Neurological Emergencies Flashcards

1
Q

What are some neurologic emergencies?

A

Mentation changes, seizures, traumatic brain injury, tetanus and Botulism and Toxins

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2
Q

What are the types of mentation changes and what part of the brain do they effect?

A

Obtunded (Decreased response to stimuli and consciousness) - forebrain or brainstem
Stuporous (Dulled) - Brainstem
Comatose (prolonged loss consciousness) - Brainstem

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3
Q

What is the ARAS (Ascending Reticular Activating System) Responsible for?

A

Wake and dreaming states (effects consciousness)

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4
Q

What are some causes of mentation cahnge?

A

Toxins, Metabolic, Cardiovascular, neurologic, hydrocephalus, inflammation (abscess, MUE, neoplasia, Trauma, Vascular

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5
Q

What is your clinical approach to mentation change?

A

Hx: rule out trauma, toxin or metabolic, signalment (hypoglycemia puppy), previous diagnosis
Ex: systemic hypothermia, pulse, pale, neuro
Min Database: CBC, Biochem (hypernatremia)

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6
Q

How do you confirm diagnosis of a stroke?

A

MRI or CT, CSF analysis

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7
Q

What are the 2 types of stroke?

A

Ischaemic or Haemorrhagic

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8
Q

What are some underlying causes of stroke?

A

Cushings (too much cortisol), Hypothyroidism, Hyperthyroidism, PLN, Liver Disease, Idiopathic, Hypertension, Neoplasia, Heart Disease

Toxin, vWD, Haemophilia, Neoplasia, Thrombocytopenia, Liver Disease, HYpertension

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9
Q

What is your triage treatment for Mentation Change?

A

Correct patient temp, correct metabolic derangements, treat toxin if indicated, Hypo/hypertension treatment, look for signs increased intracranial pressure
Hypothermic warm up

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10
Q

What do you do if you think the animal has gotten into a toxin that is causeing the neurological signs?

A

Decontaminate, treat if possible (call pet poison helpline), treat symptoms (muscle relaxer, anti-seizure), non-specific - IV fluids, Intravenous lipids, Ion trapping, Hemodialysis

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11
Q

What is the equation for Cerebral Perfusion Pressure?

A

CPP = MAP-ICP
(Want around 50mmHG)

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12
Q

What is normal ICP? Why so low?

A

ICP is normally 0-15mmHg
Low because there is not a lot of room between the skull and thehinflammation

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13
Q

What are some things that increase intercranial pressure?

A

Edema, Inflammation, CSF, Tumor and trauma

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14
Q

How can you decrease CPP?

A

Increase MAP or decrease CPP needed to perfuse brain

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15
Q

If ICP 200-300mmHg what occurs?

A

Reflex bradycardia

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16
Q

What is the Cushing’s Reflex?

A

When you have decreased cerebral blood flow (b/c increased ICP), raised Co2, meduallary vasomotor center, symatheric stimulation, increase MAP that increase CPP and ICP and Carotid baroreceptor that increased vagal stimulation and leads to reflex bradycardia

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17
Q

What are some signs of increased ICP?

A

Pupil Changes (myotic or mydriatic non-responsive) , Tetraparesis, ataxia, proprioception defects, cranial nerve defects, decerebrate posture

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18
Q

How do we decrease ICP?

A

Decrease edema (manitol, hypertonic saline, steroids, diuretics), Craniectomy, remove space occupying lesion (tumor, granuloma, depressed skull fracture)

18
Q

How does the brain try to decrease ICP?

A

Push out skull

19
Q

What are some primary neurologic diseases?

A

Encephalitis, Brain tumor, vascular accident, head trauma

19
Q

If it is primary neurologic what do you do?

A

Stabilize or decrease ICP to buy time and send to neurologist

20
Q

When is surgery the only option?

A

BP over 300

21
Q

What is status epilepticus?

A

Failure of seizures to terminate, meaning last longer than 5 min, or more than 2 without return to normal conciousness
TRUE EMERGENCY

22
Q

What the cascade that leads to brain damage?

A

Glutamate release, NMDA receptor - calcium influx, 2nd messencer, ca release and mitocondrial damage or Cosium influx, cytotoxic edema, cell death

23
What are the systemic effects of brain damage?
Hypertension, tachycardia, arrhythmia, hyperglycemia, respiratory compromise (inadequate ventilation, noncardiogennic edema, aspiration pneumonia, hyperthermia, acidosis, myoglobinuria
24
What leads to death with Status Epilepticus?
Brain herniation, ventricular arrhythmia, respiratory compromise, renal failure
25
What is Emergency triage for status epilepticus?
Check temp (active cooling), Oxygen supplementation, Anti-seizure therapy
26
What are some antiseizure therapies that can be used?
Diazepam (rectal or IV) Midazolam (Nose or IV) 3 failed benzo go to Propofol (intubate) Phemobarbitol and levetiracetam needed long term
27
What are the 2 types of seizures?
Epilepsy and Reactive
28
Reactive seizures are caused by what?
Metabolic and toxins (treatable)
29
What are some differntials for structural epilepsy?
Cognitive dysfunction, hydrocephalus, prencephaly, neuronal ceroid lipofuscinosis, brain tumor, meningioencphalitis, traumatic brain injury, cerebral vascular accident
30
What is traumatic brain injury?
Increased intracranial pressure that damages the cells -Space occupying lesion -Ischemia (K, Ca, EAA, Free Radical, mitochonria failure) - cytotoxic edema, necrosis and increase ICP) -Injury - damage parenchyma and vasculature - contusion - increase tissue osmolar loat ICP
31
When a traumatic brain injury occurs what are you look for? How do you triage it?
Seizures? (benzo/ASD) -No seizures then evaluate ABS and then neuro eval (Airway (oxygen), Breathing (ventilation) and Cardio (perfusion) TPR and metabolic evaluaiton -Check spine, thorax, abdomen -May need fluids and oxygen -No imporvement then manitol and elevate head -No improvement - surgical decompensation, hypersalivation and hypothermia
32
What does the glagow comma scale tell you?
severity of coma (Normal is high 15-18) -Use to monitor trends (evaluate every 4-24 hours
33
What is the causative agent of tetanus?
Clostridium tetani (ubiquitous)
34
How long does it take to see signs of Tetanus and what are they?
5-10 days post infection, generalized more common in dogs, stiffness, rigid, sardastic grim
35
How do you treat tetanus?
Antimicrobials (metronidazole) and antitoxin
36
What are the signs of botulism?
Flaccid paralysis (LMN) within 12 hours of exposure Diaphragm resistant to toxin
37
What's the treatment for botulism?
supportive care
38
Where is the causative agent of botulism?
Clostridium botulinum
39
What is the pathophysiology of these clostridiums?
Botulism - bind at neuromuscular junction - peripheral nerves affected Tetanus - bind at brain stem (Renshaw cells)
40
What are some clinical signs of a metabolic encephalopathies?
Seizure, behavioral change, aggression, anxiety, dementia, mania, mentation change, cortical blindness
41
What are some etiologies of metabolic encephalopathies?
Hypoglycemia, hyponatremia, hypocalcemia, hepatic encephalopathy, thiamine deficiency