Acute Brain Injury Flashcards
(28 cards)
what is the key to managing head trauma cases
there are minimal effective interventions
many will resolve with TIME and you need to provide supportive care
primary vs secondary injury after head trauma
primary: initial traumatic event causing parenchymal damage and vascular disruption
secondary: later stage effects of trauma leading to edema, inflammation, hypoxia, ischemia, neurotoxicity, and death
what happens when brain volume increases (ex. with inflammation)
increases ICP leading to decreased CPP –> less O2 –> ischemia, necrosis, death
cerebral blood flow (CBF)
amount of blood coming into and out of the cerebrum
depends on arterial inflow, venous outflow, and cerebrovascular resistance
cerebral perfusion pressure (CPP)
CPP = MAP - ICP
if ICP increases –> CPP decreases –> less O2 supply to the brain
volume buffering capacity of the brain
compensatory mechanisms of the intracranial contents to accommodate changes in volume without changing ICP
immediate: displaces CSF and blood OUT of the brain to decrease volume
long term: decrease ECF space, brain atrophy
Cushing’s reflex
global response of the brain to dangerously high ICP
brain trauma –> increase ICP –> brain tries to increase arterial pressure via peripheral vasoconstriction to compensate –> hypertension –> reflex bradycardia
clinical signs of intracerebral hemorrhage
cerebral signs
1. altered mentation
2. brainstem dysfunction
3. loss of motor control
4. abnormal posturing
what should you always assume about head trauma patients prior to treatment
assume they are on the upper end of the ICP vs ICV curve - so small increases in volume will cause dramatic increases in pressure
how does herniation happen
increased ICP –> creates large pressure gradient between intra and extracranial space –> brain herniates into lower pressure space
what are the most common sites of herniation
- foramen magnum: cerebellum herniates out the back of the skull
- transtentorial: cerebrum herniates under the tentorium cerebelli into the space of the cerebellum causing MIDBRAIN damage
- can lead to blown pupils (fixed and dilated) if becomes decerebrate
what are the ways to measure ICP
exam - look for the clinical signs associated with high ICP
direct ICP monitors
imaging (rare)
what is the goal of brain trauma treatment
maintain cerebral perfusion pressure by altering
- PaCO2
- MAP
- PaO2
- CMR
- drugs
- venous outflow
PaCO2 effect on ICP and treatment
most significant factor controlling ICP/CBF
high PaCO2 –> vasodilation –> increased ICP
tx: ensure airway is patent
- keeps PaCO2 at physiologic levels
MAP effect on ICP and treatment
brain has autoregulation mechanisms to keep pressure stable despite changes in MAP between 50-150 mmHg
tx: only treat HYPOTENSION with fluids
- do NOT treat hypertension (brain will resolve on its own)
PaO2 effect on ICP and treatment
decreased PaO2 causes cerebral vasodilation –> increases CBF –> increases ICP
tx: use flow by O2
cerebral metabolic activity (CMR) effect on ICP and treatment
metabolic activity causes production of metabolic byproducts that decrease pH and cause vasodilation –> increases ICP
high CMR –> fever, pain, seizures
tx: control fever, pain, seizures to lower metabolic activity of the brain
what drugs should be avoided in head trauma cases
inhalant anesthetics
- causes vasodilation and increased ICP
what drugs are good to use in head trauma cases
- barbituates
- propofol
- dexmedetomidine
what are ways to ensure adequate venous outflow
- keep head above the heart
- avoid jugular compression (catheters, blood draws)
what are the steps of treating a head trauma patient
- stabilize
- examine
- determine severity
- treat secondary injury
- supportive therapy
- diagnose and treat primary disease
- determine prognosis
what to do to stabilize patient
A: airway patency
B: breathing
C: compressions if needed
- immobilize if patient is showing signs of instability
- get a PCV, TP, BUN, glucose, and electrolytes
- get a history
what should you examine in a head trauma patient
PE: check for bleeding, signs of CV status, and other external injuries
Neuro: localize the lesion
do NOT dilate the eyes - need to be able to assess pupils
what are clinical signs of increased ICP
- declining mentation
- dilated and unresponsive pupils
- CN dysfunction - decreased gag, absent physiologic nystagmus, declining motor
- abnormal respiratory patterns
- abnormal posturing (decerebrate, decerebellate, schiff-sherrington)
