Traumatic subarachnoid hemorrhage
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Traumatic Subarachnoid Hemorrhage. 4FI Ri 尤彥棻 Feb.13, 2006. Severe Head Injury (1). Head-injured patients reached ED alive. 10%. Severe brain injury. 25%. Have lesions requiring neurosurgical evacuation. Severe Head Injury (2).

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Traumatic Subarachnoid Hemorrhage

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Traumatic subarachnoid hemorrhage

Traumatic Subarachnoid Hemorrhage

4FI Ri 尤彥棻

Feb.13, 2006


Severe head injury 1

Severe Head Injury (1)

Head-injured patients

reached ED alive

10%

Severe brain injury

25%

Have lesions requiring neurosurgical evacuation


Severe head injury 2

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.


Initial resuscitation of patient with severe head injury

Initial resuscitation of patient with severe head injury

J Neurotrauma 17:465, 2000.


Traumatic sah

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


Traumatic sah1

Traumatic SAH

  • SAH found on head injury

    • Increase the severity

      (more skull fr and contusion)

    • Unfavorable outcome

      With SAH:60%

      Without SAH:30%


Management of tsah 1

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


Management of tsah 2

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)


  • Management of tsah 3

    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)


    Does delayed vasospasm happen in traumatic subarachnoid hemorrhage

    Does Delayed Vasospasm Happen in Traumatic Subarachnoid Hemorrhage?


    Factors of vasospasm

    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


    Vasospasm in tsah and asah

    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


    Traumatic subarachnoid hemorrhage

    Neurosurg 43(5): 1040-1048, 1998

    Neurosurg 85: 82-89, 1996


    Why sah is considered as a poor prognostic factor of head injury

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


    Relation between tsah and head injury

    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


    Traumatic subarachnoid hemorrhage

    24 hours later

    2 hours after injury


    Traumatic subarachnoid hemorrhage

    90 mins

    after injury

    8 hours later


    In short

    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


    Nimodipine in tsah 1

    Nimodipine in TSAH (1)

    • ↓46% unfavorable outcome

      (Even in mild SAH)

    • ↓Mortality reduction

    • ↓Vegetative state

    • ↓Severe disability

    J Neurosurg 85: 82-89, 1996


    Nimodipine in tsah 2

    Nimodipine in TSAH(2)

    • Mechanism undertermined

    • Neuroprotective effect, collateral circulation??

    J Neurosurg 85: 82-89, 1996


    Outcome parameter in traumatic subarachnoid hemorrhage

    Outcome Parameter in Traumatic Subarachnoid Hemorrhage


    Traumatic subarachnoid hemorrhage

    Neurosurgery 56:671-680, 2005


    Traumatic subarachnoid hemorrhage

    • Fisher scale

      • Index of vasospasm risk based upon a CT-defined hemorrhage pattern


    Prognostic factors

    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


    Take home message

    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.


    Thanks for your attention

    THANKS FOR YOUR ATTENTION !!!


    Pulsatility index

    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


    Reference

    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


    Outcome predictors

    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


    Traumatic subarachnoid hemorrhage

    • Hunt and Hess classification

      • most commonly used in the United States

      • level of consciousness , focal deficit

      • Too subjective


    Traumatic subarachnoid hemorrhage

    • World federation of neurological surgeon

      • GCS, focal deficit


    Outcome of asah

    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%


    A case

    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


    Common complication

    Common Complication

    • Vasospasm

    • Hydrocephalus

    • Hyponatremia

    • Rebleeding

    • Antiepileptic drug therapy


    Initial resuscitation of patient with severe head injury1

    Initial resuscitation of patient with severe head injury

    J Neurotrauma 17:465, 2000.


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