Hypocalcemic tetany why

However, discrepancies may arise in alkalotic and hypoalbuminemic horses. Alkalosis increases albumin binding of calcium, which results in a decreased concentration of ionized calcium.

Thus, alkalotic horses may have normal total serum calcium while exhibiting signs of hypocalcemia. Likewise, hypoalbuminemic or acidotic horses may have decreased total serum calcium without developing signs of hypocalcemia. Total serum calcium can be adjusted for albumin concentration by the following formula:. An increased intensity of heart sounds is expected.

If arrhythmias or bradycardia develop, the IV treatment should be discontinued immediately. Once the heart rate has returned to normal, the infusion may be resumed at a slower rate. If the horse does not improve within 1—2 hr of the initial infusion, a second dose may be given, although laboratory verification of hypocalcemia is indicated. Some horses require repeated treatments over several days to recover from hypocalcemic tetany.

Mildly affected horses may recover without specific treatment. If the tetany is associated with physical exertion, incorporating magnesium into the solution may be advisable. A balanced feed ration should be provided to supply adequate amounts and ratios of calcium and phosphorus throughout gestation. In times of increased calcium demand such as lactation, fasting should be avoided and high-quality forage such as alfalfa or calcium-containing mineral mixes should be provided.

Stress and fasting during transport should be minimized. In endurance horses, water and electrolyte deficits associated with prolonged exercise and sweating may be prevented by provision of a sufficient water supply and electrolyte supplementation.

From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. Few months after the patient begun his treatment he showed clinical, neurophisiological and laboratorial improvement.

The association of the patient's symptoms and physical findings with an EMG and a muscle biopsy that showed a non-specific, non-inflammatory muscle lesion and a significant hypocalcemia and hyperphosphatemia with a very low PTH, are consistent with the diagnosis of hypocalcemic myopathy secondary to idiopathic hypoparathyroidism. Myopathy associated with hypocalcemia is better described in the literature when associated with osteomalacia. In this cases, however, CK tends do be normal 7 , whereas in our case it was strikingly elevated.

Since the first description by Wolf et al. The reason for the increased CK levels found in these myopathies is not completely established. It has been proposed that it could be due to tetany, but there are reports of enzyme elevations unrelated to its occurrence 4, Our patient, for example, had elevated CK levels with no evidence of tetany, and his Trousseau's and Chvostek's signs were negative.

Another hypothesis is that hypocalcemia could induce functional alterations in the sarcolemma, leading to the release of CK and myoglobin 4,8. Kruse 1 suggests that hypocalcemia can change the enzyme content of striated muscle with no significant morphologic or structural abnormalities.

If this is the case, then the CK increase would not be secondary to tetany alone, and hypocalcemic myopathy would represent a distinct pathological entity 4. The histological findings in our case are in agreement with the literature descriptions of mild alterations and no structural or inflammatory lesions at biopsy, indicating a mild, non-specific myopathy which supports the hypothesis of a functional change in striated muscle 4,11,13, The very low serum levels of PTH, hypocalcemia and hyperphosphatemia seen in the patient are the characteristic findings of IHP.

Mitochondrial myopathies, such as Kearn-Sayres syndrome KSS are also associated with endocrine and metabolic abnormalities such as hypoparathyroidism In KSS, however, the classic triad of pigmentary retinopathy, ophtalmoplegia and cardiac muscle conduction defects is almost always present before age 20, and frequently appears in the first decade of life 15, None of these findings was seen in our case, and the onset of fatigue, weakness and bilateral cataracts at age 20 were the first symptoms of the patient's disease.

Subsequently, there was the report of seizures and cognitive slowing. It is important to realise that, despite the patient's symptoms, a serum calcium measurement was not obtained until he was 30 years old. Barber et al. An early measurement of serum calcium is even more important when one consider that cases of proximal weakness with increased CK can be misdiagnosed as polymyositis and treated with corticosteroids.

Besides being ineffective, steroids inhibit intestinal calcium absorption and increase renal calcium excretion, leading to a worsening of the hypocalcemia and, consequently, of the patient's symptoms.

The pathophysiology of the muscle lesion in IHP is not completely understood 14 , although it probably relates to hypocalcemia. The decrease in calcium concentration causes an increase in excitability at the neuromuscular junction, with a smaller degree of depolarization being needed to generate an action potential 14 , and these alterations can occasionally lead to tetany 4.

In addition, it is likely that there are ultrastructural modifications, which occur in response to the metabolic abnormalities and cause muscle function to be less effective. Therefore, we suppose that every patient with IHP or another disease causing chronic hypocalcemia probably suffers some degree of muscle damage We believe, therefore, that IHP-associated myopathy, although rare, can occur with a greater frequency than the one described in the literature.

This is probably due to the fact that this myopathy is rarely diagnosed, even in patients with chronic hypocalcemia, as the clinical manifestations of these patients, except for those developing tetany, are subjective and non-specific. In some patients, for example, the only objective sign of disease might be myoglobinuria Two recommendations should be made, therefore, to allow an early diagnosis of this disease and a better understanding of its pathophysiology.

The first is to obtain CK measurements in every patient with a diagnosis of hypoparathyroidism or other conditions leading to chronic hypocalcemia. One should also keep in mind the possibility of performing EMG and muscle biopsy in these cases.

The second recommendation is to perform serum calcium measurements in patients with myoglobinuria or nonspecific complaints suggesting muscle disease, such as fatigue, muscle aches and weakness, especially those with proximal weakness of unknown aetiology.

We emphasise that the diagnosis of hypocalcemic myopathy secondary to IHP is important not only for obtaining a better understanding the pathophysiology of this condition, but fundamentally because of the availability of unexpensive and effective treatment options for this disease, with a few simple measures leading to a great improvement in the patient's quality of life. E-mail: dbnora terra.

Abrir menu Brasil. Arquivos de Neuro-Psiquiatria. Abrir menu. Key words: myopathy, hypocalcemia, hypoparathyroidism. Palavras-chave: miopatia, hipocalcemia, hipoparatireoidismo. Tetany can be the result of an electrolyte imbalance. Tetany can also be caused by magnesium deficiency or too little potassium. Having too much acid acidosis or too much alkali alkalosis in the body can also result in tetany.

What brings on these imbalances is another matter altogether. This can lead to dramatically lowered calcium levels, which can trigger tetany. Sometimes kidney failure or problems with the pancreas can interfere with calcium levels in the body. Low blood protein , septic shock , and some blood transfusions can also adversely affect blood calcium levels. Sometimes toxins can cause tetany. One example is the botulinum toxin found in spoiled foods or bacteria in soil that enter the body through cuts or injuries.

Ideally, your doctor will know what caused the tetany, enabling them to treat the condition at its source. In the short term, treatment goals are to correct the imbalance. This might include supplementing with calcium or magnesium , for example. Injecting calcium directly into the bloodstream is the most common approach. However, taking calcium orally along with vitamin D , for absorption may be required to prevent it from reoccurring. Once a doctor determines what was at the root of the tetany, they may consider more serious treatments.

For instance, if tumors on the parathyroid are to blame, they can be surgically removed. In some cases, such as kidney failure, ongoing treatment with calcium supplements may be required to treat the condition that led to the tetany. As with most serious conditions, early detection and treatment make the biggest difference when it comes to your outlook regarding tetany.

Treating the mineral imbalance early enough can prevent the onset of severe symptoms such as seizures and heart problems. Speaking to your doctor right away is the best course of action.