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3. Food Animal 2 > hypocalcemia > Flashcards

hypocalcemia Flashcards

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1
Q

metabolic challenges of the transistion period for a dairy cow

A
  • decreased feed intake
  • energy deficit
  • lipolysis
  • hypocalcemia
  • reduced neutrophil function
    <><>
    > immune competence decreased surrounding parturition
    > increased inflammation after parturition
    > increased oxidative stresss after perturition
    > lowered calcium spike at parturution
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2
Q

how common is subclinical and clinical milk fever?

A

clinical ~5%
subclinical ~40-60%

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3
Q

calcium requirements in early lactation

A
  • Body pool of Ca: 99% in bone
  • Extreme Ca requirements for lactation:
    = roughly 9x plasma pool of Ca required per milking in early lactation
  • 10 kg of colostrum = 23 g Ca loss!
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4
Q

calcium playes a role in what body systems

A
  • nerve impulses
  • muscle contraction
  • immune system
  • colostrum and milk production
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5
Q

mechanisms of Ca regulation

A
  • PTH acts on kidney, produces more 1,25 Vit D > more intestinal absorption of dietary Ca
  • PTH acts on bone > moves Ca to blood (inadequate Mg will mitigate this/0
    <><>
  • High dietary K+, alkalosis, positive DCAD > less Ca moved from bone to blood
  • metabolic acidosis, negative DCAD > more Ca moved from bone to blood
    <><>
    milk draws Ca from blood
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6
Q

PATHOPHYSIOLOGY OF MILK FEVER

A

 Normal hormonal response occurs in hypocalcemic cows, but… Reduced PTH and Vitamin D receptors (with age, breed)
> think ‘old Jerseys’
> Ability to mobilize Ca from bone and absorb Ca from gut decreases with age
<><>
- Ca absorption in intestine is critical to minimize hypocalcemia
- Ca++ absorption occurs in the proximal small intestine
> reduced DMI at parturition can lead to
decreased Ca++…
> decreased Ca++ causes decreased intestinal motility…
> exacerbation of hypocalcemia
<><>
 Poor PTH receptor function at target tissues when alkalotic or hypomagnesemic

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7
Q

how to metabolic alkalosis and hypomagnesemia affect Ca levels

A

metabolic alkalosis - interferes with PTH binding to receptor > no effects on vit D, etc > hypocalcemia
<><>
hypomagnesemia - prevents signalling to vitamin D from PTH receptor, even through PTH is bound.

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8
Q

RISK FACTORS AND INCIDENCE for milk fever

A

 Incidence of 5 to 10% (in 3rd+ parity)
 -24 hours to +72 postpartum
 Breed predisposition: Jerseys higher incidence
 Age predisposition: increased parity (3rd +): Older cows have fewer gut receptors for Vit D3 and higher milk yield
High producing dairy cattle
Milk fever in previous lactation
Fat (BCS > 3.75)

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9
Q

HYPOCALCEMIA RISK - SIMPLIFIED
demand vs supply model

A

Demand - milk yield
Supply - dry matter intake, ability to absorb Ca, ability to mobilize Ca

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10
Q

DIETARY RISK FACTORS for hypocalcemia

A
  • Dry cow diet with high potassium
  • metabolic alkalosis induced by excess cations (eg. K+, Na+, Ca++)
  • grass or legume hay - especially from heavily fertilized fields - high in potassium
  • DCAD = (Na+ + K+) - (Cl- + S2-)
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11
Q

incidence of milk fever by parity and serum calcium levels by week of lactation and parity

A
  • spiked at parity =3
  • serum Ca always decline around parturition, but year 3 decline much greater than previous years
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12
Q

clinical signs of milk fever
- effects on body temp, skeletal muscle, and smooth muscle

A
  • Rectal temperature (No Fever)
    Effects of Hypocalcemia on:
  • Body temperature:
    > Shifted circulation
    > Cold skin (especially skin of the ears)
  • Skeletal muscle: recumbency
  • Smooth muscle:
    – decreased gastrointestinal motility
    – decreased strength of myocardial contraction
    – poor vasomotor tone
    – decreased uterine contraction
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13
Q

stages of milk fever and main signs from each

A

STAGE 1 (“Prodromal Stage”)
 Able to stand; weak

STAGE 2
 Sternal recumbency

STAGE 3
 Lateral recumbency

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14
Q

clinical signs of stage 1 milk fever

A

 Able to stand; weak
 Decreased feed intake
 Hyperexcitable, restless
 Decreased urination, defecation
 Fine muscle tremors
 Reduced rumen contractions and strength
 Slight ataxia
 Mild tachycardia
 Sometimes: dystocia, retained placenta

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15
Q

clinical signs of stage 2 milk fever

A

 Sternal recumbency, focal muscle tremors ‘S’ shaped curve in neck
 Rectal T° variable with ambient temperature  Poor peripheral perfusion
 increased Heart rate, weak pulse
 Mydriasis, slow PLR
<><>
 Lack of manure behind cow
 Decreased rumen and intestinal motility, bloat
> Two most diagnostic clinical
signs in a recently calved 3+ lactation cow

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16
Q

clinical signs of stage 3 milk fever

A

 Lateral recumbency
 Flaccid paralysis
 Very poor cardiac function
 Bloat, may aspirate
 Poor anal tone
 Unresponsive > coma
 Death

17
Q

milk fever diagnosis?

A

 History
> NOT in 1st Lactation Animals!
 Clinical signs
 PE excludes other possible causes of recumbency
 Response to treatment
<><>
 Serum Ca:
– Pre-treatment blood sample!
– Total serum calcium (tCa) is fine
* ionized calcium (iCa) – technically better, but not necessary
 Hypocalcemia is often accompanied by:
– Alterations in P (low), Mg (high), K (normal to
low), glucose (high)
– Elevated muscle enzymes (CK, AST)

18
Q

Ddx for milk fever / other causes of recumbency

A
  • metabolic (milk fever, HypoMg, HypoP)
  • Toxemic (severe clinical mastitis, other source)
  • traumatic - musculoskeletal (nerve damage, other)
  • prolonged recumbency > pressure induced damage
19
Q

Milk fever treatment? what should we be careful of?

A
  1. Blood Sample
  2. Intravenous Ca
    >Calcium borogluconate 23% (1x500 ml bottle)
    > No need to exceed 1 x 500mL bottle IV
    Cardiotoxicity: Administer slowly!
    - Concurrent cardiac auscultation
    > Arrhythmias, tachycardia
    > Beware of endotoxemic cows
    If present, stop. Administer more slowly
  3. Subcutaneous Ca OR Oral Bolus
    - Calcium borogluconate 23% (1X 500 ml bottle)
    *** Do Not Give SQ Dextrose or Ca containing Dextrose (ie Cal Dex, CalPlus, etc)
    - Alternative is oral bolus e.g. Bovikalc (1 bolus + 1 in 6 h)
20
Q

effect of Ca supplements for milk fever

A
  • IV big Ca spike, and then levels go low again, and slowly rise to baseline
  • oral ( 2 Bovikalc 12 h apart) levels rise and remain stable
21
Q

RESPONSE TO CALCIUM THERAPY in milk fever

A

 Immediate
 Muscle tremors initially
 Stronger myocardial contractions, decreased heart rate
 Gastrointestinal motility returns (defecation, eructation)
 Urination
 Stand within 0 - 2 hours (reassess if > 4 hours)
 25 - 30% relapse in next 24 - 48 hours

22
Q

PREVENTION OF MILK FEVER RELAPSES?considerations?

A

Subcutaneous calcium
- Avoid calcium solutions with high dextrose
- Risk of abscesses

Oral calcium
- Ca propionate
- Bovikalc (calcium chloride + calcium sulphate)
- Pastes/gels (irritating!)
- DO NOT give if DOWN and Untreated IV

23
Q

Oral boluses vs SC calcium

A
  • SC big initial spike, then levels fall
  • oral remains more stable over time, higher levels at 48h post calving than SC
24
Q

NURSING CARE for milk fever - CRITICAL
> bedding? protection? etc.

A

Clean, dry bedding
Non-slip surface
Frequent shifting side-to-side
Protect from elements
Access to water and feed
Lifting: hip lifter, float tank, sling

25
Q

follow up for milk fevertreatment? what if poor response?

A

 Did not respond to treatment?
> Pre-treatment blood sample, analyze results
 Early decisions on re-treatment
> More Ca within 12 hours, lifting (within 4 hours), etc
 Recommend Euthanasia if no response within 24-48 hours
> Our responsibility to help ensure cow welfare is upheld

26
Q

HYPOCALCEMIA – COMPLICATIONS

A

 Dystocia
 Retained placenta, metritis, prolapsed uterus
 LDA – comes days later and probably associated with other health issues
 Teat trauma, mastitis
 Ischemic muscle necrosis
 Nerve compression > dysfunction
 Musculoskeletal trauma when trying to rise
 Aspiration pneumonia

27
Q

HOW DO WE DEFINE SUBCLINICAL HYPOCALCEMIA?
 Ionized Calcium or Total Calcium?
 Threshold and Sampling time (days in milk)

A

IONIZED CALCIUM (iCA)
 Bioactive form of blood calcium, capable of intracellular access
 Cow-side testing
 High cost of the device + Cartridges
 Cut-point SCH <1.17 mmol/L
- in a healthy cow, ~50% of Ca in circulation >but iCa-tCa relationship changes around parturition
Few studies base postpartum disease prediction on iCa, perhaps due to its cost and practicality
<><>
TOTAL CALCIUM (tCA = iCa + Ca bound to proteins)
 Affected by serum Total Protein concentration
 Ca is bound to albumin; this relationship is pH-dependent
 Inexpensive
 SCH cut-point found: from 1.88 to 2.35 mmol/L
 Cow-side testing not valid/available
 Most studies base postpartum disease prediction on tCa
- send to lab, results in ~24h Or
Benchtop Clinical Chemistry Analyzer

28
Q

SUBCLINICAL HYPOCALCEMIA – IS IT ALWAYS A BAD THING?

A

-there is a transient presentation which may not be bad in the long run
- but also persistant and delayed forms…

29
Q

hypocalcemia prevention and control
- take-homes for prevention
- threshold blood level for clinical signs? what do blood levels mean? supplements?

A
  • Milk fever can almost entirely be prevented through diligent implementation of a DCAD program
    > There is no clear threshold of blood [Ca] for clinical signs
  • The of 2.0 mmol/L blood total Ca soon ~ 1 day after calving to define subclinical hypocalcemia is not well supported by evidence
  • Maintenance of blood Ca > 2.15 mmol/L at 1-4 DIM is a more desirable target
  • There is mixed, but generally scant evidence for calcium supplements to prevent disease other than milk fever
  • Supplements should be targeted to multiparous/high-risk cows
30
Q

supplementation of oral calcium after calving use? supplements use in treatment? effects of supplements on risk of disease

A
  • One study supplemented cows with oral calcium after calving found:
    > an increase in milk production in higher producing cows
    > decrease in health problems among lame cows
  • Calcium supplements can reduce clinical milk fever
  • Calcium supplements can modestly increase blood [Ca] in cows with low blood [Ca] (Miltenburg et al, 2016; Blanc et al 2016; Martinez et al 2016; Amanlou et al 2016)
  • Effects of calcium supplements on risk of disease:
    > None Miltenburg et al, 2016
    > None to worse Martinez et al 2016 a, b
    > Better Amanlou et al 2016
31
Q

Limited dietary calcium intake goals for preventing hypocalcemia?

A

An old approach to control hypocalcemia
CHALLENGING
GOAL: negative calcium balance in the last weeks pre calving
> Increase concentrations of PTH
<><>
some try to use calcium binder in GI tract to acheive this… (Zeolite A)

32
Q

negative DCAD for hypocalcemia prevention? mechanism?

A

Negative DCAD > milkd metabolic acidosis > quicker response to low blood CA
-Provide excess anions in ration in order to counteract potassium effects on blood pH… improved response to PTH
<><>
Acidify diet in late dry cow period:
1. Reduced potassium (K)
- Forages = high potassium (vs. corn silage is lowest)
- Reduce crop fertilization with manure
2. Calculate “DCAD”
…and Add Urine Acidifiers to Diet
<><>
- anioic supplement added to the prepartum ration
> lower pH
> Increase urinary Ca excretion
> Around parturition
↑ bone resorption
↑ efficiency of intestinal Ca absorption
> Quicker response to low blood Ca

33
Q

when to start negative DCAD for hypocalcemia prevention? what to use?

A

Acclimatize 3 - 4 weeks pre-partum
<><>
Anionic salts
 Magnesium/calcium/ammonium sulfate
 Magnesium/calcium/ammonium chloride
 HCl
<><>
Other considerations:
 Limit intake of strong cations (Na+ and K+)
 Limit concentration of P (high concentration of P decreases calcitriol concentration)
 Magnesium level - necessary for bone resorption
 Dietary Ca % – High vs Low – Lack of consensus
 Palatability (?)

34
Q

Negative dietary cation-anion difference (DCAD) pros and cons

A

PROS
- decreased Milk fever
- decreased Subclinical hypocalcemia
- decreased Peripartum diseases
- decreased Culling
- increased Reproductive performance
- increased Milk yield

CONS
- costly product
- palatability?
- extra labour (monitoring)

35
Q

negative DCAD effectiveness - Acidification Meta-analysis: Clinical disease

A

40 to 50% reduction in cases

36
Q

Acidification
Meta-analysis:
Intake and milk
yield

A
  • Assessed effect of reduced DCAD (not necessarily negative)
  • Reduced DMI prepartum but greater postpartum
  • Overall, benefits in multiparous, not heifers
37
Q

what to monitor if feeding acidifying diet to Pre-fresh Cows

A

Urine pH in close-up group

 Close-up group
(within 3wks before parturition)
 Once per week
 Target urine pH:
– 6.0 - 6.5 Holstein
– 5.8 - 6.2 Jerseys
– ≥ 80% of cows in range

38
Q

Hypocalcemia in Beef and Sheep
- when does it occur? contributing factors?

A

Also occurs in older beef cows and ewes during late pregnancy
– Particularly when carrying twins!
– Decreased osteoclastic activity
– Often poor nutrition contributes
– Precipitated by a stress (climate change, feed shortage, etc)

3. Food Animal 2 (20 decks)

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