X-Message-Number: 27347
Date: Thu, 10 Nov 2005 13:55:35 +0100
From: Eugen Leitl <>

Subject: [: Re: [ccm-l] therapeutic hypothermia in ventricular
fibrillationcardiac arrest]

----- Forwarded message from Tom Bleck <> -----

From: Tom Bleck <>
Date: Thu, 10 Nov 2005 07:50:01 -0500
To: , Mustapha Ezzeddine <>
Cc: Ccm-L <>
Subject: Re: [ccm-l] therapeutic hypothermia in ventricular
	fibrillationcardiac arrest
X-Mailer: Microsoft Outlook Express 6.00.2900.2180

Thomas,

For the most recent analysis of these data consult:

Holzer M, Bernard SA, Hachimi-Idrissi S, Roine RO, Sterz F, Mullner M; on 
behalf of the Collaborative Group on Induced Hypothermia for Neuroprotection 
After Cardiac Arrest. Hypothermia for neuroprotection after cardiac arrest: 
systematic review and individual patient data meta-analysis.  Crit Care Med 
2005;33:414-8.

OBJECTIVE: Only a few patients survive cardiac arrest with favorable 
neurologic recovery. Our objective was to assess whether induced hypothermia 
improves neurologic recovery in survivors of primary cardiac arrest. DATA 
SOURCE: Studies were identified by a computerized search of MEDLINE, EMBASE, 
CINAHL, PASCAL, the Cochrane Controlled Trial Register, and BIOSIS. STUDY 
SELECTION: We included randomized and quasi-randomized, controlled trials of 
adults who were successfully resuscitated, where therapeutic hypothermia was 
applied within 6 hrs after arrival at the emergency department and where the 
neurologic outcome was compared. We excluded studies without a control group 
and studies with historical controls. DATA EXTRACTION: All authors of the 
identified trials supplied individual patient data with a predefined set of 
variables. DATA SYNTHESIS: We identified three randomized trials. The 
analyses were conducted according to the intention-to-treat principle. 
Summary odds ratios were calculated using a random effects model and 
translated into risk ratios. More patients in the hypothermia group were 
discharged with favorable neurologic recovery (risk ratio, 1.68; 95% 
confidence interval, 1.29-2.07). The 95% confidence interval of the 
number-needed-to-treat to allow one additional patient to leave the hospital 
with favorable neurologic recovery was 4-13. One study followed patients to 
6 months or death. Being alive at 6 months with favorable functional 
neurologic recovery was more likely in the hypothermia group (risk ratio, 
1.44; 95% confidence interval, 1.11-1.76). CONCLUSIONS: Mild therapeutic 
hypothermia improves short-term neurologic recovery and survival in patients 
resuscitated from cardiac arrest of presumed cardiac origin. Its long-term 
effectiveness and feasibility at an organizational level need further 
research.

Tom
Tom Bleck (Thomas P. Bleck MD FCCM) 
Louise Nerancy Eminent Scholar in Neurology and
Professor of Neurology, Neurological Surgery, and Internal Medicine
Chair, Critical Care Subcommittee
Director, Neuroscience Intensive Care Unit
The University of Virginia

Past President, The Neurocritical Care Society 
(http://www.neurocriticalcare.org)

Those who believe that regulation is a substitute for evidence will find
that even the most meticulous regulation of nonsense must still result in
nonsense.
--E. Ernst BMJ 2000;321:1133-1135


----- Original Message ----- 
From: <>
To: "Mustapha Ezzeddine" <>
Cc: "Ccm-L" <>
Sent: Thursday, November 10, 2005 4:57 AM
Subject: Re: [ccm-l] therapeutic hypothermia in ventricular 
fibrillationcardiac arrest


>Quoting Mustapha Ezzeddine <>:
>
>>Dear list members. I am interested in your opinion and your current 
>>practice
>>regarding the therapeutic use of hypothermia in cardiac arrest survivors.
>>I am sure it must have been vigorously discussed in the past on this 
>>list,
>>prior to me joining.
>>specifically:
>>- do you think the current evidence supports its routine use in the the
>>highly selected patient population studied in the NEJM trials.
>>- If the your are convinced by the data, what are the hurdles of
>>implementing this in your practice?
>>- if you believe the data is insufficient, what kind of evidence you are
>>waiting for?
>>- use in other types of anoxic brain injury?
>>
>>I would greatly appreciate your response and comments
>>
>>regards,
>>
>>Mustapha Ezzeddine, MD
>>Director, Neurociritcal Care Service
>>UMDNJ, Newark
>>
>
>
>
>From my personal opinion I cannot really understand the mechanism which is
>assumed to contribute to cereral protection or outcome. In focal ischemia 
>you
>see an area of necrosis and a penumbra, which is somehow perfused by
>collaterales. If reperfusion is reestablished, that region of penumbra is
>functionally restorable. In cardiac arrest the patient has a total 
>cerebral
>ischemia, if an adequate circulation is re-established and no hemmorhage 
>or
>anything leading to an elevated ICP is present, then reperfusion should 
>lead to
>a restitution of the function. What makes me wonder: Slowing metabolism by
>cooling probably also will decrease cerebral perfusion too (metabolism 
>drives
>flow). Can't cerebral metabolism be reduced by deep sedation more 
>effectively?
>Comparing patient groups after cardiac arrest, to my personal opinion some
>factors must be taken into account 1. the cause of the arrest 2. do the
>patients after ROSC have an adequate cerebral perfusion or is  MAP - ICP
>insufficient for cerebral re-perfusion (e.g.. its a difference if the 
>cause for
>cardiac arrest was a temporary arrhythmia or an MI with consecutive low 
>output)
>3. the medications administered during CPR (probably some were 
>neuroprotective
>or vice versa). I think its not really a good idea just to randomize 
>patients
>after cardiac fibrillation and CPR. The groups probably are too different. 
>And
>the authors in the NJM made a statistic error, which I think they have
>corrected later in a letter. Recalculating the results gives a small 
>positive
>(0.043) significance in neurologic outcome in "cooled" patients and 
>mortalites
>are not different (if you referred on the "Cooling after cardiac arrest 
>study"
>from 2002). This is not an outstanding result urgently requesting changes 
>in
>all strategies. Here the answer is: "No". We don't cool patients after 
>cardiac
>arrest. I think here generally the strategy is to maintain an adequate 
>CPP.
>
>Thomas
>


----- End forwarded message -----
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Eugen* Leitl <a href="http://leitl.org">leitl</a>
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