hypocalcemia Flashcards
metabolic challenges of the transistion period for a dairy cow
- decreased feed intake
- energy deficit
- lipolysis
- hypocalcemia
- reduced neutrophil function
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> immune competence decreased surrounding parturition
> increased inflammation after parturition
> increased oxidative stresss after perturition
> lowered calcium spike at parturution
how common is subclinical and clinical milk fever?
clinical ~5%
subclinical ~40-60%
calcium requirements in early lactation
- 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!
calcium playes a role in what body systems
- nerve impulses
- muscle contraction
- immune system
- colostrum and milk production
mechanisms of Ca regulation
- 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
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milk draws Ca from blood
PATHOPHYSIOLOGY OF MILK FEVER
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
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- 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
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Poor PTH receptor function at target tissues when alkalotic or hypomagnesemic
how to metabolic alkalosis and hypomagnesemia affect Ca levels
metabolic alkalosis - interferes with PTH binding to receptor > no effects on vit D, etc > hypocalcemia
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hypomagnesemia - prevents signalling to vitamin D from PTH receptor, even through PTH is bound.
RISK FACTORS AND INCIDENCE for milk fever
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)
HYPOCALCEMIA RISK - SIMPLIFIED
demand vs supply model
Demand - milk yield
Supply - dry matter intake, ability to absorb Ca, ability to mobilize Ca
DIETARY RISK FACTORS for hypocalcemia
- 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-)
incidence of milk fever by parity and serum calcium levels by week of lactation and parity
- spiked at parity =3
- serum Ca always decline around parturition, but year 3 decline much greater than previous years
clinical signs of milk fever
- effects on body temp, skeletal muscle, and smooth muscle
- 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
stages of milk fever and main signs from each
STAGE 1 (“Prodromal Stage”)
Able to stand; weak
STAGE 2
Sternal recumbency
STAGE 3
Lateral recumbency
clinical signs of stage 1 milk fever
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
clinical signs of stage 2 milk fever
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
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Lack of manure behind cow
Decreased rumen and intestinal motility, bloat
> Two most diagnostic clinical
signs in a recently calved 3+ lactation cow
clinical signs of stage 3 milk fever
Lateral recumbency
Flaccid paralysis
Very poor cardiac function
Bloat, may aspirate
Poor anal tone
Unresponsive > coma
Death
milk fever diagnosis?
History
> NOT in 1st Lactation Animals!
Clinical signs
PE excludes other possible causes of recumbency
Response to treatment
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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)
Ddx for milk fever / other causes of recumbency
- metabolic (milk fever, HypoMg, HypoP)
- Toxemic (severe clinical mastitis, other source)
- traumatic - musculoskeletal (nerve damage, other)
- prolonged recumbency > pressure induced damage
Milk fever treatment? what should we be careful of?
- Blood Sample
- 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 - 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)
effect of Ca supplements for milk fever
- 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
RESPONSE TO CALCIUM THERAPY in milk fever
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
PREVENTION OF MILK FEVER RELAPSES?considerations?
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
Oral boluses vs SC calcium
- SC big initial spike, then levels fall
- oral remains more stable over time, higher levels at 48h post calving than SC
NURSING CARE for milk fever - CRITICAL
> bedding? protection? etc.
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
follow up for milk fevertreatment? what if poor response?
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
HYPOCALCEMIA – COMPLICATIONS
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
HOW DO WE DEFINE SUBCLINICAL HYPOCALCEMIA?
Ionized Calcium or Total Calcium?
Threshold and Sampling time (days in milk)
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
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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
SUBCLINICAL HYPOCALCEMIA – IS IT ALWAYS A BAD THING?
-there is a transient presentation which may not be bad in the long run
- but also persistant and delayed forms…
hypocalcemia prevention and control
- take-homes for prevention
- threshold blood level for clinical signs? what do blood levels mean? supplements?
- 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
supplementation of oral calcium after calving use? supplements use in treatment? effects of supplements on risk of disease
- 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
Limited dietary calcium intake goals for preventing hypocalcemia?
An old approach to control hypocalcemia
CHALLENGING
GOAL: negative calcium balance in the last weeks pre calving
> Increase concentrations of PTH
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some try to use calcium binder in GI tract to acheive this… (Zeolite A)
negative DCAD for hypocalcemia prevention? mechanism?
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
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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
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- 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
when to start negative DCAD for hypocalcemia prevention? what to use?
Acclimatize 3 - 4 weeks pre-partum
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Anionic salts
Magnesium/calcium/ammonium sulfate
Magnesium/calcium/ammonium chloride
HCl
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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 (?)
Negative dietary cation-anion difference (DCAD) pros and cons
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)
negative DCAD effectiveness - Acidification Meta-analysis: Clinical disease
40 to 50% reduction in cases
Acidification
Meta-analysis:
Intake and milk
yield
- Assessed effect of reduced DCAD (not necessarily negative)
- Reduced DMI prepartum but greater postpartum
- Overall, benefits in multiparous, not heifers
what to monitor if feeding acidifying diet to Pre-fresh Cows
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
Hypocalcemia in Beef and Sheep
- when does it occur? contributing factors?
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)
