Thyroid diseases and surgery for thyroid neoplasms are both very common. Several complications of thyroidectomy are well known. Some of these are quite disturbing, such as recurrent laryngeal nerve injury and permanent hypoparathyroidism. However, postoperative hematoma often in the recovery room may be fatal. Close observation and early intervention are of utmost necessity in the post-thyroidectomy period. In a series of 600 thyroidectomies performed over a period of 11 years, eight patients developed postoperative hematoma. Seven of them underwent re-exploration, while one patient was treated conservatively. Two patients had second re-exploration for hematoma reaccumulation. All patients recovered very well after re-exploration except one elderly patient who required ventilatory support due to poor pulmonary reserve; after a week of ventilatory support and a tracheostomy, she too recovered well. One patient had the hematoma re-explored as late as 24 hours after the operation, while the remainder were re-explored within 4-6 hours after the initial procedure. Because of the extent of edema of the larynx and pharyngeal wall, it is very important that a senior, experienced person perform intubation in these patients. It is also very important to recognize that when the patients lie down flat, they may develop acute airway distress; hence, one must be prepared to intubate them emergently. We recommend close recovery room observation after thyroidectomy and early exploration and evacuation of hematoma in all patients who develop postoperative hematoma. A conservative approach may be considered in selected patients with minimal hematoma and no progression. However, it generally takes a long time for the hematoma to resorb. A better understanding of the complications of thyroidectomy will minimize morbidity and make thyroidectomy a safer procedure and a surgical triumph.
Permanent hypoparathyroidism is one of the most distressing complications of thyroid surgery. The incidence of this iatrogenic complication varies between 3 and 25 percent among patients undergoing total thyroidectomy. Parathyroid injury may be caused by inadvertent removal of the parathyroids, ligation of the blood supply, or destruction secondary to capsular hematoma. Attention to such technical details as identification of the parathyroids, dissection close to the thyroid gland, preservation of the blood supply to the parathyroids, and avoiding manipulation of parathyroids reduces the incidence of temporary and permanent hypoparathyrodism. However, if the parathyroids are injured, the best method of preserving their function is by autotransplantation. Over the past 7 years we have performed 250 thyroidectomies. An attempt was made to identify and preserve parathyroid gland in each case. Even during lobectomy procedures, the ipsilateral parathyroids were identified and preserved. Whenever any of the parathyroids was devascularized or separated from the surrounding structures, it was autotransplanted into the sternomastoid muscle. The sternomastoid was chosen for autotransplantation rather than forearm muscles to avoid an added incision and because selective measurement of parathormone is not essential in this group of patients. Prior to autotransplantation, confirmation of the nature of the tissue was made by frozen section of a small portion of the parathyroid gland. Parathyroid autotransplantation was performed in 15 instances, even when only one parathyroid was injured. Only one member of this group of 15 patients developed temporary hypoparathyroidism, which disappeared after 4 weeks of calcium supplementation. The remaining patients had an uncomplicated recovery. Autotransplantation of the parathyroid glands should be performed whenever the parathyroid is devascularized or damaged by retraction or hematoma. It is essential for every thyroid surgeon to be familiar with the technique of parathyroid autotransplantation.
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