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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
slide8
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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