Neurologic Emergencies Flashcards
What should be considered prior to neuro localization in an animal with mentation changes?
Ruling out systemic disease (toxin, metabolic, cardiovascular)
What is the clinical approach to mentation change?
- History (r/o systemic disease; signalment; previous dx)
- Examination (physical + neuro)
- Minimum Database (CBC/Chem/UA)
What are the two types of strokes?
Strokes = Vascular accident where blood clots form, depriving the brain of oxygen
- Ischemic (Cushing’s, hypo/hyperthyroid, PLN, liver dz, hypertension, neoplasia, heart dz, idiopathic)
- Hemorrhagic (toxin, vWD, hemophilia, neoplasia, thrombocytopenia, liver dz, hypertension)
Tx of neurological toxins
Decontaminate (activated charcoal) + treat symptoms + supportive care
What is the pathophysiology behind a primary neurological condition causing mentation changes?
Cerebral Perfusion Pressure (CPP) has been altered via increased intracranial pressure (ICP) from things like edema, inflammation, space-occupying lesions (tumor, granuloma, depressed skull fx)
Top DDx for 1º neuro mentation change
- Encephalitis (infectious v. autoimmune)
- Brain tumor
- Vascular accident
- Head trauma/TBI
What mentation changes are considered emergencies?
- obtunded
- stuporous
- comatose
Equation for CPP
MAP - ICP = CPP
Define Cushing’s Reflex
Aka “vasopressor response” or “CNS ischemic response”
- Physiological CNS response to acutely increased ICP. In order to perfuse the brain/relieve pressure and overcome increased ICP, body must increase systemic pressure (MAP) via vasoconstriction.
https://www.veterinary-practice.com/article/traumatic-brain-injury-in-companion-animals
What are the 3 triad indicative of Cushing’s Reflex?
- Vasoconstriction -> reflex hypertension
- Vagal stimulation -> reflex bradycardia
- Irregular breathing (increased ICP compresses brainstem, distorting respiratory centers)
https://www.veterinary-practice.com/article/traumatic-brain-injury-in-companion-animals
Other clinical signs of increased ICP
- pupil changes
- tetraparesis & ataxia
- proprioceptive deficits
- cranial nerve deficits
- decerebrate posture
Treatments for decreasing ICP
- Decrease edema & inflammation (mannitol; 7.2% hypertonic saline; corticosterioids @ anti-inflammatory dose)
- Remove space-occupying lesion via craniectomy PRN
Define Status Epilepticus
Any seizure lasting longer than 5 minutes, or >2 seizures without return to normal consciousness
These are true emergencies
Effects of status epilepticus on the brain
Brain damage from neuron death
- Glutamate release (major excitatory NT) causes aberrant neuronal signaling -> cytotoxic edema + mitochondrial damage -> -> neuron death
Systemic effects of status epilepticus on:
1. BP
2. HR
3. Heart rhythm
4. BG
5. Respiration
6. Body temperature
7. Tissue perfusion
8. Muscle breakdown
- hypertension
- tachycardia
- arrhythmias
- hyperglycemia
- respiratory compromise
- hyperthermia
- metabolic acidosis
- myoglobinuria (excessive myoglobin in urine due to muscle breakdown during convulsions)
ER Tx for status epilepticus
Stabilize the pt w/ anti-seizure therapy
1. Fast-acting benzodiazepine (Diazepam rectal or IV, Midazolam IN or IV)
2. If 1. fails 3x, Propofol IV to effect
3. Once SE stops, start loading dose of long-acting ASD (Phenobarbital; Levetiracetam)
4. Treat systemic signs (hyperthermia, hypoxia, hypovolemia)
Start CRI of benzo or propofol if seizures continue/think of etiolog
A toxin or metabolic disturbance causes what type of seizure?
Reactive
Seziure from CNS insult or systemic illness (extracranial)
3 types of epileptic seizures:
- Idiopathic Epilepsy (genetic)
- Epilepsy of Unknown Origin
- Structural Epilepsy (tumor, trauma, meningitis)
TBI: 1º vs 2º brain injuries
1º = concussions, lacerations; immediate results of traumatic events
2º = occurs during hours-days post trauma, and is caused by complex series of bichemical events (inflammatory mediators, excitatory NTs, changes in cell membrane permeability) that ultimately lead to neuronal cell death
compromised CPP from 1º, 2º, & systemic effects ALL worsen injury
2º brain injury = insults that lead to neuronal cell death:
- Systemic insults (hypo-tension,xemia,capnia, hyperthermia, e-lyte imbalances, acid-base disturbances)
- Intracranial insults (incr. ICP, compromise of BBB, mass lesions, cerebral edema, infection, vasospasm, seizures)
Immediately post TBI, there is massive release of excitatory NTs (ACh, glutamate, epi, norepi) –> influx of Na & Ca into neurons -> -> further depolarization + release of excitatory NTs. Ca influx eventually overwhelms removal, -> severe intracellular damage -> -> neuronal cell death.
Excessive metabolic activity also depletes ATP stores in the brain.
Hypoperfusion & local tissue acidosis favor ROS production post TBI. Hemorrhage (iron) favors -OH radicals. ROS cause oxidation of lipids (brain = lipid-rich environment), proteins, and DNA -> further destruction of neurons.
Nitric Oxide (NO) perpetuates 2º brain injury post trauma b/c of its vasodilatory effects + participation in free radical rxns.
Inflammatory Mediators perpetuate 2º brain injury via NO production, triggering influx of inflamm. cells, activating arachidonic acid & coagulation cascases, and disrupting BBB.
Pathophysiology of increased intracranial pressure after head trauma
TBI -> Elevated ICP:
1. Edema and/or hemorrhage cause volume of the meninges to increase –> CSF and cerebral blood flow compensatorily shunt blood away from brain –> Capacity of compensation exhausted -> intracranial volume increases -> dramatic elevations of ICP -> immediate onset of clinical signs
Meninges = 3-layered tissue compartment
The Meninges:
1. Pachymeninges (thick membrane)
- Dura mater: tough & fibrous outer layer, encompasses venous sinuses, function = protection
2. Leptomeninges (light membranes)
- Arachnoid mater: spiderweb appearance, small aa. location, function = cushioning, absorption of CSF
- Pia mater: delicate membrane that follows the gyri & sulci of brain, function = BBB, blood vessel penetration
What are the ABCs of ER therapy?
- Oxygenation
- Ventilation
- Perfusion
- TPR
- Metabolic Evaluation
A HBC dog presents with head trauma but no active seizures. What is your initial TX plan?
- Immediate systemic evaluation + ABC ER therapy
- Perform neuro exam//MGCS
Modified Glasgow Coma Scale
- A modification of the coma scale used in humans (for assessment of consciousness post brain injury) and can be useful for any pt w/ intracranial signs (eval. q4-24h, severity-dependent)
- 3 categories: level of consciousness, motor activity, brainstem reflexes
Wht are the 3 tiers associated with head trauma therapy?
Tier 1
1. IVF therapy
2. O2 therapy, manage ventilation
Tier 2 (deterioration, no improvement, MGCS < 8)
1. Mannitol or hypertonic NaCl
2. Elevation of head 30º
Tier 3 (contd. tier 2 progress)
1. Surgical decompression
2. Hyperventilation
3. Hypothermia
What two clostridial agents cause neurotoxicity?
- Clostridium tetani (Tetanus)
- Clostridium botulinum (Botulism)
Pathogenesis of Clostridia tetani
Clostridia tetani : irreversible binding of EXOTOXINS in the CNS prevents release of inhibitory NTs (glycine/GABA) -> Spastic paralysis
incr. muscle tone, rigidity, spasms; clinical signs 5-10d post infection
Pathogenesis ofClostridia botulinum
Clostridia botulinum: irreversible binding of EXOTOXINS at NMJ of peripheral nerves blocks release of excitatory NTs (ACh) -> Flaccid (LMN) paralysis
- Cats are resistant to effects of botulinum toxin, so botulism is RARE
respiratory failure usual cause of death; clinical signs within 12h
Clinical signs of metabolic encephalopathies (4)
- Seizures
- Behavior changes (aggression, anxisty, dementia, mania)
- Mentation change (obtunded, stuporous, coma)
- Cortical blindness (non-ophthalmic cause; normal PLRs, absent CN II lesions)
Common etiologies of metabolic encephalopathies (5)
- hypoglycemia
- hyponatremia
- hypocalcemia
- hepatic encephalopathy (ammonia)
- thiamine deficiency (B1 – CHO metabolism)
