Controlling hypocalcaemia Flashcards

1
Q

What is hypocalcaemia?

A
  • Metabolic disorder
  • Occurs due to net efflux of calcium from the extracellular fluid in greater quantities than the intestines or bones can replace
  • Normal plasma Ca 2.1-2.8 mmol/l.
  • Hypocalcaemic <2.0 mmol/l.
  • Sets in usually 48-72h postpartum
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2
Q

How is calcium supply controlled?

A
  • By the parathyroid gland
    – mobilising calcium from the bone when blood calcium is low and mineralising or excreting it where supply is in excess.
  • PTH triggers calcitrol (active vit D) release from kidneys
    – acts on intestines and kidneys to increase absorption.
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3
Q

What is calcium used for?

A
  • muscle contraction
  • immune function
  • nerve impulse transmission
  • bones and teeth
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4
Q

Effects of hypocalcaemia

A
  • Reduce muscle contraction
  • Increased neuromuscular irritability.
  • Decreased smooth muscle contraction.
  • Decreased skeletal muscle contraction.
  • Affects posture & gait.
  • Reduced cardiac muscle contractility.
  • Affects function and circulation.
  • Risk of mastitis is increased so sphincter muscles in teat are reduced, and she spends more time lying down, so risk of infection getting into the teat is higher.
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5
Q

Calcium requirements of the cow (maintenance, at calving, peak lactation, late pregnancy)

A
  • maintenance: (650 kg cow, 20 Kg DMI), 25 g Ca/day
  • at calving: 12 litres of colostrum, +30 g Ca/day, Total: 55 g Ca/day
  • peak lactation: 40 litres of milk +73 g Ca/day, Total: 98 g Ca/day
  • late pregnancy: Late pregnancy + 13.9 g Ca/day, Total: 38.9 g Ca/day
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6
Q

What hormones act to increase blood calcium?

A
  • PTH
  • Calcitrol
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7
Q

Risk factors

A

Around calving; Ca demand increases rapidly, endocrine control takes a few days to adjust.
- Resorption from the kidneys is the fastest repletion followed by increased intestinal absorption.
- Release of Ca from bone is the slowest.

Age of cow; Older cows have reduced calcium reserves and mechanisms respond slower.

Milk fever risk increases with parity as milk yield increases
- Peaking around 3-4

Other increased risk factors include;
- C-section, dystocia, BCS ≥4, hereditary.

Herd risk factors important too
- Eg, dairy crosses (Limousin x Holstein), channel island breeds, autumn calving cows.

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8
Q

Clinical signs of hypocalcaemia

A
  • Skeletal muscle
  • Weakness
  • S-bend neck
  • Smooth muscle
  • Rumen atony
  • GI stasis
  • Poor uterine involution
  • Cardiac muscle
  • Poor contractility
  • Slightly increased HR (c.f. “toxic” cow)

All associated with calciums role in muscle contraction.

  • Tremors
    – Early sign that is often missed
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9
Q

Treatment plan

A

400ml 40% calcium borogluconate slowly IV
- If given too fast inc. risk of hypercalcaemic relapse.
- Reverses physiological mechanisms.
- Halts PTH release and triggers calcitonin secretion due to surplus in blood.
- ~25%-40% relapse within 12 to 24 hours unless dose is managed.

Monitor heart rate and rhythm.

Consider blood sample in case no response.

Outcome of treatment:
- Eructation, defecation, urination & standing within ~20-30 mins
- If no response, consider alternatives and complications (e.g. “downer cow”)

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10
Q

Additional Ca options

A

Sub-cut
- Poor absorption
- Negative feedback
- Easy
- Relatively common

Oral
- Well absorbed
- Requires GI uptake
- Relatively easy
- Becoming more common
- Ensure she’s up before giving oral Ca

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11
Q

Additional treatment

A

NSAID
- 700 kg cow down
- Trauma common complication
- Why not?

Phosphorus
- P often low with milk fever
- Common preparation not active
- Should increase with Ca

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12
Q

Herd management: Ca restriction

A
  • Effective nutritional management during the dry period and early lactation can decrease clinical cases to ~1%
  • Restricting Ca intake during the late dry period can prevent hypoCa.
    – Reduce dietary calcium to ~100g Ca/day.
  • Dry cows on high Ca diets reduce absorption from the diet and excrete excess.
    – She cannot meet Ca demand as the mechanisms are already down-regulated.
  • Limiting Ca prior to calving, up-regulates PTH mechanisms
    – Starts resorption from bone, increases dietary absorption etc,
  • Over 2-3 weeks cow is better prepared for increased demand.
  • Must increase dietary Ca at calving.
  • Difficult to keep Ca low enough.
  • Can use Ca binder.
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13
Q

Herd management: Controlling DCAB

A
  • Lowering blood pH can prevent hypocalcaemia.
  • This is achieved through reducing DCAB in the dry period.
    – Decrease Na+ and K+ (cations), increase Cl- and S- (anions).
  • Resulting slight acidosis increases binding of PTH and other effects.
  • Improves the cow’s ability to mobilize calcium from the bones and to absorb dietary calcium from the small intestines.
  • Must provide adequate Ca as increased mobilisation.
  • Partial or full DCAB approach.
  • Anionic salts can reduce palatability (↓DMI).
  • Monitor for efficacy:
    – urine pH using DCAB should be 6.0-6.5.
  • Grass can be high in K.
  • Basically want to push her into slight acidosis
    – By triggering this it will increase the binding of PTH
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14
Q

What is DCAB?

A
  • Dietary cation-anion balance
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