3. DISCUSSION
Hypoparathyroidism is the commonest postoperative complication after
thyroid surgery and is characterized by hypocalcemia, elevated serum
phosphorus levels, and low or inappropriately normal plasma levels of
parathyroid hormone.1,4 Postoperative permanent
hypoparathyroidism is characterized by the persistence of hypocalcemia
beyond six months of surgery.1,6 Its incidence depends
on the extent of thyroidectomy and lymph node
dissection.1-3 Similarly, it occurs more frequently
after surgeries done for thyroid cancer than those done for benign
diseases.4
Hypocalcemia presents classically with muscle twitching, spasms,
tingling, and numbness. Carpopedal spasm is characteristic and, in
severe cases, can progress to tetany, seizures, and cardiac
dysrhythmias. Signs of neuromuscular excitability can be observed on
provocation tests: Chvostek’s sign and Trousseau’s
sign.7 Hypocalcemia associated with chronic
hypoparathyroidism exhibits several unique features such as basal
ganglia calcifications, neuropsychiatric symptoms, and
cataracts.7 Calcification of the brain occurs less
frequently in postoperative hypoparathyroidism than in other causes of
hypoparathyroidism; one reason behind this is believed to be the earlier
detection of hypoparathyroidism resulting in earlier supplementation of
calcium and Vitamin D following surgery.5,8 The
calcifications typically involve caudate nucleus, putamen, globus
pallidus, thalamus, and dentate nucleus; calcifications beyond these
areas are rare.5,9 Our patient had extensive bilateral
intracranial calcifications, which involved the basal ganglia, thalamus,
periventricular region, subcortical fronto-pareito-occipital region, and
cerebellum. Some patients with basal ganglia calcifications develop
Parkinsonism, while others, like our patient, do
not.5,9,10 She had also undergone cataract surgery of
both eyes eight years ago.
Patients with permanent hypoparathyroidism require life-long calcium
supplementation. The goal is to maintain serum calcium in the low normal
range, and serum calcium should be checked every three to six months or
when the medical regimen is changed.6 The synthesis of
1, 25-dihydroxyvitamin D requires parathyroid hormone; therefore, it is
deficient in patients with hypoparathyroidism and needs to be
supplemented. Commonly available vitamin D preparations contain
ergocalciferol or cholecalciferol, both of which are ineffective in
hypoparathyroidism for the reason mentioned above.7Our patient stopped checking her calcium levels one year ago, and due to
her general good condition, she stopped taking calcium and vitamin D
supplements as well, five months ago. Within a month of stopping the
supplements, she experienced carpopedal spasm, which was empirically
treated with calcium and cholecalciferol supplements without checking
calcium levels. She was not prescribed calcitriol. This probably led to
the severe hypocalcemia that she had on presentation.