Hypocalcemia after thyroid and parathyroid surgery and its’ treatment

Abstract

Hypocalcemia after thyroid and parathyroid surgery and its’ treatment Hypocalcemia is a frequent complication after thyroid and parathyroid surgery. This study aims to evaluate the incidence, pathophysiology, early diagnosis, differential diagnosis, clinical and biochemical predictive factors, treatment of hypocalcemia. Hypocalcemia may be transient, that recovers within 6 months of surgery and permanent that persists more than 6 months after surgery. Postoperative hypocalcemia arises from hypoparathyroidism, hungry bone syndrome, hemodilution due to surgical stress and alkalosis which is caused by hyperventilation due to postoperative pain. The most common cause of postoperative hypocalcemia is hypoparathyroidism. Hypoparathyroidism is characterized by a parathyroid hormone (PTH) deficient leading to hypocalcemia, hyperphosphatemia and hypercalciuria. Postoperative hypoparathroidism occurs usually due to inadvertent or unavoidable the parathyroid gland or damage to it/its blood supply. Hungry bone syndrome can occur after surgery for hyperparathyroidism and Graves disease. The clinical manifestations of postsurgical hypocalcemia depend on the degree of hypocalcemia and rapidity of hypocalcemia onset. The classic symptoms of hypocalcemia is associated with neuromuscular excitability. They vary from numbness and tingling in the fingertips, toes and circumoral region in mild hypocalcemia to paraesthesias of the upper and lower extremities in moderate hypocalcemia. In the most severe forms, tetanic muscle cramps can occur in the form of carpopedal spasm or diffuse tetany. Some cases can occur bronchospasm and laryngospasm. Neurological symptoms such as confusion, disorientation, delirium or seizure, and cardiac abnormalities such as prolonged QT interval on electrocardiogram, arrhythmias, congestive heart failure can also occur. In patients without overt signs, underlying neuromuscular excitability can become evident with provocation tests such as Chvostek’s sign and Trousseau’s sign. Diagnostic workup for hypocalcemia includes measuring serum intact PTH, phosphorus, albumin, magnesium, 25-OH Vit D, and calcium. Clinical predictive factors of hypocalcemia include female sex, inadvertent excision of the parathyroid gland, parathyroid autotransplantation, Graves’ disease, surgery for recurrent goitre, reoperation for bleeding, and heavier thyroid specimens. Perioperative PTH and postoperative changes in calcium levels can be used as biochemical predictors of hypocalcemia. The management of hypocalcemia is best accomplished by identifying high-risk patients preoperatively, preserving function of parathyroid gland during surgery, identifying hypocalcemia via early predictors and implementing appropriate treatment if necessary. Moreover prevention or early identification and appropriate management of hypocalcemia prevents hypocalcemia-related complications and allows patients to be discharged from the hospital earlier. Treatment for hypocalcemia is based on combined theraphy with calcium and vitamin D analoques. Formal guidelines for the management of hypocalcemia are not available. However, there are some common procedures existing in clinical practice. According to the degree and speed onset of hypocalcemia and the severity symptoms, intravenous calcium may be needed until an oral regimen is established. The goal of theraphy is to control hypocalcemic symptoms and achieve and maintain a serum calcium level in the low normal range. The oral dose of calcium and vitamin D analogues should be individually tailored by checking serum calcium, phosphate, and PTH initially every week, and then every 2-3 weeks or monthly. Hypercalcemia must be avoided. New drugs such as recombinant human PTH currently in clinical trials offer promising treatment options.