1. Traumatic Brain Injury
Gill Sviri MD, M.Sc

2. Contents Epidemiology Biomechanics of primary brain injury
Mechanisms of secondary brain injury
Clinical classification of head injury
Treatment modalities – past, present, and future
Controversies

3. Epidemiology 2 million pts/year evaluated in US (ED)
admissions/year
100,000 temporary or permanent disability
Additional 30-50,000 die before ED arrival
Peaks y.o and > 65
Death 3.4 x more common in males
Most common – MVC’s and gun-shot

4. Physiology – Hemodynamics
Oxygen consumption - 20% of total body
Requires 15% of normal cardiac output
CBF – 50 ml/100g/min
Autoregulation
maintained btwn MAP 60–150 or CPP
hyperTN, alkalosis, hypocarbia = v/c
hypoTN, acidosis, hypercarbia, hypoxia = v/d

5. Physiology - ICP Craniospinal space non-expandable
Sum of brain, CSF, and blood constant
Insults
brain volume – edema
CSF – obstruction
blood volume – ICH, hematoma, v/d, congestion
compensation – up to 50–100 ml
CSF displacement 1st
brain elasticity

6. Physiology - CPP CPP = MAP – ICP
<  autoregulation lost/vasoparalysis  vasodilation  incr. ICP  decr. CPP
As ICP approaches MAP  CPP ceases  cell death

7. Brain Injury dynamic process of… primary injury secondary injury
occurs at time of head trauma
irreversible
prevention strategies
secondary injury
minutes to days post injury
therapy directed at limiting this further brain cell death

8. Biomechanics – primary injury
direct injury
impact by object or compression mechanism
external signs of trauma
skull plastic deformity  absorbs energy fracture if force sufficient
transmitted force to brain tissue
injury pattern – skull #, epidural, contusion
associated indirect injury  other injury pattern

9. Biomechanics – primary injury
indirect injury
cranial contents set into vigorous motion
acceleration/deceleration, rotational, angular forces
bridging subdural vessel strain
differential acceleration – shear injuries
impact of brain on inner aspect of skull
injury pattern – subdural, DAI, concussion, countercoup

10. Secondary injury
This is where we intervene to limit further brain cell damage
mechanisms
systemic insults
intracranial lesions
neuroendocrine disturbance
membrane failure
abnormal ion fluxes
edema

11. Secondary injury

12. PATHOPHYSIOLOGY OF TBI
Primary Brain Damage
Energy
Failure
Glutamate
Release
Lactate
Acidosis
Membrane
Failure
Massive Ca
entry
Brain
Edema
Free radicals
release
Vasodilatation
Increased
CBV
Increased
ICP
Neuronal
Death
Secondary Brain Damage

13. Secondary injury - preventable
Treatable secondary insults to the brain in trauma patients include…
CPP (goal > 60 mmHg)
hypotension (goal SBP > 90) - not related to head injury!
ICP (goal < )
hypoxia (goal PaO2 > 60mmHg)
can be head injury (brainstem) or other airway/breathing/oxygenation/ventilation
anemia (goal Hct > 30%)
seizures – increased metabolic demand

14. Secondary injury - ?preventable
Edema – local/global CBF disturbance
diffuse - comprimise ventricles, loss of sulci, effaced basal cisterns
focal – hypodensity around lesion +/- shift
vasogenic – BBB failure, direct injury to cell membranes, pinocytosis incr. osmotic gradient
cytotoxic – membrane pump failure, hypoxia, ischemia

15. Clinical Classification
determined by post-resucitation GCS
Minimal – GCS 15 and no LOC/amnesia
Mild – GCS 13/14-15 with LOC/amnesia
Moderate – GCS 9-12/13
Severe – GCS 8 or less

16. Severe head injury Severe – GCS 8 or less 10% of all TBI 40% mortality
25% require neurosurgical intervention

17. Severe head injury CT findings subdural – 30% epidural – 0.5 – 1%
subarachnoid – 33%
intracerebral hematoma – 12%
subdural hygroma – 10%

18. Treatment airway and breathing BP Hyperventilation
Hyper-osmotic agents
CSF drainage
Surgery
Seizure prophylaxis

19. Moderate head injury moderate = GCS 9-12/13 10% of all TBI
20% mortality

20. CLASSIFACTION OF CLOSE TBI
Diffuse TBI
Focal TBI
Skull
fractures
Intracranial
Hemorrhages
Brain
Contusions
Brain
Concussion
Diffuse Axonal
Injury
EDH
SDH
ICH
Brain Edema
Increased ICP

21. A MAJOR THREAT: INCREASED ICP

22. LINEAR SKULL FRACTURES

25. DEPRESSED SKULL FRACTURES
Skull deformation
Compression of brain
Higher risk of bleeding

33. DEPRESSED SKULL FRACTURES
Complications:
Wound and CSF infections
CSF leak
Neural injury and deficit

34. BASE SKULL FRACTURES High energy loading CSF leak and infection
Cranial nerve damage

36. ACUTE EPIDURAL HEMATOMA
Lucid interval is suggestive
Good prognosis

37. ACUTE EPIDURAL HEMATOMA
Most often due to skull fracture
Brain damage is uncommon

38. ACUTE EPIDURAL HEMATOMA

41. ACUTE SUBDURAL HEMATOMA
Always associated with significant TBI
Often grim prognosis

42. ACUTE SUBDURAL HEMATOMA
Massive edema is the rule
Disproportionate midline shift
High mortality and morbidity

45. BRAIN CONTUSIONS:
COUP AND CONTRE-COUP

46. BRAIN CONTUSIONS:
PATHOPHYSIOLOGY

47. BRAIN CONTUSIONS: PATHOLOGY

48. EVOLVING BRAIN CONTUSIONS: THE PATIENT WHO TALK AND DIE

50. SUBARACHNOID HEMORRHAGE

52. DIFFUSE AXONAL INJURY:
PATHOPHYSIOLOGY

53. DIFFUSE AXONAL INJURY: “THE DISCONNECTED BRAIN”

54. DIFFUSE AXONAL INJURY: “THE DISCONNECTED BRAIN”

55. DIFFUSE AXONAL INJURY: “THE DISCONNECTED BRAIN”

57. GUN SHOT WOUNDS: E=mc2

58. GUN SHOT WOUNDS: E=mc2 Directly depends on velocity missile
Through and through usually fatal
Associates focal and diffuse TBI