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.