1. The Key to Survival Dr Tong WL Associate Consultant
Intensive Care Unit
17 March 2009

2. Case 1 Male, 49 yr old Chronic smoker and drinker P/H
DM on Mixtard HM for 2 years
Newly diagnosed HT in China few months ago, on amlodipine 5mg QD

3. Case 1 Admitted on 5 June 2008 Sudden collapse on Nathan Road
No pulse on ambulance at 1305
CPR with AED connected (not fired)
A&E at 1319: asystole
Intubated
Adrenaline x 3 + atropine 3mg + IV NaHCO3
ROSC at 1330

4. Case 1 A&E  ICU pH 6.77 HCO3 7.2 BE -28.4 PaO2 14.2 PaCO2 6.7
RFT 120/6.1/10.9/235
Glucose 32.7 ( H’stix in A&E 26.3)
Urine ketone 4+
Temp C

5. Case 1

7. CK LDH 948
Tn I 12.5ng/ml
Bedside echo: inferior posterior wall hypokinesia, satisfactory biventricular systolic fx

8. Case 1 Diagnosis Post cardiac arrest Acute inferior MI DKA
Aspiration pneumonia

9. Case 2 F/44 A cleansing worker, NDNS P/H: R hemiparesis in China ,
good recovery 1992
Travel: returned to HK 2 days ago from China, where she developed diarrheoa and dizziness. IV medication was given.

10. 04 Jan 2008 Sudden collapse while at work Asystole at the scene
Started CPR upon EMS arrival
Ambulance: VF, defibrillation x 2
Case 2

11. A&E Dept VF, adrenaline 8mg, defibrillation x 3, Amiodarone IV
Intubation
CPR x 30min
Temp 34.8C
Pupils fixed and dilated
BP157/105
Case 2

12. Case 2 A&E to ICU pH 7.08 HCO3 16.4 BE –14.0 PaO2 34.8 PaCO2 7.5
RFT 140/2.8/4.9/126
Glucose (H’ stix in A&E 8.8)
CK LDH 493
Case 2

13. Case 2 QTc msec

14. Case 2

15. Case 2 Bedside echo: TnI 0.2 ng/ml (D1)
4 chambers normal size, satisfactory biventricular systolic fx ; mild AR;
no RWMA
TnI 0.2 ng/ml (D1)
CT brain: hypodensity over left frontal lobe
otherwise unremarkable

16. Case 2 Diagnosis VF
Post cardiac arrest
Aspiration pneumonia

17. Outlines Cases 1 & 2 (part 1) Mortality data
Post cardiac arrest syndrome
Post cardiac arrest care
Cases 1 & 2 (part 2)
Prognostication
Summary

18. In-hospital mortality
Year
Country
Adults (n)
Rate
Remark
1/2000 to 3/2004
USA
/Canada
36902 (IHCA)
72%
12/1995 to
11/2005 UK
12172 (IHCA)
(OOHCA)
75.2%
71.4%
Admitted to ICU
11/1998
to 2/2002
Canada
1277 (IHCA)
1483 (OOHCA)
69%
65%
JAMA 2006, 295:50-57
Anaesthesia 2007, 62:
Crit Care Med 2007, 35:
UK study: ICU mortality 55-60%

19. KWH ICU 2007 & 2008 N 33
M : F
21 : 12
Age
18 –88 (67)
Post cardiac arrest patients
ICU mortality %
In-hospital mortality 79%
Cardiac arrest (N)
In-hospital mortality
In-hospital
90%
Out-of-hospital 11
55%

20. Outcome of in-hospital cardiac arrest is very poor
The goal of treatment should be to intervene early before the patient deteriorates to develop unexpected arrest

21. 2007 AHA Statistics. Adult OOH cardiac arrest survival = 6
2007 AHA Statistics Adult OOH cardiac arrest survival = 6.3% Australian OOHCA data:
Initial rhythm
survival VF
1-10 %
asystole
1-2 %

22. Survival of OOH CA patients in HK
Hospital
Year of study
Patient
No.
Initial VT/VF
Survival to hospital discharge
KWH
1990 to
1992
263
12% 3%
QMH/TSK
PYNEH
1999
320
14%
4.9%
PWH
2002
(Jul-Dec)
124
18%
0.8%
Journal of Accident and Emergency Medicine 12, 34-39
Hong Kong Med J Vol 8 No 5 October 2002
Hong Kong J. Emerg. Med. Vol. 12(3) Jul 2005

23. Variability between reports on in-hospital mortality
Brief, fleeting or sustained ROSC
Care during transport, ED or ICU
Limitation set on subsequent resuscitation efforts
Timing of therapy withdrawal

24. ROSC
Resumption of spontaneous circulation (ROSC) after prolonged, complete, whole-body ischemia is an unnatural pathophysiological state created by successful CPR

25. over the past half-century, focus was on improving the rate of ROSC
interventions improve ROSC without improving long-term survival
translation of optimized BLS and ALS interventions into the best possible outcomes is contingent on optimal
post– cardiac arrest care

26. Post-cardiac arrest syndrome
brain injury
myocardial dysfunction
systemic ischemia/reperfusion response
the unresolved pathological process that caused the cardiac arrest

27. Post-cardiac arrest syndrome
brain injury
myocardial dysfunction
systemic ischemia/reperfusion response
the unresolved pathological process that caused the cardiac arrest

28. Anoxic brain injury ( 3 phases)
Cardiac Arrest
ROSC
CPR
Low flow
High, normal or low flow
No flow
Cerebral blood flow

30. Brain injury

31. Secondary brain injury
Hypotension
Hypercapnia
Impaired cerebrovascular autoregulation
Brain edema
Pyrexia
Hyperglycemia
Seizure

32. Clinical manifestation
Coma
Seizures
Myoclonus
Cognitive dysfunction
Vegetative state
Secondary parkinsonism
Stroke
Brain death

33. Post-cardiac arrest syndrome
brain injury
myocardial dysfunction
systemic ischemia/reperfusion response
the unresolved pathological process that caused the cardiac arrest

34. Post-cardiac arrest myocardial dysfunction
detectable within minutes
manifest as hypotension, low CI, arrhythmia
stunning phenomenon rather than permanent injury or infarction
responsive to therapy and reversible
Cardiac index values reached their nadir at 8
hours after resuscitation, improved substantially by 24 hours, and almost uniformly returned to normal by 72 hours in survivors
Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest.J Am Coll Cardiol. 2002;40:2110 –2116

35. Post-cardiac arrest syndrome
brain injury
myocardial dysfunction
systemic ischemia/reperfusion response
the unresolved pathological process that caused the cardiac arrest

36. Systemic Ischemia/Reperfusion Response
represent the most severe shock state
inadequate tissue DO2 can persist even after ROSC
because of myocardial dysfunction, pressor-dependent hemodynamic instability, and microcirculatory failure
generalized activation of immunologic and coagulation pathways  endothelial dysfunction, hypercytokinemia
 increase risk of multiple organ failure and infection
manifest as intravascular volume depletion, impaired vasoregulation, impaired oxygen delivery and utilization, increased susceptibility to infection

37. Post-cardiac arrest syndrome
brain injury
myocardial dysfunction
systemic ischemia/reperfusion response
the unresolved pathological process that caused the cardiac arrest

38. Unresolved Precipitating Pathology
Cardiovascular disease
CAD accounts for two thirds of sudden cardiac deaths
Pulmonary disease (COPD, asthma)
CNS disease (CVA)
Thromboembolic disease (PE)
Toxicological (overdose, poisoning)
Infection (sepsis, pneumonia)
Hypovolemia (hemorrhage, dehydration)

39. Post-cardiac arrest care
time sensitive, both in and out of the hospital
multidisciplinary team execute a comprehensive clinical pathway tailored to available resources
a spectrum of patients, ranging from the awake, hemodynamically stable survivor to the unstable
comatose patient with persistent precipitating pathology
focus on reversing the patho-physiological
manifestations of the post– cardiac arrest syndrome with proper prioritization
Avoid premature withdrawal of care before long-term prognosis can be established

40. Therapeutic Strategies
General Measures
Monitoring
Oxygenation and Ventilation
Hemodynamic Optimization
Circulatory Support
Managing Underlying Pathology
Therapeutic Hypothermia
Seizure Control and Prevention
Glucose Control
Infection Management
Long-Term Rehabilitation

41. Monitoring options General intensive care monitoring Arterial catheter
Oxygen saturation by pulse oximetry
Continuous ECG
CVP
ScvO2
Temperature
Urine output
Arterial blood gases
Serum lactate
Blood glucose, electrolytes, CBC, and general blood sampling
CXR
More advanced hemodynamic monitoring
Echocardiography
Cardiac output monitoring (either noninvasive or PA catheter)
Cerebral monitoring
EEG (on indication/continuously): early seizure detection and treatment
CT/MRI

42. Management after cardiac arrest

43. Airway and ventilation
Intubation / Airway protection
PaCO2
Although cerebral autoregulation is either absent or dysfunction, cerebrovascular reactivity to changes in arterial carbon dioxide
tension appears to be preserved
Minimal FIO2 to maintain SaO %

44. Circulation early hemodynamic optimization
restoring and maintaining the balance between systemic oxygen delivery and demands
initiation of monitoring and therapy asap and achievement of goals within hours of presentation
Early goal-directed
hemodynamic optimization

45. ↓

46. EGDHO within 6 hr
Resuscitation 2009,80: 418–424

47. STEMI : Restoration of coronary perfusion is a priority
Primary PCI is preferred over thrombolysis
Prior CPR is not a contraindication to thrombolysis
Non-cardiac arrest patient
Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. The Lancet 2003; 361, 9351

48. Management of STEMI in post cardiac arrest patient
early primary PCI
average intervals from symptom onset or CPR to balloon inflation : 2 to 5 hours
angiographic success rates : 78% to 95%
overall in-hospital mortality: 25% to 56%
Circulation 2007;115:
Resuscitation. 2007;74:227–234

49. Post cardiac arrest patients with STEMI undergo PCI
Resuscitation (2007) 72, 379—385

50. Outcome of comatose & conscious survivors of cardiac arrest with STEMI
Resuscitation (2007) 72, 379—385

51. Predictors of 6-month survival after emergency PCI in resuscitated patients after cardiac arrest complicating AMI
Circulation 2007;115:

52. NSTEMI in post-cardiac arrest
PCI is normally delayed until more information on neurological outcome is available
However, survivors from OOHCA without obvious non cardiac causes of cardiac arrest show a high prevalence of acute coronary occlusions, which are predicted poorly by clinical and electrocardiographic findings .

53. Survivors from OOHCA
77% of all survivors of OOHCA with presumed cardiac origin
underwent immediate coronary angiography, which revealed
CAD in 97%
of these, 80% had total occlusion of a major coronary artery.
Nearly half of these patients underwent reperfusion interventions, with the majority by PCI
Results:
overall in-hospital mortality rate 72%  44% (P< 0.001) after introduction of a comprehensive post– cardiac arrest care
90% of survivors were neurologically normal
Early PCI in patients after cardiac arrest without STEMI but with suspected acute coronary symptom
Resuscitation. 2007;73:29 –39
Current Opinion in Critical Care 2008,14: 305– 310

54. Control temperature

55. Control temperature
Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome
# If cooling not possible, prevent hyperthermia
Risk highest 48 hours after resuscitation
Poorer neurologic outcome each 1 °C > 37°C
Treatment: Antipyretics or active cooling
Arch Int Med 2001;161(16)

56. Hypothermia protects from ischemia-reperfusion injury
Postulated mechanisms:
Reduction in cerebral O2 consumption
Retard destructive enzymatic reactions
Suppress free radical reactions
Protection the fluidity of lipoprotein membranes
Reduction of O2 demand in low flow region
Reduction of intracellular acidosis
Inhibit biosynthesis, release & uptake of excitatory neurotransmitters

57. Therapeutic hypothermia
a standardized treatment strategy for comatose survivors of cardiac arrest
increase survival rates
improve neurological outcome

58. Two Landmark Studies

59. Hypothermia asso. lower CO, higher SVR and hyperglycemia
T 33.5 C
within 2 hr
Lasted 12 hr
Hypothermia asso. lower CO, higher SVR and hyperglycemia
SA Bernard et al. NEJM 2002; 246(8)

60. Good neurological outcome ( CPC 1 & 2 ) unadjusted OR 2.65 (p=0.046)
49% vs 26% p=0.046
unadjusted OR (p=0.046)
adjusted** OR (p= 0.011), LR** age & time (collapse  ROSC)

61. 32-34 C
Within 4 hrs
Lasted 24 hrs
Rewarm 8hr

62. Inclusion in HACA Initial pulseless VT / VF Witnessed arrest
Presumed cardiac origin of arrest
Age 18-75
collapse to CPR : <15 min
collapse to ROSC : <1hr

63. Exclusion in HACA <30 C
Coma before cardiac arrest, persistent hypotension, or hypoxemia >15 min after ROSC

64. HACA

65. Meta-analysis on long and short- term neurological recovery
NNT = 6
Crit Care Med. 2005;33(2):

66. Impact of therapeutic hypothermia & duration of cardiac arrest
Irrespective to presence of shock or initial rhythm, the predicted benefit of TH strong dependent on duration of cardiac arrest
Oddo M. Crit Care Med 2006;34(7):1885

67. Therapeutic Hypothermia
Only therapy shown to increase survival
?? Ideal patients, technique, target temperature,
duration, and rewarming rate not yet
established
Neuroprotection may decrease as the delay
in initiation of therapy increases
Time to target temperature = 2 to 8 hours

68. Patient selection Duration of cardiac arrest Initial arrest rhythm
treat all VF
treat non-VF if short duration of cardiac arrest
Circulatory shock
not a contraindication

69. Not suitable candidate
Improving neurological state after ROSC
Arrest due to non-cardiac factors ( CVA / Drug overdose)
Severe coagulopathy
Pregnancy

70. Therapeutic Hypothermia
Induction
Maintanence
Rewarming

71. Therapeutic Hypothermia: Induction
“Auto-cooling” within 1st hour
Ice chilled cold fluids (30 ml/kg NS or LR)
Ice packs (head, neck, axilla, groin)
Shivering prevention (sedation, NMB)

72. Therapeutic hypothermia: Maintenance
Continuous temperature feedback
Surface or internal cooling
Cooling blankets or pads
Convective air cooling device (Polar Air)
Central Intravascular cooling catheters
Cold wet blankets and ice
(time consuming and less reliable)
CRRT
Cold fluid infusions alone are not adequate
Lasted 12 to 24 hours

73. Therapeutic hypothermia: Rewarming
Passive rewarming
Active rewarming
Internal or external devices
Other heating systems
Goal 0.25 °C – 0.5 °C ↑ per hour
Careful monitoring
Plasma electrolyte concentrations
Hemodynamics

74. Complications of mild hypothermia
Increase infection
Cardiovascular instability
Coagulopathy
Hyperglycemia
Increase plasma amylase
Hypophosphatemia & hypomagnesemia

75. Seizure & Myoclonus
occur up to 1/3 of adult after ROSC during the hospital course
Commonly within first 24hr
Strong association of status epilepticus with mortality
Myoclonus associated with poor outcome
Treat seizure promptly & effectively
No studies that directly addressed the use of prophylactic anticonvulsant drugs after cardiac arrest
Maintenance therapy after the first event once
Exclude potential precipitating causes (e.g. intracranial haemorrhage, electrolyte imbalance, etc)

76. Seizure & Myoclonus Myoclonus phenytoin : ineffective
Clonazepam : most effective
sodium valproate and levetiracetam also effective
Shivering may require the use of sedation or neuromuscular blocking drugs
Continuous EEG monitoring for patients requiring sustained neuromuscular blockade

77. Glucose Control
Strong association between high blood glucose after resuscitation from
cardiac arrest and poor neurological outcome
Persistent hyperglycaemia after stroke is associated with a worse neurological outcome

78. Glycemic control vs mortality in ICU setting (1)
Patients group
Study type
outcome
key results
All adults [N=1548] admitted to the surgical ICU unit Feb Jan 2001.
Groups:
Intensive insulin therapy [N=765] (glucose maintained mmol/l) vs
Conventional insulin therapy (glucose maintained mmol/l)[N=783]
Prospective randomised controlled trial
ICU mortality
In-hospital mortality
4.6% (N=35) vs 8% (N=63)
(p<0.04)
7.2% (N=55) vs
10.9% (N=85)
(p=0.01)
Van den Berghe G et al. Intensive insulin therapy in critically ill patients
NEJM 2001; 34(19)

79. Glycemic control vs mortality in ICU setting (2)
Patients group
Study type
outcome
key results
1200 adult patients admitted to medical ICU for ≥ 3 days.
Groups:
Strict glucose control ( mmol/l) N=595] vs
Conventional therapy (insulin administered when glucose >11.9mmol/l) [N=605]
Prospective randomised controlled trial
In-hospital mortality
No significant association 37.3% (N=222) vs 40% (N=242) (p=0.33)
ICU mortality
No significant association 24.2% (N=144) vs 26.8% (N=162) (p=0.31)
ICU mortality in patients admitted ≥3 days
43.0% (N=166) vs 52.5% (N=200) (p=0.009)
Van den Berghe et al. Intensive Insulin Therapy in the Medical ICU
NEJM 2006; 354 (5);

80. Losert H et al. (Austria) Strict normoglycemic control within 12hr after cardiac arrest might not be necessary
Patients group
Study type
outcome
key results
234 patients
witnessed VF or pulseless VT cardiac arrest with ROSC therapeutic cooling x 24hr,
Aged years,
Non-diabetic,
Grouped by 12 hour glucose:
mmol/l [N=58] vs
mmol/l [N=59] vs
mmol/l [N=48] vs
mmol/l [N=39]
Retrospective analysis of prospective multi-centre trial on mild
therapeutic hypothermia
Good neuro-
Recovery
(CPC 1-2)
at 6 m
64% vs 75% vs 29% vs 18% (p<0.001)
OR of good recovery at 6m
8.05 (95% CI ) vs (95% CI ) vs 1.88 (95% CI ) vs 1
Survival at 6m
78% vs 76% vs 42% vs 31% (p<0.001)
Resuscitation 2008 Feb;76(2):

81. Losert weakness
Potential inter-laboratory glucose imprecision as multi-centre trial.
Study cannot comment on hypoglycaemic incidence as one-off 12 hour blood glucose measurements used.
Study can only comment on non-diabetic patients.
Underestimate of diabetics as diagnoses assumed from medical notes, not verified with HbA1C.
Retrospective analysis of previous multi-centre trial unable to determinine optimal glucose level or comment on causality.

82. Modest glucose control avoid hypoglycemia Oksanen T et al. (Finland)
Patients group
Study type
outcome
key results
99 patients OHH VF cardiac arrest with ROSC treated with therapeutic hypothermia.
Groups:
strict glucose control (blood glucose 4-6 mmol/l) (N=39) vs moderate glucose control (6-8 mmol/L) (N=51)
Randomised
controlled trial
Mortality at 30 days
No significant association
33% (N=13) vs 35% (N=18) (p=0.846)
Moderate hypoglycaemia (<3mmol/l)
18% (N=7) vs
2% (N=1) (p<0.01)
Severe hypoglycaemia (<2.2mmol/l)
0% vs 0%
Intensive Care Medicine 2007; 33,

83. Oksanen weakness
Similar glucose levels between groups. Ethical issues prevent groups being randomized to blood glucose levels >8 mmol/l.
Groups not blinded.
Study ceased prematurely due to small mortality differences between groups. Small sized study groups with only ~10% power to detect ~8% mortality difference

84. Glucose Control in post cardiac arrest patient
Clinical bottom line
mmol/L
glucose trigger insulin therapy?
monitor blood glucose frequently
avoid hypoglycemia and hyperglycemia

85. Implement of PCAR care protocol
N=137 OHHCA
Observational study comparing prospective case period with retrospective control period in Norway
All were admitted to ICU
Rx protocol: TH
Reperfusion by PCI
Hemodynamic control
Seizure
Ventilation
Glucose 5-8 mmol/L
Implementation of a standardised treatment protocol for post resuscitation care after
out-of-hospital cardiac arrest. Sunde et al. Resuscitation 2007 ;73:29-39

87. Interventonal period (n=61)
Control period (n=58)
P value
Age <70
71%
48%
0.022
Male
82%
79%
0.89
Glucose at 12hr
(mmol/L)
8.0 +/- 3.5
9.7 +/- 3.3
0.033
Glucose at 24hr
6.4 +/- 1.6
7.5 +/- 2.7
0.028
Temp at 12 hr
33.9 +/- 1.7
37.5 +/-1.1
<0.001
Temp at 24 hr
34.0 +/- 1.9
38.4 +/- 1.3
Therapeutic
hypothermia
66% 0%
< 0.001
Reperfusion
49%
3 %
p<0.001

88. Interventonal period
(n=61)
Control period (n=58)
Favourable neurological outcome
at discharge
56%
31%
OR 3.61
95% CI
p= 0.001
Survival to discharge
26%
OR 2.8
95% CI
p=0.007
Survival
at 1 yr
P=0.001

89. Limitations Single centre Hawthorne effect Age might be a confounder
Non-randomized
Improved survival may be a result of a total improvement across the entire
chain of survival
Increased focus, enthusiasm, and introduction of new treatment strategies
generally improve quality and outcome

90. Case 1 Progress Diagnosis on ICU admission: Post cardiac arrest
Acute inferior MI
DKA
Aspiration pneumonia

91. Case 1 DOA on 5/6 Medications: Aspirin, PPI IV amiodarone
Dopamine, morphine infusion
IV insulin, IV Sodium bicarbonate
IV Augmentin
Metoprolol (6/6), enteral feeding
Hypothermia
(33-34C) x 12hr
Last over 48 hr (at 36C because of fever)

92. Case 1 ICU Progress D1 D2 D3 D4 D5 Temp 35.6 34 37.8 37.6 37.3 36.4
37.8
37.6
37.3
36.4
GCS
(EMV)
1/1/1
3/3/1
2/1/1
Pupils
4/4
fixed
3/3
brisk
5/3
4/3
MAP 82 84
100 74 85
H’stix
32.2
8.0
7.9
12.2
9.2
Dopamine + -
morphine
Day 3 CT brain: hypodensity at brainstem and cerebellum
CT brain
Extubated

93. Case 1

94. Case 1 General ward (3 weeks)
DM control
14/6 FU CT brain
16/6 AROU, E. coli UTI, Rx Augmentin
GCS 7/15 ( E4M2V1)
To WTSH on 3/7/08
Outcomes:
Survived to hospital discharge Vegetative

95. Case 2 progress
Dx : VF
Post cardiac arrest
Aspiration pneumonia

96. A&E  ICU (4.1) D1 D2 D3 D4 D5
Temp.
34.7
38.3
35.9
36.6
37.6
35.6
EMV
1/4/1 4/4/1
2/1/1
4/2/1
2/2/1
Pupils
3/3 S
3/3 B
3/3 S
4/4 B
4/4
MAP 91 98
106
103 97
H’stix
19.3
7.4
5.9
7.6
4.1
Seizure + -
Dopamine
Dormicum
+/-
CT Brain
CT Brain
CT Brain
Case 2

97. CT brain follow up on D4 Case 2
CT brain (D1): hypodensity over left frontal lobe
Case 2

98. ICU Mx Mechanical ventilation
Therapeutic hypothermia D1, cooling blanket all along (fever)
Correction of K
IV Augmentin
Glycemic control
Seizure control
Case 2

99. Progress in ICU (1 week) 9.1 percutaneous tracheostomy 11.1
Remained vegetative, GCS 2/4/1
Tracheostomy mask 40% O2
Normal RFT/ LFT
To general ward
Case 2

100. Toxicology Urine (by HPLC) Ranitidine Phenytoin Paracetamol
Ciprofloxacin
Some were unidentified
Empty bottle by name
Cefprozil
An orange oval pill
( by HPLC and GC)
nifedipine

101. In general ward Cardiac team  Amiodarone > ICD for recurrent VF
Episode of GTC
Recurrent fever: rocpehin /flagyl levofloxacin( twitching) sulperazone
Septic work-up ( CSU, line/ tracheal aspirate) –ve
No neurological recovery, GCS 7/15
Case 2

102. On 22.1.08 Outcome: In-hospital mortality
Desaturation followed by cardiac arrest within an hr.
PEA CPR (x 20min)
Outcome:
In-hospital mortality
Case 2

103. Poor outcome was defined as
death or persisting unconsciousness after 1 month or
severe disability requiring full nursing care after 6 months
Neurology 2006;67:

104. Prognostication
clinical circumstances of the cardiac arrest and resuscitation
patient characteristic
neurologic examination
electrophysiologic studies
biochemical markers
neuroimaging

105. 1. Circumstances surrounding CPR
Association between peri-arrest factors
outcomes
first monitored rhythm
no flow time (arrest to start of CPR)
duration of CPR
False +ve rate: %
Age
Comorbidity B

106. 2. Neurological examination
motor component of the GCS
brainstem reflexes (pupil light reflexes corneal reflexes )
presence of convulsions or myoclonic status epilepticus
to consider pathologic (hypotension, shock, severe metabolic abnormalities) or clinical interventions (paralytics, sedatives, and hypothermia) that will alter or mask the presentation of neurologic signs

107. Most reliable predictors for poor outcome
On day 3 after CPR
absence of the pupillary light response
(FPR on first 24hr : 18-36%)
absence of corneal reflex
Glasgow motor score ≤ 2 (i.e., extensor or absent)
Within day 1
myoclonic status epilepticus :
spontaneous, repetitive, generalised multifocal clonus involving the face, limbs, and axial musculature in comatose patients
Single convulsions and sporadic focal myoclonus do not predict poor outcome accurately A B

108. 3. Electroencephalogram
Strong but not invariably asso. poor outcome:
Generalised suppression to < 20μV,
burst-suppression pattern with generalised epileptiform activity, or
generalised period complexes on a flat background
#Malignant EEG pattern had FPR for poor outcome 3% (95% CI: 0.9% to 11%).
Timely access to EEG recording and interpretation may be a problem on many ICU
presence or absence of a burst-suppression pattern and of epileptiform activity
(absent, sporadic, frequent, status). C

109. 4. Somatosensory evoked potentials
the first cortical response (N20 component) of SSEPs with median nerve stimulation is the best studied waveform
minimally influenced by drugs and metabolic derangements
predicting poor outcome in comatose patients within 3 days after cardiac arrest
FPR of 0.7% (95% CI: 0.1 to 3.7) for poor outcome by meta-analysis
absence of the N20 during the first week:
positive likelihood ratio of 12 (95%CI 5.3–27.6) for poor outcome
presence of the N20 response is not helpful in predicting outcome as reflected in a pooled sensitivity of only 46%
test the integrity of the neuronal pathways from a peripheral nerve, spinal cord, brainstem, & cerebral cortex B

110. 5. Neurological biochemical markers
NSE
S-100
is a dimeric acidic calcium-binding protein present in high concentrations in glial cells and Schwann cells
CK-BB
neurons and astrocytes

111. Neuron-specific enolase (NSE)
located in neurons and neuroectodermal cells
peaks in the serum and CSF at 72 h after injury
the cut-off points range from 20 to 65 μg/dl
60% of 231 patients had NSE 33 g/L at day 1 to 3 after CPR. All these patients had a poor outcome
(FPR of 0, 95% CI: 0 to 3)
a decrease in NSE levels between 24 and 48 h has been associated with good neurologic outcome after OHCA in patients treated with hypothermia (Oksanen. ICM 2007)
NOT RELIABLE:
variability in trial designs,
sampling times,
cut-off levels.
Related to the biologic aspect of NSE and the regions of the brain
that are injured during cardiac arrest:
The level of serum NSE reflects the volume of neuronal injury, irrespective
of the location and function of the neuronal population.
With the greatest neuronal mass in the cortex, serum NSE largely reflects cortical
injury which may or may not have a direct impact on recovery
of arousal.
Smaller areas with critical roles in arousal, such as the midbrain or thalamus, may be injured with little spillage of NSE.
Specificity 100% ,sensitivity ~50% B

112. 6. Radiological studies U
Not enough evidence to define lesions that would predict poor outcome with precision
on CT, MRI and nuclear magnetic resonance spectroscopy
25 comatose post cardiac arrest patients were compared with the scans of normal controls :
A difference in GM/WM ratio of < 1.18 at the basal ganglia level was 100% predictive of death.
This single study is not enough to recommend CT scanning as a means of predicting outcome in
individual cases U

113. In 2006, AAN practice parameters provided prognostication on poor outcome in nonhypothermia-treated patients

114. Effect of induced hypothermia
modify the course of brain injury
delay the clearance of sedatives/NM drugs
which may mask neurological recovery
delay the recovery of motor responses by up to 6 days
motor responses no better than extension at day 3 regained awareness, giving a FPR of 14% (95% CI: 0. 03– 0.44)
Predictors of poor neurologic outcome after induced mild hypothermia following cardiac arrest. Neurology 2008;71:1535–7.

115. SSEPs and NSE predict functional outcome after therapeutic hypothermia
Bilateral absence of cortical N20 responses predicted permanent coma, with specificity 100% (95% CI: 92–100%), sensitivity of 75% (95% CI: 30–95%) in the hypothermia group and 80% (95% CI 49–94%) in the normothermia group
Curr Opin Crit Care :261–268
TH-treated patients had lower serum NSE over the first several days after cardiac arrest, &
associated with better functional outcome than normothermic gp Oksanen. ICM 2007

116. Proposed strategy in hypothermia- treated patients
After ROSC
24hr
48hr
72hr
Neurology 2006;66:62–68

117. Summary
Post-cardiac arrest syndrome is characterized by ROSC after prolonged complete whole body ischemia
Therapeutic mild hypothermia which improve neurological recovery and mortality is now a standard of care in selective patients
Growing evidence of modest glycemic control improving outcomes
Care bundle concept on post cardiac arrest care should be