Hypoparathyroidism in Emergency Medicine 

Updated: Aug 05, 2015
Author: Agnieszka Gliwa, MD; Chief Editor: Erik D Schraga, MD 



Hypoparathyroidism describes a condition in which there are low circulating levels of parathyroid hormone (PTH) or insensitivity to its action.[1] The causes of hypoparathyroidism vary; however, they all share a common feature of hypocalcemia. The presentation of hypoparathyroidism also varies depending on the chronicity of the resultant hypocalcemia. Muscle spasms/tetany, paresthesias, and seizures may occur in an acute onset, whereas chronic hypoparathyroidism may only be evidenced by visual impairment due to cataract formation.

See Hypocalcemia for more information.


Many underlying pathologic etiologies of hypoparathyroidism exist.

  • The most common causes are neck surgery and autoimmune processes. Hypoparathyroidism resulting from thyroid or parathyroid surgery can become clinically apparent 1-2 days after the procedure or follow the operation by many years. The incidence of permanent hypoparathyroidism varies with the extent of the procedure, the surgeon’s experience, and the underlying disease process being treated. Rarely, hypoparathyroidism can be a complication of radioactive iodine treatment of external localized radiotherapy.[2]

  • Autoimmune insult to the parathyroid gland can be isolated or associated with a variety of polyglandular syndromes. Antibodies to the parathyroids have been detected in up to 30% of patients with isolated hypoparathyroidism and 40% of patients with polyglandular disease.[3] The calcium sensor-receptor is another target of autoantibodies in hypoparathyroidism. In patients with polyglandular autoimmune syndrome type 1, more than 50% will have this antibody. See Polyglandular Autoimmune Syndrome, Type I.

  • Maternal hyperparathyroidism can result in transient neonatal hypoparathyroidism.[4, 5, 6] Maternal PTH suppresses neonatal parathyroid activity; however, this resolves rapidly after birth and removal from excessive maternal PTH.

  • Both hypermagnesemia and hypomagnesemia can result in decreased PTH secretion. In the case of hypermagnesemia, elevated magnesium levels result in stimulation of a calcium-sensing receptor on the pituitary. This, in turn, attenuates PTH secretion. In the case of chronic alcoholics with hypomagnesemia, there is diminution of PTH secretion levels and a resistance to hormone activity.[7, 8] See Hypermagnesemia and Hypomagnesemia.

  • This condition is characterized by thymus and parathyroid dysgenesis, cardiac malformation, and facial dysmorphogenesis.[9] Other complex syndromes associated with hypoparathyroidism have been described and include Sanjat-Sakati syndrome, HDR syndrome, Kenny-Caffey syndrome, Kearns-Sayre syndrome, and Pearson marrow-pancreas syndrome.[10] See DiGeorge Syndrome and Kearns-Sayre Syndrome.

  • Infiltration of the parathyroid gland can lead to clinically significant hypoparathyroidism. Causes include metastatic carcinoma, hemochromatosis, transfusion-related iron overload, Wilson disease[11] , and sarcoidosis[12] . See Hemochromatosis, Wilson Disease, and Sarcoidosis.

PTH functions to maintain plasma calcium levels by withdrawing calcium from bone tissue, glomerular filtrate reabsorption, and indirectly through increased intestinal absorption of calcium by activation of vitamin D-1,25. Insufficient production of PTH is known as true hypoparathyroidism, while decreased action on target tissues is called pseudohypoparathyroidism.[3] See Pseudohypoparathyroidism.



United States

Primary hypoparathyroidism is rare. Familial cases occur with autosomal dominant, autosomal recessive, and X-linked transmission.


Acute hypocalcemia can be treated with good outcome. The mortality rate of hypoparathyroidism depends on the underlying cause.


With the exception of X-linked transmitted syndromes, no sex predilection exists.


See the list below:

  • Maternal hyperparathyroidism resulting in newborn hypoparathyroidism usually manifests by the third week of life;[4, 5] however, cases have been reported as late as 2 months of age.[6]

  • Patients with DiGeorge syndrome present for clinical evaluation between birth and 3 months of age with a variety of symptoms.

  • Patients with polyglandular autoimmune syndrome type I present early in life. These patients typically have candidiasis by age 5 years and hypoparathyroidism by age 10 years.

  • For other forms of hypoparathyroidism, no age predilection is noted.




See the list below:

  • A full surgical and family history is essential in cases of suspected hypoparathyroidism.

  • Neuromuscular irritability, arising from hypocalcemia, is the hallmark of the condition. These features can range from mild-to-moderate paresthesias of the extremities or lips to painful muscle cramps. In severe cases, tetany can result in carpopedal spasm, laryngospasm,[13] or generalized seizures.[14] Recurrent laryngospasm should prompt an investigation of underlying hypoparathyroidism.[15]

  • Additionally, severe hypocalcemia can result in neuropsychiatric and cardiovascular abnormalities. Neuropsychiatric manifestations include irritability, anxiety, psychosis, dementia, hallucinations, depression, and confusion. The cardiovascular effects of hypocalcemia are usually bradydysrhythmias or prolongation of the QT interval. Severe hypocalcemia can rarely mimic myocardial infarction.[16]

  • Gastrointestinal complaints may result from hypocalcemia as well. Smooth muscle spasms can result in intestinal and biliary cramping. Several cases of dysphagia have been described in the setting of hypocalcemia.[17]

  • Symptoms are rare unless the ionized calcium level drops below 2.8 mg/dL.[3]


The clinical manifestation of hypoparathyroidism is due to hypocalcemia.

  • Head, ears, eyes, nose, and throat signs

    • Surgical/traumatic scars

    • Mucocutaneous candidiasis (in the setting of polyglandular failure type 1[18] )

  • Neurologic signs

    • Hyperreflexia

    • Tetany

    • Chvostek sign - Chvostek sign has low sensitivity and specificity. Twenty-five percent of healthy persons will have a positive result; 29% of hypocalcemic patients will have a negative result.[3]

    • Trousseau sign (carpal spasm caused by occluding the brachial artery) - Trousseau sign is more reliable. Only 1-4% of healthy persons will have a positive sign; 94% of hypocalcemic persons will have a positive sign.[3]

    • Seizures

    • Altered mental status

  • Cardiovascular signs

    • Heart failure[19, 20, 21]

    • Bradycardia[22]

    • Hypotension not responsive to fluids or pressors[23]

  • Ophthalmologic signs - Cataracts[24]

  • Signs in infants

    • Vomiting

    • Abdominal distention

    • Apneic spells

    • Intermittent cyanosis

    • Twitching, tremors, and seizures


Hypoparathyroidism has multiple etiologies:

  • Postsurgical

  • Autoimmune

  • Sporadic[25]

  • Polyglandular syndromes

  • Activating antibodies to the calcium-sensing receptor[26, 27]

  • Infiltration

  • Parathyroid destruction

  • Copper[11]

  • Malignancy

  • Granulomatous disease[12]

  • Mitochondrial neuropathies

  • Inactivating mutations of the PTH gene[25]

  • DiGeorge syndrome[9]

  • Impaired secretion and/or action of PTH

  • Hypomagnesemia[28]

  • Pseudohypoparathyroidism

  • Hemochromatosis[29]

  • Infarction[30]

  • Hypermagnesemia[31]

  • Medication induced (aluminum,[32] doxorubicin,[28] aminoglycoside,[33] cimetidine,[34] alendronate[35] , omeprazole[36] )





Laboratory Studies

See the list below:

  • The diagnosis of hypoparathyroidism is supported by hypocalcemia, hyperphosphatemia, and low parathyroid hormone levels in the absence of renal failure or intestinal malabsorption.

  • Both total and ionized calcium are decreased. Normal total serum calcium levels range from 9-10.5 mg/dL (2.2-2.6 mmol/L). Normal ionized calcium levels are 4.5-5.6 mg/dL (1.1-1.4 mmol/L).

  • Serum magnesium level can be low, high, or normal.

  • Transient symptomatic hypocalcemia can occur immediately after thyroid surgery; normal PTH levels 3 hours after surgery and a normal serum calcium level on the postoperative day one rules out persistent hypoparathyroidism.[37]

Imaging Studies

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  • Radiography: Bone density is increased[38] ; tooth enamel and root abnormalities have been described.[39] Ossification of the paravertebral ligaments is frequently observed.[40]

  • CT scan: Calcification of subcortical nuclei, dentate nucleus,[41] and basal ganglia[42] can occur.

Other Tests

See the list below:

  • ECG may show prolonged QT interval[43] , bradycardia, or rarely ST-segment elevations.[16]

  • For D-xylose absorption test, the results are usually normal.[44]


See the list below:

  • Slit lamp examination for cataracts[24]



Prehospital Care

See the list below:

  • Address and stabilize ABCs.

  • Obtain intravenous access.

  • Control seizures with benzodiazepines.

Emergency Department Care

Acute, symptomatic hypocalcemia is a medical emergency. The main goal of treatment is to restore serum calcium levels to alleviate symptoms of acute hypocalcemia. In the setting of severe symptoms, calcium therapy should be given even if serum levels are only mildly reduced.

Recent guidelines on chronic hypoparathyroidism by the European Society of Endocrinology are below:[45]

  • Consider a diagnosis of chronic hypoparathyroidism (HypoPT) in a patient with hypocalcemia and inappropriately low parathyroid hormone (PTH) levels.
  • Consider genetic testing and/or family screening in a patient with HypoPT of unknown etiology.
  • Treatment targeted to maintain serum calcium level (albumin adjusted total calcium or ionized calcium) in the lower part or slightly below the lower limit of the reference range (target range) is suggested, with patients being free of symptoms or signs of hypocalcemia.
  • Treat patients with chronic HypoPT with symptoms of hypocalcemia and/or an albumin adjusted serum calcium level <2.0 mmol/L (<8.0 mg/dL/ionized serum calcium levels [S-Ca 2] <1.00 mmol/L).
  • Offer treatment to asymptomatic patients with chronic HypoPT and an albumin adjusted calcium level between 2.0 mmol/L (8.0 mg/dL/S-Ca 2+ 1.00 mmol/L) and the lower limit of the reference range in order to assess whether this may improve their well-being.
  • Use activated vitamin D analogues plus calcium supplements in divided doses as the primary therapy.
  • If activated vitamin D analogues are not available, treat with calciferol (preferentially cholecalciferol).
  • Titrate activated vitamin D analogues or cholecalciferol in such a manner that patients are without symptoms of hypocalcaemia and serum calcium levels are maintained within the target range.
  • Provide vitamin D supplementations in a daily dose of 400–800 IU to patients treated with activated vitamin D analogues.
  • In a patient with hypercalciuria, consider a reduction in calcium intake, a sodium-restricted diet, and/or treatment with a thiazide diuretic.
  • In a patient with renal stones, evaluate renal stone risk factors and management according to relevant international guidelines.
  • In a patient with hyperphosphatemia and/or an elevated calcium-phosphate product, consider dietary interventions and/or adjustment of treatment with calcium and vitamin D analogues.
  • In a patient with hypomagnesemia, consider measures that may increase serum magnesium levels.
  • The routine use of replacement therapy with PTH or PTH analogues is not recommended.

Care to prevent long-term complications from hypocalcemia or hypercalcemia[46] should be coordinated with an endocrinologist.

  • Intravenous calcium: 100-300 mg elemental calcium diluted in 150 mL D5W over 10 minutes (10-30 mL of 10% calcium gluconate [9.3 mg/mL elemental calcium])

    • This solution raises ionized calcium level by 0.5-1.5 mmol. Calcium chloride may be used if infused through a central line, as it can be harmful when given in a peripheral vein.

    • Initial rate of infusion is 0.3-2 mg elemental calcium/kg/h. This scale is not exact; base subsequent adjustments on serial calcium measurements every 2-4 hours.

    • Infuse children with 2 mg/kg elemental calcium, or about 0.2 mL of 10% calcium gluconate/kg, IV.

  • Oral therapy: Calcium carbonate, 1-2 grams or more per day, in 3-4 divided doses.

    • May be appropriate for patients with mildly lowered calcium levels and mild or no symptoms.


Consult an endocrinologist.



Medication Summary

Hypoparathyroidism is treated primarily with vitamin D.[47] Dietary supplementation with Ca2+ may be necessary.

Electrolyte supplements

Class Summary

Hypoparathyroidism manifests as hypocalcemia. As a result, calcium supplementation may be indicated.

Calcium gluconate (Kalcinate)

Can be given IV initially, then maintained as high-calcium diet. Some patients require calcium supplementation. The 10% IV solution provides 100 mg/mL of calcium gluconate that equals 9 mg/mL (0.46 mEq/mL) of elemental calcium. One 10-mL ampule contains 93 mg of elemental calcium.

Vitamin D Analog

Class Summary

Vitamin D enhances absorption of calcium and maintains calcium homeostasis.

Calcitriol (Calcijex, Rocaltrol)

Stimulates absorption of calcium and phosphate from small intestine and promotes release of calcium from bone into blood.



Further Outpatient Care

See the list below:

  • High-calcium diet

  • Calcium supplementation

  • Calcitriol

Further Inpatient Care

See the list below:

  • Effects of 1 bolus of intravenous calcium will wane after 2 hours; therefore, subsequent continuous infusion is required to control hypocalcemia.

  • Cardiac monitoring is indicated for patients with hypoparathyroidism.


Complications of hypoparathyroidism may include the following:

  • Neuromuscular symptoms

  • Cataracts[24]

  • Intracranial calcifications[41, 42]

  • Growth stunting (with HDR syndrome)[48]

  • Tooth malformation[39]

  • Mental retardation (with HDR syndrome)[48]

  • Hypothyroidism

  • Cardiomyopathy[46]

  • Parkinsonian symptoms[49]

  • Ossification of paravertebral ligaments[40]

  • Adhesive capsulitis[50]


See the list below:

  • Prognosis is determined by the underlying cause of hypoparathyroidism.

Patient Education

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  • Educate patients concerning regulation and effects of calcium on the body.

  • Educate patients about the importance of periodic blood chemistry evaluation.