8/29/2011. Brain Injury Incidence: 200/100,000. Prehospital Brain Injury Mortality Incidence: 20/100,000

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1 Traumatic Brain Injury Almario G. Jabson MD Section Of Neurosurgery Asian Hospital And Medical Center Brain Injury Incidence: 200/100,000 Prehospital Brain Injury Mortality Incidence: 20/100,000 Hospital Admissions by Severity: Mild: 80% Moderate: 10% Severe: 10% RACE AND GENDER DIAGNOSIS Peak Incidence: years old Secondary Peak Incidence: Infants and children Elderly HISTORY DOI: DATE OF INJURY TOI: TIME OF INJURY POI: PLACE OF INJURY MOI: MECHANISM OF INJURY M:F = 2-3:1 1

2 MECHANISM OF INJURY HISTORY MVA/TRANSPORT RELATED FALLS INTERPERSONAL VIOLENCE SPORTS RELATED WORK RELATED HEADACHE LOSS OF CONSCIOUSNESS AMNESIA NAUSEA/VOMITTING SEIZURES ALCOHOL INTAKE DIAGNOSIS GLASGOW COMA SCALE PHYSICAL/NEUROLOGIC EXAM RAPID INITIAL ASSESSMENT SYSTEMIC NEUROLOGIC (GCS, LATERALIZING SIGNS, INC. INTRACRANIAL PRESSURE) COMPREHENSIVE PHYSICAL AND NEUROLOGIC EXAM POINTS BEST EYE BEST VERBAL BEST MOTOR 6 OBEYS 5 ORIENTED LOCALIZES PAIN 4 SPONTANEOUS CONFUSED WITHDRAWS TO PAIN 3 TO SPEECH INAPPROPRIATE DECORTICATE 2 TO PAIN INCOMPREHENSIBLE DECEREBRATE 1 NONE NONE NONE 2

3 INITIAL NEUROLOGIC EXAM DIAGNOSIS LATERALIZING SIGNS PUPIL SIZE AND REACTIVITY WEAKNESS INCREASED ICP CUSHING S TRIAD INCREASING BP DECREASING HR DECREASING RR DIAGNOSTIC WORK-UP LABORATORY WORK-UP RADIOGRAPHIC EVALUATION X-RAYS CT-SCAN X-RAYS CT SCAN SKULL AP-LATERAL CERVICAL FILMS CERVICAL AP-LATERAL OPEN MOUTH VIEW EMERGENT CONDITIONS DETECTED ON PLAIN CT SCAN BLOOD HYDROCEPHALUS CEREBRAL SWELLING CEREBRAL ANOXIA SKULL FRACTURES ISCHEMIC INFARCTION PNEUMOCEPHALUS MIDLINE SHIFT 3

4 PATHOLOGIES IN HEAD INJURY CLOSED HEAD INJURY PRIMARY INJURY SECONDARY INJURY PENETRATING HEAD INJURY GUNSHOT WOUND NONGUNSHOT WOUND INJURY PRIMARY INJURY/IMPACT DAMAGE FOCAL INJURIES CONTUSIONS LACERATIONS FRACTURES HEMATOMAS DIFFUSE INJURIES DIFFUSE AXONAL INJURY CONCUSSION SECONDARY INJURY SPECIFIC PATHOLOGIES EVENTS WHICH OCCUR AFTER ONSET OF PRIMARY INJURY AGGRAVATING CONDITIONS ISCHEMIA HYPOXEMIA EDEMA COMPRESSION FROM MASS LESIONS SCALP INJURIES LACERATION CONTUSION HEMATOMA AVULSION 4

SPECIFIC PATHOLOGIES SPECIFIC PATHOLOGIES SKULL

COMMINUTED BASAL SKULL DIASTATIC INTRACRANIAL LESIONS

INTRAVENTRICULAR SUBARACHNOID HEMORRHAGE CONTUSIONS

5 SPECIFIC PATHOLOGIES SPECIFIC PATHOLOGIES SKULL FRACTURES LINEAR PINGPONG DEPRESSED OPEN CLOSED COMMINUTED BASAL SKULL DIASTATIC INTRACRANIAL LESIONS HEMATOMAS EPIDURAL SUBDURAL INTRACEREBRAL INTRAVENTRICULAR SUBARACHNOID HEMORRHAGE CONTUSIONS HEMORRHAGIC CONTUSION CONTUSION HEMATOMA Epidural Hematoma Acute Subdural Hematoma 5

6 Chronic Subdural Hematoma Contusion Hematoma Penetrating Injury MANAGEMENT RESUSCITATION/CABs IMMOBILIZATION AS NEEDED MEDICATIONS SURGERY PREVENTION 6

7 MANAGEMENT MANAGEMENT ISSUES PRIMARY INJURY SURGICAL VS. NONSURGICAL SECONDARY INJURY MINIMIZE/PREVENT DELETERIOUS EFFECTS OF FACTORS CAUSING SECONDARY INJURY MANAGEMENT OF INTRACRANIAL PRESSURE ( ICP ) CEREBRAL BLOOD FLOW ( CBF ) INDIRECTLY MEASURED BY CEREBRAL PERFUSION PRESSURE ( CPP ) CPP = MEAN ARTERIAL PRESSURE ( MAP ) - INTRACRANIAL PRESSURE ( ICP ) ROUTINE MEASURES SPECIFIC MEASURES POSITIONING ELEVATE HOB TO DEGREES KEEP HEAD MIDLINE LIGHT SEDATION AVOID HYPOTENSION CONTROL HYPERTENSION PREVENT HYPERGLYCEMIA INTUBATE IF GCS < 8 OR WITH RESPIRATORY DISTRESS AVOID EXCESSIVE HYPERVENTILATION DVT Prophylaxis if possible HEAVY SEDATION AND/OR PARALYSIS CSF DRAINAGE OSMOTIC THERAPY MANNITOL FUROSEMIDE SERUM OSMOLARITY HYPERVENTILATION STEROIDS NOT RECOMMENDED 7

8 MANAGEMENT ISSUES INTRACRANIAL PRESSURE MONITOR Although ICP monitor is widely used, the overall outcome of severe HI hasn t been improved by its use. MANAGEMENT ISSUES HYPERVENTILATION Chronic use (>24 hours) of hyperventilation correlates with poor outcome in sever HI Recommended for acute ICP increase Class I Evidence AACNS/Brain Trauma Foundation MANNITOL MECHANISM OF ACTION INCREASE CBF AND O2 DELIVERY BY IMMED. PLASMA EXPANSION, REDUCED HCT AND VISCOSITY DOSE 0.25g/kg to 1gm/kg/dose ONSET OF ACTION 1-5 MINUTES DURATION OF ACTION PEAKS IN MINUTES FUROSEMIDE MECHANISM OF ACTION INCREASE SERUM TONICITY MAY SLOW PRODUCTION OF CSF ACTS SYNERGISTICALLY WITH MANNITOL DOSE ADULTS: MG IV PEDS: 1MG/KG PRECAUTIONS SERUM OSMOLARITY DEHYDRATION 8

9 MECHANISM OF ACTION HYPERVENTILATION INDICATIONS TO TIDE PATIENT OVER IF UNRESPONSIVE TO OTHER MEASURES HYPEREMIA MANAGEMENT ISSUES CORTICOSTEROIDS The use of corticosteroids does not cause a decrease in ICP nor does it improve outcome of HI. ONSET OF ACTON < 30 SECONDS DURATION OF ACTION PEAKS IN 8 MINUTES, EFFECT LESSENED BY 1 HOUR PRECAUTIONS Class I Evidence AANS/Brain Trauma Foundation MANAGEMENT: Concussion Special Circumstances in Concussive Injuries Impact Seizure 12% (more common than in adults) not predictive of early or late epilepsy anticonvulsant treatment is not needed MANAGEMENT ISSUES ANTICONVULSANT Lewis et al, 1993 Pedia HI Post-traum traum Sz GCS % GCS>8 3.8% Pxs with low GCS, prophylactic treatment reduces post- traumatic seizures 9

10 MANAGEMENT: Discharge Criteria When Does Surgery Come In? Basic Principle To lessen the Impact of Primary Injury and Prevent Secondary Injury Normal level of alertness Tolerates oral intake Usual gait 10

Pre-hospital Response to Trauma and Brain Injury. Hans Notenboom, M.D. Asst. Medical Director Sacred Heart Medical Center

Pre-hospital Response to Trauma and Brain Injury Hans Notenboom, M.D. Asst. Medical Director Sacred Heart Medical Center Traumatic Brain Injury is Common 235,000 Americans hospitalized for non-fatal TBI