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Traumatic Brain Injury Gill Sviri MD, M.Sc. Contents ► Epidemiology ► Biomechanics of primary brain injury ► Mechanisms of secondary brain injury ► Clinical.

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Presentation on theme: "Traumatic Brain Injury Gill Sviri MD, M.Sc. Contents ► Epidemiology ► Biomechanics of primary brain injury ► Mechanisms of secondary brain injury ► Clinical."— Presentation transcript:

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  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 Vasodilatation Primary Brain Damage Energy Failure Glutamate Release Neuronal Death Free radicals release Membrane Failure Lactate Acidosis Massive Ca entry Brain Edema Increased ICP Increased CBV 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 Focal TBI Diffuse TBI Skull fractures Brain Contusions Intracranial Hemorrhages Brain Concussion Diffuse Axonal Injury EDHSDHICH Brain Edema Increased ICP

21 A MAJOR THREAT: INCREASED ICP

22 LINEAR SKULL FRACTURES

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

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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

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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

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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

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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

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50 SUBARACHNOID HEMORRHAGE

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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”

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57 GUN SHOT WOUNDS: E=mc 2

58 Directly depends on velocity missile Through and through usually fatal Associates focal and diffuse TBI

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