Naslov
Treatment of postoperative hypocalcemia

Autori
Karner, Ivan ; Štefanić, Mario ; Wagenhofer, Vlado ; Mihaljević, Ivan

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, stručni

Izvornik
Acta Clinica Croatica 46 (Suppl 2):57-58 (2007) / Kusić, Zvonko - Zagreb : Klinički bolnički centar Sestre milosrdnice ; Institut za medicinska istraživanja i medicinu rada, 2007

Skup
1st Congress of Croatian Thyroid Society: Thyroid Cancer

Mjesto i datum
Split, Hrvatska, 26.10.2007. - 28.10.2007

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Thyroid Neoplasms; Hypocalcemia; Postoperative Complications

Sažetak
Postoperative hypocalcemia is one of the most common complications of thyroid surgery. It is related to the type of disease (malignant or benign), number of parathyroid glands identified during surgical procedure, re-operation and the surgeon's experience. Postoperative hypoparathyroidism can be temporary or permanent. The incidence of permanent hypoparathyroidism has been reported to range from as high as more than 20%, when total thyroidectomy and radical neck dissection are performed, to as low as 0.9% ; however, there are reports on an even lower incidence of permanent hypoparathyroidism. Operative strategies to prevent postoperative hypoparathyroidism include preservation of parathyroid glands in situ and autotransplantation of parathyroid glands during total thyroidectomy. Postoperative hypoparathyroidism results in hypocalcemia, hyperphosphatemia, and low parathyroid hormone (PTH) level. Intraoperative PTH at 20 to 30 minutes after total thyroidectomy can predict impending postoperative hypocalcemia. Acute hypocalcemia directly causes increased neuromuscular irritability, and this pathophysiology underlies the most prominent symptoms. Tetany is seen in more severe hypocalcemia. If there is any doubt, the presence of hypocalcemia needs to be confirmed by the measurement of serum ionized calcium. The diagnosis is confirmed by a finding of serum calcium <2.05 mmol/L or ionized calcium <1.1 mmol/L. Patients with acute symptomatic hypocalcemia (serum calcium <0.8 mmol/L) should be treated promptly with IV calcium. Calcium gluconate is preferred to calcium chloride because it causes less tissue necrosis if extravasated. The first 100 to 200 mg of elemental calcium (1 to 2 g calcium gluconate) should be given over 10 to 20 minutes. Faster administration may result in cardiac dysfunction, or even arrest. This should be followed by slow calcium infusion at 0.5 to 1.5 mg/kg/h. Calcium infusion should be continued until the patient can receive effective doses of oral calcium and vitamin D. Chronic hypocalcemia is treated by the administration of oral calcium and, if it is insufficient, vitamin D supplementation (0.25 to 0.50 mg of 1, 25-(OH)2 vitamin D3 is the usual initial daily dose). Appropriate doses of calcium and vitamin D are established by gradual titration. The serum calcium level should be targeted to about 2.0 mmol/L. Most patients will be entirely asymptomatic at this level, and further elevation will lead to hypercalciuria because of the lack of PTH effect on the renal tubules. Chronic hypercalciuria may lead to the development of nephrocalcinosis, nephrolithiasis, renal impairment, and should be avoided. With the recent availability of synthetic PTH preparations (1-34 PTH, teriparatide), several reports have described successful control of hypocalcemia with a lower risk of hypercalciuria using twice-daily subcutaneous administration.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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