Head Injury

Anthony G. Hillier, D.O. St. John West Shore Emergency Medicine Resident

Head Injury-Epidemiology Injury      1.5 million Non-fatal TBI¶s Non370,000 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 15- 

Causes of TBI
± Young: GSW ± Old: Falls

Head Injury-Anatomy Injury    Scalp Blood supply Calvaria Brain
± Occupies 80% of calvarium

Head Injury-Pathophysiology Injury 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 Injury    Brain consumes 20% of total O2 Receives 15% of Cardiac Output Brain tissue perfusion CPP versus CBF ± CPP=MAP-ICP CPP=MAP MAP=(SBP-DBP/3) + DBP MAP=(SBP± ICP=IVM  Autoregulation ± 50-150 mm Hg 50- .

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ICP .

01 mg/kg Pretreatment Induction-Etomidate 0. Vecuronium 0.5 mg/kg Paralysis- .3 mg/kg.Head Injury-Initial Evaluation Injuryand 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 ICP and maintain adequate MAP  Pretreatment-Lidocaine 1. Induction3Thiopental 3-5 mg/kg.5 mg/kg. Fentanyl 3-5 mcg/kg. Propofol 1-4 mg/kg 31 Paralysis-Succinylcholine 1.

Head Injury-Initial Evaluation Injuryand Management  Circulation ± Maintain MAP at 90 mm Hg ± Aggressive fluid resuscitation  Does not increase ICP ± Vasopressors if crystalloids inadequate ± Transfuse if hypotensive and Hct <30 ± Hypertension-Assume Cushing Reflex Hypertension If ICP is normal. gradually reduce MAP no more than 30% .

amnesia. vomiting or diffuse HA  Less than 0. 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 ± GCS 14-15 14± 80% of all TBI ± Low Risk  GCS 15 and no LOC. amnesia.1% risk of hematoma requiring evacuation ± Medium Risk  GCS 15 and LOC.

epilepsy. drug/alcohol consumption.Spectrum of Traumatic Brain Injury  Mild TBI ± High Risk     GCS 14-15 14Neurologic deficits Up to 10% risk of hematoma requiring evacuation Anyone with coagulopathy. age >60 and previous neurosurgery ± Disposition  No CT indicated or negative CT with GCS 15-Home 15 GCS 14 and negative CT-Observation admit CT- .

Spectrum of Traumatic Brain Injury  Moderate TBI ± GCS 9-13 9± 10% of all TBI ± <20% mortality ± 50% morbidity ± 40% positive CT ± 8% NS intervention ± <10 make moderate recovery  Severe TBI ± GCS <9 ± 10% of all TBI ± 40% mortality .

Intracerebral Pressure  Normal <15 mm Hg  ICP >20-25 mm Hg >20± Increases morbidity and mortality  ICP monitoring rarely available in the ED  Must use physical findings ± Neurologic deterioration ± Unilaterally dilated pupil ± Hemiparesis ± Posturing .

Hennepin County Medical Center . Defillo.4% over 15 minutes A. hypovolemia or HTN ± 30 mL of 23.Increased ICP-Management ICP Hypertonic Saline ± Improves CPP and brain tissue O2 levels ± Decreased ICP by 35% (8-10 mm HG) (8± CPP increased by 14% ± MAP remained stable ± Greatest benefit in those with higher ICP and lower CPP ± Repeated doses were not associated with rebound.

reduces hypotension ± Dosage  0.25- .25-1 gm/kg bolus 0. CPP and brain metabolism ± Free radical scavenger ± Reduces ICP within 30 minutes.Increased ICP-Management ICP Mannitol ± Osmotic agent ± Effects ICP. last 6-8 hours 6± Volume expansion. CBF.

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

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Increased ICP-Management ICP Barbiturate Coma ± Not indicated in the ED ± Lowers ICP. cerebral metabolic O2 demand  Anticonvulsants ± Reduce occurrence of post-traumatic seizures post± No improvement in long-term outcome long-  ICP Monitoring ± Should be performed on TBI with GCS <9 ± Increased ICP 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 table- .

commonthe EAC and TM  Dural tear ± ± ± ± CSF otorrhea CSF rhinorrhea Battle Sign Raccoon Sign ± ± ± ± Hemotympanum Vertigo Hearing loss Seventh nerve palsy  CSF testing ± Ring sign.Specific Head Injuries  Skull Fractures ± Basilar Fracture  Most common-petrous portion of temporal bone. glucose or CSF transferrin  Should be started on prophylactic antibiotics ± Ceftriaxone 1-2 gm 1- .

STUDY OBJECTIVE: To study the development of a ring sign when blood is mixed with various fluids.22(4):718 The 'ring sign': is it a reliable indicator for cerebral spinal fluid? Dula DJ. and the specimens were examined after ten minutes for the development of a ring. METHODS: One drop of blood and one drop of either spinal fluid.22(4):718-20. coffee filters. tap water. of filter paper did not affect the development of a ring. Pennsylvania. including standard laboratory filter paper. A variety of filter paper agents were used. W. RESULTS: All fluids. blood alone did not. when mixed with blood.The Ring Sign  Ann Emerg Med. paper towels. DJ. or rhinorrhea fluid were placed simultaneously on filter paper. Apr. the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid. Department of Emergency Medicine. . The type sign. gave rise to a ring sign. Danville. CONCLUSION: In this experimental setting. saline. Geisinger Medical Center. and bed linens. Fales W. 1993 Apr.

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Specific Head Injuries  Brain Herniation ± Four Types     Uncal Transtentorial Central Transtentorial Cerebellotonsillar Upward Posterior Fossa .

Case 1 .

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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  Traumatic Subarachnoid Hemorrhage ± Most common CT finding in moderate to severe TBI ± If isolated head injury. may present with headache.

Case 2 .

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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 accelerationtearing of bridging veins ± Common in elderly and alcoholics ± Classified as acute. subacute or chronic  Acute <2 weeks  Chronic >2 weeks .

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diffuse abnormalities .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.

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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 .

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Headache .ComplicationsComplications-Long Term Sequela  Seizure Disorder ± 2% Early post-traumatic incidence post± Increased to 30% in children.Photophobia . alcoholics and with intracranial hematoma  Prophylactic antiepileptics reduce early occurrence  Use not supported by the literature  Concussion .Vomiting .Brief LOC .Nausea .Cognitive/Memory dysfunction .Dizziness .Vertigo .

Low socioeconomic status .Litigation .ComplicationsComplications-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 85± Risk factors: .Female .

ComplicationsComplications-Long Term Sequela  Infection ± Skull fracture ± CSF leak ± Intubation ± History of Fracture  Fever  Signs of meningitis ± 3rd generation cephalosporin ± Vancomycin ± ICU ± Treatment  Prophylactic antibiotics .

Questions? .

Lecture Questions 1. d. Hypertonic saline Hyperventilation to CO2 of <30 mm Hg Mannitol ICP monitoring Barbiturate coma . c. Which of the following modalities is not recommended for head injured patients with elevated ICP? a. b. e.

It is expensive to society c. Post-concussive symptoms are common Postb. Which of the following are true regarding TBI? a.2. Preventing secondary brain injury is critical in the management d. All of the above are correct .

Epidural hematomas are associated with all of the following except: a. Trauma to the temporoparietal region Extremes of age Have classic presentation only 30% of the time Damage to the middle meningeal artery Damage to a venous sinus . c. d. b. e.3.

Mortality is reduced with nimodipine c. Most common CT finding in TBI e. Size of bleed is unrelated to mortality .4. Has a higher mortality than an equal aneurysmal SAH b. Surgical drainage is usually unnecessary d. Traumatic subarachnoid hemorrhage has all the following features except: a.

d. Concerning basilar skull fractures which of the following is not true? a. e. a . Most commonly occurs in the temporal bone b. b. The ring sign is both sensitive and specific for CSF otorrhea/rhinorrhea b. The only physical exam finding may be a hemotympanum c. Battle and Raccoon signs are usually not initially present in the ED d.5.

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