亡，但傳統的治療手術死亡率約3成。
縫合血管還得花上半小時，出血量大約3000c.c.，但人工血管接環，縫合只要2分鐘，出血量也降到500c.c.。魏崢：「兩個東西要連在一起，大家都可以想到很簡單的道理，兩個東西在一起一定要用縫的，那不要用縫的話，就用套的套在裡面，一邊固定到人工血管，一邊固定到主動脈就這麼簡單。」
除了典型主動脈剝離患者會出現胸痛現象外，醫生還提醒，下肢癱瘓、腰痛都是主動脈剝離的徵兆，民眾要是出現這些症狀要盡早就醫。
2009年1月14日 星期三
Antipsychotics can cause sudden death
Atypical Antipsychotic Drugs and Sudden Death
It is known that the use of typical antipsychotic agents (e.g., haloperidol) is associated with an increased risk of sudden cardiac death. This study shows that the same association applies to the newer atypical antipsychotic agents (e.g., risperidone) and is dose-related.
Mechanism of Cardiac Toxicity
Typical antipsychotic drugs block repolarizing potassium currents in vitro and prolong the QT interval, one important mechanism for the ventricular tachyarrhythmias that may be seen with these agents. Such tachyarrhythmias, once induced, often lead to sudden death. There are numerous case reports of torsades de pointes and sudden death in conjunction with the use of typical antipsychotic agents. Several atypical antipsychotic drugs also block repolarizing potassium currents and prolong ventricular repolarization as well. Typical and atypical antipsychotic drugs may carry similar increased risks of sudden cardiac death and suggest that other mechanisms may be involved, such as autonomic effects, inhibition of other ion channels, and other acute cardiotoxic effects such as myocarditis. Clozapine, an atypical antipsychotic drug, is associated with an increased risk of myocarditis.
Long QT Interval
The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study showed that 3% of patients with schizophrenia (mean age, 40 years) who were treated with risperidone and quetiapine had prolongation of the QT interval. The risk of this finding was doubled (6%) among patients with dementia (mean age, 78 years); these proportions are probably even higher among elderly users of high-dose antipsychotic drugs. Once prolongation of the QT interval is detected, a reduction of the dose or discontinuation of the drug should be attempted. Additionally, concurrent medications should be examined for known interactions and other risk factors for sudden death reduced. Follow-up electrocardiograms should be obtained.
Tips:
Given the data concluding that current users of typical and atypical antipsychotic drugs had a similar, dose-related increased risk of sudden death from cardiac causes, researchers believe that it is reasonable to obtain an electrocardiogram (ECG) before and shortly after initiation of treatment with an antipsychotic drug.
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New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009
It is known that the use of typical antipsychotic agents (e.g., haloperidol) is associated with an increased risk of sudden cardiac death. This study shows that the same association applies to the newer atypical antipsychotic agents (e.g., risperidone) and is dose-related.
Mechanism of Cardiac Toxicity
Typical antipsychotic drugs block repolarizing potassium currents in vitro and prolong the QT interval, one important mechanism for the ventricular tachyarrhythmias that may be seen with these agents. Such tachyarrhythmias, once induced, often lead to sudden death. There are numerous case reports of torsades de pointes and sudden death in conjunction with the use of typical antipsychotic agents. Several atypical antipsychotic drugs also block repolarizing potassium currents and prolong ventricular repolarization as well. Typical and atypical antipsychotic drugs may carry similar increased risks of sudden cardiac death and suggest that other mechanisms may be involved, such as autonomic effects, inhibition of other ion channels, and other acute cardiotoxic effects such as myocarditis. Clozapine, an atypical antipsychotic drug, is associated with an increased risk of myocarditis.
Long QT Interval
The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study showed that 3% of patients with schizophrenia (mean age, 40 years) who were treated with risperidone and quetiapine had prolongation of the QT interval. The risk of this finding was doubled (6%) among patients with dementia (mean age, 78 years); these proportions are probably even higher among elderly users of high-dose antipsychotic drugs. Once prolongation of the QT interval is detected, a reduction of the dose or discontinuation of the drug should be attempted. Additionally, concurrent medications should be examined for known interactions and other risk factors for sudden death reduced. Follow-up electrocardiograms should be obtained.
Tips:
Given the data concluding that current users of typical and atypical antipsychotic drugs had a similar, dose-related increased risk of sudden death from cardiac causes, researchers believe that it is reasonable to obtain an electrocardiogram (ECG) before and shortly after initiation of treatment with an antipsychotic drug.
---
New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009
Necrotizing fasciitis
What is necrotizing fasciitis?
Necrotizing fasciitis is defined pathologically by necrosis of the deep soft tissue, including fascia, with relative sparing of skeletal muscle. It results in extensive necrosis that often largely spares the overlying skin. It is most often caused by group A streptococcus.
What other organisms besides group A streptococcus can cause necrotizing fasciitis?
The most common presentations of necrotizing fasciitis involve the abdominal wall or perineum, often with polymicrobial infection due to spontaneous, traumatic, or surgical disruption of bowel integrity, particularly in a patients with diabetes or immunosuppression. In a patient who is healthy and has not recently undergone surgery, a monomicrobial infection is the rule with group A streptococcus or Staphylococcus aureus, including methicillin-resistant S. aureus, implicated most frequently. Necrotizing fasciitis arising as a complication of infection in the setting of drug abuse is often caused by clostridium species, notably Clostridium sordellii in association with black-tar heroin.
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New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009
Necrotizing fasciitis is defined pathologically by necrosis of the deep soft tissue, including fascia, with relative sparing of skeletal muscle. It results in extensive necrosis that often largely spares the overlying skin. It is most often caused by group A streptococcus.
What other organisms besides group A streptococcus can cause necrotizing fasciitis?
The most common presentations of necrotizing fasciitis involve the abdominal wall or perineum, often with polymicrobial infection due to spontaneous, traumatic, or surgical disruption of bowel integrity, particularly in a patients with diabetes or immunosuppression. In a patient who is healthy and has not recently undergone surgery, a monomicrobial infection is the rule with group A streptococcus or Staphylococcus aureus, including methicillin-resistant S. aureus, implicated most frequently. Necrotizing fasciitis arising as a complication of infection in the setting of drug abuse is often caused by clostridium species, notably Clostridium sordellii in association with black-tar heroin.
---
New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009
Sepsis：定義和治療
Severe Sepsis and Septic Shock
Severe sepsis is based on a diagnosis of a temperature greater than 38.0ºC, a heart rate of more than 90 beats per minute, respirations of more than 20 breaths per minute, a white-cell count of more than 12,000 per cubic millimeter, and evidence of organ dysfunction. Septic shock is defined by the presence of persistent hypotension (systolic blood pressure <90 mm Hg) despite adequate volume resuscitation.
Treating Septic Shock
The keys to treating septic shock are restoring tissue perfusion, providing prompt administration of antimicrobial therapy, and removing the source of infection. The first objective in early goal-directed therapy intended to restore tissue perfusion is to provide adequate volume resuscitation with saline and crystalloid fluid, if necessary. If initial fluid resuscitation fails to restore adequate tissue perfusion, the second step in early goal-directed therapy is to use vasopressors, such as norepinephrine, to maintain mean systemic arterial pressure above 65 mm Hg. The third objective is to achieve adequate tissue perfusion as measured by central venous oxygen saturation, which is the difference between oxygen delivery to peripheral tissues and oxygen consumption by those tissues. Other strategies can include increasing the concentration of oxygen-carrying hemoglobin or increasing cardiac output with an inotropic agent such as dopamine. Norepinephrine was used in this case; it is the vasopressor of choice because it results in peripheral vasoconstriction without causing clinically significant tachycardia.
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New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009
Severe sepsis is based on a diagnosis of a temperature greater than 38.0ºC, a heart rate of more than 90 beats per minute, respirations of more than 20 breaths per minute, a white-cell count of more than 12,000 per cubic millimeter, and evidence of organ dysfunction. Septic shock is defined by the presence of persistent hypotension (systolic blood pressure <90 mm Hg) despite adequate volume resuscitation.
Treating Septic Shock
The keys to treating septic shock are restoring tissue perfusion, providing prompt administration of antimicrobial therapy, and removing the source of infection. The first objective in early goal-directed therapy intended to restore tissue perfusion is to provide adequate volume resuscitation with saline and crystalloid fluid, if necessary. If initial fluid resuscitation fails to restore adequate tissue perfusion, the second step in early goal-directed therapy is to use vasopressors, such as norepinephrine, to maintain mean systemic arterial pressure above 65 mm Hg. The third objective is to achieve adequate tissue perfusion as measured by central venous oxygen saturation, which is the difference between oxygen delivery to peripheral tissues and oxygen consumption by those tissues. Other strategies can include increasing the concentration of oxygen-carrying hemoglobin or increasing cardiac output with an inotropic agent such as dopamine. Norepinephrine was used in this case; it is the vasopressor of choice because it results in peripheral vasoconstriction without causing clinically significant tachycardia.
---
New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009
2009年1月12日 星期一
有 agonal respiration 之 CPR 預後佳
Gasping During Cardiac Arrest Is Associated with Improved Survival
Gasping is common and should not delay initiation of CPR.
Early and uninterrupted bystander cardiopulmonary resuscitation is often critical to patient survival after cardiac arrest. However, the presence of agonal or gasping respirations might delay recognition of arrest and, therefore, delay initiation of CPR. Researchers retrospectively reviewed cardiac arrest reports from Arizona emergency medical services systems to assess the frequency of gasping respirations in adults with out-of-hospital nontraumatic cardiac arrest.
Patients were excluded if they had obvious signs of death, do-not-resuscitate orders, or arrest secondary to drowning. Overall, 44 of 113 patients (39%) had reports of gasping. Although similar proportions of patients with and without reports of gasping received bystander CPR, the group with gasping had a significantly higher rate of survival to hospital discharge (odds ratio for survival, 3.4). The authors conclude that abnormal breathing is common after cardiac arrest and that the public and medical dispatchers should be made aware of this finding.
Comment:
Agonal or gasping respirations are hallmarks of cerebral hypoperfusion. Although this retrospective study likely underestimated the incidence of gasping, the findings suggest that it is common immediately after cardiac arrest. As we learn more about the meaning and prognostic significance of gasping, the challenge will be to help the public to understand that CPR should be initiated even when gasping is present.
—
Aaron E. Bair, MD, MSc, FAAEM, FACEP
Published in Journal Watch Emergency Medicine January 9, 2009
Citation(s):
Bobrow BJ et al. Gasping during cardiac arrest in humans is frequent and associated with improved survival. Circulation 2008 Dec 9; 118:2550
Gasping is common and should not delay initiation of CPR.
Early and uninterrupted bystander cardiopulmonary resuscitation is often critical to patient survival after cardiac arrest. However, the presence of agonal or gasping respirations might delay recognition of arrest and, therefore, delay initiation of CPR. Researchers retrospectively reviewed cardiac arrest reports from Arizona emergency medical services systems to assess the frequency of gasping respirations in adults with out-of-hospital nontraumatic cardiac arrest.
Patients were excluded if they had obvious signs of death, do-not-resuscitate orders, or arrest secondary to drowning. Overall, 44 of 113 patients (39%) had reports of gasping. Although similar proportions of patients with and without reports of gasping received bystander CPR, the group with gasping had a significantly higher rate of survival to hospital discharge (odds ratio for survival, 3.4). The authors conclude that abnormal breathing is common after cardiac arrest and that the public and medical dispatchers should be made aware of this finding.
Comment:
Agonal or gasping respirations are hallmarks of cerebral hypoperfusion. Although this retrospective study likely underestimated the incidence of gasping, the findings suggest that it is common immediately after cardiac arrest. As we learn more about the meaning and prognostic significance of gasping, the challenge will be to help the public to understand that CPR should be initiated even when gasping is present.
—
Aaron E. Bair, MD, MSc, FAAEM, FACEP
Published in Journal Watch Emergency Medicine January 9, 2009
Citation(s):
Bobrow BJ et al. Gasping during cardiac arrest in humans is frequent and associated with improved survival. Circulation 2008 Dec 9; 118:2550
2009年1月5日 星期一
RSI 會殺人？
Salicylate Overdose: When RSI Can Kill A Patient
Management of severe salicylate poisoning is uniquely within the scope of EM practice, but it is also an example where routine RSI can get you into trouble. Intubation may be necessary in the setting of acute salicylate intoxication for a number of reasons (altered mental status, hypoxia, patient tiring, etc.).
Severe salicylate intoxication is typically associated with metabolic acidosis and a concomitant respiratory alkalosis. It is important to keep in mind that the degree of alkalosis is actually high compared to the degree of metabolic acidosis because of associated hyperventilation, a primary CNS effect of salicylate, NOT a simple compensatory response to the metabolic acidosis.
An acidic environment facilitates the ability of the salicylate molecule to cross biologic membranes. Hence, anything that interrupts hyperventilation will worsen the acidemia and result in deterioration of the patient. There are documented cases where rapid sequence intubation has resulted in catastrophe and cardiac arrest because the patient was not ventilated rapidly enough to maintain the pH at alkaline levels; suppression of the patient's respiratory drive can be rapidly life threatening in this setting.
As stated in Goldfrank’s Toxicologic Emergencies: "Endotracheal intubation followed by assisted ventilation of a salicylate-poisoned patient poses particular risks and may contribute to mortality in several ways.........Few healthcare providers are trained or skilled at maintaining the appropriate concentration of hypocarbia and hyperventilation necessary.(3)"
If a patient with acute severe salicylate intoxication requires intubation, the goal should be to maintain the pCO2 at pre-intubation levels, or possibly even lower if CNS depression was already evident. Be cautions not to use typical ventilator settings which can result in worsening acidosis and death.
References:
(1) Greenberg MI, et al. Deleterious effects of endotracheal intubation in salicylate poisoning Ann Emerg Med. 2003;41: 583-4.
(2) Berk WA, Andersen JC. Salicylate-associated asystole: report of two cases. Am J Med. 1989;86: 505-6.
(3) Goldfrank’s Toxicologic Emergencies. 8th edition. Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Nelson L, Hoffman RS (eds.). Appleton and Lange, Norwalk, CN, 2005.
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其實我覺得原文標題有點太過聳動
其實不是RSI殺人，而是不會設定ventilator而殺人
PS: 感謝小侯醫師提供此資訊。
這裡也有提到此觀念，見第二個『A』：
http://jack119.blogspot.com/2008/08/blog-post_18.html
Management of severe salicylate poisoning is uniquely within the scope of EM practice, but it is also an example where routine RSI can get you into trouble. Intubation may be necessary in the setting of acute salicylate intoxication for a number of reasons (altered mental status, hypoxia, patient tiring, etc.).
Severe salicylate intoxication is typically associated with metabolic acidosis and a concomitant respiratory alkalosis. It is important to keep in mind that the degree of alkalosis is actually high compared to the degree of metabolic acidosis because of associated hyperventilation, a primary CNS effect of salicylate, NOT a simple compensatory response to the metabolic acidosis.
An acidic environment facilitates the ability of the salicylate molecule to cross biologic membranes. Hence, anything that interrupts hyperventilation will worsen the acidemia and result in deterioration of the patient. There are documented cases where rapid sequence intubation has resulted in catastrophe and cardiac arrest because the patient was not ventilated rapidly enough to maintain the pH at alkaline levels; suppression of the patient's respiratory drive can be rapidly life threatening in this setting.
As stated in Goldfrank’s Toxicologic Emergencies: "Endotracheal intubation followed by assisted ventilation of a salicylate-poisoned patient poses particular risks and may contribute to mortality in several ways.........Few healthcare providers are trained or skilled at maintaining the appropriate concentration of hypocarbia and hyperventilation necessary.(3)"
If a patient with acute severe salicylate intoxication requires intubation, the goal should be to maintain the pCO2 at pre-intubation levels, or possibly even lower if CNS depression was already evident. Be cautions not to use typical ventilator settings which can result in worsening acidosis and death.
References:
(1) Greenberg MI, et al. Deleterious effects of endotracheal intubation in salicylate poisoning Ann Emerg Med. 2003;41: 583-4.
(2) Berk WA, Andersen JC. Salicylate-associated asystole: report of two cases. Am J Med. 1989;86: 505-6.
(3) Goldfrank’s Toxicologic Emergencies. 8th edition. Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Nelson L, Hoffman RS (eds.). Appleton and Lange, Norwalk, CN, 2005.
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其實我覺得原文標題有點太過聳動
其實不是RSI殺人，而是不會設定ventilator而殺人
PS: 感謝小侯醫師提供此資訊。
這裡也有提到此觀念，見第二個『A』：
http://jack119.blogspot.com/2008/08/blog-post_18.html
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