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.