Correspondence
Neurologic Prognosis after Cardiac Arrest
N Engl J Med 2009; 361:1999-2000November 12, 2009
- Article
To the Editor:
We are concerned that Young (Aug. 6 issue)1 did not emphasize the considerable help provided by the clinical history in predicting the prognosis for a patient after cardiac arrest. Elements of the clinical history — such as the location of the arrest (home or outdoors), the presence or absence of witnesses, and the chronology (delays in delivery of cardiopulmonary resuscitation and the first therapeutic shock) — are generally easy to collect and are strongly associated with outcomes.2,3 Therefore, such information may assist clinicians in making the difficult decision to withdraw life support. In these situations, it seems to us that the value of basic medical practices should not be underestimated.
3 ReferencesNicolas Nesseler, M.D.
Guillaume Leurent, M.D.
Philippe Seguin, M.D., Ph.D.
Rennes University Hospital, Rennes, France
nicolas.nesseler@chu-rennes. fr 1
Young GB . Neurologic prognosis after cardiac arrest. N Engl J Med 2009;361:605-611
Full Text | Web of Science | Medline2
Haukoos JS ,Lewis RJ ,Niemann JT . Prediction rules for estimating neurologic outcome following out-of-hospital cardiac arrest. Resuscitation 2004;63:145-155
CrossRef | Web of Science | Medline3
Oddo M ,Ribordy V ,Feihl F , et al. Early predictors of outcome in comatose survivors of ventricular fibrillation and non-ventricular fibrillation cardiac arrest treated with hypothermia: a prospective study. Crit Care Med 2008;36:2296-2301
CrossRef | Web of Science | Medline
To the Editor:
On the basis of recent publications and our own experience, we would advise great caution in the use of levels of neuron-specific enolase (NSE) to predict outcome after cardiac arrest. NSE is not specific for neurocellular damage. Most important, NSE levels can be clinically significantly influenced by hemolysis, which now occurs more frequently given the expanding use of ventricular assist devices1,2 in resuscitated patients.
In addition, the use of therapeutic hypothermia seems to decrease the prognostic value of NSE,3 a fact not adequately reflected in the 2006 algorithm of the American Academy of Neurology (AAN). We would underscore the importance of Young's comment that the introduction of therapeutic hypothermia requires modification of this algorithm. Hypothermia attenuates the metabolism of sedating drugs, rendering estimations based on normal half-lives inaccurate, especially in the case of drugs affected by cytochrome P-450 enzymes.4 In our practice, we have excluded the use of NSE levels in clinical decision making.
4 ReferencesSebastian Grundmann, M.D., Ph.D.
Hans-Joerg Busch, M.D.
University Hospital Freiburg, Freiburg, Germany
sebastian.grundmann@uniklinik-freiburg. de 1
Johnsson P ,Blomquist S ,Luhrs C , et al. Neuron-specific enolase increases in plasma during and immediately after extracorporeal circulation. Ann Thorac Surg 2000;69:750-754
CrossRef | Web of Science | Medline2
Pfeifer R ,Ferrari M ,Borner A ,Deufel T ,Figulla HR . Serum concentration of NSE and S-100b during LVAD in non-resuscitated patients. Resuscitation 2008;79:46-53
CrossRef | Web of Science | Medline3
Tiainen M ,Roine RO ,Pettila V ,Takkunen O . Serum neuron-specific enolase and S-100B protein in cardiac arrest patients treated with hypothermia. Stroke 2003;34:2881-2886
CrossRef | Web of Science | Medline4
Tortorici MA ,Kochanek PM ,Poloyac SM . Effects of hypothermia on drug disposition, metabolism, and response: a focus of hypothermia-mediated alterations on the cytochrome P450 enzyme system. Crit Care Med 2007;35:2196-2204
CrossRef | Web of Science | Medline
Author/Editor Response
Nesseler et al. are correct in stating that the occurrence of out-of-hospital cardiac arrests and delays in the delivery of cardiopulmonary resuscitation are significantly related to poor outcome. However, if we select variables associated with a false positive rate that is close to zero for such prediction, then these and several other clinical factors are not sufficiently robust to be prognostically useful in the individual case.
The AAN practice parameters1 are based on reports produced before the advent of hypothermic treatment for comatose survivors of cardiac arrest. Grundmann and Busch appropriately underscore concerns about the potential modifying effect of hypothermia on the various parameters found to have predictive value in the AAN document.1 As noted in my Clinical Practice article, hypothermia can delay the return of the motor response for up to 6 days in patients who do eventually recover conscious awareness.1,2
Grundmann and Busch also have concerns about the validity of the measurement of NSE levels in patients who have received hypothermic treatment. Serum concentrations of more than 33 μg per liter obtained in a large series of patients from 1 to 3 days after cardiac arrest were found to be predictive of poor outcome.3 Hypothermia can decrease the rise in NSE levels and may lead to reduced sensitivity for poor outcome, but the drop in NSE levels in patients who have had hypothermic treatment may also reflect increased neuroprotection.4 It seems unlikely that NSE levels would rise after hypothermic treatment to produce a higher rate of false positives for poor outcome; elevated serum levels of NSE should still have prognostic value for poor outcome. The clearance rate of some drugs may be affected by hypothermia, but this effect would not significantly compromise the results of testing in patients paralyzed with cisatracurium or sedated with propofol (drugs commonly used during hypothermia), which are still cleared quickly, especially once patients are normothermic.
Prospective data are needed to examine the validity of the AAN practice parameters in a group of patients who receive hypothermic treatment after having cardiac arrest. It is highly likely that the factors that have been shown to be reliable predictors in the past — such as loss of pupillary and corneal reflexes and of somatosensory-evoked responses — will be validated. However, the timing of the testing of some variables may require adjustment.
4 ReferencesG. Bryan Young, M.D.
University of Western Ontario, London, ON, Canada
bryan.young@lhsc. on. ca 1
Wijdicks EF ,Hijdra A ,Young GB , et al. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2006;67:203-210
CrossRef | Web of Science | Medline2
Al Thenayan E ,Savard M ,Sharpe M ,Nortin L ,Young B . Predictors of poor neurologic outcome after induced mild hypothermia following cardiac arrest. Neurology 2008;71:1535-1537
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Zandbergen EG ,Hijdra A ,Koelman JH , et al. Prediction of poor outcome within the first 3 days of postanoxic coma. Neurology 2006;66:62-68[Erratum, Neurology 2006;66:1133.]
CrossRef | Web of Science | Medline4
Tiainen M ,Roine RO ,Pettila V ,Takkunen O . Serum neuron-specific enolase and S-100B protein in cardiac arrest patients treated with hypothermia. Stroke 2003;34:2881-2886
CrossRef | Web of Science | Medline
