traumatic subarachnoid hemorrhage 4fi ri 尤彥棻 feb.13, 2006
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Traumatic Subarachnoid Traumatic Subarachnoid HemorrhageHemorrhage
4FI Ri 4FI Ri 尤彥棻尤彥棻Feb.13, 2006Feb.13, 2006
Head-injured patientsHead-injured patients reached ED alivereached ED alive
25%25%
10%10%
Have lesions requiring Have lesions requiring neurosurgical neurosurgical evacuation evacuation
Severe brain injurySevere brain injury
Severe Head Injury (1)Severe Head Injury (1)
Severe Head Injury (2)Severe Head Injury (2)
Presenting with a GCS score of 8 or less at Presenting with a GCS score of 8 or less at the acute presentation the acute presentation after injury.after injury.
Severe head injury as TBI manifested by a Severe head injury as TBI manifested by a postresuscitationpostresuscitation GCS of 8 or less within 4 GCS of 8 or less within 48 hours. 8 hours.
Initial resuscitation of Initial resuscitation of patient with severe head patient with severe head injuryinjury
J Neurotrauma 17:465, 2000.J Neurotrauma 17:465, 2000.
Traumatic SAHTraumatic SAH SAH: Blood within CSF and SAH: Blood within CSF and meningeal intima meningeal intima 30%-40% of severe 30%-40% of severe traumatic brain injury traumatic brain injury TSAH TSAH
– convexity of the cerebral hemisphereconvexity of the cerebral hemisphere– Presence of contusions and SDHPresence of contusions and SDH– Basal cisterns were less involvedBasal cisterns were less involved
Rosen's Emergency Medicine p. 310J Neurosurg 85: 82-89, 1996J Neurosurg 85: 82-89, 1996
Traumatic SAHTraumatic SAH
SAH found on head injurySAH found on head injury– Increase the severityIncrease the severity (more skull fr and contusion)(more skull fr and contusion)– Unfavorable outcome Unfavorable outcome With SAH:60% With SAH:60% Without SAH:30%Without SAH:30%
Management of TSAH Management of TSAH (1)(1)
Keep at bedrestKeep at bedrest Check GCS, Vital signs, neurological deficitCheck GCS, Vital signs, neurological deficit ICP and BPICP and BP
– Cerebral perfusion pressure (CPP=MAP-ICP)Cerebral perfusion pressure (CPP=MAP-ICP) (CPP control above 70-80mmHg)(CPP control above 70-80mmHg)
(1) ICP Monitor(1) ICP Monitor– BP control (SBP<140) BP control (SBP<140) (↓rebleeding, ↑infarction)(↓rebleeding, ↑infarction)– Avoid direct vasodilator; Labetalol is preferredAvoid direct vasodilator; Labetalol is preferred
J Trauma 30:933-941, 1990 Uptodate: SAH management
Management of TSAH Management of TSAH (2)(2) (2) No ICP Monitor (2) No ICP Monitor
– Withheld Withheld antihypertensive antihypertensive – unless severe elevation in BPunless severe elevation in BP– cerebral ischemia and compensatory nature of acute hycerebral ischemia and compensatory nature of acute hy
pertensionpertension Constant hemodynamic monitoring. Constant hemodynamic monitoring. Analgesia (↓hemodynamic fluctuations) Analgesia (↓hemodynamic fluctuations) Stool softeners Stool softeners Transcranial Doppler measurements (baseline)Transcranial Doppler measurements (baseline)
Management of TSAH Management of TSAH (3)(3) Seizure prophylaxisSeizure prophylaxis
– minimized whenever possibleminimized whenever possible– AED exposure may be associated with worAED exposure may be associated with wor
se neurologic and cognitive outcome after se neurologic and cognitive outcome after SAHSAH
Prevent delayed ischemia?Prevent delayed ischemia?– Monitor with transcranial doppler (TCD)Monitor with transcranial doppler (TCD)
Stroke 2005; 36:583
Does Delayed Vasospasm HaDoes Delayed Vasospasm Happen in Traumatic Subarachppen in Traumatic Subarach
noid Hemorrhage?noid Hemorrhage?
Factors of vasospasmFactors of vasospasm
Site of subarachnoid blood (location of spSite of subarachnoid blood (location of spasm)asm)
Massive SAHMassive SAH Direct stretching or mechanical irritation oDirect stretching or mechanical irritation o
f the cerebral arteriesf the cerebral arteries
J Neurosurg 84:762-768, 1996J Neurosurg 84:762-768, 1996
Vasospasm in TSAH and Vasospasm in TSAH and ASAHASAH
Vasospasm inVasospasm in
Traumatic SAHTraumatic SAHVasospasm in Vasospasm in Aneurysmal SAHAneurysmal SAH
CourseCourse Post-traumaticPost-traumatic Day7-12Day7-12
MechanisMechanismm
Mechanical stimulationMechanical stimulation
Neurological Neurological mechanismmechanism
Hematoma atHematoma atcircle of williscircle of willis
DurationDuration Shorter Shorter Longer Longer
SymptomSymptom Subclinical*Subclinical* Clinical deficit or Clinical deficit or
CT evidenceCT evidence
*Symptoms of ischemia appeared only on day 4 or late; could exert unfavorable global effect on critically injured trauma patients
Vasospasm inVasospasm in
Traumatic SAHTraumatic SAHVasospasm in Vasospasm in Aneurysmal SAHAneurysmal SAH
NeurologicNeurological al deterioratideteriorationon
Day 0 (Acute phase)Day 0 (Acute phase)
(cerebral edema, ICH)(cerebral edema, ICH)Day 0 & Day 8Day 0 & Day 8
(Two peaks)(Two peaks)
Infarction aInfarction arearea(LDAs on C(LDAs on CT)T)
Deep-seated Deep-seated contusioncontusion
Gliding contusionGliding contusion
Vascular territoryVascular territory
OthersOthers No impressive efficacy tNo impressive efficacy to hyperdynamic therapo hyperdynamic therapyy(Modest hemodilution, In(Modest hemodilution, Induced hypertension Hyperduced hypertension Hypervolemia)volemia)
Neurosurg 43(5): 1040-1048, 1998Neurosurg 43(5): 1040-1048, 1998Neurosurg 85: 82-89, 1996Neurosurg 85: 82-89, 1996
Why SAH is considered as Why SAH is considered as a poor prognostic factor of a poor prognostic factor of head injury?head injury?
Relation between Relation between TSAH and Head InjuryTSAH and Head Injury
Poor outcome predictor of head injury: Poor outcome predictor of head injury: – Older age, lower GCS and SAH Older age, lower GCS and SAH
Low-density areas observed on follow-Low-density areas observed on follow-up CT located at the site of earlier up CT located at the site of earlier contusions but not the vascular contusions but not the vascular territory territory (Fukuda et al, 1998)(Fukuda et al, 1998)
TSAH is only an indicator of greater TSAH is only an indicator of greater initial brain damageinitial brain damage
Neurosurg 56:671-680, 2005Neurosurg 56:671-680, 2005Neurosurg 50:261-269,2002Neurosurg 50:261-269,2002
24 hours 24 hours laterlater
2 hours after injury2 hours after injury
8 hours later8 hours later
90 mins 90 mins after injuryafter injury
In ShortIn Short
Initial contusion contribute to the severity Initial contusion contribute to the severity of brain damage. of brain damage.
TSAH means greater initial damage than nTSAH means greater initial damage than non-TSAHon-TSAH
Unlike aneurysmal SAH, the effect of vasosUnlike aneurysmal SAH, the effect of vasospasm was usually subclinical and short aftpasm was usually subclinical and short after injuryer injury
Neurosurg 56:671-680, 2005Neurosurg 56:671-680, 2005Neurosurg 50:261-269,2002Neurosurg 50:261-269,2002
Nimodipine in TSAH (1)Nimodipine in TSAH (1) ↓↓46% unfavorable outcome46% unfavorable outcome
(Even in mild SAH)(Even in mild SAH) ↓↓Mortality reductionMortality reduction ↓↓Vegetative stateVegetative state ↓↓Severe disabilitySevere disability
J Neurosurg 85: 82-89, 1996J Neurosurg 85: 82-89, 1996
Nimodipine in TSAH(2)Nimodipine in TSAH(2) Mechanism underterminedMechanism undertermined Neuroprotective effect, collateral circulatiNeuroprotective effect, collateral circulati
on??on??
J Neurosurg 85: 82-89, 1996J Neurosurg 85: 82-89, 1996
Outcome Parameter in TraumOutcome Parameter in Traumatic Subarachnoid Hemorrhaatic Subarachnoid Hemorrha
gege
Neurosurgery 56:671-680, 2005
Fisher scaleFisher scale– Index of vasospasm risk based upon a CT-Index of vasospasm risk based upon a CT-
defined hemorrhage pattern defined hemorrhage pattern
Prognostic factorsPrognostic factors
Amount of subarachnoid blood at admissiAmount of subarachnoid blood at admissionon
GCS scoreGCS score Increase in volume of contusion Increase in volume of contusion
– TSAH with parenchymal damage have poor ouTSAH with parenchymal damage have poor outcometcome
Neurosurgery 56:671-680, 2005
Take Home MessageTake Home Message
Poor prognostic factors of head injuryPoor prognostic factors of head injury– Old age, low GCS, SAHOld age, low GCS, SAH
Outcome predictor of TSAHOutcome predictor of TSAH– Initial GCS and contusion, fisher classificationInitial GCS and contusion, fisher classification
Management of TSAHManagement of TSAH– ICP, BP and ↓ ICP, BP and ↓ hemodynamic fluctuationhemodynamic fluctuation
Vasospasm in TSAH and ASAH: Vasospasm in TSAH and ASAH: – mechanism, distribution, clinical mechanism, distribution, clinical
Nimodipine can decrease unfavorable outcome oNimodipine can decrease unfavorable outcome of TSAH.f TSAH.
THANKS FOR YOUR THANKS FOR YOUR ATTENTION !!!ATTENTION !!!
Pulsatility IndexPulsatility Index
Normal PI: 0.5~1.1 (0.7~1.02) Normal PI: 0.5~1.1 (0.7~1.02) --pooled data --pooled data PI for MCA ACA PCA PI for MCA ACA PCA 0.69 0.11~0.710.13 0.69 0.11~0.710.13 EC-ICA: 0.74 0.13 EC-ICA: 0.74 0.13 ----J Ultrasound Med,1990 J Ultrasound Med,1990
ReferenceReference
Claassen, J, Vu, A, Kreiter, KT, et al. Effect of acutClaassen, J, Vu, A, Kreiter, KT, et al. Effect of acute physiologic derangements on outcome after sue physiologic derangements on outcome after subarachnoid hemorrhage. Crit Care Med 2004; 32:8barachnoid hemorrhage. Crit Care Med 2004; 32:832. 32.
Barker FG, 2nd, Ogilvy, CS. Efficacy of prophylactiBarker FG, 2nd, Ogilvy, CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after suc nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurobarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405. surg 1996; 84:405.
FACTORS ASSOCIATED WITH NEUROLOGICAL OUTCOME AND LESION PROGRESSION IN TRAUMATIC SUBARACHNOID HEMORRHAGE PATIENTS Neurosurgery 56:671-680, 2005
Outcome predictors Outcome predictors SAH Physiologic Derangement Score (SASAH Physiologic Derangement Score (SA
H-PDS; range, 0–8) :H-PDS; range, 0–8) :– Arterio-alveolar gradient, 3 points; Arterio-alveolar gradient, 3 points; – Bicarbonate, 2 points; Bicarbonate, 2 points; – Glucose, 2 pointsGlucose, 2 points– Mean arterial pressure, 1 pointMean arterial pressure, 1 point
Hunt and Hess classification – most commonly used in the United States– level of consciousness , focal deficit– Too subjective
World federation of neurological surgeon– GCS, focal deficit
Outcome of ASAHOutcome of ASAH
Carter and Ogilvy (Gr. 0-4)Carter and Ogilvy (Gr. 0-4)– Age greater than 50Age greater than 50– Hunt and Hess grade 4 to 5 (in coma)Hunt and Hess grade 4 to 5 (in coma)– Fisher scale score 3 to 4 Fisher scale score 3 to 4 – Aneurysm size >10 mmAneurysm size >10 mm
Outcome prediction and therapy substratifyOutcome prediction and therapy substratify– Good to excellent outcomes Good to excellent outcomes
Grades 0-2: >78% Grades 0-2: >78% Grade 3: 67%Grade 3: 67% Grade 4: 25% Grade 4: 25%
A CaseA Case
23 y/o woman, no underlying23 y/o woman, no underlying Found unconsciousness at the scene of coFound unconsciousness at the scene of co
llision to llision to 安全島 安全島 by driving a carby driving a car At ED: GCS E1M5V1 At ED: GCS E1M5V1 Right knee open fracture Right knee open fracture Head CT: diffuse SAH with brain swellingHead CT: diffuse SAH with brain swelling Right knee radiograph: transverse fractureRight knee radiograph: transverse fracture Angiography: no definite intracranial vascAngiography: no definite intracranial vasc
ular abnormality ular abnormality
Common ComplicationCommon Complication
VasospasmVasospasm HydrocephalusHydrocephalus Hyponatremia Hyponatremia Rebleeding Rebleeding Antiepileptic drug therapyAntiepileptic drug therapy
Initial resuscitation of Initial resuscitation of patient with severe head patient with severe head injury injury
J Neurotrauma 17:465, 2000.J Neurotrauma 17:465, 2000.