Hypocalcaemia is an acute complication of hypomagnesaemia. Characteristically, hypocalcaemia is unresponsive to intravenous calcium therapy, and resolves itself when the magnesium deficiency returns to its normal state (DiBartola 11).
The mechanism is considered to be as a result of suppression of PTH secretion or inhibition of the peripheral action of PTH or to both. This disease is not widespread in all other species but more in dogs and horses compared to cats and cows.
The causative agent/organism or mechanism
The cause of hypocalcaemia is generally undetermined, but it could result from such problems as maternal calcium loss to the fetal skeletons and to the milk, poor absorption of dietary calcium, and parathyroid gland atrophy caused by reprehensible diet or dietary supplements. The commonest cause of hypocalcaemia is hypoalbuminaemia, closely followed by renal failure.
The breakdowns of causative agent/organism of hypocalcaemia are:
Hypoalbuminaemia or Vitamin D deficiency
- Malnutrition
- Malabsorption
- Renal disease
- Drugs (phenytoin, barbiturates)
- Vitamin D deficiency
Hypoparathyroidism
- Congenital
- Idiopathic
- Parathyroid ablation (surgery, infarction)
- Magnesium deficiency
- Pseudohypoparathyroidism
Increased bone uptake (hungry bone syndrome)
- Post-parathyroidectomy for hyperparathyroidism
- Post-thyroidectomy
- Osteoblastic secondaries (lung, prostate, breast)
Hyperphosphataemia
- Renal failure
- Phosphate therapy
- Tumor lysis
Drug therapy
- Frusemide, EDTA, calcitonin, mithramycin.
Clinical signs and symptoms
The Clinical signs and symptoms of hypocalcaemia include panting, trembling, muscle fasciculation, weakness, and ataxia (James et al 603). These early clinical signs quickly progress to tetany with tonic-clonic spasms and opisthotonos. Heart rate, respiratory rate, and rectal temperature increases, particularly during tetany. Clinical signs rapidly advance in severity and may be fatal if the animal goes untreated.
Diagnostic tests
Hypocalcaemia is diagnosed on the basis of the typical clinical signs in a heavily lactating female. It can be established by measuring the serum concentrations of calcium, which naturally are below the reference range (Bushinsky and Monk 1998).
Because the clinical signs in postpartum dogs are so suggestive, treatment is usually started before, or without, laboratory confirmation. Laboratory confirmation would be required in a prepartum animal. Although severe hypoglycemia could cause similar clinical signs, it is a rare postpartum disorder in the animal (James et al. 603).
Treatment of Hypocalcaemia
Hypocalcaemia associated with tetany or carpopedal spasm should be treated with an intravenous infusion of calcium.
The typical procedure is to infuse 10-20 mL of 10% calcium gluconate over 2-3 minutes and repeated if required (calcium chloride is also available for infusion but is to be avoided due to the possibility of thrombophlebitis). If the hypocalcaemic symptoms persist despite calcium infusion, the possibility of hypomagnesaemia should be considered.
The continuing treatment of hypocalcaemia (e.g. that of hypoparathyroidism or severe vitamin D deficiency) should be managed by vitamin D therapy supplemented with oral calcium, e.g. vitamin D; dihydrotachysterol 5 mg daily, 1,25-dihydroxycholecalciferol: 2.5 ug daily; calcium: 2-4 g of elemental calcium daily (James et al 604; Papich 2010). During treatment with these medications a careful watch should be kept on the plasma calcium levels.
Prevention and/or control programs
Several steps can be taken to prevent hypocalcaemia in large and small animals. First, a high-quality, nutritionally balanced and complete diet should be fed to the animal during pregnancy and lactation. Second, oral calcium supplementation during gestation is contraindicated since it may worsen, rather than prevent, hypocalcaemia. Finally, the animal should have access to food and water ad libitum during lactation.
If necessary, the dam can be physically separated from the neonates for 30 to 60 minutes several times a day to encourage her to eat. Supplemental bottle-feeding of the litter with milk replacer early in lactation and with solid food after 3 to 4 weeks of age may be helpful, especially for large litters.
Clients Education
Client education is essential since they need to be made aware of signs of hypocalcaemia, including weakness, lethargy, muscle fasciculation, and facial pruritus. It must be emphasized that signs may be noted at any time and that urgent intervention is necessary.
Clients must also be aware that monitoring blood calcium levels, on a regular basis, requires measurement of ionized calcium, as opposed to total calcium (Haskell 110). Clients should identify veterinary practices that can provide domestic and accurate ionized calcium measurements. Clients must also be aware of signs of hypocalcaemia (PU/PD).
Works Cited
Bushinsky DA, and Monk RD. Calcium (review). Lancet, 1998; 352:306-311.
DiBartola, Stephen. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. New York, NY: Elsevier Health Sciences, 2011. Print.
James, Fox, Anderson Lynn, Franklin Loew, and Fred Quimby. Laboratory Animal Medicine. San Diego, California: Academic Press, 2002. Print.
Haskell, Scott. Blackwell’s Five-Minute Veterinary Consult: Ruminant. Denvers, MA: John Wiley & Sons, 2011. Print.
Papich, Mark. Saunders Handbook of Veterinary Drugs: Small and Large Animal. New York, NY: Elsevier Health Sciences. 2010. Print.