Neuro Emergencies Flashcards
If you have a mentation change in a patient what should you look for primarily?
Signs of increased intracranial pressure
You then want to maintain cerebral perfusion pressure -> MAP - ICP = CPP. Increased MAP or decreased CPP needed to perfuse brain.
A patient comes in with severe hypertension and reflex bradycardia, what might you be worried about?
Cushings reflex
Signs of increased intracranial pressure
Pupil changes
Tetraparesis and ataxia
Proprioception deficits
Cranial nerve deficits
Decerebrate posture
How would you decrease intracranial pressure if you can’t get to a neurologist?
Decrease edema with mannitol or hypertonic saline for a fast onset and short duration. Then for long term management use corticosteroids and diuretics
Status epilepticus is an ___and is any seizure lasting longer than ___ or >2 seizures without return to normal consciousness
EMERGENCY, 5 minutes,
Mitochondrial damage during status epilepticus is mostly due to what?
Ca+ release from the ER
Systemic effects of status epilepticus
Profound:
- hypertension
- tachycardia
- arrhythmias
- hyperglycemia
Other:
- respiratory compromise
- hyperthermia
- acidosis
- Myoglobinuria
How should you treat a patient with status epilepticus?
- Start with benzodiazepine
- Move on to propofol if needed
- Add in long acting seizure meds (pheno or Keppra)
- Start CRI of benzo or propofol if the seizures continue
- Treat systemic signs (hyperthermia, hypoxia, hypovolemia)
After 3 failed attempts of stopping status epilepticus in a patient with benzodiazepines, what should you reach for?
Propofol IV
In a case of ivermectin toxicity you should not use what?
Benzo’s -> reach for propofol
Reactive seizures are associated with __ and __ while epilepsy is associated with what?
Toxins and metabolites
Idiopathic or structural epilepsy
A dog comes into your emergency clinic with head trauma but is not experiencing seizures, what should you do?
ABC’s:
Oxygen
Ventilation
Perfusion
TPE
Metabolic evaluation
Modified Glasgow Coma Scale
Can be used to monitor trends for any patient with intracranial signs but the prognosis is only helpful for traumatic brain injuries over 48 hours before prognosis is helpful
Briefly explain tetanus
It’s caused by clostridium tetanus from the environment and causes diffuse rigidity with eyelids pulled back after 5-10 days of infections. It should be treated with antimicrobials +/- antitoxin
__ tetanus is more common in dogs while __ is more common in cats
Generalized, localized
Briefly describe Botulism
Botulism is caused by clostridium botulinum and results in flaccid (LMN) paralysis within 12hrs of exposure. There is not specific treatment other than supportive care.
Why do botulinum and tetanus cause difference clinical signs if they’re both clostridia’s toxins?
They bind to different docking proteins which causes tetanus to cause CNS disease and botulinum to cause peripheral nerve disease
How does hypoglycemia effect metabolic encephalopathies?
During a seizure sodium is going into the cell while phosphorus is going out. If there is little glucose within the the cell then ATP is not being produced by the TCA cycle, therefore the ATPase pump doesn’t allow the membrane to relax which causes the seizure
How does hyponatremia effect metabolic encephalopathies?
A systemic hyponatremia means that sodium that is in the cells draw water in causing edema but you want to correct this slowly
Hypocalcemias effect on metabolic encephalopathies
Hypocalcemia effects the sodium channels. Calcium normally binds to sodium channels but in these cases it unbinds which allows the channels to open more causing depolarization of the membrane
NH3 is needed for __ to become __. What happens if there’s too much NH3?
Glutamine to become glutamate
Too much NH3 results in glutamate to become glutamine
NH3 is needed for __ to become __. What happens if there’s too much NH3?
Glutamine to become glutamate
Too much NH3 results in glutamate to become glutamine
