TBI Flashcards
Primary brain injury involves:
injury includes
Direct vascular damage also occurs leading to
Laceration is the most severe form of primary brain
axial hematomas
extraaxial hematomas in the
leading to compression of the brain and severe neurologic dysfunction
Historically it has been believed that extraaxial hemorrhage is rare in dogs and cats suffering from TBI. However, more recent evidence suggests that this type of hemorrhage occurs in up to _____% of animals with mild head injury and in >_____% with severe injury
physical disruption of intracranial structures
contusions, hematomas, lacerations
intracranial hemorrhage and vasogenic edema
within the brain parenchyma
subarachnoid, subdural, and epidural spaces
10%
>80%
excitatory neurotransmitters:
which excitatory NT should you remember and what does it do?:
- massive release of excitatory NT
- influx of Na & Ca
- depolarization, further release of excitatory NT ie (glutamate)
- glutamate mediates accum. of Ca activates numerous intracellular enzymes =ultimately cell death
- depletion of ATpP = cell death
glutamate - increase intracell. Ca
ROS
3 main triggers:
MoA:
acidosis
hypoperfusion
hemorr./iron triggering Haber-Weiss reaction
- local tissue acidosis and hypoperfusion trigger ROS formation
- ROS preferentially damaging to cell membranes w high levels of polyunsaturated fats and cholesterol .:. brain tissue
- hemorrhage may serve as an iron source
- which favors the production of OH (hydroxyl) radicals via the Haber‐Weiss reaction of the xanthine oxidase pathway
NO/CK
NO contributes to ROS‐ & glutamate‐med tissue damage
- release of inflammatory CK
- followed by accum. inflammatory cells
- activate AA andcoagulation cascades, disrupting the BBB, and …
- inducing nitric oxide (NO) production
=excessive vasodilation leading to the loss of pressure autoregulation
worse primary injury ranked
laceration>contusion>concussion
Systemic insults that contribute to secondary brain injury:
HHHHH
hypotension, hypoxemia, hyperglycemia, hypoglycemia, hypercapnia, hypocapnia, hyperthermia
electrolyte imbalances, and acid-base disturbances
ICP explained via Monroe‐Kellie doctrine holds that the skull is a rigid compartment that contains 3 components:
normal circum, these components exist in state of:
increase occurs in the volume of one component:
accommodation is known as:
and accomplished by:
limit to intracranial compliance results in:
severe increases in ICP trigger the:
brain parenchyma
arterial and venous blood
CSF
balanced dynamic equilibrium
one or more of the other components must decrease or an elevation in ICP will result
intracranial compliance
fluid shifts in the brain vasculature and CSF pathways
= ICP
= ischemia of brain tissue
cerebral ischemic response, or Cushing reflex
Cushing reflex MoA:
why the increased MAP:
why the decreased HR:
CPP equation:
cushing’s reflex occurs when:
- > ICP result in decreased cerebral blood flow (CBF)
- increased CO2
- sensed at the vasomotor center
- initiates a SNS response leading to massive catecholamine release and > MAP
attempt to increase cerebral perfusion pressure (CPP)
hypertension is detected by baroreceptors
= reflex bradycardia
CPP = MAP - ICP
late = life‐threatening elevation in ICP
Blood flow to the brain per unit time, or cerebral blood flow (CBF), is a function of CPP:
normal brain CBF autoreg.:
How does this change with trauma:
“Monro-Kellie Doctrine,” developed in the early nineteenth century to describe intracranial dynamics:
CPP is driving pressure in brain
MAP 50 to 150 mm Hg
loses much of this autoregulatory capacity
=susceptible to ischemic injury w small decreases in MAP
V intracranial = V blood + V parench + Vcsf + V lesion
primary determinant of CBF:
Blood flow to the brain per unit time, or cerebral blood flow (CBF), is a function of CPP:
normal brain CBF autoreg.:
How does this change with trauma:
“Monro-Kellie Doctrine,” developed in the early nineteenth century to describe intracranial dynamics:
CPP
CPP is driving pressure in brain
MAP 50 to 150 mm Hg
loses much of this autoregulatory capacity
=susceptible to ischemic injury w small decreases in MAP
V intracranial = V blood + V parench + Vcsf + V lesion
Tx priorities:
ABC the systemic stuff first
Tx priorities:
- ABC the systemic stuff first
2. vertebral, skull
Initial neurologic assessment includes evaluation of (5):
level of consciousness
pupil size and responsiveness/ocular position & movem.
skeletal motor responses
breathing pattern
In human patients TBI is graded as mild, moderate, or severe based on the Glasgow coma scale
MGCS for TBI has been evaluated with respect to survival over a 48‐hour period:
MGCS incorporates 3 categories:
assigns a score from:
- estimate of prognosis for the veterinarian and owner
- higher better px
- **better utilized as obj assessment of progression of neurologic signs rather than as a prognostic indicator (SIS for individual vs group)
level of consciousness
motor activity
brainstem reflexes
1 to 6, total score of 3–18
motor activicty:
-affected by the animal’s level of consciousness
decerebrate rigidity
decerebellate rigidity
main determination between cerebral and cerebellar injury is ____
decerebrate patient, results in a comatose state = damage to ____ & associated w grave prognosis
opisthotonus with hyperextension of all four limbs
= cerebral damage
variable flexion and extension of the hind limbs
= cerebellar damage
level of consciousness
RAS within the midbrain
brainstem reflexes:
Pupils that respond appropriately to light indicate adequate function of:
Miotic pupils indicate:
Progression to mydriasis may indicate:
Transtentorial herniation places pressure on:
resulting in:
Fixed, unresponsive and midrange pupils are seen with:
Brain herniation is associated with severe disability and death if not treated rapidly and aggressively
Repeated neurologic assess recommended every ____
rostral brainstem, optic chiasm, optic nerves, and retinae
diffuse forebrain injury
brain herniation
CN III, interrupting parasympathetic input to the eye resulting in a dilated pupil
cerebellar herniation
30–60 minutes to monitor tx efficacy/assess deterior.
Tx:
1.
2.
Extracranial stabilization: correction perfusion, optimizing systemic oxygenation and ventilation
Intracranial stabilization: optimizing cerebral perfusion, decreasing ICP, and minimizing elevations in the cerebral metabolic rate
Initial Extracranial Therapy
Fluid therapy:
restoration of intravascular volume to ensure ___
discuss hx recommendations for fluid restriction:
hypotension has been shown to be associated with:
In 1 prospective study, hypotension was associated with a ____% increase in mortality
adequate CPP
little/no data to support idea that dehydration diminishes cerebral edema and these recommendations for fluid restriction are firmly contraindicated
significant increases in morbidity and mortality in human TBI patients
150% increase in mortality
fluid type controversy:
It is the _____, rather than the plasma _____ pressure, that determines water movement between the vascular and extravascular compartments
.:. uninjured brain, minimal concern that aggressive crystalloid resuscitation may produce cerebral edema b/c
injured brain the BBB may be disrupted regionally or globally. This disruption may result in increased permeability to both ions and _____ particles
regaurdless, benefit obtained by the restoration of CPP with either crystalloids or colloids outweighs the potential risks
osmolality vs oncotic pressure
isoosmolar .:. no fluid shifts
colloidal
Hypertonic saline is superior why?
> osmolarity promotes transcapillary shift of interstitial and intracellular fluid into the vasculature
marked volume expansion exceeds the volume infused
4mL/kg of 7.5% sodium chloride
< ICP and >MAP
after resusc. then what?
continued fluid therapy is mandatory
hypertonic solutions act to dehydrate
maint. + ongoing
Oxygenation and ventilation
decreased oxygen delivery is a main perpetrator of:
human studies in TBI patients have shown that mortality for patients with documented hypoxia after injury is ____that of patients w.out doc. episodes of hypoxia
lethal level of hypoxemia - pulse os 75% = PaO2
Nasal oxygen cannulas and transtracheal oxygen catheters supply approximately 40% inspired oxygen concentration with flow rates of:
secondary brain insult
double
40mmHg
50–100mL/kg/min
what is the most imortant fctor controlling CBF?:
Plasma CO2 tension regulates cerebral blood vessel diameter -
hypercapnia vs hypocapnea:
most accurate method to monitor PaCO2 levels:
rak VBG, ABG, ETCO2 highest to lowest CO2:
PaCO2
dilation vs constriction
ABG
VBG > ABG > ETCO2
hypoventilating patients may require:
Hyperventilation has traditionally been viewed as a method of decreasing ICP. Hyperventilation:
However, it has been shown that even moderate hypocapnia (CO2 <34mmHg) leads to excess vasoconstriction, perpetuating cerebral hypoperfusion
When can aggressive hyperventilation be considered:
MV
cerebral vasoconstriction < CBV < ICP
brief periods of time in patients with acute deterioration but still not below a PaCO2 of 30
Initial Intracranial Therapy
Minimizing increases in ICP
Positioning the head such that it is elevated:
must prevent:
15–30° angle
-reduce CBV by increasing venous drainage
bending of neck .:. stiff board
Hyperosmotic agents
Mannitol:
____is considered the first‐line therapy
dose ____
mannitol
0.5 to 1.5g/kg over 15–20 minutes
study showed that high‐dose (∼1.4g/kg) = significant neurologic improv. vs (∼0.7g/kg) therapy
Hyperosmotic agents
Mannitol:
____is considered the first‐line therapy
dose ____
MoA
rheologic mechanism:
onset
duration
Osmotic mechanism:
onset
duration
limit in trauma:
Free radical scavenging properties:
furosemide + mannitol?
mannitol
0.5 to 1.5g/kg over 15–20 minutes
study showed that high‐dose (∼1.4g/kg) = significant neurologic improv. vs (∼0.7g/kg) therapy
controversy exists MoA
-transient plasma expansion decreasing blood viscosity
=cerebral vascular vasoconstriction to maint. CBF
.:. ICP decreases secondary to a decreased CBV despite maintained CBF
- rheologic mechanism most profound effect on ICP
- occurs immediately, persists for approx 75 min
-osmotic effects delayed for 15–30 min
-nontraumatized brain mannitol promotes the shift of water ICS, ISS to IVV
= osmotic diuresis, reducing cerebral edema
-peaks 1 hour - persist for 6–8 hours
-traumatized brain decreased perfusion of parenchyma
- reported to have free radical scavenging properties
- limit secondary oxidative injury
-addition of furosemide has no effect + risk of worsening hypovolemia
Mannitol administration is contraindicated in:
being freely filtered, it retains fluid within the renal tubules resulting in wasting of _____
hypovolemic patients
electrolytes and water
only to normo‐volemic followed w crystalloid
exacerbation of ongoing intracranial hemorrhage:
- by its osmotic effect. However, there is no clinical evidence to prove this theory and, as the benefits of treatment far outweigh the theoretical risks, it may be:
Mannitol may cause increased permeability of the blood-brain barrier:
disregaurded
worse when in circ long time .:. no CRI rather boluses
reverse osmotic shift:
-In situations of prolonged contact (multiple bolus doses or continuous infusions) mannitol can accumulate in the extravascular compartment exceeding the intravascular concentration and leading to brain edema and an increase in ICP. However:
reverse osmotic shift is less likely to occur with appropriate bolus use of mannitol
Hypertonic saline
intact BBB is relatively ______ to sodium and chloride
hyperosmolar concentrations:
- creates a driving force shifting
- improves regional CBF via
- excitotoxicity by promoting reuptake of excitatory amino acids, such as:
duration:
must exclude ____ before treatment:
Risk of aggravating _____:
risk exists for mannitol as well and may be worse than hypertonic saline in the patient with pulmonary contusions
Studies comparing mannitol and hypertonic saline
When equimolar doses of mannitol, 3% NaCl, and 23.4% NaCl were compared in a ovine model of intracerebral hemorrhage, ICP reduction was most prominent after:
However, after 2 hours only ___ had a sustained effect on ICP and the ICP in the ____ animals exceeded the pretreatment ICP
- this study suggests that hypertonic saline may actually be favored over mannitol
- rodent model = 23.4% hypertonic greater ICP decrease and a more sustained effect than mannitol
- human patients w increased ICP = hypertonic saline‐dextran solution lowered ICP more effectively and longer than mannitol
impermeable
-shifting water from the interstitial and intracellular spaces of the brain into the intravascular compartment thus reducing brain water content and ICP
-dehydration of cerebrovascular endothelial cells
reduction of endothelial edema = increase in vessel diameter = improving CBF
-reduction in ICP
-and enhanced cerebral oxygen delivery
- glutamate, into the intracellular space
l- reducing adhesion of polymorphonuclear cells to microvasculature modulating the inflammatory response
volume expansion 15–75 minutes
beneficial effects on ICP are maintained far longer
hyponatremic
pulmonary edema or contusions
prominent after 23.4% NaCl administration
3% NaCl had a sustained effect
mannitol‐treated animals exceeded the pretreatment ICP
At this time The Brain Trauma Foundation Guidelines still consider ______to be first line treatment for ICP TBI
recent studies support the growing clinical literature that hypertonic saline may in fact be superior to mannitol in controlling ICP with fewer untoward effects
especially valuable in situations of shock and hypotension when administered with an artificial colloid.
mannitol
untoward effects
NaCl similar rheologic and osmotic effects to mannitol
-hypotension is a less likely sequela why?:
Na reabsorbed in the kidneys
