2009年1月21日 星期三

OHCA 低溫處置不見長期療效?

The impact of therapeutic hypothermia on neurological function and quality of life after cardiac arrest

To assess the impact of therapeutic hypothermia on cognitive function and quality of life in comatose survivors of out of Hospital Cardiac arrest (OHCA).

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.

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.

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.

Resuscitation, Volume 80, Issue 2, February 2009, Pages 171-176

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:
  1. Hemoglobin level >12.9 g/dL (men) or >11.9 g/dL (women)
  2. Systolic blood pressure >109 mm Hg
  3. Pulse <100/minute>
  4. Blood urea nitrogen level <18.2>
  5. No melena or syncope
  6. No past or present liver disease or heart failure
In phase 1 of this multicenter study (data collection), 16% of 630 consecutive outpatients who were evaluated for UGIB scored "0" on the GBS; all but 3 were admitted, and none died or required interventions. In phase 2 of the study (GBS-driven admissions), 572 consecutive outpatients with UGIB were evaluated; of 123 (22%) who scored "0" on the GBS, 84 were sent home with appointments for outpatient endoscopy. Twenty-three of these patients underwent their planned endoscopies (none of which led to interventions); among patients who missed their planned endoscopies, no hospital admissions or deaths had occurred at 6 months.

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
  1. Happy people tend to be at the centre of large groups of other happy people
  2. 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)
  3. Happiness ripples through social networks, spreading like a contagious disease
  4. You don't have to be friends with people just like you.
I think this means we should stay connected to lots of different people - preferably happy ones but not necessarily all the same.

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

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
  1. 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
  2. Treat severe Bell's palsy with oral prednisolone
  3. 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-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.


主動脈剝離新術 用「套」的有救!







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.

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.

New England Journal of Medicine - Vol. 360, No. 3, January 15, 2009


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.

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.

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

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.

(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.


PS: 感謝小侯醫師提供此資訊。