61例尿毒症患者甲状旁腺全切加前臂移植术后低钙血症的发生与处理

目的针对内科治疗无效的继发性甲状旁腺功能亢进（sHPT）的尿毒症患者行甲状旁腺全切加前臂移植术，分析术后患者低钙血症的发生与处理。方法61例患者术后立即监测血钙浓度，并静脉补充葡萄糖酸钙，使血钙维持在1．8～2．2mmol／L之间，统计手术前、后患者的全段甲状旁腺激素（iPTH）、血清钙磷乘积和碱性磷酸酶（AKP）水平以及手术切除的总的腺体质量。结果56例患者（占91．7％）术后12-24h即出现血钙低于1．8mmol／L，静脉立即补充葡萄糖酸钙，约合元素钙（18±6）g，补钙剂量与术前血iPTH（r=0．621，P〈0．01）、钙磷乘积（r=0．719，P〈0．01）、AKP（r=0．606，P〈0．01）及总的切除腺体质量（r=0．716，P〈0．01）相关。结论低钙血症是患者甲状旁腺术后的常见表现，与SHPT的严重程度有关，术后及早监测血钙和静脉补钙可有效、安全预防严重低钙血症的发生。

Occurrence and management of hypocalcemia following total parathyroidectomy with autotransplantation in 61 cases of uremia with secondary hyperparathyroidism

Objective To investigate postoperative hypocalcemia following total parathyroidectomy with forearm autotransplantation （PTX） for severe secondary hyperparathyroidism （SHPT） in patients with uremia and to evaluate relevant factors associated with intravenous calcium regimen. Methods Between 1996 and 2006, PTX was performed on 61 cases of uremia with SHPT. The concentration of serum calcium was monitored and the infusion dosage of calcium gluconate according to the target total calcium range between 1.8 to 2. 2 mmol/L was recorded. The levels of intact parathyroid hormone （iPTH）, calcium-phosphorus product （Ca x p） and alkaline phosphatase （AKP） were measured before and after PTX. Total parathyroid gland weight was also obtained. Results Hypocal- cemia occurring 12 to 24 h postoperatively was found in 91.7% （n = 56/61 ） of patients whose serum calcium concentration was 1.7 mmol/L or less. For keeping total calcium level within 1.8 to 2. 2 mmol/L, the dosage of element calcium due to the infusion of calcium gluconate was （18 ± 6）g, which was correlated positively with preoperative iPTH level （r = 0. 621, P〈0. 01 ）, Ca× P value （r = 0. 719, P〈0. 01）, AKP level （r= 0. 606, P〈0. 01） and total parathyroid gland weight （r= 0. 716, P 〈0. 01 ）, respectively. Conclusions Postoperative hypocalcemia was a common complication developed in uremia patients with severe SHirr receiving PTX. Closely monitoring along with correcting serum calcium level plays an essential role in preventing clinical symptoms related to hypocalcemia.