#EMConf: Head Injuries


General Terminology:

  • Traumatic Brain Injury: Brain function impairment that results from external force
  • Glasgow Coma Scale: Says nothing about underlying structural brain injury, but provides a common language across consultants and is effective for measuring recovery and response over time
  • Primary vs secondary brain injuries:

Classification of TBI

  • Mild (GCS 14-15) = 80% of TBIs; can be a concussion, but can lead to significant debilitating long term sequelae
  • Moderate (GCS 9-13) = 10% of TBIs; 20% mortality for isolated injury, but only 40% will have an abnormal CT finding
  • Severe TBI (GCS 3-8) = 40% mortality, often in the first 48 hours; <10% have good neurologic recovery

Goals for Management of Elevated ICP Secondary to Traumatic Brain Injury: Prevent Secondary Injury!

  • Elevate HOB 30 degrees to decrease ICP and improve oxygenation
  • PaCO2 is the most powerful determinant of cerebral blood flow, with a goal of 35-45 mmHg (NORMAL)
  • Goal PaO2 >60mmHg with SpO2 >90%, basically avoiding hypoxia
  • Also want to avoid hypotension (GOAL CPP >60mmHg; CPP = MAP-ICP so you want MAP 100-110)

Management of Elevated ICP Secondary to Head Bleed

  • Head CT (sometimes serial imaging)
  • Early neurosurgery consult 
    • Bolt” = EVD / Ventriculostomy/ parenchymal pressure monitor to directly measure ICP
    • Emergent Decompressive Craniectomy: Removal of a portion of the skull to allow for brain edema and to avoid downward herniation
  • Reverse anticoagulation
    • Heparin: Protamine
    • Warfarin: PCC or FFP or IV vitamin K
    • DOACs: PCC; for particular DOACs = Idarucizumab for Dabigatran, Andexanet Alfa for Xa inhibitors (Rivaroxaban and Apixaban) 
    • ASA or Clopidogrel: Platelet transfusion
  • Consider seizure prophylaxis
  • Mannitol or Hypertonic saline 

Patterns of Hematomas

  • Epidural: Direct blow to head, usually at pterion, injury to middle meningeal artery
    • Brisk bleeding
    • Initial LOC then lucid interval, then neuro deterioration
    • Need urgent neurosurg consult and possible intervention
    • Lens shaped bleed does not cross suture line
  • Subdural: Elderly, sudden acceleration-deceleration injury
    • Tearing of bridging veins, SLOW venous ooze, therefore may not be symptomatic until days or weeks after initial injury
    • Elderly or alcoholic
    • Crescent shaped, crosses suture lines
    • Acute bleed = < 2 weeks vs chronic bleed >2 weeks 
    • Usually these do not require surgical intervention; greater mortality if they do
  • Traumatic SAH: Sudden deceleration injury causing shearing of blood vessels into the subarachnoid space
    • Most common CT abnormality in moderate to severe TBI
    • Most sensitive is CT 6-8 hours AFTER injury, can be missed on early CT
    • Rebleeding is very common
    • Large traumatic SAH may dissect into the ventricles, causing hydrocephalus
    • Traumatic SAH blood tends to collect on the brain periphery (in the cerebral sulci) vs. spontaneous SAH causes central collection of blood in the basal cisterns (star pattern)
  • Cerebral Hematomas/Contusions: Deceleration injury, severe trauma, penetrating trauma, shaken baby syndrome
    • Collections of blood WITHIN the brain parenchyma and along the base of the brain (irregular contour)
    • Most commonly= frontal and temporal
    • White lesions with surround edema (darker) that expand overtime and can result in mass effect and herniation
    • No real surgical management; just do serial CTs 

DAI = Diffuse Axonal Injury:

  • Occurs as a result of traumatic deceleration
  • Shearing of AXONS in the deep white matter
  • Typical clinical picture: Comatose patient with no or minimal signs of injury on initial head CT; MRI shows extent of the damage!
  • Devastating prognosis, can progress to massive swelling and herniation within hours or days after injury
  • Treatment is supportive

Skull Fractures: