Neuro Emerg 20: Head Trauma Flashcards
What is the normal ICP in a dog?
5-12 mm Hg
What regulates cerebral blood flow?
- partial pressure of carbon dioxide
- partial pressure of oxygen levels
- cerebral metabolic activity
What is the relationship between CBF, CPP, and CVR?
CBF = CPP/CVR
CBF - c blood flow
CPP - c perfusion pres.
CVR - c vascular resistance
What is cerebral compliance?
the ability of the cranial contents to decrease in volume - in an attempt to reduce ICP
How do you define concussion?
a traumatic reversible paralysis of the neurologic function
immediate in onset
does not describe the underlying brain pathology
How do you define brain contusion?
bruising of the brain surface, without rupture of the pia-arachinoid or interruption of the brain architecture
How much of the total CO supplies the brain?
15-20%
What are the 3 components of CBF autoregulation?
- Myogenic mechanisms
- Chemical mechanisms
- Neurogenic mechanisms
At what MAP range can the autoregulation achieve a constant CBF?
50-150 mm Hg
outside this range CBF depends on systemic arterial circulation
How does arterial oxygen concentration affect CBF?
decrease in PaO2 leads to cerebral vasodilation –> increased blood flow
increaed PaO2 vice versa
How does partial pressure of arterial CO2 affect CBF?
increased PaCO2 leads to vasodilation –>increased blood flow
decreased PaCO2 vice versa
Ischemia and loss of autoregulation occur at a CPP < _____
< 40 mm Hg
What are the chemical mechanisms of autoregulation of CBF?
- arterial O2 cc
- arterial CO2 cc
- nitric oxide
Explain the Cushing’s reflex in detail
reduced CBF –> reduced CO2 removal –> vasomotor centres –> sitmulates sympathetic nervous system –> increasing MAP –> baroreceptors in the carotid sinus and aorta –> vagal centres of the brainstem –> reflex bradycardia
What are the different types of forces affecting the brain during primary injury from TBI?
Acceleration and Deceleration
* grey matter is most susceptible
* hemorrhage or contusion
* tearing of neuronal tissue
* “whiplash”
Rotational
* spherical shape of skull direct rotational forces into the deeper brain tissue
* white matter most susceptible
* concussive injuries and axonal damage
What structure may be fractured in a patient suffering TBI and secondary vestibular signs?
Bulla fracture
What are locations of extra-axial and intra-axial bleeding in TBI?
Extra-axial:
* epidural
* subarachnoid
* subdural space
Intra-axial: brain parenchyma
What is the most common location for bleeding in TBI?
brain parenchyma
subarachnoid space
How do epidural and subdural hemorrhage differ in their nature of bleeding?
Epidural bleeding - from meningeal arteries - more acute
Subdural hematomas - slower venous bleeding - slower to accumulate
What are the primary mediators involved in secondary brain injury from TBI?
- oxygen free radial
- excitatory amino acids (e.g., glutamate)
- nitric oxide
Explain how mediators lead to secondary brain injury
Trauma –> neurons release excitatory amino acids (primarily glutamate) –> glutamate –> neuronal depolarization + cellular Ca++ influx –> excessive IC Ca++ –> more free radical production –> stimulates NO production + more excitatory AA release
ROS + NOS –> lipid peroxidation of cellular membranes –> further excitatory AA release and damage
Self-perpetuating vicious cycle
At what time after trauma is brain edema typically most severe?
24-48 hours after injury
What are the two types of edema in TBI?
Vasogenic edema
* due to failure of the BBB and vasodilation
* vasodilation typically from hypercapnia
Cytotoxic edema
* failure of the cellular ion pumps
* cellular membrane damage
* cellular death
Describe the Monro-Kellie doctrine
Describes how the volume components (brain parenchyma, CSF, blood) can adjust to increases in each others volume
* compliance of the brain during increased intracranial pressure
* CSF shunted out of the intracranial cavity to the spinal subarachnoid space
* decreasing CSF production, increasing CSF absorption
* vasoconstriction decreasing cerebral blood volume
