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SA Optho/Neuro > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

1
Q

Compare and contrast the meaning of obtunded, stuporous and comatose

A

Obtunded: Abnormal response to stimuli due to a state of reduced consciousness

Stuporous: unresponsive but still aware of surroundings

Comatose: Of or in a state of deep unconsciousness

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2
Q

Of the 3 mentation changes, which is commonly localized to the forebrain?

A

Obtunded

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3
Q

What are the causes of mentation changes in small animals?

A

DAMNITTV:
Degenerative
Anomalous- hydrocephalus can lead to mild mentation changes
Metabolic- hypoglycemia, sodium changes, ketoacidosis etc
Neoplasia- very common
Infectious- bacterial, fungal, protozoal
Immune Mediated- MUE very common
Trauma- very common
Toxin- very common
Vascular- less common than N I or T

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4
Q

What is the first thing you should rule out from your history?

A

Trauma toxic or metabolic cause
-hypoglycemia if puppy thats not eating

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5
Q

What is the initial clinical approach for patients with mentation changes?

A

First check the patients temperature, then correct any metabolic derangements, treat for toxin if indicated, check blood pressure, and look for signs of increased intracranial pressure

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6
Q

What is the treatment for a neuro toxin case?

A

DECONTAMINATE (activated charcoal, induce vomiting), give specific treatment if possible, treat symptoms (muscle relaxer, anti-seizure meds)
- non specific treatments: IV fluids, IV lipids, ion trapping, hemodialysis
-call the pet poison hotline!

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7
Q

If it is determined to be a primary neurologic cause, what is the most important thing you can do for treatment?

A

Help to maintain cerebral perfusion pressure

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8
Q

What is the equation for CPP and what is the range it should always be between?

A

MAP-ICP=CPP
Range: 70-120 mmHg

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9
Q

Describe the cushings reflex

A

Increased ICP leads to reduced cerebral bloodflow. This raises the amount of CO2 in the blood which causes the medullary vasomotor center to send out sympathetic signals to increase MAP. This INCREASES CPP leading to a further increased Intracranial pressure. The increase in MAP also stimulates the carotid baroreceptors and induces vagal stimulation resulting in reflex bradycardia

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10
Q

What are some signs of increased intracranial pressure besides reduced mentation?

A

Pupil changes (if myotic=hypothalamus, if myiadriatic=brainstem=badd), tetraparesis and ataxia, proprioception defects, cranial nerve deficits, decerebrate posture

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11
Q

Describe the decerebrate posture?

A

Increased muscle tone in all 4 limbs

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12
Q

What are the fastest ways to decrease intracranial pressure in neuro cases?

A

Decrease edema with mannitol or 7.2% hypertonic saline

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13
Q

What are the options for long-term management in patients with increased ICP?

A

Corticosteroids and Diuretics (carbonic anhydrase inhibitor)

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14
Q

If pressure cannot be normalized with medical management, what are the next steps?

A

Craniectomy and remove the space occupying lesion (tumor, granuloma, or depressed skull fracture)

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15
Q

What are the symptoms of strokes?

A

Focal non-progressive or convulsive brain signs

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16
Q

How do you confirm that a stroke has occurred?

A

Imaging of the brain (CT or MRI) and CSF analysis

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17
Q

What are some causes of ischemic strokes vs hemorrhagic strokes?

A

Ischemic: cushings, hypothyroidism, hyperthyroidism, protein losing nephropathy, Liver disease, Idiopathic, hypertension, neoplasia, heart disease

Hemorrhagic: Toxic, von-Willibrand’s disease, hemophilia, neoplasia, thrombocytopenia, liver disease, hypertension

18
Q

Which cause of brain masses usually has an acute presentation?

A

Vascular accident

19
Q

Define status epilepticus

A

-Failure of seizures to terminate
-any seizure lasting longer than 5 minutes
->2 seizures without return to normal consciousness within 24 hours
-this is a true EMERGENCY

20
Q

Describe how seizures lead to brain damage

A

Excitatory neurotransmitter glutamate excites the NMDA receptors opening either sodium or calcium channels. Sodium influx leads to cytotoxic edema and cell death vs calcium influx leads to mitochondrial damage and cell death

21
Q

What systemic affects often accompany seizures and can worsen the effects of them?

A

Hypertension, tachycardia, arrythmias, hyperglycemia, respiratory compromise, hyperthermia, acidosis, myoglobinuria

22
Q

What are the most common ways that death accompanies seizures?

A

Ventricular arrythmias, respiratory compromise or renal failure

23
Q

What are the 3 things you should implement as soon as possible when a patient presents for status epilepticus?

A
  1. Check temperature, and implement active cooling if indicated
  2. Oxygen supplementation
  3. Anti-epileptic therapy
24
Q

What are the most commonly used drugs for anti-epileptic therapy?

A

IV diazepam or midazolam is first choice, if doesnt work 3 times in a row, move to IV propofol

25
Q

What are the options for long term treatment after a seizure patient has been stabilized?

A

Phenobarbital, levetiracetam

26
Q

What are some common causes of reactive seizures?

A

Medications, plants, food, rodenticides/insecticides, illicit drugs

27
Q

Using the DAMNITV scheme, describe the common causes of structural epilepsy

A

D- cognitive dysfunction syndrome
A- hydrocephalus/porencephaly
M- neuronal ceroid lipofuscinosis
N- brain tumors
I- meningoencephalitis of unknown etiology
T- traumatic brain injury
V- cerebral vascular accident

28
Q

Describe the pathogenesis of traumatic brain injury

A

Damage to the parynchema and vasculature can lead to contusions, axonal injury, increased BBB permeability, vascular dysregulation, vasogenic edema, and ischemia. All of these can lead to increased intracranial pressure.

29
Q

What is the treatment for traumatic brain injury?

A

If no seizures are present, evaluate systemically and implement ABC emergency therapy before a neurologic evaluation. If seizures are present, administer ASD and then do the same as above.

30
Q

What can the Modified Glasgow coma scale be used for?

A

Can be useful to monitor trends for any patient with intracranial signs (evaluate every 4-24 hours). Can be used to determine prognosis if assessed over 48 hours.

31
Q

Which species is generalized tetanus more common in-dogs or cats?

A

Generalized more common in dogs, localized more common in cats

32
Q

How long does it take for clinical signs of tetanus to be observed?

A

5-10 days after initial infection

33
Q

What is the most common treatment for tetanus?

A

Metronidazole +/- antitoxin. Penicillin can also be used

34
Q

What is the main difference in clinical signs between tetanus and botulism?

A

Tetanus results in rigid paralysis vs botulism results in flaccid paralysis

35
Q

How soon after exposure due clinical signs develop with botulism?

A

12 hours

36
Q

What is the treatment for botulism?

A

Supportive Care

37
Q

How do clostridium toxins interfere with SNARE proteins to result in the clinical signs seen?

A

Clostridium binds to synaptotagmin and prevents fusion of the Ach vesicle to the plasma membrane

38
Q

What are the common clinical signs of metabolic encephalopathies?

A

Seizures, behavior changes, mentation changes, cortical blindness

39
Q

How does hypoglycemia lead to seizures?

A

Lack of glucose–> lack of phosphorus (ATP) to power atpase pumps in order to restore resting membrane potentials

40
Q

How can hyponatremia lead to nerve damage

A

Water will be drawn into cells due to low sodium in the plasma leading to swelling or death of neurons

41
Q

How can hypocalcemia lead to tremors or seizures?

A

Calcium bound to sodium channels will disassociate making it easier for excitatory channels to open

42
Q

How can hepatic encephalopathy lead to neuronal dysfunction?

A

NH3 is necessary for glutamine to be created from glutamate. If too much NH3 there will be conversion of glutamate to glutamine

SA Optho/Neuro (8 decks)

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