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
What are the 4 types of brain herniation?
- Falcine herniation - hernation of one of the cerebral hemisphere ventral to the falx cerebri
- Transtentorial herniation - herniation of the parahippocampal gyrus below the tentorium cerebelli –> compression of the midbrain –> mydriasis, unresponsive pupils, loss of consciousness death from cardiopulmonary arrest
- Foramenal herniation - cerebellar herniation into the foramen magnum death from compressing the respiratory centres of the medulla
- Calvarial herniation - herniation of the brain through a defect
How does body temperature increase cerebral metabolic rate?
increases or decreases proportionately by 5% per Celsius degree changes
What are the three categories of the MGCS?
- Motor activity
- Brainstem reflexes
- Level of cnsciousness
Explain Decerebrate and Decerebellate rigidity
Decerebrate rigidity
* indicates loss of communication between cerebrum and brainstem
* opisthotonus with hyperextension in all 4 limbs
* stuporous or comatose
* abnormal PLR
Decerebellate rigidity
* acute cerebellar injury
* flexion or extension of the hindlimbs
* consciousness usually normal
Response of the pupils to light indicates function of the following structures:
- Retina
- optic nerves
- optic chiasm
- rostral brainstem
What are your differentials for causes of miosis in TBI?
- Injury to the diencephalon - sympathetic innervation originates in the hypothalamus
- injuries to structures of the peripheral sympathetic innervation to the eye (brachial plexus, cranial mediastinum, cervical soft tissues, tympanic bulla)
- ocular injury and spasm of the ciliary muscles of the iris
What are your differentials for mydriasis in TBI?
Bilateral:
* midbrain damage
* brain herniation
* decreased cerebral perfusion
* postictal changes
Unilateral:
* trauma to the iris or retina
* periorbital trauma or hematoma
* previous ocular disease
* CN III injury/paralysis
Absent oculocephalic reflexes indicate injury to which structure?
absence –> brainstem
delayed –> cerebral injuries
What is a period of hyperventilation followed by apnea referred to and what does it indicate?
Cheyne-Stokes respiration
usually from diencephalic injury and reduced responsiveness to paCO2
What are your differentials for hyperventilation in TBI patients?
- cerebral acidosis
- cerebral hypoxia
- mesencephalic injury
- transtentorial herniation
- primary respiratory injury (pulmonary contusions, pneumothorax, hemithorax)
- pain, anxiety
What type of injury does ataxic respiraiton indicate?
brainstem injury
What is the recommended angle for elevating a TBI patient’s head?
30 degree ange
What are the PaO2 and PaCO2 goals for patients with head trauma?
PaO2 greater than or equal to 90 mm Hg
PaCO2 between 35 and 45 mm Hg
How does mannitol improve CBF?
- decreases edema
- expands plasma volume and reduces blood viscosity –> improves CBF and O2 delivery to the brain –> vasoconstriction in response to O2 increase –> ICP decreases
- assists in scavenging free radicals
- osmotic effect –> drawing water from extravascular to intravascular space and diuresis
How does hyperglycemia prognosticate outcome in TBI?
dogs and cats:
* recent study showed association between degree of hyperglycemia and severity of head trauma
* no association between outcome and degree of hyperglycemia
A MGCS of 8 is associated with a ____% survival chance
50%
