Calcium regulation is critical for normal cell function, membrane stability, neural transmission, bone structure and blood coagulation. The normal total calcium concentration in the plasma is 8.9 - 10.1 mg/dL (4.5–5.1 mEq/L).2 Hypocalcemia is an electrolyte derangement commonly encountered on surgical and medical services.1, 2 It may be transient, reversing with addressing the underlying cause, or chronic and even lifelong, when due to a genetic disorder or the result of irreversible damage to the parathyroid glands after surgery or secondary to autoimmune destruction.1–3 After thyroidectomy, transient hypoparathyroidism occurs in 5–10% of patients; incidence of transient hypocalcaemia ranges 19–38% and permanent hypocalcemia occurs in 1% of patients.1
Clinical symptoms of hypocalcemia can be due to increased neuromuscular excitation resulting in tetany, paresthesia or seizure.1 It can also be because of deposition of calcium in soft tissues producing reduced vision due to cataract, papillaedema or calcification of basal ganglia.4–8 It has been reported that longstanding hypocalcaemia has been remarkably asymptomatic or minimal symptoms like paresthesia.4 Symptomatic long term hypocalcemia can occur after thyroid surgery with tetany, paresthesia, seizure and confusion.1, 2, 4 The patient presented here had most of the above systemic manifestations which improved with supplemental calcium gluconate.
Hypocalcaemic cataracts are bilateral, punctate, iridescent opacities in the anterior and posterior cortex lying beneath the lens capsule which are usually separated from the lens capsule by a zone of clear lens. The opacities may remain stable or mature into complete cortical cataracts.3 The morphology and bilaterality of the cataract with-out other concomitant primary ocular conditions in the case described here suggests the cause of the cataract to be long-term depreciation of serum calcium level in her body. The proposed mechanism of cataract formation in hypocalcemia is membrane damage with low calcium level in the aqueous humor and sodium content increase in the lens.9 As far as the authors’ knowledge; there are few reported cases of bilateral cataract secondary to hypocalcemia.5, 6, 8 Freedman and et al. reported bilateral cataract secondary to hypocalcaemia presenting 4 years after total thyroidectomy.5 Our patient developed long-term hypocalcemia after total thyroidectomy which took longer time to return back to normal. Her serum calcium level at the time of diagnosis was very low. It took 7 years of treatment to raise her serum calcium level. Chronic hypocalcemia due to hypoparathyroidism is treated with calcium supplements (1000–1500 mg/d elemental calcium in divided doses) and either vitamin D2 or D3 (25,000–100,000 U daily) or calcitriol (1,25(OH)2D, 0.25–2 g/d).2 The patient described here has been on calcium gluconate 500 mg tid which is according to the recommended dose; was not taking vitamin D and calcitriol because they were not available in our setup and they are expensive to buy from abroad.
Other causes of bilaterally symmetrical cataract include metabolic disturbances like hyperphosphatemia, calcitonin reduction, vitamin D insufficiency and renal failure. Idiopathic hypoparathyroidism is another important cause of bilaterally symmetrical cataract. The patient presented here had a clear history of total thyroidectomy and was diagnosed to have hypocalcemia 7 years prior to her presentation to eye department. In addition the investigations were not suggestive of the above differential diagnoses.