tatiana helena rech, Hospital de Clinicas de Porto Alegre
28 November 2006
Tatiana H Rech, Silvia Regina Rios Vieira and Janete Salles Brauner
The search for very specific prognostic tests to define unfavorable outcomes early in the course of cardiac arrest has been a major focus of critical care research, and the need for more prognostic accuracy is successfully highlighted by David Tirschwell in “Optimizing neurologic prognosis after cardiac arrest” [1].
As suggested by Tirschwell, withholding and withdrawing therapy might influence outcomes. Indeed, one of our concerns [2] was to make sure that all patients would receive full life support. The non-survivors died of sepsis and multiple organ failure; would they have died had they received full support or entered a vegetative state? Would this have affected the cutoff values for NSE? Meynaar and colleagues designed a study where primary caregivers were blinded to NSE measurements, but they interrupted care based on somatosensory evoked potentials (SSEP) in 48 hours [3]. Zingler and colleagues published three case reports of diagnostic pitfalls in patients with hypoxic brain damage, where two patients had significantly increased concentrations of NSE (up to 90 ng/ml on day 3) and normal SSEP. Those patients were in a persistent vegetative state after three months of follow-up [4]. Zandbergen and colleagues also used SSEP results to make treatment decisions at 72 hours after the arrest, but their study shows that NSE levels and SSEP results overlap only partially [5]. An additional question surrounding this issue is how therapeutic hypothermia after cardiac arrest could influence NSE cutoff values. Tiainem and colleagues have raised the hypothesis that therapeutic hypothermia could reduce the prognostic value of serum NSE [6].
Initial answers to many of these question could probably be reached, as suggested by Tirschwell, through an international prospective study to test a predefined cutoff value for NSE using multiple samples (at 24, 24, 72 and 96 hours). Such a study should include patients treated with therapeutic hypothermia and with no restrictions of life support. It is not always so easy to find a course of action — let us not miss this opportunity.
References
1. Tirschwell D: Optimizing neurologic prognosis after cardiac arrest. Crit Care 2006, 10:171-172.
2. Rech TH, Rio Vieira SR, Nagel F, Brauner JS, Scalco R: Serum neuron-specific enolase as early predictor of outcome after in-hospital cardiac arrest: a cohort study. Crit Care 2006, 10:R133-R138.
3. Meynaar IA, Straaten HM, van der Wetering J, Verlooy P, Slaats EH, Bosman RJ, van der Spoel JI, Zandstra DF: Serum neuron-specific enolase predicts outcome in post-anoxic coma: a prospective cohort study. Intensive Care Med 2003, 29:189-195.
4. Zingler VC, Pohlmann-Eden B: Diagnostic pitfalls in patients with hypoxic brain damage: three case reports. Resuscitation 2005, 65:107-110.
5. Zandbergen EG, Hijdra A, Koelman JH, Hart AA, Vos PE, Verbeek MM, de Haan RJ: Prediction of poor outcome within the first 3 days of postanoxic coma. Neurology 2006, 66:62-68.
6. 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.
Competing interests
The authors have no competing interests to declare.
Critical Care
A clear course of action
28 November 2006
Tatiana H Rech, Silvia Regina Rios Vieira and Janete Salles Brauner
The search for very specific prognostic tests to define unfavorable outcomes early in the course of cardiac arrest has been a major focus of critical care research, and the need for more prognostic accuracy is successfully highlighted by David Tirschwell in “Optimizing neurologic prognosis after cardiac arrest” [1].
As suggested by Tirschwell, withholding and withdrawing therapy might influence outcomes. Indeed, one of our concerns [2] was to make sure that all patients would receive full life support. The non-survivors died of sepsis and multiple organ failure; would they have died had they received full support or entered a vegetative state? Would this have affected the cutoff values for NSE? Meynaar and colleagues designed a study where primary caregivers were blinded to NSE measurements, but they interrupted care based on somatosensory evoked potentials (SSEP) in 48 hours [3]. Zingler and colleagues published three case reports of diagnostic pitfalls in patients with hypoxic brain damage, where two patients had significantly increased concentrations of NSE (up to 90 ng/ml on day 3) and normal SSEP. Those patients were in a persistent vegetative state after three months of follow-up [4]. Zandbergen and colleagues also used SSEP results to make treatment decisions at 72 hours after the arrest, but their study shows that NSE levels and SSEP results overlap only partially [5]. An additional question surrounding this issue is how therapeutic hypothermia after cardiac arrest could influence NSE cutoff values. Tiainem and colleagues have raised the hypothesis that therapeutic hypothermia could reduce the prognostic value of serum NSE [6].
Initial answers to many of these question could probably be reached, as suggested by Tirschwell, through an international prospective study to test a predefined cutoff value for NSE using multiple samples (at 24, 24, 72 and 96 hours). Such a study should include patients treated with therapeutic hypothermia and with no restrictions of life support. It is not always so easy to find a course of action — let us not miss this opportunity.
References
1. Tirschwell D: Optimizing neurologic prognosis after cardiac arrest. Crit Care 2006, 10:171-172.
2. Rech TH, Rio Vieira SR, Nagel F, Brauner JS, Scalco R: Serum neuron-specific enolase as early predictor of outcome after in-hospital cardiac arrest: a cohort study. Crit Care 2006, 10:R133-R138.
3. Meynaar IA, Straaten HM, van der Wetering J, Verlooy P, Slaats EH, Bosman RJ, van der Spoel JI, Zandstra DF: Serum neuron-specific enolase predicts outcome in post-anoxic coma: a prospective cohort study. Intensive Care Med 2003, 29:189-195.
4. Zingler VC, Pohlmann-Eden B: Diagnostic pitfalls in patients with hypoxic brain damage: three case reports. Resuscitation 2005, 65:107-110.
5. Zandbergen EG, Hijdra A, Koelman JH, Hart AA, Vos PE, Verbeek MM, de Haan RJ: Prediction of poor outcome within the first 3 days of postanoxic coma. Neurology 2006, 66:62-68.
6. 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.
Competing interests
The authors have no competing interests to declare.