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Head Injury

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

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Head Injury

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

  2. 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

  3. Head Injury-Anatomy • Scalp • Blood supply • Calvaria • Brain • Occupies 80% of calvarium

  4. 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

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

  6. ICP

  7. Prevent Secondary Brain Injury Hypoxemia Hypotension Anemia 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 1.5 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 Hyperglycemia Evacuation of mass Head Injury-Initial Evaluation and Management

  8. Head Injury-Initial Evaluation and 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 • If ICP is normal, gradually reduce MAP no more than 30%

  9. 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

  10. 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 admit

  11. 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 Spectrum of Traumatic Brain Injury

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

  13. Increased ICP-Management • Hypertonic Saline • Improves CPP and brain tissue O2 levels • Decreased ICP by 35% (8-10 mm HG) • CPP increased by 14% • MAP remained stable • Greatest benefit in those with higher ICP and lower CPP • Repeated doses were not associated with rebound, hypovolemia or HTN • 30 mL of 23.4% over 15 minutes A. Defillo, Hennepin County Medical Center

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

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

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

  17. 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

  18. 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 CSF testing Ring sign, glucose or CSF transferrin Should be started on prophylactic antibiotics Ceftriaxone 1-2 gm Hemotympanum Vertigo Hearing loss Seventh nerve palsy Specific Head Injuries

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

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

  21. Case 1

  22. 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%

  23. Case 2

  24. 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

  25. 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

  26. 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

  27. 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

  28. 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 supported by the literature • Concussion - Brief LOC - Vertigo - Nausea - Dizziness - Headache - Vomiting - Photophobia - Cognitive/Memory dysfunction

  29. 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

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

  31. Questions?

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

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

  34. Epidural hematomas are associated with all of the following except: • 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

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

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

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