Head Injuries Flashcards
Brain anatomy
Cranium - skull
Dura mater - thick membrane around brain
Subarachnoid - between Pia and dura
epidural space - above dura mater
Subdural space - below dura mater
Monro-Kellie hypothesis
The cranial vault is a fixed space
3 intracranial components:
1. Brain
2. CSF
3. blood
Any increase in one component requires a decrease in another (and/or an increase in pressure)
Intracranial Pressure (ICP)
Measurement of pressure inn the intracranial vault
Normal: 0-15 mmHg
Estimate high when calculating cerebral perfusion pressure (CPP)
Cerebral Blood Flow (CBF)
Requires 15-20% of cardiac output to meet metabolic demands.
Maintained by cerebral autoregulation; despite changes in CPP
Cerebral Perfusion Pressure (CPP)
Gradient driving cerebral blood flow (CBF)
Calculated as CPP = MAP - ICP
( MAP = [[DBP x 2]+SBP] / 3 )
Assume ICP = 20
Normal CPP averages 60-80 mmHg
Brain requires 60-70 for optimal CBF
Strive to maintain CPP at:
>70 mmHg for adults
>60 mmHg for peds
CPP <50 mmHg = infarction
If goal is CPP of 70:
CPP = MAP - ICP
70 = MAP - 20
MAP = 90…. 90 is the minimum MAP for TBI
For kids, can target a MAP of 80 for CPP 60
Mean Arterial Pressure (calculation)
MAP = [[DBP x 2]+SBP] / 3
Cushing’s Triad
Clinical sign of increased ICP due to herniation
Bradycardia
Hypertension (widening pulse pressure)
Cheyne-stokes respirations
Increased ICP signs
tachycardia
Hypertension (widening pulse pressure)
Cheyne-stokes respirations
Change in LOC, pupil size and reaction, motor response.
Signs of herniation:
decorticate - flexion of upper extremities towards core
Decerebrate (more ominous) - extension of upper extremities
Blown pupil(s)
Traumatic Brain Injuries (primary vs secondary)
Primary Injuries
precipitating injury resulting in immediate injury
…Direct trauma
…inracerebral bleed
Can be localized or diffuse.
Secondary injuries
Biochemical and cellular responses to the injury
Can exacerbate the primary injury and cause loss of brain tissue that was not initially injured.
3 H’s of secondary brain injury
Hypoxia
Hypo/hyper-tension
hypo/hyper-capnia
Ischemia
Edema
Increased ICP
Vasodilation - body’s attempt to increase blood supply to the ischemic tissue.
Maintain EtCO2 between 35-40 mmHg
What to do if increased ICP
Reduce stimulation:
Reduce noise, light, sound
Suction only if necessary
Good fluid balance
Temperature regulation
Sedation and analgesia
Head of bed at 30 degrees
Osmotherapy with mannitol or hypertonic saline
Concave vs convex appearance of BLOOD on head CT
Subdural hematoma = concave (banana)
Epidural hematoma = convex (lemon)
Subdural hematoma
Occurs between the dura mater and the arachnoid membrane
Concnave appearance on CT like banana
Venous bleeding
Acute <4 days (bright white on CT)
Subacute 4-21 days blended black/white
Chronic >21 days black blood appearance.
Causes:
hypertensive hemorrhage
ruptured aneurysm
Trauma
Can have immediate LOC
Can be acute, subacute, or chronic
Acute subdural bleeds have a 40-60% mortality rate.
Falx cerebri
Brain midline
Should be a vertical line from 12-6 o’clock
Subdural hematoma treatment
Advanced airway management
…any hypoxia, hypotension, or aspiration can lead to increased mortality… (up to 50% mortality with each)
maintain EtCO2
Adequate fluid resuscitation
Osmotherapy:
mannitol, lasix, 3% saline
Maintain serum Na at upper limit of 155 mEq/L…high Na pulls volume out of cells
Anticonvulsants for seizure prevention
epidural hematoma
Convex appearance on CT like lemon
Usually trauma related
Occurs between the cranium and dura mater; often associated w/skull fracture.
Often injury to pterion region near temple.
Usually arterial bleeding from middle meningeal artery but sometimes venous
Cause rapid compression of brain stem
Classic presentation:
…LOC –> ‘lucid interval’ –> neuro deterioration
Remember: MMA artery like MMA fighter
Deterioration after lucid period
Airway issues during second period of unresponsiveness…always intubate
subarachnoid hemorrhage
Occurs between arachnoid and Pia mater
Causes:
trauma
ruptured cerebral anneurysm
Rupture of arteriovenous malformation (AVM)
Signs/symptoms:
Decreased mental status to coma
Seizures
Sudden onset of severe headache
N/V
Most commonly originate in circle of willis
Anterior communicating artery (40% of subarachnoid hemorrhages)
Treatment:
Maintain SBP <140 mmHg (nicardipine)
Decrease ICP
Complications:
rebreeding, cerebral ischemia, vasospasm, hydrocephalus
Overall mortality is high
Intraventricular hemorrhage
Primarily caused by trauma (shearing forces), aneurysm, vascular malformation
Found in frontal and temporal lobe injuries
Treatment:
Prevent further injury
Maximize CPP >70 mmHg
Maintain SBP <160 mmHg
…for slightly higher perfusion pressure
Control ICP
Diffuse Axonal Injury (DAI)
Occurs when nerve fibers are shorn, torn, or stretched as the result of head impact (frontal-occipital impacts).
Treatment: aimed at preventing secondary injuries.
Avoid hypotension, hypoxia, cerebral edema, and elevated ICP
CT scans don’t pick up on these injuries
MRI needed to show injury
Anterior Cord Syndrome
Least common type of SCI
Causes:
Iatrogenic
Anterior spinal artery embolus
aortic dissection repair
Hyperflexion injury of cervical spine (head coming forward/down
Signs/Symptoms
Injury below T10
Fecal/urinary incontinence
Spastic paralysis
Loss of pain, pressure, temp, crude touch
Brown-sequard syndrome
Causes:
penetrating trauma (stabbing, GSW)
Spinal cord tumor (ipsilateral)
Signs/symptoms
Ipsilateral loss of fine touch, proprioception, vibration.
Contralateral loss of pain and temp; 1-2 segments below lesion level.
+ babinsky sign
Central Cord Syndrome
Causes:
Hyperestension injury (head back)
MVA, diving, minor fall
Syringomyelia (Chiari malformation)
Cervical-thoracic injuries
Upper motor neuron related
Affects upper extremities more often than lower extremities
SCIWORA
Often associated as swelling of spinal cord
Spinal Cord Injury Without Radiograph Abnormality
F/U MRI 6-9 days after injury to exclude evolving cord edema in pts with ongoing sx
SCI S/S pearls
Pt feels hot (I’m burning up)
Can pt lift legs?
Hot + can’t lift legs –> likely SCI
Spinal shock
Acute SCI
Loss of voluntary reflexes below level of injury.
Lasts days to months.
Neurogenic shock
Acute SCI: C1 - C5
Loss of vasomotor and sympathetic nervous system tone below level of injury
Hypotension, bradycardia, temp regulation issues.
Lasts up to 6 weeks.
Levophed is first line med.
Autonomic dysreflexia
Lesions at T6 and above
Triggered by (pain) stimulus below level of SCI
Over-reaction of ANS which can induce hypertensive crisis, slowed HR
Hypoxia or hypotension in TBI
one episode of either can increase mortality by 50%
Hypercarbia in TBI
Leads to increased cerebral blood flow and increased ICP
Target EtCO2 40
hypocarbia in TBI
caused by hyperventilation
Leads to decreased cerebral blood flow and possible cerebral ischemia
Target EtCO2 40
