Carpopedal spasm (post-thyroidectomy hypoparathyroidism)

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141 Carpopedal spasm (post-thyroidectomy hypoparathyroidism)

Instruction

Look at this patient’s hands.

Salient features

History

• History of thyroid surgery

• Paraesthesias of fingers, toes and circumoral region

• Muscle cramping, carpopedal spasm, laryngeal stridor, convulsions.

Examination

• Spasm of the hands: fingers are extended, except at the metacarpophalangeal joints, and the thumb is strongly adducted.

Proceed as follows:

• Look at the feet for spasm

• Investigate as follows:

• Tap over the facial nerve (in front of the tragus of the ear): there is contraction of the lips and facial muscles (Chvostek’s sign or Chvostek–Weiss sign)
• Inflate the BP cuff to just above the systolic pressure for 3 min; this will cause the hand to go into spasm: Trousseau’s sign (Fig. 141.1)
• Look into the mouth for candidiasis (may be seen in primary hypoparathyroidism) and defective teeth
• Finger nails may be thin and brittle
• Check for thyroidectomy scar
• Look for cataracts.

• Tell the examiner that you would like to perform the following tests:

• Do a skull radiograph (looking for basal ganglia calcification)
• Check serum total and ionized calcium, albumin, phosphorus, magnesium and parathromone (PTH)
• ECG for prolonged QT intervals and T wave abnormalities
• Slit-lamp examination for early posterior lenticular cataract formation.
image

Fig. 141.1 Trousseau’s sign.

(With permission from Burnside, McGlynn 1987.)

Diagnosis

This patient has carpopedal spasm (lesion) caused by hypoparathyroidism as a complication of thyroidectomy (aetiology).

Advanced-level questions

Mention any drugs that you would use cautiously in hypoparathyroidism

Furosemide, as it may enhance hypocalcaemia, and phenothiazine drugs, because they may precipitate extrapyramidal symptoms.

How would you manage an acute attack of hypoparathyroid tetany?

• Maintain airway

• Slow intravenous calcium gluconate and oral calcium

• Vitamin D preparations

• Magnesium (if associated hypomagnesaemia)

• Outpatient therapy with calcium carbonate three times daily and calcitriol once or twice daily adjusting the dose to maintain a target level of albumin-corrected serum calcium at the lower end of the normal range (approximately 80–85 mg/l (2.00–2.12 mmol/l)), a 24-hour urinary calcium level of <300 mg, and a calcium–phosphate product <55.

What are the causes of hypoparathyroidism?

• Damage during thyroid or neck surgery (Lancet 1960;ii: 1432)

• Idiopathic

• Destruction of the parathyroid gland caused by the following:

• Radioactive iodine therapy
• External neck irradiation
• Haemochromatosis and Wilson’s deficiency
• Metastatic disease from the breast, lung, lymphoproliferative disorder.

• Dysembryogenesis (DiGeorge syndrome)

• Polyglandular autoimmune syndrome (PGA type 1), which is also known as autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECD).

How is corrected total calcium calcuated?

Albumin-corrected total calcium is calculated as follows:

image

where calcium is measured in milligrams per decilitre and albumin is measured in grams per decilitre.

What is the mechanism of hypocalcaemia?

Hypocalaemia results from PTH secretion that is inadequate to:

• mobilize calcium from bone

• reabsorb calcium from the distal nephron

• stimulate renal 1α-hydroxylase activity; as a result, insufficient 1,25-dihydroxyvitamin D (1,25-dihydrocholecalciferol) is generated for efficient intestinal absorption of calcium.

What are the biochemical features of hypoparathyroidism?

Typically it consists of low serum calcium (with intact PTH), high serum phosphate, normal alkaline phosphatase levels and reduced urine calcium excretion.

Remember: Hypomagnesaemia causes resistance to effects of PTH and when severe may decrease PTH release as well. Hypermagnesaemia may also decrease PTH release.

What do you know about pseudohypoparathyroidism?

It is a condition characterized by end-organ resistance to PTH. The biochemistry is similar to that of idiopathic hypoparathyroidism except that patients with pseudohypoparathyroidism have elevated PTH levels do not respond to injected PTH. These patients are moon-faced, short statured and mentally retarded and may have short fourth or fifth metacarpals. Patients without hypocalcaemia but who have these phenotypic abnormalities are said to have ‘pseudopseudohypoparathyroidism’.

What are the main physiological effects of parathyroid hormone?

It results in a net increase of ionized calcium in the plasma through:

• increased bone osteoclastic activity, resulting in increased delivery of calcium and phosphorous to the extracellular compartment

• enhanced renal tubular absorption of calcium

• inhibited absorption of phosphate and bicarbonate by the renal tubule

• stimulated synthesis of 1,25-dihydrovitamin D by the kidney.

Frantisek Chvostek (1835–1884) was Professor of Medicine in Vienna, Austria.

Nathan Weiss (1851–1883), an Austrian physician.

Armand Trousseau (1801–1867), a Parisian physician, was the first to refer to adrenal insufficiency as Addison’s disease.

Professor Karim Meeran, qualified from the Royal Free Hospital and trained in Endocrinology at Hammersmith Hospital and St Bartholomew’s Hospital. He is Professor of Endocrinology, Imperial College Deputy Director of Medical Education and Lead Clinician for Endocrinology, Hammersmith Hospital. He is involved with the Abu Dhabi Imperial College London Diabetes Centre. Professor Meeran’s clinical focus is in all aspects of Endocrinology and Diabetes including thyroid, adrenal, hirsuitism, PCOS, prolactin and pituitary diseases, calcium and bone metabolism and neuroendocrine tumours.

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