10/25/2014 1 Scott P. Sherry, MS, PA-C, FCCM Assistant Professor Department of Surgery Division of Trauma, Critical Care and Acute Care Surgery Traumatic Brain Injuries DISCLOSURES – Nothing to disclose – Discussion of off label medication use Objectives • Overview of the cerebral anatomy • Description of the epidemiology of TBI • Understand and describe different types of TBI • Understand and describe management strategies of patients with suspected or known traumatic brain injury including intercranialhypertension • Understand “prognosis” in the TBI patient
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10/25/2014
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Scott P. Sherry, MS, PA-C, FCCM
Assistant Professor
Department of Surgery
Division of Trauma, Critical Care and Acute Care Surgery
Traumatic Brain Injuries
DISCLOSURES
– Nothing to disclose
– Discussion of off
label medication use
Objectives
• Overview of the cerebral anatomy
• Description of the epidemiology of TBI
• Understand and describe different types of TBI
• Understand and describe management strategies
of patients with suspected or known traumatic
brain injury including intercranial hypertension
• Understand “prognosis” in the TBI patient
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Meningeal Anatomy Review
•
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Traumatic Brain Injury
• 500,000 cases each year in the US
• 10% die before reaching medical care
• Severity:
• 80% mild
• 10% moderate
• 10% severe
• Broad injury pattern
– Concussion, DAI, SAH, SDH, IPH, IVH, EDH
Head Injury Epidemiology
• Trauma mortality: 40 % secondary to brain
injury
• Overall mortality: 7 - 36 % (head injury alone)
• Annual mortality: 100,000
Head Injury Disability
• Survivors of TBI and permanent disability:
• 10 % of those with a mild injury
• 66 % of those with a moderate injury
• ~100 % of those with a severe injury
• 90,000 newly disabled per year
• For those who survive gunshot wounds:
• 10 % have severe disabilities
• 20 % have moderate disabilities
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Traumatic SAH
• Scattered appearance
• Has a risk of vasospasm
– Less incidence than aneurysmal SAH
Pedestrian Struck: SDH, SAH
Fall from Car: IPH, SDH, SAH
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Epidural Hematoma
• Usually an arterial injury
• Has a “classic presentation”
– DO NOT MISS THIS
• Lens shaped appearance to lesion
– Suture attachments
• Urgent surgical intervention is warranted
• Temporal bone fx with middle menigeal artery
• Generally good recovery with prompt intervention
Epidural Hemorrhage
Epidural Hemorrhage
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Epidural Hemorrhage
Epidural Hemorrhage
Epidural Hemorrhage
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Epidural Hemorrhage
Epidural Hemorrhage
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Subdural Hematoma
• Venous injury generally
– Bridging Veins
• Crescent shaped lesion
• Follows subdural tact
– Has attachment points at the front / back.
• Some are acute, chronic and acute on chronic
bleeds
• Most common traumatic mass effect lesion
Subdural Hematoma
Subdural Hematoma
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Subdural Hematoma
Subdural Hematoma
Subdural Hematoma
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Subdural Hematoma
Subdural Hematoma
Subdural Hematoma
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Subdural Hematoma
Subdural Hematoma
Subdural Hematoma
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Subdural Hematoma
Subdural Hematoma
Subdural Hematoma
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Motor Vehicle Crash: SDH
Unwitnessed Fall: SDH
Fall from Barstool: IPH, SDH
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Pedestrian Struck: IPH, SDH
Diffuse Axonal Injury
• Active process triggered by the injury that
takes about 24 hours
• Frequently without radiographic abnormality
• Frequently seen in areas of radiographically
apparent “shear injury”
– this latter finding usually occurs at the grey-white
junction
– MRI is diagnostic
• Major cause of long-term disability
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MVC: IPH, DAI, IVH, SAH
Thalamic Bleed
Cerebral Edema
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MVC: IPH, DAI, IVH, SAH
Assault: IPH
PedestrianStruck: IPH
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ATV Crash: Skull Fx, ICH
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“Found Down”
Suspected Fall
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“Found Down”
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head
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GSW Head
GSW Head
GSW Head (BONE)
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GSW Head (BONE)
GSW Head (BONE)
GSW Head (BONE)
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GSW Head (BONE)
GSW Head (BONE)
GSW Head (BONE)
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GSW Head (BONE)
GSW Head (BONE)
GSW Head (BONE)
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GSW Head (BONE)
GSW Head (BONE)
GSW Head (BONE)
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GSW Head (BONE)
GSW Head (BONE)
Shot Gun Wounds
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Prehospital Care
• High index of suspicion
• Trauma Center Transport
– Immediate
• Prevention of secondary insults
– Hypoxia / Hypotension
Hospital Care
• Immediate CT
– Any LOC
– Amnesia to event
• If e/o TBI
– Neurosurgical Consult
– Prompt transfer if needed
– Frequent neuro checks
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PREVENT Secondary Injury
• Hypoxia and hypotension
– 2 major causes of secondary CNS injury following
head trauma
– These complications occur frequently
• Prevention could have the greatest effect of
any currently available treatment for head
trauma
Outcome from Severe Brain Injury
• Univariate predictors of poor outcome:
– ICP > 25 mm Hg
– MAP < 70 mm Hg or
– CPP < 60 mm Hg and fluid balance < -594 mL
Clifton et al. Crit Care Med 2002;30:739–745.
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Increased Intracranial Pressure
• Monroe Kellie
– Volume of the skull is a constant
• Brain ~ 85%
• Blood ~5%
• CSF ~ 10%
• An increase in the volume of any of these will
raise ICP
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Important Formulas
• Cerebral Perfusion Pressure (CPP)
= Mean Arterial Pressure – Intercranial Pressure
– Goal CPP > ~ 60
– Guidelines = 50-70mm Hg
Increased Intracranial Pressure
• Management
– Correct the underlying pathophysiology if possible
– Airway control and prevention of hypercapnea are crucial
• Posture and head position
– ICP monitoring
– Avoid jugular vein compression
• Head in neutral position with body
• Head of bed elevated > 30 deg
• Cervical collars loose or remove
• No circumferential ETT Tape
Increased Intracranial Pressure
• Hyperventilation (PaCO2 < 35 mmHg)
• Works by decreasing blood flow
– should be reserved for emergency treatment and
only for brief periods.
• Avoid Severe Hyperventilation < 30
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Increased Intracranial Pressure
• Pharmacologic options
– Mannitol 1G / KG
– Follow up doses
• 0.25-0.5 gm/kg q4h
• Follow Serum OSM < 320
– Hypertonic Saline
• 3%
• 7.5%
• 23.4%
– Lasix / Diuretics
Increased Intracranial Pressure
• Sedation and Analgesia
– Opiods
– Benzodiazepines
– Propofol
• Decrease cerebral metabolic rate, which is coupled to blood flow
– Prevent hyperthermia
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Slide 118
Increased Intracranial Pressure
• Neuromuscular junction blockade
– Titrate with train-of-four stimulator to 1 or 2
twitches
• High-dose barbiturates
– E.g., pentobarbital 5 – 12 mg/kg load followed by
infusion to control ICP
– Risk of infection
Slide 119
Increased Intracranial Pressure
Surgical options
• Resect mass lesions if possible
• Ventriculostomy Drainage
• Craniectomy
– Lateral for focal lesions
– Bifrontal (Kjellberg) for diffuse swelling
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CCM April 2013
Recovery - Trajectory
• Emergence of conscious awareness
• Recovery of higher processing
• Return of functional capacity
Recovery from COMA
• Vegetative state
• Minimally conscious state
• Emergence from minimally conscious state
– Functional communication
– Object use
• Time course variable
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Natural History of VS / MCS
• Not well studied
– 50% MCS / 3% VS had no or mod disabilities when
evaluated after 1 year of injury
– More rapid improvement in the traumatically
injured
• After recovery of awareness
– May have significant neurologic impairments
– Motor, dystonic, movement disorders, aphasia.
– Attention, mood, memory, seizure disorders
Organ Donation
• Treat all traumatic brain injuries to the fullest