Exam 2 - Intracranial Disease 2 Flashcards
how would you describe metabolic encephalopathy in terms of disease onset, progression, and pain?
onset - can be episodic, slowly progressive, or rapidly progressive
progression - typically worsens over time
pain - not usually painful
T/F: in metabolic encephalopathy, it’s usually forebrain predominant & systemic effects are usually evident
true
what is the ‘minimum database’ in regards to metabolic encephalopathy?
hypoglycemia - check glucose
hyper/hyponatremia
hypocalcemia - check ionized calcium
ammonia, bile acids - hepatic encephalopathy
what is the general description given for metabolic encephalopathy?
waxing/waning forebrain disease with normal neurological exam and vague or symmetrical neurological signs
how low is too low with hypoglycemia?
<50mg/dL
what are some common underlying causes of hypoglycemia?
excess insulin or insulin-like substances (insulinoma)
decreased glucose production - neonates or severe hepatic insufficiency
excess glucose utilization - sepsis
how high is too high with hypernatremia?
> 180mEq/L
what are some causes of free water deficit causing hypernatremia?
no intake - denied water or hypodipsic hypernatremia
loss from disease - vomiting/diarrhea or diabetes insipidus
iatrogenic loss - mannitol or activated charcoal
what are some causes of sodium excess causing hypernatremia?
sodium rich diet - seawater, jerky, play dough
sodium rich drugs
how does hypernatremia develop?
excess sodium causes cells to shrink & you have an increased concentration gradient
when fluids are rapidly given, idiogenic osmoles are created, and the cell rapidly expands causing cerebral edema
how low is too low with hyponatremia?
<125 mEq/L
what are some causes of free water excess causing hyponatremia?
hypovolemic - cavitary effusions, excessive gi loss, or urinary loss
addison’s
hypervolemic - left heart failure or very severe renal failure
what should you do if you give fluids to a hypernatremic patient & they develop neurological clinical signs?
d/c fluids, check their sodium, & give lasix
what happens if there a rapid decrease in free H2O when trying to correct hyponatremia?
irreversible demyelination of nerves
T/F: clinical signs of demyelination from rapidly decreasing free H2O in a hyponatremic patient will appear > 24 hours after treatment
true
what should you do if an animal with hyponatremia develops clinical signs 24 hours after you started treating it?
stop giving high sodium fluids & give free H2O
what clinical signs are associated with severe hepatic insufficiency in dogs and cats with hepatic encephalopathy?
increased protein intake, gi disease (hemorrhage or obstruction), acute-or-chronic hepatic injury, dehydration, & sepsis
what medical management/emergency treatment can be used for hepatic encephalopathy patients?
lactulose - traps ammonia in the colon & decrease bacterial ammonia production
metronidazole (antibiotics) - decreases ammonia producing bacteria
what is the treatment used for metabolic encephalopathy?
correction of the metabolic abnormality should improve neurological signs - diagnostic confirmation
successful resolution of underlying cause can resolve neuro signs but residual seizures are possible if they became epileptic during the incident
what animal is most commonly affected by nutritional encephalopathy caused by thiamine deficiency?
cats
how would the onset, progression, and pain status of thiamine deficiency be described?
onset - slowly develops
progression - gets worse over time
pain - not usually painful
what are the common neurological localizations given to thiamine deficiency?
forebrain, brainstem, & cerebellar - multifocal
T/F: systemic disease may be a risk factor for thiamine deficiency
true
what is the most common cause of thiamine deficiency?
inadequate dietary intake - cats have a higher requirement
what are the mechanisms that lead to thiamine deficiency?
- inadequate dietary intake
- increased elimination because of increased GFR - hyperthyroid cats
- decreased absorption in chronic enteropathy - IBD
what would you expect to see on imaging in a patient with thiamine deficiency?
patches in the gray matter
what test is used for diagnosing thiamine deficiency & why?
high pressure liquid chromatography send out test
more sensitive, specific, & stable
what is the prognosis of thiamine deficiency?
good
what is the treatment for thiamine deficiency?
parenteral supplementation given SQ every 3-5 days - not IV!!!
oral supplementation for at least 2-4 weeks & diet change
how would the onset, progression, and pain status of toxic encephalopathy be described?
onset - variable
progression - single exposure may be static to improving over time while chronic exposure can worsen over time
pain - not usually painful
what clinical signs are associated with metronidazole toxicity?
central vestibular signs
what is metronidazole toxicity associated with?
higher doses & longer duration treatments
T/F: damage from metronidazole toxicity is reversible
true - may resolve faster with oral diazepam treatment
a high dose of bromethalin will cause what clinical signs?
seizures & death within hours of ingestion
a low dose of bromethalin will cause what clinical signs?
paresis/paralysis & potentially coma within 1-2 days of ingestion
what is the treatment for bromethalin toxicity?
gastric lavage with activated charcoal if recent ingestion
what is the prognosis of bromethalin toxicity?
guarded to poor
what anatomic changes are seen with cerebral atrophy?
widening of cortical sulci
enlargement of ventricles
thinning of cortex
shrinking of hippocampus
how would the onset, progression, and pain status of canine cognitive dysfunction be described?
onset - insidious onset with varied/vague signs in older adults
progression - relentlessly progressive
painful - not really
what clinical signs are seen if they are confined to the forebrain in canine cognitive dysfunction?
disrupted sleep-wake cycle, anxiety, decreased interaction with the owner, and rare seizures
how can you confirm canine cognitive dysfunction?
rule out systemic & structural brain disease
& distinguishing normal aging from a pathological small interthalmic adhesion
T/F: there is a cure for canine cognitive dysfunction
false - no cure
what treatments/therapies can be used for an animal with suspected canine cognitive dysfunction?
l-deprenyl, monoamine oxidase inhibitors (careful of interactions)
diet - combo of high fatty acids, anti-oxidants, & l-carnitine suggested
environmental enrichment in dogs
what is a congenital brain malformation?
malformation present at birth that may or may not show signs at birth
what is the progression of congenital brain malformations causing intracranial disease?
underlying problem doesn’t progress but clinical signs may progress
what neurological signs are seen with congenital brain malformations?
depends on the location of the malformation
what animals are typically affected by hydrocephalus?
young animals under 6 months of age
inherited - toy breeds & brachycephalic
in utero insult - trauma, toxin, infection, or nutritional deficiency
how is hydrocephalus diagnosed?
MRI, CT, or even ultrasound - use CSF to rule out meningoencephalitis
what treatment can be used for congenital hydrocephalus?
omeprazole, glucocorticoids, diuretics - decrease CSF production
control seizures
surgery - ventriculoperitoneal shunt
what are the complications associated with the ventriculoperitoneal shunt surgery?
blockage, breakage, or infection
what is the typical presentation of a traumatic brain injury?
emergency - peracute onset & progressive
how is a traumatic brain injury diagnosed?
based on clinical signs & the recognition of progressive neurological dysfunction after known or suspected trauma because of the increased intracranial pressure
why is increased intracranial pressure so bad?
causes caudal herniation of the brainstem as it pushes the cerebellum/medulla through the foramen magnum & midbrain under the osseous tentorium
what are the clinical signs associated with increased intracranial pressure?
progressive signs of forebrain disease, new signs of brainstem disease, central vestibular signs, pupillary/ocular reflex abnormalities, & hypertension with reflex bradycardia (cushing’s reflex)
how is increased intracranial pressure diagnosed?
neurological exam & indirect diagnostic data
what is tier 1 of managing increased intracranial pressure?
basic systemic stabilization
what is tier 2 of managing increased intracranial pressure?
medical reduction of intracranial pressure - mannitol & head elevation
what is tier 3 of managing increased intracranial pressure?
possible surgical intervention
what is the treatment for increased intracranial pressure?
maintain normal PO2, PCO2, temperature, perfusion, control seizure activity, & elevate the head without compressing jugular veins
what are you looking for on imaging if you suspect increased intracranial pressure?
depressed fractures, hematomas, ongoing bleeding (CT) - surgical targets
what is a common cause of slowly progressive intracranial disease in older dogs?
canine cognitive dysfunction
what is a common cause of peracute intracranial disease in older dogs?
vascular insult
what are the 2 most important parts of managing a traumatic brain injury?
systemic stabilization
management of intracranial pressure
