hypothermic resuscitation
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Hypothermic Resuscitation
Sombat Muengtaweepongsa M DSombat Muengtaweepongsa, M.D.Division of NeurologyFaculty of Medicine
Thammasat UniversityThammasat University
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ScopeScope• Therapeutic hypothermia after cardiac arrest• Therapeutic hypothermia in ischemic strokeTherapeutic hypothermia in ischemic stroke• Fever control in critical care neurology
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2005 ILCOR2005 ILCOR
• There seems to be good evidence (level 1) to recommend the use of induced )mild hypothermia in comatose survivors of-out-hospital cardiac arrestsurvivors of out hospital cardiac arrest caused by VF.
Level 1 evidence indicates one or more randomized clinical trials in which benefit was shown
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Therapeutic Hypothermia after CardiacTherapeutic Hypothermia after Cardiac
Arrest
(N Engl J Med 2002;346:557-63.)
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Th RCT f TH ft di tThe RCT of TH after cardiac arrest
HACA (European) Bernard trial (Australia)
Sample N=275 N=77Cooled verses normothermia
137 cooled138 normothermia
43 cooled34 normothermia
Intervention Cooling blankets and ice packs
Ice packs
Target temperature 32-34 degrees 33 degreesInitiation Prehospital ERpDuration 24 hours 12 hoursFollow up 6 months 30 daysFollow up 6 months 30 days
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BenefitBenefit
• NNT of 7 to prevent 1 death with TH• NNT of 6 to reduce neurologicNNT of 6 to reduce neurologic
impairment with TH
The NNT is the number of patients who need to be treated in order to prevent one additional bad outcome
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Ad E tHACA study group, 2002. New England Journal of
Medicine 346(8).
Adverse Events• Bleeding, pneumonia, sepsis, pancreatitis,
renal failure, pulmonary edema, seizures, , p y , ,arrhythmias and pressure sores were recorded in both trials with no significant gadverse events.
“ Sepsis was more likely to develop in the patients ith h pothermia than those in normothermiawith hypothermia than those in normothermia,
although this difference was not statistically significant” (HACA study group 2002)significant (HACA study group, 2002)
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Sid ff t f d t h th iSide effects of moderate hypothermia on various organ systems
Variable Normothermia Hypothermia After-rewarming
Plt tPlt count 183 (145-310) 110 (20-180) 160 (50-210)
aPTT 27 (20-45) 34 (25-50) 30 (20-55)
lipase 140 (60-190) 250 (140-1200) 200 (135-1000)
K+ 4.1 (3.5-4.7) 3.4 (3.1-3.9) 4.4 (4.0-5.2)K+ 4.1 (3.5 4.7) 3.4 (3.1 3.9) 4.4 (4.0 5.2)
Na+ 139 (134-145) 140 (138-150) 145 (139-155)
C ClCr Clearance 81 (60-100) 65 (45-90) 70 (45-95)
Norepinephrine 0 0.32 (0.0-0.45) 0.08 (0.0-0.24)
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What is the purpose of TH?What is the purpose of TH?• Aimed at minimizing the effects of
anoxic neurologic injury following g j y gcardiac arrest
• Other than supportive care TH it is the• Other than supportive care TH it is the only identified measure to improve
f fquality of life post resuscitation
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So why is TH notSo why is TH not done more often?
Both of these studies involved a highly selected group ofpatients, excluding up to 92% of patients with out-of-hospitalcardiac arrest initially assessed for eligibility
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Suggested Inclusion Criteriagg• TH is indicated if the patient meets all of the
following criteria:following criteria:1. Witnessed arrest2. Initial rhythm VF or pulseless VT…. But3. Time to ACLS was less than 15 minutes and total
of ACLS time less than 60 minutes4. GCS of 8 or below4. GCS of 8 or below5. SBP of > 90 with or without vasopressors6 Less than 8 hours have elapsed since return of6. Less than 8 hours have elapsed since return of
spontaneous circulation (ROSC)
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Suggested Exclusion Criteriagg1. Pregnancy2. GCS 10 and improving3. Down time of > 30 minutes4. ACLS preformed for > 60 minutes5 Known terminal illness5. Known terminal illness6. Comatose state prior to cardiac arrest7 P l d h t i (i MAP 60 f 307. Prolonged hypotension (ie MAP < 60 for >30
minutes)8. Evidence of hypoxemia for > 15 min following
ROSC9. Known coagulopathy that cannot be reversed
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M h i f t ti bMechanisms of neuroprotection by hypothermia
• counteract ischemic brain damage by several mechanisms– prevention of the blood–brain-barrier
disruptiondisruption– oxygen-based free-radical production excitotoxicneurotransmitter release– excitotoxicneurotransmitter release
– anti-inflammatory action– delayed apoptosis
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Historical ObservationsHistorical Observations
• Not Dead till Warm and Dead– Cold patients would wake up in the Morguep p g
• Kids / Hockey Players- fall through ice, long rescue times but good recoverylong rescue times, but good recovery
• Hibernation: state of low oxygen, acidosis, yglow energy supply
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Ideal temperature curve
Induction
erat
ure
Rewarming
Tem
pe Sustainment Rewarming
Timee
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Methods to Control Brain Temperature in Stroke
PatientsPatients
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Methods of CoolingMethods of Cooling
• Selective head cooling– Cooling helmet: ineffective in adultg
• Internal cooling by intravenous and intraarterial ice cold salineintraarterial ice-cold saline– Need large volume
• Surface cooling• Endovascular cooling• Endovascular cooling
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Surface blanketSurface blanket
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Surface coolingSurface cooling
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Surface coolingSurface cooling
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Figure 1. The Reprieve Endovascular Temperature Management System
De Georgia, M. A. et al. Neurology 2004;63:312-317
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Endovascular catheterEndovascular catheter
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Intravascular Hypothermic Machine
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Intravascular Hypothermic Catheter
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Thermoregulatory Defenses Against Hypothermia
• Vasoconstriction– Primary autonomic defensesy– Threshold: 36.5o C
• Shivering• Shivering– “last resort” response– Threshold: 35.5o C
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Introduction of thermoregulatory tolerance
• Nonpharmacological treatments– Whole body surface warmingy g
• Pharmacological treatmentsA th ti d M l l t– Anesthetics and Muscle relaxants
– Meperidine– Drug combination
• Meperidine and Buspironep p• Meperidine and Dexmedetomidine
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Reductions in the shivering threshold (compared with the control day) for the dexmedetomidine (Dex), meperidine (Mep), and 2-drug combination (Combo) days
Copyright ©2003 American Heart Association
Doufas, A. G. et al. Stroke 2003;34:1218-1223
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RewarmingRewarming
Th t iti l i d f i k l t d t• The most critical period of risk related to therapeutic hypothermia
• Vasodilation• Hypermetabolic responseHypermetabolic response
– Systemic inflammatory response syndrome (SIRS)(SIRS)
• Passive controlled rewarmingSt i i t 0 1 0 5 oC h– Stepwise rewarming rate: 0.1-0.5 oC per hr
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RewarmingRewarming
C b l id ff t• Cerebral side effects– Rebound edema and ICP elevation
E b l id ff• Extracerebral side effects– Infection
P i• Pneumonia• Sepsis
– CardiopulmonaryCardiopulmonary• Elevation of catecholamines: arrhythmia
– Hematologic• Induced thrombosis
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Therapeutic Hypothermia for
Ischemic StrokeIschemic Stroke
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A case scenarioA case scenario
69 y/o woman presented to an outside h it l ith dd t f i ht id dhospital with sudden onset of right sided weakness and speech impairment. She arrived at the OSH at 20 minutes after onset. CT-brain was negative. TPA wasonset. CT brain was negative. TPA was started at 90 minutes after the onset before she was transferred to SLUHbefore she was transferred to SLUH.
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A case scenario (cont )A case scenario (cont.)
Sh l t d k b t h iShe was alert and awake, but aphasic. NIHSS was 8 with:
LOCb 2, partial hemianopiapartial hemianopia, right arm drifting, some effort against gravity on right legsome effort against gravity on right leg, partial sensory loss on the left sidemoderate aphasiamoderate aphasia.
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A case scenario (cont )
With t ith i t b ti d ti
A case scenario (cont.)
Without either intubation or sedation, therapeutic hypothermia with endovascular cooling technique was started at 5 hours after onset. Target core temperature of 33oC was reached within 3 hrs. Shivering was under control with combination of surface warming and meperidine plus buspirone. Gradual p p prewarming was applied after target temperature was maintained for 24 hrs.
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Temperature and stroke
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For each 1 degrees C increase in body temperature the relative risk of poor outcome rose by 2.2 (95of poor outcome rose by 2.2 (95 percent CI 1.4-3.5) (p less than 0.002).
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She was discharged to a rehab after 5 days of admission with NIHSS of 5 and mRS of 3.
At day 30 She walked by herself to followAt day 30, She walked by herself to follow up at DOB. NIHSS was only 3 including
Shemianopia and partial sensory loss. mRS was 2.
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Hypothermia for MalignantHypothermia for Malignant MCA Infarction
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Fever-related Brain Injury in the
C b l I f tiNeuro-ICU
• Cerebral Infarction• Elevated temperature is associated with
t ft t kpoor outcome after strokeHajat et al, Stroke 2000;31:410
• Subarachnoid Hemorrhage• Subarachnoid Hemorrhage• Fever burden independently associated with
mortality & poor functional outcome.y pMayer et al, Crit Care Med 2003 (Suppl);30:A5
• Intracerebral HemorrhageD ti f f ( 37 5° C) ithi th fi t• Duration of fever (>37.5° C) within the first 72 hours is independently associated with poor outcomeSchwarz et al, Neurology 2000;54:354
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Treatment of fever in the neurologic intensive care unit with a th t b d h t h tcatheter-based heat exchange system
Diringer MN, CCM 2204;32:559
• 296 patients with T ≥38° C for at least 2 ioccasions
– SAH, TBI, ICH and cerebral infarction• Alsius Cool Line endovascular heat exchange• Alsius Cool Line endovascular heat exchange
catheter plus standard surface cooling• Fever Burden >38 °CFever Burden 38 C
– 7.92 °C-hours – 2.87 °C-hours
64% relative reduction (P<0.01)
• Shivering “of concern” in four patients (3.7%)
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Clinical Trial of a Novel Surface Cooling System for Fever Control in Neurocritical Care Patientsfor Fever Control in Neurocritical Care PatientsMayer, et al, Crit Care Med 2004
• 47 patients with T ≥38.3° C for >2 consecutive hours after receiving acetaminophen
Median GCS 8 0– Median GCS 8.0– SAH, ICH, infarction, TBI– Mean 42 hours >38 3° C prior to– Mean 42 hours >38.3 C prior to
randomization• Interventions
– Standard SubZero cooling blanket– Medivance Artcic Sun surface cooling
system• Main outcome measure
24 h f b d– 24 hour fever burden
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Clinical Trial of a Novel Surface Cooling System for Fever Control in Neurocritical Care Patients
P=0.001
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Change in Glasgow Coma ScaleChange in Glasgow Coma Scale
P=.038, GEE model
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ConclusionConclusion
• TH is a standard treatment in selected patients after cardiac arrest.p
• TH should be benefit for penumbra salvaging in acute ischemic strokesalvaging in acute ischemic stroke.
• TH is one of treatments for increase ICP.• Fever control is essential, particularly in
such a bad neurological conditionssuch a bad neurological conditions.
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Take home messageTake home message
“ No evidence” doesn’t meandoesn t mean
“Evidence does not exist”.
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Thank you for your attentionThank you for your attention