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Small Animal Optho/Neuro > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

1
Q

If a patient has an obtunded mentation, where is the likely location of the lesion?

A

forebrain or mild disease of the brainstem

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2
Q

if a patient has a stuporous or comatose mentation, where is the likely location of the lesion?

A

brainstem
or really large forebrain lesion

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3
Q

T/F: a really large lesion within the forebrain can cause brainstem disease which can lead a patient to being stuporous or comatose

A

true

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4
Q

Match the following with the correct mentation change:
_______: able to respond to the environment, but response is abnormal
________: has heartbeat, but is non-responsive and may or may not be breathing
________: applying noxious stimuli elicits an abnormal response

A

obtunded: able to respond to the environment, but response is abnormal
comatose: has heartbeat, but is non-responsive and may or may not be breathing
stuporous: applying noxious stimuli elicits an abnormal response

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5
Q

What are the 4 most common categorical causes of mentation change?

A
  1. neoplasia
  2. immune-mediated (MUE)
  3. trauma
  4. toxin
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6
Q

You give a patient with a suspected toxicity intravenous lipids. Now that patient is seizing. Why can you not give it an anti-seizure medication?

A

the AED will bind to the lipids and will not work.

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7
Q

T/F: most CNS toxins are CNS depressants

A

false – most are excitatory (caffeine, chocolate, insecticides, moldy food/garbage, lead, some rodenticides)

only a few are depressants (some rodenticides, antifreeze, and ivermectin)

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8
Q

Cerebral blood flow needs to be maintained around ____ ml/100g/min

A

50

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9
Q

T/F: cerebral blood flow can be maintained at 50 mL/100g/min within a large range of the cerebral perfusion pressure.

A

True.
The cerebral perfusion pressure can be between ~70-100.

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10
Q

If a patients intracranial pressure is increasing (>20 mmHg), then the cerebral perfusion pressure is – increased or decreased?

A

decreased. If it goes below 50 mmHg, then its dangerous.

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11
Q

If a patients intracranial pressure is increasing, their cerebral perfusion pressure is decreased. What can you do to help correct this?

A

increase the MAP or decrease the ICP in order to appropriately perfuse the brain.

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12
Q

Describe the Cushings Reflex

A

when intracranial pressure (ICP) is INCREASED (due to inflammation, trauma, etc.), then the cerebral blood flow is DECREASED.
As a result, the PaCO2 is increased within the brain to activate the medullary vasomotor center.
This causes sympathetic stimulation and INCREASES the mean arterial pressure (MAP).
When MAP increases, cerebral perfusion pressure (CPP) is INCREASED which can lead to further increased intracranial pressure (ICP).
Additionally, the increase in MAP causes activation of the carotid baroreceptors, which leads to vagal stimulation and subsequent reflex bradycardia.

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13
Q

Your patients blood pressure is 240 and their heart rate is 30. What can you interpret from this information?

A

There is likely a Cushings reflex occurring… the protective mechanism is failing.

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14
Q

Which is WORSE to see in regard to increased intracranial pressure – mydriatic pupils or miotic pupils?

A

Mydriatic is worse.

Miotic pupils mean that the lesion is within the hypothalamus. Mydriatic pupils indicate that the lesion is involving more than just the hypothalamus and brainstem.

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15
Q

what are signs of increased intracranial pressure?

A

hypertension
bradycardia
pupil changes
tetraparesis and ataxia
proprioceptive deficits
cranial nerve deficits
decerebrate posture

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16
Q

How do we treat mentation changes induced by increased intracranial pressure?

A

we need to decrease intracranial pressure by giving medications that can decrease edema.

  • Decrease edema: mannitol or hypertonic saline (if pt is dehydrated) + corticosteroids (AI dose) + diuretics
  • Perform craniectomy if meds do not work alone
  • Remove the space-occupying lesion if able
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17
Q

what are the 2 types of strokes?

A
  1. ischemic stroke
  2. hemorrhagic stroke
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18
Q

What is status epilepticus?

A

failure of a seizure to terminate within 5 minutes or greater than 2 seizures without return to normal consciousness
This is TRUE EMERGENCY

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19
Q

What pathophysiology supports the idea that status epilepticus is a true emergency?
(2 reasons)

A
  1. Seizures cause glutamate release (excitatory NT), which leads to excitement of NMDA receptors.
    This causes a calcium ad sodium influx which leads to cytotoxic edema, mitochondrial damage, and ultimately cell death/brain damage.
  2. Seizures activate the sympathetic nervous system and thus have profound systemic effects (hypertension, tachycardia, arrhythmias, hyperglycemia, resp compromise, hyperthermia, acidosis, and myoglobinuria)
20
Q

How can seizures cause respiratory compromise? (3 reasons)

A

they can cause convulsion of the intercostal muscles and diaphragm and lead to inadequate ventilation.

they activate the sympathetic nervous system, which causes vasodilation and can lead to non-cardiogenic pulmonary edema

they activate the autonomic nervous system and can cause vomiting or regurgitation which can cause aspiration pneumonia

21
Q

what are the MOST common causes of death associated with seizures? (3)

A
  1. ventricular arrhythmias
  2. respiratory compromise
  3. renal failure
22
Q

A patient enters your ER in status epilepticus. How do you approach and treat this patient?

A
  1. check their temperature and actively cool them
  2. provide O2 supplementation
  3. give anti-seizure meds (diazepam, or midazolam)
  4. if AEDs fail 3 times, give propofol
  5. start a loading dose of pheno or keppra (long term AEDs)
23
Q

What are the 2 types of seizures?

A
  1. epileptic seizures (can be idiopathic epilepsy, structural epilepsy, or epilepsy of unknown cause)
  2. reactive seizures (toxins or metabolic causes)
24
Q

what are the 3 components/categories of the modified glasgow coma scale?

A
  1. motor activity (ambulation and muscle tone)
  2. brain-stem reflexes (PLRs, OCRs, pupil size)
  3. level of consciousness (mentation)
25
Q

T/F: higher modified glasgow coma scale scores have grave prognosis

A

false – lower scores carry grave prognosis. Anything above 15 has a good prognosis.

26
Q

what is modified glasgow coma scale used for?

A
  1. monitor trends in patients with intracranial signs
  2. for prognosis for traumatic brain injuries (must assess over 24 hr for reliability)
27
Q

A patient with head trauma presents to your clinic and is having seizures. You start by administering appropriate AEDs to stop the seizure. Then you assess the patient using the MGCS. What should be next in order to determine the extent of the injury?

A

imaging – survey spine, thorax, and abdominal radiographs

meanwhile providing tier 1 treatment (fluid therapy and oxygen supplementation). Monitor this patient for 72 hrs and repeat the MGCS every 6 hrs.

28
Q

If a patient with a traumatic brain injury has been receiving tier 1 treatment (supportive care) and then their MGCS goes DOWN (ie the patient deteriorates), what is you next line of treatment?

A

tier 2 treatment – interventional
give mannitol or hypertonic saline
elevate head 30 degrees.

29
Q

If a patient with a traumatic brain injury has been receiving tier 2 treatment (mannitol and elevation of the head) and then their MGCS goes DOWN (ie the patient deteriorates), what is you next line of treatment?

A

tier 3 treatment – invasive
surgical decompression, hyperventilation, and hypothermia.

30
Q

T/F: patients with very severe TBI an do well

A

true

31
Q

what does clostridium tetani cause?

A

5-10 days post-infection with C. tetani, it causes rigidity of all limbs.

32
Q

localized tetanus is more common in cats or dogs? why?

A

cats
they are more resistant to the toxin produced by C. tetani

33
Q

what is the treatment for tetanus?

A

metronidazole or penicillin +/- antitoxin (if severe)

34
Q

what does C. botulinum cause?

A

flaccid LMN paralysis and often autonomic signs within 12 hours of infection

35
Q

T/F: in cases of botulism, we should worry that our patients will have respiratory compromise due to diaphragmatic paralysis.

A

false – the diaphragm is resistant to the toxin

36
Q

what is the treatment for botulism?

A

nothing! just supportive care.

37
Q

Botulinum and tetanus cause very different clinical signs. How are the mechanisms different?

A

botulinum binds to tje SNARE complex and inhibits the acetylcholine vesicle from fusing to the axon terminal, subsequently leading to NO release of Ach and therefore no excitation/muscle contraction

Tetanus binds to inhibitory interneurons (Renshaw cells) and blocks the release of inhibitory NTs
–> no relaxation –> spastic paralysis

38
Q

What are clinical signs of metabolic encephalopathies?

A

seizures
behavior changes
mentation changes
cortical blindness

39
Q

How does hypoglycemia cause seizures?

A

Lack of glucose leads to inability for the Na/K ATPase pump to work. Na will accumulate within the cell and K will accumulate outside of the cell. The membrane will be UNABLE to relax and therefore a seizure will occur.

40
Q

T/F: it does not take much Na change to change serum osmolality

A

true

serum osmolality = 2Na + Glucose/18 + BUN/2.8

41
Q

How does hyponatremia cause seizures?

A

less sodium outside of cells –> water flows INTO cells –> neuronal edema –> seizures

42
Q

why must we SLOWLY correct sodium deficiencies?

A

if we give too much too fast, then water will flow out of the cells TOO QUICKLY and cause neuronal death.

43
Q

T/F: calcium does not play a role in the resting membrane potential itself, butit does have an effect on sodium channels.

A

true

44
Q

How does hypocalcemia cause seizures?

A

if there is LESS calcium outside of cells, then the calcium that is bound to sodium channels will dissociate. This makes it easier for the Na channels to open which causes depolarization and seizures.

45
Q

How does hepatic encephalopathy cause seizures?

A

glutamate binds to NMDA receptors, unbinds from NMDA receptors, and gets taken up by astrocytes. Once here, it gets converted to glutamine with the help of NH3. Once it is glutamine, it cna be transported back to presynaptic terminal and be converted back to glutamate.

However, if there is too much ammonia (NH3) in cases of hepatic encephalopathy, then the conversion of glutamate to glutamine will continue and cause neuronal dysfunction.

Small Animal Optho/Neuro (12 decks)

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