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Neurologic Emergencies > Neuro Emerg 20: Head Trauma > Flashcards

Neuro Emerg 20: Head Trauma Flashcards

1
Q

What is the normal ICP in a dog?

A

5-12 mm Hg

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2
Q

What regulates cerebral blood flow?

A
  • partial pressure of carbon dioxide
  • partial pressure of oxygen levels
  • cerebral metabolic activity
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3
Q

What is the relationship between CBF, CPP, and CVR?

A

CBF = CPP/CVR

CBF - c blood flow
CPP - c perfusion pres.
CVR - c vascular resistance

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4
Q

What is cerebral compliance?

A

the ability of the cranial contents to decrease in volume - in an attempt to reduce ICP

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5
Q

How do you define concussion?

A

a traumatic reversible paralysis of the neurologic function
immediate in onset

does not describe the underlying brain pathology

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6
Q

How do you define brain contusion?

A

bruising of the brain surface, without rupture of the pia-arachinoid or interruption of the brain architecture

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7
Q

How much of the total CO supplies the brain?

A

15-20%

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8
Q

What are the 3 components of CBF autoregulation?

A
  1. Myogenic mechanisms
  2. Chemical mechanisms
  3. Neurogenic mechanisms
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9
Q

At what MAP range can the autoregulation achieve a constant CBF?

A

50-150 mm Hg

outside this range CBF depends on systemic arterial circulation

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10
Q

How does arterial oxygen concentration affect CBF?

A

decrease in PaO2 leads to cerebral vasodilation –> increased blood flow
increaed PaO2 vice versa

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11
Q

How does partial pressure of arterial CO2 affect CBF?

A

increased PaCO2 leads to vasodilation –>increased blood flow
decreased PaCO2 vice versa

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12
Q

Ischemia and loss of autoregulation occur at a CPP < _____

A

< 40 mm Hg

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13
Q

What are the chemical mechanisms of autoregulation of CBF?

A
  • arterial O2 cc
  • arterial CO2 cc
  • nitric oxide
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14
Q

Explain the Cushing’s reflex in detail

A

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

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15
Q

What are the different types of forces affecting the brain during primary injury from TBI?

A

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

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16
Q

What structure may be fractured in a patient suffering TBI and secondary vestibular signs?

A

Bulla fracture

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17
Q

What are locations of extra-axial and intra-axial bleeding in TBI?

A

Extra-axial:
* epidural
* subarachnoid
* subdural space

Intra-axial: brain parenchyma

18
Q

What is the most common location for bleeding in TBI?

A

brain parenchyma
subarachnoid space

19
Q

How do epidural and subdural hemorrhage differ in their nature of bleeding?

A

Epidural bleeding - from meningeal arteries - more acute
Subdural hematomas - slower venous bleeding - slower to accumulate

20
Q

What are the primary mediators involved in secondary brain injury from TBI?

A
  • oxygen free radial
  • excitatory amino acids (e.g., glutamate)
  • nitric oxide
21
Q

Explain how mediators lead to secondary brain injury

A

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

22
Q

At what time after trauma is brain edema typically most severe?

A

24-48 hours after injury

23
Q

What are the two types of edema in TBI?

A

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

24
Q

Describe the Monro-Kellie doctrine

A

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

25
Q

What are the 4 types of brain herniation?

A
  • 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
26
Q

How does body temperature increase cerebral metabolic rate?

A

increases or decreases proportionately by 5% per Celsius degree changes

27
Q

What are the three categories of the MGCS?

A
  • Motor activity
  • Brainstem reflexes
  • Level of cnsciousness
28
Q

Explain Decerebrate and Decerebellate rigidity

A

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

29
Q

Response of the pupils to light indicates function of the following structures:

A
  • Retina
  • optic nerves
  • optic chiasm
  • rostral brainstem
30
Q

What are your differentials for causes of miosis in TBI?

A
  • 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
31
Q

What are your differentials for mydriasis in TBI?

A

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

32
Q

Absent oculocephalic reflexes indicate injury to which structure?

A

absence –> brainstem
delayed –> cerebral injuries

33
Q

What is a period of hyperventilation followed by apnea referred to and what does it indicate?

A

Cheyne-Stokes respiration
usually from diencephalic injury and reduced responsiveness to paCO2

34
Q

What are your differentials for hyperventilation in TBI patients?

A
  • cerebral acidosis
  • cerebral hypoxia
  • mesencephalic injury
  • transtentorial herniation
  • primary respiratory injury (pulmonary contusions, pneumothorax, hemithorax)
  • pain, anxiety
35
Q

What type of injury does ataxic respiraiton indicate?

A

brainstem injury

36
Q

What is the recommended angle for elevating a TBI patient’s head?

A

30 degree ange

37
Q

What are the PaO2 and PaCO2 goals for patients with head trauma?

A

PaO2 greater than or equal to 90 mm Hg
PaCO2 between 35 and 45 mm Hg

38
Q

How does mannitol improve CBF?

A
  • 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
39
Q

How does hyperglycemia prognosticate outcome in TBI?

A

dogs and cats:
* recent study showed association between degree of hyperglycemia and severity of head trauma
* no association between outcome and degree of hyperglycemia

40
Q

A MGCS of 8 is associated with a ____% survival chance

A

50%

Neurologic Emergencies (3 decks)

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