Hypocalcemia (Milk Fever)

normal calcium metabolism

etiology

risk factors

clinical signs

diagnosis

treatment

prophylaxis/prevention

high risk individuals

whole damn herd

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

function

sources

hormones

mm contraction

nerve impulse transmission

dietary

active

active

skeletal stores

parathyroid hormone (PTH)

increases

calcitonin

decreases

  1. 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

  1. 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)

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

high milk production

parity

rare in fist lactation heifers

breed

Jerseys

Guernsey

stage 1: prodromal, standing but wobbly

stage 2: sternal recumbancy

stage 3: lateral recumbency

usually not noticed

muscle tremors

bellowing, open mouth breathing

excitable

hyperesthetic

ataxic

no urine or defecation

tachycardic

flaccid paralysis

tachcardia

weak, lethargic, depressed

bloat, tympany, decreased rumen contractions

cool extremities

lateral kink s-shaped neck

decreased temperature

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

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

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

🚫 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

🚫

udder insufflation

skipping milkings

prophylactic Ca administration by prducer

🚫

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

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

buffering blood

respiratory system regulation of acid-base status (rapid)

kidneys (slower)

restrict cation sources in feedstuff

supplement additional anions

monitor

urine pH

dry matter intake

7.5-8.0 inadequate acidification

6.2 - 6.8 optimal

<5.8 excessive acidification

transition ration 3w prepartum

unrestricted access to food and water

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