Traumatic Subarachnoid Hemorrhage

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

2. 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 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. J Trauma 30:933-941, 1990 Uptodate: SAH management Management of TSAH (1) • 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

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. Stroke 2005; 36:583 Management of TSAH (3) • Seizure prophylaxis • minimized whenever possible • AED exposure may be associated with worse neurologic and cognitive outcome after SAH • Prevent delayed ischemia? • Monitor with transcranial doppler (TCD)

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 84:762-768, 1996

12. Vasospasm in TSAH and ASAH *Symptoms of ischemia appeared only on day 4 or late; could exert unfavorable global effect on critically injured trauma patients

13. Neurosurg 43(5): 1040-1048, 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 56:671-680, 2005 Neurosurg 50:261-269,2002

16. 24 hours later 2 hours after injury

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 56:671-680, 2005 Neurosurg 50:261-269,2002

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 56:671-680, 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 56:671-680, 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 • 0.69 0.11~0.71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 56:671-680, 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 • 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.