Traumatic Brain Injury Gill Sviri MD, M.Sc

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

Epidemiology 2 million pts/year evaluated in US (ED) 220 000 admissions/year 100,000 temporary or permanent disability Additional 30-50,000 die before ED arrival Peaks 15-25 y.o and > 65 Death 3.4 x more common in males Most common – MVC’s and gun-shot

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 50-160 hyperTN, alkalosis, hypocarbia = v/c hypoTN, acidosis, hypercarbia, hypoxia = v/d

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

Physiology - CPP CPP = MAP – ICP < 40-50  autoregulation lost/vasoparalysis  vasodilation  incr. ICP  decr. CPP As ICP approaches MAP  CPP ceases  cell death

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

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

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

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

Secondary injury

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

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 < 15 - 20) hypoxia (goal PaO2 > 60mmHg) can be head injury (brainstem) or other airway/breathing/oxygenation/ventilation anemia (goal Hct > 30%) seizures – increased metabolic demand

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

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

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

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

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

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

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

A MAJOR THREAT: INCREASED ICP

LINEAR SKULL FRACTURES

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

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

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

ACUTE EPIDURAL HEMATOMA Lucid interval is suggestive Good prognosis

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

ACUTE EPIDURAL HEMATOMA

ACUTE SUBDURAL HEMATOMA Always associated with significant TBI Often grim prognosis

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

BRAIN CONTUSIONS: COUP AND CONTRE-COUP

BRAIN CONTUSIONS: PATHOPHYSIOLOGY

BRAIN CONTUSIONS: PATHOLOGY

EVOLVING BRAIN CONTUSIONS: THE PATIENT WHO TALK AND DIE

SUBARACHNOID HEMORRHAGE

DIFFUSE AXONAL INJURY: PATHOPHYSIOLOGY

DIFFUSE AXONAL INJURY: “THE DISCONNECTED BRAIN”

DIFFUSE AXONAL INJURY: “THE DISCONNECTED BRAIN”

DIFFUSE AXONAL INJURY: “THE DISCONNECTED BRAIN”

GUN SHOT WOUNDS: E=mc2

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