Metabolic Diseases in Food Animals - 4
Metabolic Diseases in Food Animals
Hypocalcemia: Treatment
Definitions:
Hypocalcemia: A condition marked by low levels of calcium in the blood, significant in dairy cows, especially around parturition.
Subclinical Hypocalcemia:
Focus is on the presenting disease; treatment involves calcium supplementation.
Treatment Approach:
Stage 1 Hypocalcemia:
No intravenous (IV) calcium treatment is necessary.
Cows are still standing, indicating they can manage oral calcium supplementation.
An oral calcium supplement is recommended, as it is rapidly absorbed with little risk of subsequent hypercalcemia and rebound hypocalcemia.
Use an acidogenic source of calcium (calcium chloride or calcium sulfate) in a bolus formulation, enhancing the cow's calcium homeostasis by increasing parathyroid hormone (PTH) receptor responsiveness.
Risks Associated with Treatments:
Bradyarrhythmia
Relapse rate approximately 1/3 of cases for hypocalcemia after treatment.
Stages 2 and 3 Hypocalcemia:
For cows that are recumbent, immediate correction of hypocalcemia is essential through intravenous calcium infusion.
Recommended dose: 500 mL of a 23% calcium borogluconate solution provides 10.7 g of elemental calcium, which is sufficient for normocalcemia in even the heaviest cows with severe hypocalcemia.
Many marketed hypocalcemia treatments also include phosphorus, magnesium, glucose, or potassium; however, these additional electrolytes are unnecessary and potentially harmful for parturient paresis.
Calcium gluconate alone is the best treatment option for intravenous administration during parturient paresis.
Treatment Composition for Hypocalcemia
Calcium (as calcium borogluconate, equivalent to calcium gluconate 23.2%): 10.8 g
Potassium (as potassium chloride): 8.0 g
Phosphorus (as sodium hypophosphite • H2O): 2.5 g
Magnesium (as magnesium borogluconate): 1.6 g
Dextrose • H2O: 75.0 g
Total Composition: Each 500 mL of sterile aqueous solution contains the above listed elements.
Severe, Acute Hypophosphatemia (Downer Cow)
Causes:
Often seen in lactating cows following milk fever; caused by excessive PTH leading to phosphorus loss through urine/saliva.
Clinical signs include weakness resulting from Adenosine Triphosphate (ATP) depletion.
Phosphorus plasma levels can remain critically low (<1 mg/dL) even after calcium is treated, affecting the cow's ability to rise due to prolonged hypophosphatemia.
Treatment Options:
Same treatment as for milk fever.
Intravenous Treatment: Use 6 g of phosphorus dissolved in 1 liter of saline, typically using 23 g of monosodium phosphate for a rapid increase in plasma P levels.
Oral Treatment: Administer 50 g of phosphorus via 200 g monosodium phosphate drench for slower but longer-lasting results.
Key Note: Hypophosphite-based solutions are ineffective for restoring physiological function.
Primary Prevention Strategy:
Hypophosphatemia is not usually linked to dietary phosphorus deficiency since affected cows often receive sufficient dietary phosphorus (0.4% typically).
Primary prevention involves avoiding hypocalcemia to reduce potential for hypophosphatemia development.
Magnesium's Role in Metabolic Function
Body Distribution:
70% of total body magnesium is in the skeleton; a small amount is released upon calcium release.
30% is found intracellularly.
Functions:
Acts as a cofactor for various enzymes (including kinases and ATP), critical for the release of parathyroid hormone (PTH).
Magnesium plays a regulatory role in calcium homeostasis, influencing neuromuscular function.
Effect of Magnesium on Neuromuscular Function
Magnesium as a Cofactor:
Mg2+ is required for acetylcholinesterase (AchE) activity.
It competes with Ca2+ to inhibit the release of Ach into the neuromuscular junction (NMJ).
Effects of Imbalanced Magnesium Levels:
Low Mg2+ levels lead to increased Ach accumulation at NMJ, resulting in hyperexcitability and potential tetany.
Conversely, high Mg2+ can lead to Ach blockade, resulting in paresis.
Hypomagnesemia and Grass Tetany
At Risk Cows:
Cattle on fertilized, lush pastures, especially young grasses that are low in Sodium (Na) and Magnesium (Mg) but high in Potassium (K) and Nitrogen (N).
Dairy cattle in their first 2 months of lactation, and young growing calves on a milk diet.
Stress-induced cases (transport tetany) affecting cattle/sheep.
Clinical Signs of Hypomagnesemia
Early Signs:
Muscle fasciculations, aggressive behavior, bellowing, staggering, and a nervous attitude.
Later Signs:
Heart sounds audible without a stethoscope, significant recumbency, repetitive muscle contractions, and convulsions/seizures.
Diagnosis of Hypomagnesemia
Approach:
Evaluating signalment and clinical signs, performing dietary assessments, blood chemistry panels indicating decreased Mg levels.
Diagnosis can be complicated due to variability in magnesium intake, and outputs post-milking.
Post-mortem Assessments:
Cerebrospinal Fluid (CSF) testing is reliable up to 12 hours post-mortem. Vitreous humor is viable for 24-48 hours.
Treatment of Hypomagnesemia
Acute Treatment Options:
Administer 200-300 mL of 20% IV magnesium sulfate (MgSO4); this gives 8g -12g of Mg.
Alternatively, use 200 mL of 50% MgSO4 subcutaneously (SC).
If concurrent hypocalcemia is present, a Ca/Mg combination is most effective: 500 mL of 23% calcium borogluconate solution is recommended.
CSF Levels:
It takes approximately an hour for CSF levels to normalize; during this time, avoid stimulating the cow to rise for at least 30 minutes and refrain from oral treatment before recovery.
Prevention and Treatment of Hypomagnesemia
Relapse Management:
Oral supplementation within 12 hours is crucial; must verify swallowing reflexes.
Supplementation Options:
Mg salts can be administered, with 50g Mg and Mg oxide (100 g) being effective. Better absorption occurs with Mg sulfate (200-400 mL of a 50% solution).
Preventative Strategies:
Effective pasture management and supplementation protocols to maintain adequate magnesium levels.
Potassium: Internal and External Balance
Body Distribution:
Intracellular potassium normal levels around 150 mmol/L and extracellular around 5 mmol/L.
Sources of Potassium:
Primarily obtained through diet.
Elimination occurs mainly via renal excretion, with minor losses through saliva, gastrointestinal (GI) fluid, and milk.
Hypokalemia: Clinical Signs
Symptoms:
Absent feces, decreased rumen motility, paretic gait (weakness), kyphosis (abnormal curvature of the spine), tachycardia (increased heart rate), arrhythmias, recumbency, S-shaped neck posture.
Diagnosis of Hypokalemia
Clinical Pathology:
Potassium levels below <2.5 mEq/L indicate severe deficiency.
Muscle enzymes (creatine kinase (CK), aspartate aminotransferase (AST)) can be elevated, necessitating checks for other electrolyte imbalances.
Treatment of Hypokalemia
Supplementation Options:
Potassium supplementation typically involves intravenous (IV) and oral methods. IV is effective only for severely hypokalemic cattle that are recumbent with rumen atony.
Maximum administration rate for IV potassium is 0.5 mEq/kg/hr.
Oral Supplementation:
Administer KCl salts via orogastric intubation at dosages of 125-240g up to twice daily for adult cattle, ensuring that the daily maximum does not exceed 240 g to avoid adverse effects such as diarrhea, excessive salivation, muscular tremors, and excitability.
5 Ms of Down Cows
Mastitis ✓
Metritis
Metabolic Disorders
Hypocalcemia, Mg, K, P, hypoglycemia.
Musculoskeletal/neurological disorders ✔
Massive Sepsis.
Peritonitis, pneumonia…
Clinical Approach
Different management strategies for beef vs. dairy cows, both prepartum and postpartum.
Factors including days in milk (DIM) and physical examination should be considered.
Vicious Cycle
Transition Period:
Lastting 8 weeks prior to calving begins 3 weeks before calving.
Key periods: Fresh cow, lactation preparation, dry-off periods.
After calving, transition to fresh cow management before necessary to ensure healthy lactation.
Monitoring Factors:
Blood parameters management and overall cow-side management; ensuring proper mineral and vitamin supply is vital.
Risks of Neglecting Management:
Reduced dry matter intake (DMI), negative energy balance (NEB), lipid mobilization leading to fatty liver issues.
DAMNIT-VP Framework
A diagnostic mnemonic used in veterinary medicine for identifying potential causes of down cows:
D: Degenerative
A: Anomalous
M: Metabolic
N: Neoplasia
I: Infectious, Inflammatory, Immune, Iatrogenic
T: Traumatic, Toxin
V: Vascular
P: Parasitic
Prognosis and Treatment Plans for Downer Cows
Determining prognosis is essential for outlining treatment plans based on cost, time, and expected return to productivity.
Prompt treatment with appropriate veterinary drugs and care is critical. Identify the cause of recumbency to decide treatment efficacy.
Nursing should be reserved for cows with a reasonable chance of recovery; otherwise, euthanasia may be necessary for those with poor prognoses.
Conclusion
Veterinary students, practitioners, and farmers must remain vigilant during the transition period of dairy cows to avoid metabolic diseases that can lead to severe outcomes in animal welfare and productivity.