Bailey And Love's Short Practice Of Surgery 26th Ed by Unknown

Author:Unknown
Language: eng
Format: epub
Tags: surgery

Figure 51.51 Parathyroid adenoma. Operative photograph showing normal left inferior parathyroid (IPG) and large left superior parathyroid adenoma (SPG).

Otto Werner, 1 879-1936, a German physician who had a practice in a small town near the German-Danish border. John Sipple, born 1930, Professor of Medicine, SUNY Medical Center, New York, NY, USA.

THE THYROID AND PARATHYROID GLANDS

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Figure 51.52 Parathyroid hyperplasia, (a) Mobilised right thyroid lobe showing enlarged superior and inferior parathyroid glands. Note how the superior gland has migrated posterior and inferior to the inferior thyroid artery, (b) Total parathyroidectomy specimens.

incidental findings during neck exploration. If aspirated preop-eratively the diagnosis should be suspected from the watery clear fluid aspirated- The diagnosis is confirmed by a high PTH level.

Clinical presentation

The classic quartet of 'stones, bones, abdominal groans and psychic moans' is rarely observed in developed countries when the diagnosis is usually detected on serum calcium estimation well before the full picture of severe bone disease (von Recklinghausen's disease), renal calculi and calcinosis, pancreatitis and psychiatric disorder. Incidentally detected hypercalcae-mia is rarely truly 'asymptomatic' and most patients experience an improved sense of well-being after surgery. Careful enquiry into family history is always appropriate and may reveal an index case for familial disease including familial primary HPT, MEN syndromes and familial hypocalciuric hypercalcaemia.

Diagnosis

Although ionised calcium is the physiologically active circulating element, total serum calcium is a satisfactory measure. The effect of binding to serum proteins must be corrected by

upward or downward correction to a serum albumin level of 40 g/L. Inappropriate, i.e. elevated or normal PTH levels in the presence of high serum calcium is diagnostic of primary HPT. Hypophosphataemia and elevated urine calcium excretion are confirmatory.

Other causes of hypercalcaemia must be considered and excluded (Table 51.11). Advanced malignancy is the most common cause of hypercalcaemia in hospitalised patients, due to parathyroid hormone-related peptide (PTHrP) or bone metastases. The PTH level is suppressed.

Familial hypocalciuric hypercalcaemia is an autosomal dominant disorder characterised by mild elevation of calcium and PTH levels secondary to a missense mutation in the cell membrane calcium receptor. The low urinary excretion of calcium will discriminate this from HPT. Parathyroidectomy is not required. However, neonatal hyperparathyroidism is rare but is associated with severe hypercalcaemia in homozygous patients and urgent near-total parathyroidectomy is required.

Table 51.11 Causes of hypercalcaemia.

Treatment of primary hyperparathyroidism

At present surgery is the only curative option and should be offered to all patients with significant hypercalcaemia provided they are otherwise fit for the procedure. There are a number of medical strategies and therapies, particularly in mild hyperparathyroidism, which include simple expectant treatment until the calcium level or symptoms reach a level at which surgery becomes more attractive, low calcium diet, withdrawal of drugs (diuretics and lithium) which aggravate hypercalcaemia and, more recently, calcium reducing agents such as bisphosphanates and the calcium receptor agonist cinacalcet.

Occasionally, patients present with a parathyroid crisis and severe hypercalcaemia (serum calcium greater than 3.5 mmol/L). This results in confusion, nausea, abdominal pain, cardiac arrhythmias and hypotension with acute renal failure.

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