Case Presentation:
A 61 year-old woman presented with unbearable weakness and muscle aches that progressed over the past two weeks. The patient was seen in clinic the day prior for these symptoms and overall lethargy to the point of inability to stand or walk. On examination, she had generalized weakness, dry skin, a flat affect, and a well-healed transverse surgical scar across her anterior neck. Electrolyte studies revealed a serum calcium of 6.2 mg/dL (normal: 8.9-10.3 mg/dL), total Vitamin D (VitD) 25-hydroxy <10 ng/mL (normal: 30-80 ng/mL), and a parathyroid hormone (PTH) level of 45 pg/mL (normal: 12-88 pg/mL). The remainder of her workup was normal including serum albumin, magnesium, alkaline phosphatase, thyroid stimulating hormone and kidney function.
In review of the patient’s history, she had undergone surgical resection of a thyroid lymphoma 20 years prior and was subsequently treated with local radiation. The patient was adequately replaced with thyroid hormone and had maintained normal electrolytes for many years. Replenishment of calcium and vitamin D was initiated with oral calcium carbonate, intravenous calcium gluconate, oral Vitamin D2 and oral 1, 25-dihydroxyvitamin D3. At the time of discharge, the patient’s serum calcium had improved to 8.4 mg/dL and most importantly, her mood and strength were returning to baseline.
Discussion:
The symptoms of hypocalcemia are broad as this case demonstrated a subtle presentation of weakness, muscle cramps, dry skin, and personality changes. Previous authors have suggested unique symptom profiles when comparing early and late-onset hypocalcemia in post-thyroidectomy patients. Late-onset hypocalcemia symptoms were similar to our patient, but the symptoms of early hypocalcemia in post-thyroidectomy patients typically included more overt findings of numbness, tingling, and tetany.
The additional impact of radiation in provoking late-onset hypoparathyroidism is poorly documented. Few reports conversely identify external beam radiation with hyperparathyroidism that is thought to arise from adenomatous change, hyperplasia or malignant transformation of the parathyroid glands. Unfortunately, a histological link between cases of hypoparathyroidism and radiation exposure has yet to be studied. It is well known that high-dose external beam radiation produces fibrosis and vascular insufficiency, which may predispose to late-onset parathyroid dysfunction.
Hypoparathyroidism, vitamin D deficiency, renal wasting, and concurrent electrolyte abnormalities are a few of the necessary considerations in evaluating the etiology of hypocalcemia. Primary hypoparathyroidism involves both the Surgeon and the Hospitalist. Surgical damage is the most common cause of transient or permanent primary hypoparathyroidism, but the Hospitalist is responsible to recognize the variable timeline of presenation, unique symptom profile and aggressively replace the electrolytes.
Conclusions:
1. Recognize the unique spectrum of symptoms associated with hypocalcemia in the early and late post-thyroidectomy states.
2. Consider the long-term impact of radiation therapy on the parathyroid glands.
3. Develop an approach to differentiate between the etiologies of hypocalcemia and initiate appropriate treatment.