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Outcome after cardia arrest: predictive values and limitations of the neuroproteins neuron-specific enolase and protein S-100 and the GCS R¨udiger Pfeifera , ∗, Angelika B¨ornerb, Andreas Kracka, Holger H. Siguscha, Ralf Surbera, Hans R. Figullaa. Presented by Ri 許宸睿.

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Presented by ri

Outcome after cardia arrest: predictive values and limitations of the neuroproteins neuron-specific enolase and protein S-100 and the GCSR¨udiger Pfeifera,∗, Angelika B¨ornerb, Andreas Kracka, Holger H. Siguscha,Ralf Surbera, Hans R. Figullaa

Presented by Ri許宸睿

Resuscitation 65 (2005) 49–55


Introduction
Introduction

  • Cardiac arrest

     →Cessation of cerebral perfusion

     →Global hypoxic ischemic brain damage

  • Sever neurological damage

    • Vegetative state in 20~50% of long-term survivor


Prognostic marker in previous study
Prognostic marker in previous study

  • Pre-CPR data

    • Age >70y/o

    • Co-mobility

    • Asystole as primary cardiac dysythm

  • CPR data

    • Bystander resuscitation

    • The duration of resuscitation(30min)

    • Time of hypxia(6min)

  • Post-CPR data

    • Persistent hyperglycemia

    • Unconsciousness >48hr

    • GCS at admission or 3days after CPR


Methods
Methods

  • Enrolled 97 patient between 1998~2002

    • Non-traumatic cardiac arrest

    • ROSC, and survived >24hr

      Group 1: death or vegetative state

      Group 2: recovered cognitive brain function

  • Access the predictive value of

    • Epidemiological data


Pre cpr data

No significant differences in

mean age, co-morbidity, or initial rhythm

Pre-CPR data


Cpr data

Absence of bystander CPR

3.9-fold increased in risk

Time of hypoxia was significant shorter with Group Ⅱ

Subjective impression

CPR data


Post cpr data

Coma > 48h

60.6 fold increased in risk

Post-CPR data


GCS < 6 on D30

Marker of poor outcome

Plus coma >48h

Most reliable clinical variables

23% of Group 1

Sedation and muscle relaxation >72h

No proper NE

GCS


Neuroprotein
Neuroprotein

  • Neuron-specific enolase(NSE)

    • Neurons ; HL = 24hr

  • S-100 protein

    • Glia; HL = 2hr

  • Cerebral disease cause elevation of NSE and S-100

    • Ischemic stroke, meningoencephalitis, and head injury

  • Cerebral hypoxia

    • Death of neuronal cell and damage to BBB


Neuroprotein1
Neuroprotein

NSE

S-100


Neuroprotein2
Neuroprotein

  • The difference in the mean value were highly significant since 24hr after CPR

    • As a result of ongoing brain damage

  • Valid cut-off level – unsettled

    • NSE > 60 mg/ml on D3 – specificity 96%

    • S-100 >1.5 ug/ml on D3 – specificity 96%

  • If combine NSE, S-100, and GCS

    • Specificity 100%, sensitivity 20%



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