Traumatic Subarachnoid Hemorrhage 4FI Ri 尤彥棻 Feb.13, 2006

Head-injured patients reached ED alive reached ED alive 25% 10% Have lesions requiring neurosurgical evacuation Severe brain injury Severe Head Injury (1)

Severe Head Injury (2) Presenting with a GCS score of 8 or less at the acute presentation after injury. Presenting with a GCS score of 8 or less at the acute presentation after injury. Severe head injury as TBI manifested by a postresuscitation GCS of 8 or less within 48 hours. Severe head injury as TBI manifested by a postresuscitation GCS of 8 or less within 48 hours.

Initial resuscitation of patient with severe head injury J Neurotrauma 17:465, 2000.

Traumatic 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 hemisphere –Presence of contusions and SDH –Basal cisterns were less involved Rosen's Emergency Medicine p. 310 J Neurosurg 85: 82-89, 1996

Traumatic SAH SAH found on head injury SAH found on head injury –Increase the severity (more skull fr and contusion) (more skull fr and contusion) –Unfavorable outcome With SAH:60% With SAH:60% Without SAH:30% Without SAH:30%

Management of TSAH (1) Keep at bedrest Keep at bedrest Check GCS, Vital signs, neurological deficit Check GCS, Vital signs, neurological deficit ICP and BP ICP and BP –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) ( ↓ rebleeding, ↑ infarction) ( ↓ rebleeding, ↑ infarction) –Avoid direct vasodilator; Labetalol is preferred J Trauma 30: , 1990 Uptodate: SAH management

Management of TSAH (2) (2) No ICP Monitor (2) No ICP Monitor –Withheld antihypertensive –unless severe elevation in BP –cerebral ischemia and compensatory nature of acute hypertension 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 (3) Seizure prophylaxis Seizure prophylaxis –minimized whenever possible –AED exposure may be associated with worse neurologic and cognitive outcome after SAH Prevent delayed ischemia? Prevent delayed ischemia? –Monitor with transcranial doppler (TCD) Stroke 2005; 36:583

Does Delayed Vasospasm Happen in Traumatic Subarachnoid Hemorrhage?

Factors of vasospasm Site of subarachnoid blood (location of spasm) Site of subarachnoid blood (location of spasm) Massive SAH Massive SAH Direct stretching or mechanical irritation of the cerebral arteries Direct stretching or mechanical irritation of the cerebral arteries J Neurosurg 84: , 1996

Vasospasm in TSAH and ASAH Vasospasm in Traumatic SAH Vasospasm in Aneurysmal SAH CoursePost-traumaticDay7-12 Mechanism Mechanical stimulation Neurological mechanism Hematoma at circle of willis DurationShorterLonger SymptomSubclinical* Clinical deficit or CT evidence *Symptoms of ischemia appeared only on day 4 or late; could exert unfavorable global effect on critically injured trauma patients

Vasospasm in Traumatic SAH Vasospasm in Aneurysmal SAH Neurological deterioration Day 0 (Acute phase) (cerebral edema, ICH) Day 0 & Day 8 (Two peaks) Infarction area (LDAs on CT) Deep-seated contusion Gliding contusion Vascular territory Others No impressive efficacy to hyperdynamic therapy (Modest hemodilution, Induced hypertension Hypervolemia) Neurosurg 43(5): , 1998 Neurosurg 85: 82-89, 1996

Why SAH is considered as a poor prognostic factor of head injury?

Relation between TSAH and Head Injury Poor outcome predictor of head injury: Poor outcome predictor of head injury: –Older age, lower GCS and SAH Low-density areas observed on follow-up CT located at the site of earlier contusions but not the vascular territory (Fukuda et al, 1998) Low-density areas observed on follow-up CT located at the site of earlier contusions but not the vascular territory (Fukuda et al, 1998) TSAH is only an indicator of greater initial brain damage TSAH is only an indicator of greater initial brain damage Neurosurg 56: , 2005 Neurosurg 50: ,2002

24 hours later 2 hours after injury

8 hours later 90 mins after injury

In Short Initial contusion contribute to the severity of brain damage. Initial contusion contribute to the severity of brain damage. TSAH means greater initial damage than non-TSAH TSAH means greater initial damage than non-TSAH Unlike aneurysmal SAH, the effect of vasospasm was usually subclinical and short after injury Unlike aneurysmal SAH, the effect of vasospasm was usually subclinical and short after injury Neurosurg 56: , 2005 Neurosurg 50: ,2002

Nimodipine in TSAH (1) ↓ 46% unfavorable outcome ↓ 46% unfavorable outcome (Even in mild SAH) (Even in mild SAH) ↓ Mortality reduction ↓ Mortality reduction ↓ Vegetative state ↓ Vegetative state ↓ Severe disability ↓ Severe disability J Neurosurg 85: 82-89, 1996

Nimodipine in TSAH(2) Mechanism undertermined Mechanism undertermined Neuroprotective effect, collateral circulation?? Neuroprotective effect, collateral circulation?? J Neurosurg 85: 82-89, 1996

Outcome Parameter in Traumatic Subarachnoid Hemorrhage

Neurosurgery 56: , 2005

Fisher scale Fisher scale –Index of vasospasm risk based upon a CT- defined hemorrhage pattern

Prognostic factors Amount of subarachnoid blood at admission Amount of subarachnoid blood at admission GCS score GCS score Increase in volume of contusion Increase in volume of contusion –TSAH with parenchymal damage have poor outcome Neurosurgery 56: , 2005

Take Home Message Poor prognostic factors of head injury Poor prognostic factors of head injury –Old age, low GCS, SAH Outcome predictor of TSAH Outcome predictor of TSAH –Initial GCS and contusion, fisher classification Management of TSAH Management of TSAH –ICP, BP and ↓ hemodynamic fluctuation Vasospasm in TSAH and ASAH: Vasospasm in TSAH and ASAH: –mechanism, distribution, clinical Nimodipine can decrease unfavorable outcome of TSAH. Nimodipine can decrease unfavorable outcome of TSAH.

THANKS FOR YOUR ATTENTION !!!

Pulsatility 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 ~0.71  ~0.71  0.13 EC-ICA: 0.74  0.13 EC-ICA: 0.74  J Ultrasound Med, J Ultrasound Med,1990

Reference Claassen, J, Vu, A, Kreiter, KT, et al. Effect of acute physiologic derangements on outcome after subarachnoid hemorrhage. Crit Care Med 2004; 32:832. Claassen, J, Vu, A, Kreiter, KT, et al. Effect of acute physiologic derangements on outcome after subarachnoid hemorrhage. Crit Care Med 2004; 32:832. Barker FG, 2nd, Ogilvy, CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405. Barker FG, 2nd, Ogilvy, CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405. FACTORS ASSOCIATED WITH NEUROLOGICAL OUTCOME AND LESION PROGRESSION IN TRAUMATIC SUBARACHNOID HEMORRHAGE PATIENTS Neurosurgery 56: , 2005

Outcome predictors SAH Physiologic Derangement Score (SAH- PDS; range, 0 – 8) : SAH Physiologic Derangement Score (SAH- PDS; range, 0 – 8) : –Arterio-alveolar gradient, 3 points; –Bicarbonate, 2 points; –Glucose, 2 points –Mean 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 ASAH Carter and Ogilvy (Gr. 0-4) Carter and Ogilvy (Gr. 0-4) –Age greater than 50 –Hunt and Hess grade 4 to 5 (in coma) –Fisher scale score 3 to 4 –Aneurysm size >10 mm Outcome prediction and therapy substratify Outcome prediction and therapy substratify –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 Case 23 y/o woman, no underlying 23 y/o woman, no underlying Found unconsciousness at the scene of collision to 安全島 by driving a car Found unconsciousness at the scene of collision to 安全島 by 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 swelling Head CT: diffuse SAH with brain swelling Right knee radiograph: transverse fracture Right knee radiograph: transverse fracture Angiography: no definite intracranial vascular abnormality Angiography: no definite intracranial vascular abnormality

Common Complication Vasospasm Vasospasm Hydrocephalus Hydrocephalus Hyponatremia Hyponatremia Rebleeding Rebleeding Antiepileptic drug therapy Antiepileptic drug therapy

Initial resuscitation of patient with severe head injury J Neurotrauma 17:465, 2000.