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

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

3. Severe Head Injury (2)
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.

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

5. Traumatic SAH SAH: Blood within CSF and meningeal intima
30%-40% of severe
traumatic brain injury
TSAH
convexity of the cerebral hemisphere
Presence of contusions and SDH
Basal cisterns were less involved
TSAH convexity of the cerebral hemispheres
Presence of contusions and SDH
Rosen's Emergency Medicine p. 310
J Neurosurg 85: 82-89, 1996

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

7. Management of TSAH (1) Keep at bedrest
                                                                                 
Keep at bedrest
Check GCS, Vital signs, neurological deficit
ICP and BP
Cerebral perfusion pressure (CPP=MAP-ICP)
(CPP control above 70-80mmHg)
(1) ICP Monitor
BP control (SBP<140)
(↓rebleeding, ↑infarction)
Avoid direct vasodilator; Labetalol is preferred
nitroprusside or nitroglycerin
J Trauma 30: , 1990
Uptodate: SAH management

8. Management of TSAH (2) (2) No ICP Monitor
Withheld antihypertensive
unless severe elevation in BP
cerebral ischemia and compensatory nature of acute hypertension
Constant hemodynamic monitoring.
Analgesia (↓hemodynamic fluctuations)
Stool softeners
Transcranial Doppler measurements (baseline)

9. Management of TSAH (3) Seizure prophylaxis Prevent delayed ischemia?
minimized whenever possible
AED exposure may be associated with worse neurologic and cognitive outcome after SAH
Prevent delayed ischemia?
Monitor with transcranial doppler (TCD)
(avoid Dextrose-containing and hypotonic solutions)
Hyperdynamic therapy(triple-H)
Modest hemodilution,
Induced hypertension (with pressor agents such as phenylephrine or dopamine )
hypervolemia
Lower the risk of potential deleterious effect of seizure in aneurysm
AED exposure may be associated with worse neurologic and cognitive outcome after SAH
Relatively low risk associated with AED administration versus the potential deleterious effects of seizures on an already dysautoregulated brain
Stroke 2005; 36:583

10. Does Delayed Vasospasm Happen in Traumatic Subarachnoid Hemorrhage?

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

12. Vasospasm in TSAH and ASAH
Traumatic SAH
Aneurysmal SAH
Course
Post-traumatic
Day7-12
Mechanism
Mechanical stimulation
Neurological mechanism
Hematoma at
circle of willis
Duration
Shorter
Longer
Symptom
Subclinical*
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

13. Neurological deterioration Day 0 (Acute phase) (cerebral edema, ICH)
Vasospasm in
Traumatic SAH
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

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

15. Relation between TSAH and 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)
TSAH is only an indicator of greater initial brain damage
Neurosurg 56: , 2005
Neurosurg 50: ,2002

16. 2 hours after injury
24 hours later

17. 90 mins
after injury
8 hours later

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

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

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

21. Outcome Parameter in Traumatic Subarachnoid Hemorrhage

22. Neurosurgery 56: , 2005

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

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

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

26. THANKS FOR YOUR ATTENTION !!!

28. Pulsatility Index Normal PI: 0.5~1.1 (0.7~1.02) --pooled data
PI for MCA ACA PCA
~0.710.13
EC-ICA: 0.74 0.13
--J Ultrasound Med,1990

29. 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.
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

30. Outcome predictors
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

31. Hunt and Hess classification
most commonly used in the United States
level of consciousness , focal deficit
Too subjective

32. World federation of neurological surgeon
GCS, focal deficit

33. Outcome of ASAH Grades 0-2: >78% Grade 3: 67% Grade 4: 25%
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
Good to excellent outcomes
Grades 0-2: >78%
Grade 3: 67%
Grade 4: 25%

35. A Case 23 y/o woman, no underlying
Found unconsciousness at the scene of collision to 安全島 by driving a car
At ED: GCS E1M5V1
Right knee open fracture
Head CT: diffuse SAH with brain swelling
Right knee radiograph: transverse fracture
Angiography: no definite intracranial vascular abnormality

36. Common Complication Vasospasm Hydrocephalus Hyponatremia Rebleeding
Antiepileptic drug therapy

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