Carpopedal spasm (post-thyroidectomy hypoparathyroidism)

Look at this patient's hands.

Spasm of the hands - the fingers are extended, except at the metacarpophalangeal

joints, and the thumb is strongly adducted.

· Look at the feet for spasm and then 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

cuff just above the systolic pressure for 3 minutes; this will cause the

hand to go into spasm - Trousseau's sign.

-Look into the mouth for candidiasis (may be seen in primary hypoparathyroidism)

and defective teeth.

-Fingernails may be thin and brittle. -Check for thyroidectomy scar. -Look for

cataracts.

· Tell the examiner that you would like to perform the following tests: - Skull

radiograph (looking for basal ganglia calcification). -Measurement of serum

calcium and magnesium levels.

-ECG for prolonged QT intervals and T-wave abnormalities.

- Slit-lamp examination for early posterior lenticular cataract formation.

This patient has carpopedal spasm (lesion) due to hypoparathyroidism as a

com-plication of thyroidectomy (aetiology).

Furosemide (frusemide), as it may enhance hypocalcaemia, and phenothiazine

drags, because they may precipitate extrapyramidal symptoms.

· Maintain airway.

· Slow intravenous calcium gluconate and oral calcium.

· Vitamin D preparations.

· Magnesium (if associated hypomagnesaemia).

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

· Idiopathic.

· Destruction of the parathyroid gland due to 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).

Typically, low serum calcium, high serum phosphate and normal alkaline

phosphatase levels and reduced urine calcium excretion.

It is a condition characterized by end-organ resistance to parathyroid hormone. The

biochemistry is similar to that of idiopathic hypoparathyroidism except that patients

with pseudohypoparathyroidism do not respond to injected parathyroid hormone.

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'.

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

· Increased bone osteoclastic activity resulting in increased delivery of calcium and

phosphorus to the extracellular compartment.

· Enhanced renal tubular absorption of calcium.

· Inhibits the absorption of phosphate and bicarbonate by the renal tubule.

· Stimulates the synthesis of 1,25-dihydrocholecalciferol (vitamin D) by the kidney.

Franz 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.