Trauma Sistem Saraf Pusat 463v47

Head Injury

Head Injury-Epidemiology • • • • • •

1.5 million Non-fatal TBI’s 370,000 Hospitalizations 80,000 cases of neurological sequela 52,000 Die from TBI’s 4 billion annually for cost of treatment Peak incidence: – Males age 15-24 years

• Causes of TBI – Young: GSW – Old: Falls

Head Injury-Anatomy • • • •

Scalp Blood supply Calvaria Brain – Occupies 80% of calvarium

Head Injury-Pathophysiology • Primary injury – Irreversible cellular injury as a direct result of the injury – Prevent the event

• Secondary injury – Damage to cells that are not initially injured – Occurs hours to weeks after injury – Prevent hypoxia and ischemia

Head Injury-Normal Physiology • • • •

Brain consumes 20% of total O2 Receives 15% of Cardiac Output Brain tissue perfusion P versus CBF – P=MAP-I • MAP=(SBP-DBP/3) + DBP – I=IVM

• Autoregulation – 50-150 mm Hg

I

Head Injury-Initial Evaluation and Management • Prevent Secondary Brain Injury – Hypoxemia – Hypotension – Anemia

– Hyperglycemia – Evacuation of mass

• Airway control with cervical spine immobilization – Orotracheal Rapid Sequence Intubation • Goal is to RSI to blunt rise in I and maintain adequate MAP • Pretreatment-Lidocaine 1.5 mg/kg, Vecuronium 0.01 mg/kg • Induction-Etomidate 0.3 mg/kg, Fentanyl 3-5 mcg/kg, Thiopental 3-5 mg/kg, Propofol 1-4 mg/kg • Paralysis-Succinylcholine 1.5 mg/kg

Head Injury-Initial Evaluation and Management • Circulation – Maintain MAP at 90 mm Hg – Aggressive fluid resuscitation • Does not increase I

– Vasopressors if crystalloids inadequate – Transfuse if hypotensive and Hct <30 – Hypertension-Assume Cushing Reflex • If I is normal, gradually reduce MAP no more than 30%

Spectrum of Traumatic Brain Injury • Mild TBI – GCS 14-15 – 80% of all TBI – Low Risk • GCS 15 and no LOC, amnesia, vomiting or diffuse HA • Less than 0.1% risk of hematoma requiring evacuation

– Medium Risk • GCS 15 and LOC, amnesia, vomiting or Diffuse HA • 1-3% risk of hematoma requiring evacuation • CT should be done in medium risk mild TBI

Spectrum of Traumatic Brain Injury • Mild TBI – High Risk • • • •

GCS 14-15 Neurologic deficits Up to 10% risk of hematoma requiring evacuation Anyone with coagulopathy, drug/alcohol consumption, epilepsy, age >60 and previous neurosurgery

– Disposition • No CT indicated or negative CT with GCS 15-Home • GCS 14 and negative CT-Observation it

Spectrum of Traumatic Brain Injury • Moderate TBI – GCS 9-13 – 10% of all TBI – <20% mortality

• Severe TBI – GCS <9 – 10% of all TBI – 40% mortality

– 50% morbidity – 40% positive CT – 8% NS intervention – <10 make moderate recovery

Intracerebral Pressure • Normal <15 mm Hg • I >20-25 mm Hg – Increases morbidity and mortality

• I monitoring rarely available in the ED • Must use physical findings – Neurologic deterioration – Unilaterally dilated pupil

– Hemiparesis – Posturing

Increased I-Management • Hypertonic Saline – Improves P and brain tissue O2 levels – Decreased I by 35% (8-10 mm HG) – P increased by 14% – MAP remained stable – Greatest benefit in those with higher I and lower P – Repeated doses were not associated with rebound, hypovolemia or HTN – 30 mL of 23.4% over 15 minutes

Increased I-Management • Mannitol – Osmotic agent – Effects I, CBF, P and brain metabolism – Free radical scavenger – Reduces I within 30 minutes, last 6-8 hours – Volume expansion, reduces hypotension – Dosage • 0.25-1 gm/kg bolus

Increased I-Management • Hyperventilation – Not recommended as prophylactic intervention – Never lower than 25 mm Hg – Reduces I by vasoconstriction, may lead to cerebral ischemia – Used as a last resort measure – Maintain PaCO2 at 30-35 mm Hg

Increased I-Management • Barbiturate Coma – Not indicated in the ED – Lowers I, cerebral metabolic O2 demand

• Anticonvulsants – Reduce occurrence of post-traumatic seizures – No improvement in long-term outcome

• I Monitoring – Should be performed on TBI with GCS <9 – Increased I may be managed by drainage

Specific Head Injuries • Scalp Lacerations – May lead to massive blood loss – Small galeal lacerations may be left alone

• Skull Fracture – Linear and simple comminuted skull fractures • • • •

Exploration of wound Prophylactic antibiotics are controversial Occipital fractures have a high incidence of other injury If depressed beyond outer table-requires NS repair

Specific Head Injuries • Skull Fractures – Basilar Fracture • Most common-petrous portion of temporal bone, the EAC and TM • Dural tear – – – –

CSF otorrhea CSF rhinorrhea Battle Sign Raccoon Sign

– – – –

Hemotympanum Vertigo Hearing loss Seventh nerve palsy

• CSF testing – Ring sign, glucose or CSF transferrin

• Should be started on prophylactic antibiotics – Ceftriaxone 1-2 gm

Specific Head Injuries • Brain Herniation – Four Types • • • •

Uncal Transtentorial Central Transtentorial Cerebellotonsillar Upward Posterior Fossa

Specific Head Injuries • Traumatic Subarachnoid Hemorrhage – Most common CT finding in moderate to severe TBI – If isolated head injury, may present with headache, photophobia and meningismus – Early tSAH development triples mortality – Size of bleed and outcome – Timing of CT – Nimodipine reduces death and disability by 55%

Specific Head Injuries • Epidural Hematoma – Occurs in 0.5% of all head injuries – Blunt trauma to temporoparietal region – Eighty percent with associated skull fracture – May occur with venous sinus tears – Classic presentation only 30% of the time

Specific Head Injuries • Subdural Hematoma – Sudden acceleration-deceleration injury with tearing of bridging veins – Common in elderly and alcoholics – Classified as acute, subacute or chronic • Acute <2 weeks • Chronic >2 weeks

Specific Head Injuries • Diffuse Axonal Injury – Disruption of axons in white matter and brainstem – Injury occurs immediately and is irreversible – Seen after MVC or shaken baby syndrome – Usually have persistent vegetative state – CT usually normal – MRI with multiple, diffuse abnormalities

Specific Head Injuries • Penetrating Injury – Gunshot Wounds • Injury due to direct brain injury and cavitary effects • GCS predicts prognosis – GCS >8 and reactive pupils = 25% mortality – GCS <5 = nears 100% mortality

– Stab wounds

Complications-Long Term Sequela • Seizure Disorder – 2% Early post-traumatic incidence – Increased to 30% in children, alcoholics and with intracranial hematoma • Prophylactic antiepileptics reduce early occurrence • Use not ed by the literature

• Concussion - Brief LOC

- Vertigo - Nausea - Dizziness - Headache - Vomiting - Photophobia - Cognitive/Memory dysfunction

Complications-Long Term Sequela • Concussion – Up to 80% may have symptoms at 3 months – 15% may have symptoms at 1 year – Persistence of these symptoms is termed Postconcussive Syndrome – 85-90% recover after 1 year – Risk factors: - Female

- Litigation

- Low socioeconomic status

Complications-Long Term Sequela • Infection – Skull fracture – CSF leak – Intubation

– ICU

– Treatment • Prophylactic antibiotics

– History of Fracture • Fever • Signs of meningitis – 3rd generation cephalosporin – Vancomycin

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