Please enable JavaScript.
Coggle requires JavaScript to display documents.
Hypocalcemia (Milk Fever) - Coggle Diagram
Hypocalcemia (Milk Fever)
normal calcium metabolism
function
mm contraction
nerve impulse transmission
sources
dietary
active
active
skeletal stores
hormones
parathyroid hormone (PTH)
increases
calcitonin
decreases
etiology
early to mid-dry period
diets fed during dry period typically exceed Ca requirement
most of Ca demand easily met passively
active bone resorption mechanisms are quiescent
periparturient period
sudden increase in Ca demands
colostrum and milk production
fetal skeletal demands
rapid decrease in blood [Ca]
large increase in PTH
increases renal absorption of Ca (minutes)
increases osteoclast activity (48hrs)
stimulates vit D synthesis in kidneys (24hrs)
risk factors
high milk production
parity
rare in fist lactation heifers
breed
Jerseys
Guernsey
clinical signs
stage 1: prodromal, standing but wobbly
usually not noticed
muscle tremors
bellowing, open mouth breathing
excitable
hyperesthetic
ataxic
no urine or defecation
tachycardic
stage 2: sternal recumbancy
flaccid paralysis
tachcardia
weak, lethargic, depressed
bloat, tympany, decreased rumen contractions
cool extremities
lateral kink s-shaped neck
decreased temperature
stage 3: lateral recumbency
extreme mm flacidity
reduced/absent corneal reflexes and pupillary light reflex
stage 1 and 2 symptoms
death in few hours w/o treatment
complications
dystocia/arrested partuition
uterine prolapse
retained placenta
traumatic injury from struggling
aspiration pneumonia
metabolic disease
ketosis
DA
metritis
decreased repro performance
decreased production
diagnosis
history, signamlment, CS
response to treatment
retrospective serum biochemistry
collect blood and put it in fridge
analyze later if animal doesn't respond to treatment
clin path
hypocalcemia defined as <7.5 mg/dl
hypophospatemia defined as <3 mg/dl
hypermagnesemia defined as >2.2 mg/dl
stress leukogram
hyperglycemia
moderately elevated CPK
treatment
emergency action
500mL 23% Ca borogluconate slow IV over 5-10min
Ca is cardiotoxic so monitor
normal response
HR slows and strengthens
brighter and more alert in 10-20min
muscle function returns
usually treats accompanying hypophos
persistent hypophosphatemia
occasionally occurs even after correcting Ca
alert downer cow
IV 30g sodium monophosphate
follow with -.5kg in oral drench
fleet enema + 1L saline - give IV
must be in at least sternal recumbency
avoid IV in milk vein
preventing relapse
24-40% relapse in <48hrs
option 1
sq injection of 500mL 23% CBG
slow release
split b/w two sites
:forbidden: dextrose
option 2
oral dose w/ Ca salt gels
calcium chlorid
calcium propionate
supportive therapy
give space to lunge
provide good footing
retreat if not up in 4-6hrs
support in sternal
assistance getting up
:forbidden:
udder insufflation
skipping milkings
prophylaxis/prevention
high risk individuals
prophylactic Ca administration by prducer
:forbidden:
IV/SQ Ca treatment at calving
oral Ca gls or bolus 2-3x
1 treatment prior to calving
1 treatment at calving
1-2 tc at 12-24 hrs post-calving
use Ca-proprionate
whole damn herd
if >5-10% clinical rate, address nutrition
perpartum dietary management
manipulate dietary cation anion difference (DCAD)
minimize high K forage (legumes)
Ca binder in the diet to decrease absorbtion
zeolite A
induces slight metabolic acidosis
tight binding of PTH to receptors
prevents milk fever
restrict cation sources in feedstuff
supplement additional anions
monitor
urine pH
7.5-8.0 inadequate acidification
6.2 - 6.8 optimal
<5.8 excessive acidification
dry matter intake
transition ration 3w prepartum
unrestricted access to food and water
buffering blood
respiratory system regulation of acid-base status (rapid)
kidneys (slower)
basics
aka
parturient paresis
milk fever
non-febrile disease of adult dairy cows
acute Ca deficiency causes progressive neuromusclar dysfxn
flaccid paralysis
circulatory collapse
depression of consciousness
clinical vs subclinical
failure of mechanisms to maintain blood Ca levels during sudden Ca outflow
factors that influence adaptability to hypocalcemia
Ca intake
acid-base status
metabolic alkalosis impairs PTH
high dietary potassium
reduces PTH secretion
reduced Mg absorption
reduced PTH responsiveness
excess dietary phosphorus
high estrogen levels
other ruminants
rare in beef cows
osteoporosis if chronic
if occurs, probably late gestation
lower incidence in sheep
last 4-6w gestation
complicated by pregnancy toxemia
transport tetany
risk factors
older ewes
multiple fetuses
sudden stress
similar CS as dairy cows
clin path
hypocalcemia
+/- hypoMg/K/glycemia
increased CK, AST
similar treatment as dairy cows
dairy goats
prepartum or several weeks postpartum
risk factors
multiple fetuses
high milk production
non-parturient hypocalcemia possible