Hipocalcemia

Also known as: Parturient Hypocalcaemia — Milk Fever — Puerperal Tetany — Lactation Tetany — Periparturient Hypocalcaemia — Eclampsia

Introduction

A number of metabolic disorders have been characterised by the development of hypocalcaemia, which occurs in most animal species.

Many of these syndromes develop near the time of the increased calcium demand associated with parturition and probably are the reflection of a temporary failure of calcium homeostatic mechanisms.

Milk Fever in Dairy Cows

This is of major economic and veterinary importance, and can contribute to the Downer Cow Syndrome which has a big impact on animal welfare.

Milk fever is a metabolic disease of high-producing dairy cows characterised by the development of severe hypocalcaemia and hypophosphataemia resulting from the mineralisation of foetal bones and the initiation of lactation.

It usually occurs around the time of parturition.

Total and ionized calcium levels decrease several days before parturition. Magnesium levels may increase reciprocally as calcium levels decline. The concentration of glucose in the blood is often increased due to interference with the secretion of insulin from the beta cells of the pancreas, which requires an adequate level of calcium.

It is most common in high-producing dairy cows over the age of 5, and also more common in Channel Island breeds.

The disease can contribute to dystocia, uterine prolapse, retained fetal membranes, metritis, abomasal displacement, and mastitis.

Clinical Signs

It usually occurs within 72 hours of parturition.

Stage 1: cow is standing, shows hyperexcitability, hypersensitivity, tremors, ear twitching and ataxia.

Stage 2: sternal recumbency, S-shaped curve to the neck, depressed, dry muzzle, cold extremities, no defecation, bloat, delayed pupil responses

Stage 3: lateral recumbency, reduced consciousness, unresponsive, muscle flaccidity, reduced cardiac output, tachycardia, bloat, death

Some other diseases may occur concurrently with milk fever, such as traumatic injuries due to calving, nerve paralysis or compartment syndrome due to prolonged recumbency.

Treatment

Treatment involves restoring serum calcium levels back to normal as soon as possible, to avoid complications such as nerve and muscle damage. Calcium borogluconate is given intravenously (i/v), and sometimes also suncutaneous (s/c) to provide a more sustained release. Many solutions also contain magnesium and phosphorus, which can sometimes be helpful and is not contraindicated. Calcium solutions should be administered slowly over 10-20 minutes and the heart auscultated for arrhythmias.

The animal will respond quickly to calcium supplementation, and eructation, defecation and urination should occur once the cow rises.

A significant number of cows may relapse the following day and will require treatment again.

Prevention

Prevention of hypocalcaemia is implemented during the dry period. Dry cows should not receive feeds high in calcium such as lush spring grass, kale, sugar beet pulp. However feeding low-calcium diets prior to parturition to stimulate intestinal absorption and enhance skeletal reabsorption is not as effective as once thought.

Prophylactic treatment of susceptible cows is possible, using s/c or oral calcium supplementation.

DCAD (dietary cation-anion difference) diets are the new method of prevention. They involve decreasing the blood pH of cows in the late pre-partum and early post-partum periods by providing an excess of anions over cations. This is believed to enhance calcium absorption from the intestine and reabsorption from bone. This diet should only be fed to dry cows, and involves supplementation with anionic salts such as magnesium chloride, magnesium sulphate, calcium chloride, ammonium chloride. These salts are not palatable and reduce dry matter intake and can lead to a negative energy balance and problems such as fatty liver. DCAD diets must be used with great care and urine pH should be monitored closely.

Other methods of prevention include:

checking magnesium levels and supplementing if necessary

vitamin D3 analogues

synthetic bovine parathyroid hormone

Hypocalcaemia in Small Animals

Eclampsia

This is a hypocalcaemic tetany associated with pregnancy in bitches and queens. Calcium is lost to foetuses during gestation and through milk during lactation. Improper perinatal nutrition or the stress of lactation may result in limited calcium intake. Excessive supplementation of calcium during pregnancy causes downregulation of the calcium regulatory system and subsequent clinical hypocalcemia when calcium demand is high.

Tetany occurs as a result of spontaneous repetitive firing of motor nerve fibers. As a result of the loss of stabilizing membrane-bound calcium, nerve membranes become more permeable to ions and require a stimulus of lesser magnitude to depolarize. Hypoglycemia can occur concurrently.

Eclampsia occurs more commonly in small-breed dogs and is uncommon in cats and large-breed dogs. Bitches with a previous history of eclampsia may have recurrence with subsequent litters.

Clinical Signs

Initial signs are: restlessness, excitability, panting and irritability.

The signs can then progress to: hypersalivation, stiffness of gait and ataxia.

Severe tetany is characterised by: tonic-clonic spasms, recumbency and seizures, tachycardia, miosis and pyrexia.

Death may result from respiratory depression, hyperthermia and cerebral oedema.

Diagnosis

This is based on the history, clinical signs and response to treatment.

A pre-treatment calcium sample should be taken, but treatment should not be delayed for laboratory confirmation.

Serum glucose levels should be evaluated for concurrent hypoglycaemia.

Treatment

A slow intravenous infusion of 10% calcium gluconate is indicated immediately.

ECG monitoring can be put in place to check for arrhythmias. A portion of the calcium can also be diluted with saline and injected subcutaneously for prolonged release.

The response should be immediate following treatment. Diazepam may have to be used if the seizuring does not stop.

Oral supplementation of calcium carbonate should be continued at home and a well-balanced growth-formula diet should be fed.

Puppies older than 3 weeks should be weaned, and younger puppies should be hand-fed concurrently to reduce the strain on the bitch.

Prevention

A well-balanced growth formula diet should be fed to the bitch during the second half of gestation and through lactation.

Calcium should not be supplemented during pregnancy but can be given during lactation in bitches with a previous history of eclampsia.

Other Causes

If the animal is not in a periparturient period, other causes of hypocalcaemia should be considered:

Renal failure

Primary hypoparathyroidism

Acute pancreatitis

Ethylene glycol toxicity

Iatrogenic: following parathyroid surgery, post-transfusion, phosphate enemas

Severe malabsorption/starvation

Hypovitaminosis D

Hypoalbuminaemia

Laboratory error

Clinial Signs

Common clinical signs include: facial rubbing, muscle tremors or cramps, stiff gait, behavioural changes, pyrexia, depression, inappetance, arrhythmias, hypotension, respiratory depression, death.

Investigation of Hypocalcaemia

When the cause is not obvious, investigation of hypocalcaemia should include:

Checking albumin levels: calcium is bound to albumin and levels change together

Haematology, biochemistry and urinalysis

Imaging

Parathyroid Hormone assay

Treatment

Acute treatment involves slow intravenous injection of 10% calcium borogluconate. Concurrent monitoring for bradycardia and arrhythmias.

Chronic treatment of hypocalcaemia involves treating the underlying cause. It can involve an oral vitamin D metabolite such as calcitriol, or an oral calcium supplement such as calcium carbonate. Calcium levels should be kept slightly low to normal.

For treatment of primary hypoparathyroidism, vitamin D treatment has to be continued lifelong but oral calcium can usually be stopped.

References

Pineda, M. (2003) McDonald's veterinary endocrinology and reproduction Wiley-Blackwell

Merck and co (2008) The Merck Veterinary Manual Merial

Wingfield, W. (2001) Veterinary emergency medicine secrets Elsevier Health Sciences

Root, M. (2009) Clinical canine and feline reproduction: evidence-based answers John Wiley and Sons