Terms in this set (48)
What is the leading cause of death & disability in young adults?
Stats for TBI
Every 5 minutes 1 American dies or is disabled
Economic costs-25 billion/yr
Peak rates 15-24 y.o.
Male to female ratio for TBIs
Causes of TBI
High association w/ alcohol or drug use
What are the types of head injury based on?
Location of injury
Types of depressed skull fractures
Meninges intact (have more time) ␣ Meninges torn (immediate surgical management)
How are depressed skull fractures diagnosed?
Skull is deformed
Missile injuries may cause burst type fracture
Management of depressed skull fractures
Elevate skull fracture (don't pull foreign bodies unless directly visualizing, Abx early-staph biggest risk)
What agent is not recommended in the management of depressed skull fractures w/ general anesthesia and why?
Vancomycin (histamine release, cardiac depression)
Types of epidural hematomas
Describe arterial epidural hematomas
Rapid deterioration after a lucid period
Tentorial herniation w/ CN III involvement
Immediate surgical intervention required
Describe venous epidural hematomas
May obtain CT
Mechanism of epidural hematomas
Middle meningeal vessels, dural sinus
Types of subdural hematoma
Acute-symptomatic w/in 72˚
Sub-acute-symptmatic w/in 3-15 days
Chronic-symptomatic after 2 weeks
Mechanism of subdural hematomas
75% d/t trauma
Spontaneous 25% d/t coagulopathies, aneurysms, neoplasms
Intracerebral contusion or hemorrhage
Subarachnoid hemorrhage-prognosis poor, blood toxic to brain tissue, clots may occlude CSF drainage
May benefit from surgical drainage
Evaluation of a brain injured patient
Realize cannot change the damage, can only prevent 2˚ injury
Rapid management critical
On arrival check ABC
Perform neuro exam (GCS)
What does the glasgow coma scale (GCS) allow for?
Grading of impairment of consciousness
What is assessed w/ the GCS?
Eye opening, best motor response, verbal response
In regards to GCS, what is considered to be severe head injury?
8 or less
What is the GCS used for?
Drive algorithms, predict outcomes & morbidity
Emergency evaluation & care for TBI
Initial impact is not amenable to tx
2˚ injury is treatable (hypoxia, hypotension, delay in tx, sepsis, seizures)
Respiratory abnormalities after a TBI
Central: apnea, hypoxia, hypercarbia, neurogenic pulm edema
2˚ abnormalities after a TBI
Aspiration, multiple trauma, fat embolism, DIC, drug related problems, iatrogenic conditions
Tx of respiratory abnormalities associated w/ TBI
Always give 02, achieve Pa02 > 100 mmHg, maintain normal PaC02
<1 hr 22% mortality
>1 hr 38% mortality
Indications to intubate w/ TBI
Sp02 < 94%, Pa02 < 70 mmHg, PaCO2 >45 mmHg, RR <10 or >30, any abnormal respiratory pattern, inability to protect airway
What is the gold standard to assess breathing?
Check for ETCO2
What is hypotension in TBI usually associated with?
Other injuries: ruptured spleen or liver, brain stem injury, spinal cord shock
Common CV response to TBIs
Normal symptoms: tachycardia, HTN
Pathophysiology of tachycardia and HTN associated w/ TBIs
Activation of autonomic system
Cushings response to TBIs
What does a Cushing's response indicate?
Brainstem injury-poor prognosis
Describe EKG changes associated w/ TBI
ST segment depression
What is QT prolongation associated with?
The more the prolongation the worse the outcome
Fluid management & TBIs
Perfusion is key-requires euvolemia, adequate tissue oxygenation
E-lyte balance is important
Describe the BBB
Don't allow lg proteins or sugars to pass normally
Hydrostatic forces are not usually an issue
What do decreases in CPP lead to?
Ischemic cellular injury, ↑d cell edema->further ↑s the ICP->worsening CPP
Describe MAP and CPP
Should be preserved-HTN may not be bad, may indicate ↑d ICP, severe HTN may worsen the condition
What agents decrease MAP?
What should be avoided in the treatment of MAP and why?
Nitroprusside, hydralazine (direct arterial vasodilators as they ↑ CBF)
What can increase ICP
Cerebral vasodilation: brain swelling, ↑ in CBV (hyperemia), cerebral vasoparalysis (responsiveness to tx of vasoconstriction)
What are the effects of prolonged hyperemia?
Causes vasogenic edema, ↑d ICP, eventual herniation of the brain
What agents decrease ICP
Mannitol, diuretics (lasix), barbs, propofol, etomidate
Effects of mannitol on ICP
Lowers ICP: ↓s blood viscosity, ↑s O2 delivery, reflex vasoconstriction
Effects of lasix on ICP
Lowers ICP: ↓s brain H20 content,prolongs action of mannitol, ↓s CSF formation
What agents are not indicated in patients w/ TBI since they may worsen outcome?
Mechanical ways of decreasing ICP
Release of hematoma, drainage of CSF, craniectomy, hyperventilation, head up position
Reduction of ICP
Maintenance of CBF
↓ of CMRO2
Scavenging free radicals
Prevention of seizures
↓ of sympathetic action
↓d intravascular sludging
Prevention of Ca++ shifts