Metabolic causes of CNS disease Flashcards
electrolyte imbalances etiology
from profuse diarrhea, gastric reflux, extreme exertion, renal failure, transport stress and lactation
hyponatremia, hypernatremia, hypocalcemia and hypomagnesemia
electrolyte imbalances diagnosis
measurement of serum and sometimes CSF electrolyte concentrations
thorough PE, chem panel
electrolyte imbalances tx
correction of electrolyte disturbances via IV therapy with electrolyte supplementation
treatment of underlying disorder
what is hypomagnesemic tetany
nervous irritation or tetany associated wtih decreased levesl of serum magnesium
common in ruminants
grass tetany
grass stagger or lactation tetany
seen in dairy cattle overwintered indoors on poor quality, then turned out on lush grass pasture in spring
beef cows with calves in similar conditions
milk tetany
seen in 2-4 month old vealer calves on poor quality milk replacer diet
transport tetany
any age or species of ruminants
seen after extended truck or rail transport of 24 hour or greater duration
esp if feed and water withheld
pathogenesis of hypomagnesemic tetany
serum magnesium levesl almost always less than 1 mg/dl
the onset of clinical signs closely associated with low CSF levels of Mg
clinical findings in hypomagnesium tetany
signs limited to nervous dysfunction
hx of recent turnout onto pasture
early signs: alert, anxious expression, muscle twitching and fasciculations
progressive sxs: hyperesthesia, continuous bellowing, frenzied galloping, collapse with full blown convulsions (episodic)
death within 1-2 hours of first signs
DDx of hypomagnesium tetany
rabies
lead poisoning
nervous ketosis
diagnosis of hypomagnesium tetany
serum mg less than 1 mg/dl
clinical response to tx
polioencephalomalacia epidemiology
occurs sporadically or as a herd problem
herd outbreaks following management changes
morbidity: 25%, mortality: 50%
mostly 6-18 months of age
polioencephalomalacia pathogenesis
thiamine deficiency
inolved with glucose metabolism (esp in brain)
production may be reduced after a change in diet
high concentrate ration
thiamine analogues
decreased glucose production
thiaminase-1 producing bacteria in rumen
high dietary sulfur, amprolium, bracken fern, molasses-urea diet with no roughage
intracellular edema –>neuronal degeneration and laminar necrosis
polioencephalomalacia clinical signs
blindness
PLR normal
opsithonotic
incoordinated
depression with excitement
dorsomedial strabismus
later signs: muscle tremors
terminal signs: recumbency with opisthotonos, convulsions, coma and death
24-48 hours
clinical pathology of polioencephalomalacia
CBC normal
increased serum pyruvate levels, decreased blood lactate
CSF: normal to mild protein elevation
necropsy: diffuse cerebral edema, UV fluorescence observed in necrotic areas
polioencephalomalacia diagnosis
response to early thiamine therapy
determination of sulfur content of diet (<0.4%)
cattle: r/o lead poisoning, hypovitaminosis A, TME
sheep: r/o enterotoxemia, focal symmetrical encephalomalacia
goats: r/o caprine leukoencephalomyelitis, enterotoxemia, listeriosis, pregnancy toxemia, lead poisoning and meningoencephalitis
polioencephalomalacia treatment
thiamine q 6 hours until recovered
remove grain, put on forage ration
response in 6-8 hours
corticosteroids
severe cases response poorly
Nervous ketosis epidemiology
wasting form: more ommon
nervous form: hypoglycemia
nervous ketosis clinical signs
belligerence
delirium
awkward stance
head pressing
licking
intermittent nervous signs lasting 1-2 hours
nervous ketosis diagnosis
urine or milk ketones
reponse to IV glucose therapy
intermittent signs
nervous ketosis tx
IV glucose
oral propylene glycol
DDx of nervous ketosis
listeriosis
rabies
pseudorabies
polioencephalomalacia
lead poisoning
hypovitamosis A epidemiology
drought conditions
poor quality stored feed
young, growing animals
hypovitamosis A clinical syndromes
blindness due to stenosis of optic foramen, increase in CSF pressure, pupils dilated and unresponsive to light
encephalopathy-increasing CSF pressure, clonic tonic convulsions
progressive paresis or paralysis-destruction of peripheral nerves
