Description

A 65-year-old woman presented to the hospital with severe weakness, muscle cramps and lower extremity contractures. She had a medical history of hypertension, atrial fibrillation and heart failure with preserved ejection fraction. She also had amiodarone-induced thyrotoxicosis with multinodular substernal goitre with subsequent thyroidectomy without parathyroid tissue implant in the forearm, performed 8 months earlier. The patient mentioned recent emotional instability, difficulty performing activities of daily living and depression. She was taking metoprolol, diltiazem, apixaban, levothyroxine and furosemide. Physical examination revealed Trousseau’s sign while taking her blood pressure (video 1). Her total calcium level was 5.8 mg/dL (normal range (NR) 8.4–10.2), ionised calcium 2.96 mg/dL (NR 4.52–5.28), 25-hydroxyvitamin D 24.0 ng/mL (59.9 nmol/L, considered insufficient <30 ng/mL), parathyroid hormone less than 1.0 pg/mL (NR 15.0–65.0), thyroid-stimulting hormone (TSH) 2.66 mcIU/mL (NR 0.27–4.2), magnesium 1.2 mg/dL (NR 1.7–2.2), potassium 3.4 mmol/L (NR 3.6–5.0) and creatinine 1.3 mg/dL (NR 0.52–1.04). ECG showed sinus rhythm with QT interval prolongation, and chest radiograph showed pulmonary oedema.

The patient was diagnosed with symptomatic hypocalcaemia secondary to postsurgical hypoparathyroidism. She started treatment with calcium gluconate 3 g intravenous at admission followed by 1 g intravenous every 12 hours, calcium carbonate 2000 mg orally every 6 hours and calcitriol 3 μg orally every 6 hours. The weakness, muscle cramps and extremity contractures resolved within the first 24 hours. She received treatment for hypokalaemia and hypomagnesaemia. Furosemide, which is associated with hypokalaemia, hypomagnesaemia and hypocalcaemia, was changed to hydrochlorothiazide during the admission. The absence of parathyroid hormone leads to hypocalcaemia and hypercalciuria. Hydrochlorothiazide is greatly beneficial in the treatment of this patient because it decreases the urinary calcium and increases the serum calcium.

The patient’s length of hospitalisation was 72 hours, and at the time of discharge, the creatinine was normal. The hypokalaemia, hypomagnesaemia and pulmonary oedema resolved. The ECG showed a normal QT interval, her ionised calcium was 4.76 mg/dL and calcium level was 8.5 mg/dL. The patient was discharged home and continues treatment with furosemide 40 mg orally daily, potassium supplements, calcitriol 2 μg orally every 8 hours and calcium carbonate 1000 mg orally two times per day.

Trousseau’s sign is common in the setting of hypocalcaemia. It is observable as a carpopedal spasm induced by ischaemia secondary to the inflation of a sphygmomanometer to 20 mm Hg over the systolic blood pressure for 3 min. In our patient, it was observed in hypocalcaemia secondary to postsurgical hypoparathyroidism and worsened with furosemide. Chvostek’s sign, also observed in hypocalcaemia, was not observed in our patient. However, it is absent in about one-third of patients with hypocalcaemia.1–3

In contrast with two previous reported cases, our patient also had QT prolongation, emotional instability and depression.1 3 QT prolongation is associated with hypocalcaemia, as well as with hypomagnesaemia and hypokalaemia. Hypocalcaemia can cause psychological symptoms, particularly emotional instability, anxiety, depression and less common hallucinations and psychosis. After 8 months of follow-up with the same treatment, she is asymptomatic, she has normal calcium levels and she can perform all her activities of daily living.