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Most common cause of both acute and chronic hypoparathyroidism is surgery of the neck, including thyroidectomy, parathyroidectomy, and radical neck dissection.
Nonsurgical hypoparathyroidism is rare. Etiologies include autoimmune disease, infiltrative diseases (e.g., hemochromatosis, Wilson disease), hypomagnesemia or hypermagnesemia, and genetic disorders involving PTH biosynthesis or parathyroid development (e.g., DiGeorge syndrome).
Severe hypocalcemia leading to heart failure, hypotension, arrhythmias, laryngospasm, bronchospasm, seizure, or altered mental status
Hypocalcemia and other lyte abnormalities.
Pts on oral calcium maintenance therapy may require IV supplementation during long surgical procedures.
Watch for periop causes of hypocalcemia, including both respiratory or metabolic alkalosis and citrate toxicity from large volume RBC transfusions.
PTH is normally secreted by the parathyroid glands to maintain calcium and phosphorous homeostasis.
PTH impacts calcium and phosphorous by increasing (1) bone resorption to release calcium and phosphorous, (2) calcium reabsorption and phosphorous excretion in the kidney, and (3) vitamin D activation, indirectly resulting in an increased absorption of calcium and phosphorous by the intestines.
Hypoparathyroidism is characterized by hypocalcemia with an inappropriately low PTH level. It is usually accompanied by an elevated serum phosphorous level.
Symptoms of hypoparathyroidism are due to hypocalcemia, with the severity of symptoms dictated by disease chronicity, rapidity of calcium concentration change, and the overall severity of hypocalcemia.
Symptoms may range from mild (paresthesias, cramping, tetany) to severe (seizure, laryngospasm, altered mental status, heart failure, hypotension, cardiac arrhythmias).
Most common etiology of acute and chronic hypoparathyroidism is postsurgical, specifically following surgery on the neck.
Incidence of hypoparathyroidism after total thyroidectomy is 0.5–10%, but it is usually transient. Permanent hypoparathyroidism persisting 6 mo after surgery occurs in only 4.4% of pts.
Postsurgical hypoparathyroidism is usually evident within several h of surgery and is caused by hypoparathyroid gland damage, removal, or devascularization.
Acquired hypoparathyroidism can also be caused by isolated autoimmune destruction of parathyroid tissue or as part of an autoimmune polyendocrine syndrome, antibodies to the calcium-sensing receptor, neck radiation, 131 I therapy, and infiltrative diseases, including hemochromatosis, thalassemias, and granulomatosis diseases.
Reversible hypoparathyroidism can be caused by severe hypomagnesemia (e.g., from chronic malnutrition or alcoholism) or hypermagnesemia (e.g., from tocolytic therapy).
Congenital hypoparathyroidism is seen in genetic disorders involving parathyroid development (e.g., DiGeorge syndrome) or PTH biosynthesis.
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