This patient has presented with a first-episode tonic-clonic seizure at age 32, a highly concerning presentation. Further questioning reveals a history of episodic, abnormal twitching of his facial muscles during the preceding weeks, while examination reveals positive Trousseau's and Chvostek's signs; considered together, these findings are strongly suspicious of hypocalcemia. Thus, an ionized calcium assay is a good next step; this should be obtained in parallel with investigations to rule out other common causes of seizures, i.e. serum glucose levels, a serum electrolyte panel, a complete blood count, and non-contrast computed tomography (CT) of the brain. The investigation results confirm the presence of hypocalcemia; given the absence of signs, symptoms, or investigation results suggesting at an alternate etiology, this can be considered the cause of her symptoms. An ECG is essential, as these patients are at increased risk for arrhythmias, with the characteristic pattern being a prolonged QT interval. However, this patient's ECG turns out to be unremarkable. Serum magnesium levels should also be assayed as hypomagnesemia can precipitate hypocalcemia by suppressing the secretion of parathyroid hormone (PTH); in such individuals, correction of magnesium levels is essential to obtain a full response to calcium replacement therapy. Given the presence of seizures, it can be argued that he needs intravenous (IV) calcium replacement; calcium gluconate is usually preferred over calcium chloride, as it causes less tissue necrosis if extravasated. Note that continuous ECG monitoring should be carried out during the infusion, as rapid changes in serum calcium levels may precipitate arrhythmias. Therapy with phenytoin sodium is not indicated here, as the seizures are secondary to hypocalcemia and will not recur once calcium levels are restored. Furthermore, given the normal magnesium levels, replacement therapy with magnesium sulfate is of little value here. Last, but not least, following stabilization, the underlying etiology must be investigated; in this patient, hypoparathyroidism is a strong consideration, given the history of trauma to the head and neck.
Hypoparathyroidism is a rare endocrine disease defined as an absolute or relative deficiency of parathyroid hormone (PTH). One of the key actions of PTH is to increase serum calcium levels by promoting the release of calcium from bone, increasing the absorption of calcium from the gut, and promoting resorption of calcium in the kidneys; the hormone also promotes renal excretion of phosphate. Thus, as might be excepted, hypoparathyroidism results in hypocalcemia and hyperphosphatemia. The condition is most often transient, following surgical procedures such as thyroidectomy, anterior neck exploration, or excision of neck lesions. Functional hypoparathyroidism can also occur after an extended period of hypomagnesemia; this may be seen in patients with malabsorption. Congenital and idopathic hypoparathyroidism are the other forms of the disease, but are both rare. The signs and symptoms of hypoparathyroidism are highly varied, with the severity depending on PTH levels. Neuromuscular and neuropsychiatric features are common, including numbness, paresthesia or cramping of the lower back, legs, and feet; these are mainly a result of the hypocalcemia. Severe symptoms include seizures, bronchospasm, laryngospasm, and tetany. Rhythm abnormalities, specifically an extended QT interval, and altered mental status are also part of the clinical picture of acute, severe hypoparathyroidism. On examination, it is beneficial to look for Chvostek's and Trousseau's signs, although individuals with chronic hypoparathyroidism may be asymptomatic. Investigations are key to the diagnosis; this involves demonstrating the presence of hypocalcemia and/or hyperphosphatemia in conjunction with a low to normal serum PTH. Note that if serum total calcium levels are assayed, a corrected calcium measurement should be obtained, as a significant fraction of calcium is protein bound, and thus affected by plasma albumin levels. Alternately, serum ionized calcium levels can be used. For etiological reasons, serum magnesium, vitamin D, and 24-hour urine calcium and creatinine may also be measured; the first of these rules out hypomagnesemia as a cause of the hypoparathyroidism, while the next two rule out hypovitaminosis D, and renal disease as causes for the hypocalcemia. The goals of management are to correct the hypocalcemia and maintain serum calcium between 8.5 to 9.5 mg/dL with urinary calcium of less than 400 mg/day. Where severe hypocalcemia is present the patient may require correction with intravenous (IV) calcium until stable, in conjunction with monitoring of the cardiac rhythm and serum calcium levels. Following stabilization, conversion to oral calcium supplements and vitamin D (calcitriol) can take place. A low-phosphate diet will help treat the hyperphosphatemia. While the exact role of PTH replacement still being evaluated, it is important to note that human recombinant PTH has been granted FDA approval as of 2015, as a once-daily injection in conjunction with oral calcium and vitamin D supplementation. Complications of hypoparathyroidism are usually the result of prolonged hypocalcemia; these include growth failure, mental retardation, nephrolithiasis, cataract formation, seizures, and arrhythmias. When treated correctly and promptly, patients with hypoparathyroidism have a good prognosis; however, where complications do occur, some of these may be irreversible - particularly growth failure, and cataracts.