What is Hypocalcemia?
Hypocalcemia is an electrolyte disorder characterized by low serum calcium levels. There are a variety of causes including chronic kidney disease, inadequate PTH production (hypoparathyroidism), vitamin D deficiency, and low abnormal magnesium metabolism (hypomagnesemia). Hypoparathyroidism may be caused by surgical removal of the parathyroid glands or due to autoimmune disease. Certain medications such as bisphosphonates for osteoporosis may also contribute to hypocalcemia.
The symptoms of acute hypocalcemia usually include tetany – this is a term for neuromuscular irritability. Patients also often develop numbness and paresthesias around the mouth as well as the hand and feet. Muscle spasms are another common manifestation. Severe cases result in laryngospasm, impaired cardiac function, seizure, and life-threatening cardiac arrhythmias. Due to the importance of this condition, it is critical that patients understand its causes, symptoms, and treatment. By the end of this article, you will have the answers to these essential questions:
- What causes Hypocalcemia?
- How common is Hypocalcemia?
- What are the symptoms and signs of Hypocalcemia?
- How is Hypocalcemia diagnosed?
- How is Hypocalcemia treated?
What causes Hypocalcemia?
Calcium is important for functions such as cell signaling, hormone secretion, muscle contraction, and coagulation. Calcium levels are affected by key regulators including parathyroid hormone (PTH) and vitamin D. The kidneys are also an essential regulator of calcium metabolism. In fact, the kidneys are responsible for synthesis of vitamin D via the enzyme alpha-hydroxylase. Low serum calcium levels (hypocalcemia) can be caused by a variety of conditions including:
- Inadequate PTH production (hypoparathyroidism)
- Chronic kidney disease
- Vitamin D deficiency
- Abnormal magnesium metabolism (hypomagnesemia)
- Extravascular calcium deposition (pancreatitis, hyperphosphatemia)
Hypoparathyroidism may be caused by removal of the parathyroid glands, which often occurs during thyroid, parathyroid, or radical neck surgery. Some patients develop hypoparathyroidism from autoimmune destruction of the parathyroid glands. Certain medications are also associated with hypocalcemia including:
- Inhibitors of bone resorption
- Calcium chelators (EDTA, citrate)
How common is Hypocalcemia?
Hypocalcemia is a common condition that is often initially evaluated in the primary care clinic. The most common cause is kidney disease. Advanced cases often require referral to a nephrology (kidney) specialist, particularly if first-line measures are unsuccessful.
It is difficult to determine the precise incidence of hypocalcemia. The incidence is approximately 15%-88% in patients hospitalized in the intensive care unit. About 27% of individuals with thyroid removal surgery (thyroidectomy) have transient hypocalcemia and about 1% develop permanent hypocalcemia.
What are the symptoms and signs of Hypocalcemia?
Symptoms of hypocalcemia depend on how quickly calcium levels decrease and the severity of hypocalcemia. Acute symptomatic hypocalcemia often results in tetany, a form of neuromuscular irritability. Patients often experience:
- Numbness around the mouth
- Tingling (paresthesias) involving the hands and feet
- Muscle cramps
Non-specific symptoms often include fatigue, anxiety, and agitation. Severe cases may result painful muscle contractions in the hands and feet (carpopedal spasm), laryngospasm, seizure, decreased cardiac function, and cardiac arrhythmia.
A classic physical examination sign that can suggest acute hypocalcemia is the Trousseau sign, which is characterized by carpopedal spasm when the blood pressure cuff is inflated. Chvostek sign is another finding characterized by contraction of the facial muscles caused by tapping just anterior to the ear.
Chronic hypocalcemia from hypoparathyroidism can result in cataracts, basal ganglia calcification, and dementia. Basal ganglia calcifications can lead to movement disorders such as Parkinson disease, which usually presents with bradykinesia (slow movement), rigidity, and tremor.
How is Hypocalcemia diagnosed?
The diagnosis of hypocalcemia may be suggested based on symptoms and physical examination, but is typically confirmed with laboratory studies. Your doctor will usually obtain a CMP (comprehensive metabolic panel), which contains a serum calcium concentration. If the calcium concentration is low, the laboratory value is typically confirmed by repeating the measurement with an ionized calcium level. This study is obtained to assess for a true decrease in serum calcium. Occasionally, your doctor will use a serum albumin level to calculate the corrected serum calcium concentration.
Once hypocalcemia is confirmed, you doctor will usually order additional tests to determine its cause. This normally includes a serum parathyroid hormone (PTH). They may also obtain a serum magnesium, phosphate, and vitamin D level.
How is Hypocalcemia treated?
The treatment of hypocalcemia depends on its severity and cause. Severe, symptomatic hypocalcemia (e.g., Calcium < 7.5 mg/dL) is typically corrected with intravenous calcium therapy.
Individuals with less severe hypocalcemia accompanied by mild symptoms are often treated with oral calcium supplements (e.g., calcium carbonate, calcium citrate). Common calcium supplement brands include Caltrate, Citracel, OsCal, and Tums. Patients with hypocalcemia due to kidney disease often requires correction of hyperphosphatemia with phosphate binders (PhosLo – calcium acetate) and repletion of low vitamin D levels. Those with coexisting hypomagnesemia should typically receive intravenous magnesium sulfate or oral magnesium supplementation.
Patients with vitamin D deficiency require vitamin D supplementation. Initial treatment often includes 50,000 international units of vitamin D2 or D3 weekly for 6-8 weeks, followed by 800-1000 international units of vitamin D3 daily. Most patients with hypoparathyroidism require calcium and vitamin D supplementation for their lifetime. Individuals with hypoparathyroidism that do not maintain adequate calcium levels with calcium and vitamin D supplements may benefit from therapy with Natpara (recombinant parathyroid hormone).
Hypocalcemia Patient Summary:
- Hypocalcemia is an electrolyte disorder characterized by low serum calcium levels.
- Common causes including chronic kidney disease, inadequate PTH production (hypoparathyroidism), vitamin D deficiency, and hypomagnesemia.
- Hypoparathyroidism may be caused by surgical removal of the parathyroid glands or due to autoimmune disease.
- Medications such as bisphosphonates for osteoporosis may also contribute to hypocalcemia.
- The symptoms of acute hypocalcemia include neuromuscular irritability and numbness/paresthesias around the mouth, hands, and feet. Muscle spasm is common.
- Severe cases result in laryngospasm, impaired cardiac function, seizure, and life-threatening cardiac arrhythmias.
- Severe, symptomatic hypocalcemia is corrected with intravenous calcium therapy.
- Less severe hypocalcemia accompanied by mild symptoms are often treated with oral calcium supplements. Common brands include Caltrate, Citracel, OsCal, and Tums.
- Hypocalcemia due to kidney disease often requires correction of hyperphosphatemia with phosphate binders (PhosLo – calcium acetate) and repletion of low vitamin D.
- Coexisting hypomagnesemia should be corrected with magnesium supplements.
- Patients with vitamin D deficiency require vitamin D supplementation.
- Most patients with hypoparathyroidism require lifelong calcium and vitamin D.
- Individuals with hypoparathyroidism refractory to calcium and vitamin D supplements may benefit from therapy with Natpara (recombinant parathyroid hormone).
- Hannan FM, Thakker RV. Investigating hypocalcemia. BMJ 2013; 346:f2213.
- Thakker R. Hypocalcemia: pathogenesis, differential diagnosis, and management. In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, American Society of Bone and Mineral Research 2006; 6:213.
- Riccardi D, Brown EM. Physiology and pathophysiology of the calcium-sensing receptor in the kidney. Am J Physiol Renal Physiol 2010; 298:F485.
The above information is an educational aid only. It is not intended as medical advice for individual conditions or treatments. Talk to your doctor, nurse or pharmacist before following any medical regimen to see if it is safe and effective for you.