The course of partial parathyroid insufficiency after thyroedectomy

Wade, J. S. H.; Goodall, Peter; Deane, Lorraine; Dauncey, T. M.; Fourman, Paul

doi:10.1002/bjs.1800520705

Cited by 43 publications

(13 citation statements)

References 15 publications

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“…The incidence of transient hypocalcaemia follow¬ ing partial thyroidectomy was 30% in this study -higher than that previously reported (Michie et al 1971;Wade 1960;Wade et al 1965). This discre¬ pancy may be explained by the different criteria used for hypocalcaemia in different studies, and the varying intervals between operation and post¬ operative assessment.…”

Section: Discussioncontrasting

confidence: 71%

The mechanism of hypocalcaemia following thyroidectomy

Percival

Hargreaves

Kanis

1985

Acta Endocrinologica

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The mechanism of transient hypocalcaemia following thyroidectomy was studied in 29 consecutive patients undergoing thyroid surgery. Eight of 27 (30%) patients who had a partial thyroidectomy developed transient hypocalcaemia. Hypocalcaemia was attributable to a reduction in renal tubular reabsorption of calcium (P < 0.05), but was not associated with changes in serum values of immunoassayable parathyroid hormone or calcitonin.Thyrotoxicosis is commonly associated with abnor¬ mal calcium and skeletal homeostasis. Abnormali¬ ties include increased bone turnover, particularly bone résorption which gives rise to osteoporosis, hypercalciuria and occasionally hypercalcaemia (Adams et al. 1967;Baxter & Bondy 1967).Hypocalcaemia is a well-recognised phenomenon following thyroidectomy. Permanent and transient forms are recognised. Permanent hypocalcaemia may occur after radical thyroid surgery, which damages the parathyroid glands. The cause of transient hypocalcaemia is less clear. It has been thought to be due to functional hypoparathyroidism (Davis et al. 1961; Riddell 1962), the reversal of thyrotoxic osteodystrophy (Michie et al. 1971; Laitinen 1976), or the release of calcitonin during thyroid manipulation (Wilkin et al. 1977; Watson et al. 1981; Rasmusson et al. 1980) causing decreased efflux of calcium from the skeleton to the extra¬ cellular fluid. The aims of this study were to identify factors of importance in the causation of transient hypo¬ calcaemia and to evaluate the mechanisms whereby it arose. Patients and MethodsThe effect of thyroidectomy was studied in 29 consecu¬ tive patients referred for thyroid surgery. Twenty-seven patients had partial thyroidectomy for thyrotoxicosis (n = 9) or for a non-toxic nodular goitre (n = 18). The 2 remaining patients underwent total thyroidectomy for carcinoma of the thyroid. An additional 11 patients undergoing minor abdominal surgery were assessed and served as controls. All the thyroidectomies were per¬ formed by one surgeon (A.W. H.) using techniques de¬ scribed by Wade (1960). In each case the parathyroid glands were identified at operation and not excised. The thyrotoxic patients had been previously treated with carbimazole. Their pre-operative preparation included bed rest, oral potassium iodide and sedation (oral phenobarbitone 30 mg t.d.s. with amylobarbitone 200 mg at night) for 1 week. They were considered adequately prepared if the pulse rate awake and during sleep was consistently less than 80/min. This criterion was met in 8 of the thyrotoxic patients and the remaining patient required additional treatment with propranolol. Iv fluids including blood transfusions were not administered preor post-operatively.

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Section: Discussioncontrasting

confidence: 71%

The mechanism of hypocalcaemia following thyroidectomy

Percival

Hargreaves

Kanis

1985

Acta Endocrinologica

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“…The differences could be due to differences in the selection of patients for surgery between the institutions. The early onset of tetany after thyroidectomy may not be accounted for by parathyroid damage or infarction alone (Michie et al, 1971), which was once widely accepted as the main cause of postoperative tetany in Graves' patients (Wade et al, 1965;Parfitt, 1971;Escobar-Jimines et al, 1977). Although we previously observed a significant decrease in serum PTH level in patients with Graves' disease who suffered postoperative tetany (Murakami et al, 1989) findings support the theory that parathyroid damage may not be the sole cause because of the significant differences in the frequency of postoperative tetany between the two sexes.…”

Section: Discussionmentioning

confidence: 99%

“…Tetany is one of the postoperative complications, resulting from hyperexcitability at the neuromuscular junction, usually caused by hypocalcaemia (Brown, 1911). The mechanisms of the postoperative hypocalcaemia and tetany are disputed and have yet to be clarified: these conditions have been suggested to be due to surgical interference with the parathyroids (Wade et al, 1965;Parfitt, 1971;Escobar-Jimines et al, 1977), abnormal release of calcitonin by manipulating the thyroid gland at operation (Wilkin et al, 1977) and the sudden reversal of thyrotoxic osteodystrophy present before thyroidectomy, which leads to a rapid skeletal uptake of calcium referred to as the 'hungry bone syndrome' (Michie et al, 1971;Laitinen, 1976;Jones & Davidson, 1987). These studies were conducted focusing mainly on bone and calcium metabolism in relation to postoperative hypocalcaemia and tetany, in a relatively small number of patients with Graves' disease.…”

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confidence: 99%

Postoperative tetany in patients with Graves' disease: a risk factor analysis

Yamashita

Noguchi

Tahara

et al. 1997

Clinical Endocrinology

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These results, combined with previous observations in which a significant decline in serum parathyroid hormone level was found in patients with Graves' disease who suffered postoperative tetany, suggests that postoperative tetany may occur during the period of bone restoration due to antithyroid drug therapy and be due to continuation of a calcium flux bone concomitant with transient hypoparathyroidism induced by surgery. Calcium supplements during preoperative period and/or after surgery may be appropriate for patients who are anticipated to develop postoperative tetany based on these risk factors.

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“…As more than 80% and 90% of the blood supply of the superior and inferior parathyroid glands, respectively, is provided by the inferior thyroid artery (ITA), some authors have proposed mandatory ligature of secondary and tertiary branches of the ITA medial to the gland to avoid the ligature of truncal arteries to prevent postoperative hypocalcemia . However, since the original Wade et al study, some authors have not found differences in the rate of hypocalcemia using this technique …”

Section: Introductionmentioning

confidence: 99%