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: