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Hypocalcaemia and hypomagnesaemia - Coggle Diagram
Hypocalcaemia and hypomagnesaemia
milk fever (hypoCa)
clinical signs
24h after parturition, but can occur at or before calving
the signs then progress over a period of 12-24h
teeth grinding
muscle tremors
stiff legs
straight hocks
paddling of feet when standing during the early stages
muscle weakness
recumbency with characteristic kink 's-bend' in neck, later the head is held against the chest
gut stasis causes bloat and constipation
if left untreated the cow will become comatose and lie on her side
luminal bloat and or paralysis of respiratory muscles cause death in untreated cattle after 12-24h
complications of hypocalcaemia
uterine inertia
lead to calving problems and stillbirth
prolapse of the uterus
inhalation of rumen contents when cast causing pneumonia
pressure damage to nerve and muscles
differential diagnosis
acute toxic mastits
physical injury/nerve paralysis
uterine rupture
haemorrhage caused by dystocia
acidosis/grain overload
botulism
hypophosphataemia
diagnosis
hx, clinical signs + response to IV
calcium borogluconate
solution within minutes
Clinical signs occur when serum calcium levels fall below 1.5mmol/l (normal 2.2-2.6 mmol/l) and are often as low as 0.4 mmol/l in cattle with advanced disease.
treatment
administer 400ml of 40% calcium borogluconate solution (containing 12g calcium) warmed to body temperature, by slow intravenous injection (over 5-10 minutes) into the jugular vein using a 14 gauge needle and flutter valve with the bottle held 30-40 cm above the infusion site
prevention
cows should be 2.5-3 at calving
primary cause is usually the high potassium or calcium content of the forage content in the dry period
Low dietary magnesium may be a factor and provision of magnesium chloride will also lower the dietary cation-anion balance (DCAB) of the diet
grass staggers (hypoMg)
The amount and concentration of magnesium in the body is dependent upon
absorption
mainly from the
rumen
which varies from
10-35%
, the requirement for
milk
production - and excretion by the
kidneys
.
factors affecting availability of dietary magnesium
levels in the soil and grass which vary
high levels of potassium (e.g. fertilisers) disrupt the absorption of magnesium
high levels of ammonia (from nitrogenous fertilisers) inhibit magnesium absorption
lush pastures are low in fibre and increase the rate of passage of food material through the rumen reducing time for the absorption
clinical presentation
Sudden death without premonitory signs is encountered most commonly in older lactating beef cows 4-8 weeks after calving maintained at pasture without appropriate supplementary feeding. The cow is found dead with disturbed soil around its feet indicating paddling/seizure activity often after stormy weather.
In acute disease there is initial
excitability
with
high head carriage, twitching of muscles
(especially around the head) and
incoordination
("staggering gait"). Affected cows become separated from the group and have a startled expression, show an
exaggerated blink reflex
and
frequent grinding of the teeth
There is rapid progression to periods of seizure activity. During
seizure
activity there is frenzied
paddling
of the limbs, sudden eye movements,
rapid pounding heart
, and
teeth grinding
with
frothy salivation
differential diagnoses in adult cows
sudden death
electrocution/lightning
anthrax
clostridial disease e.g. blackleg
acute disease
lead poisoning
hypocalcaemia
nervous acetonaemia (dairy cow)
diagnosis
Plasma magnesium less than 0.8mmol/l indicate subclinical hypomagnesaemia and an increased risk of developing acute hypomagnesaemia.
dead on arrival
• If the animal is dead on arrival collect aqueous or vitreous humor samples for laboratory analysis to confirm the diagnosis
• Mg <0.33mmol/l in aqueous humor or <0.55 mmol/L in vitreous humor of are indicative of hypomagnesemia.
• Vitreous humor sampling is best
as it is much more stable fluid and
therefore a more reliable test
prevention/control measures
The total diet should contain 2.5g/kg DM of magnesium to meet requirements of the majority of lactating cows at pasture. The best method is to use 60g magnesium oxide (calcined magnesite) per cow per day in high-magnesium cobs. Magnesium salts are relatively inexpensive and the cost of supplementation 100 cows for two months will be less than the loss on one animal due to hypomagnesaemia.
The sole water supply can be medicated with soluble magnesium salts such as chloride, sulphate or acetate. Pastures may be dusted during high-risk periods with finely ground calcined magnesite every 10-14 days. Intra-ruminal boluses give a slow release of relatively small amounts of magnesium into the rumen over a period of four weeks. Magnesium salts and minerals are unpalatable therefore ad-lib minerals are not satisfactory. Supplementation is especially important during stormy weather when roughage, such as straw, can be beneficial for beef cows.