Hypocalcemia resident survival guide

Hypocalcemia Resident Survival Guide
Diagnostic Criteria
Causes
Focused Initial Rapid Evaluation
Complete Diagnostic Approach
Dos
Don'ts

Main article: Hypocalcemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, M.D. [2]; Vidit Bhargava, M.B.B.S [3]; Ammu Susheela, M.D. [4]

Overview

Hypocalcemia is the lowering of serum calcium level in blood. Clinically it can present as acute or chronic hypocalcemia. It could be due to low level of calcium production or low calcium circulation. Hypoparathyroidism and vitamin D deficiency are the two most common causes of hypocalcemia. Acute hypocalcemia is treated with Intravenous calcium gluconate while chronic hypocalcemia is treated with oral calcium supplements and correcting the underlying cause.

Diagnostic Criteria

• About 50% calcium in serum is bound to proteins especially albumin. Hence serum albumin level is measured while evaluating for hypocalcemia.

• Normal level of total calcium is between 8.5-10.5 mgl/dl (2.12-2.62mmol/L). The normal range of ionized calcium is 4.65-5.25mg/dl(1.16 to 1.31 mmol/L).
• Hypocalcemia is defined as corrected serum total calcium level <8.5 mg/dl (2.12mmol/L)..
• It could be acute or chronic.

Causes

Common

• Surgery induced hypoparathyroidism.
• Autoimmune disease induced hypoparathyroidism.
• Malabsorption induced vitamin D deficiency.
• Vitamin D deficiency due to low dietary intake or exposure to ultraviolet light.

Rare

• Hypomagnesaemia.
• Vitamin D resistance.
• Sclerotic metastasis.
• Parathyroid hormone resistance.
• Autosomal dominant hypocalcemia.

Others

• Critical illness.
• Hungry bone syndrome after parathyroidectomy for hyperparathyroidism.
• Post high dose IV treatment with bisphosphonates in vitamin D deficient patients.
• Infusion of phosphates or calcium chelators, such as citrate, with massive blood transfusion.
• Fanconi syndrome.

• Post irradiation of parathyroid gland.

• Pseudohypoparathyroidism.

FIRE: Focused Initial Rapid Evaluation

Focused Initial Rapid Evaluation (FIRE) should be undertaken to identify patients requiring urgent intervention.

Symptomatic hypocalcemia is characterized by neuromuscular irritability, perioral numbness, carpopedal spasm, laryngospasm, paresthesia of hands and feet, focal or generalized seizures, diaphoresis, bronchospasm, billiary colic, cognitive impairment, personality disturbances, prolonged QT interval and ECG changes that mimic heart failure or myocardial infraction. Symptomatic hypocalcemia or serum calcium <7.6 mg/dL (1.9mmol/L) with unknown cause?

No

Yes

Proceed to Complete Diagnostic Approach

10ml of 10% solution of calcium gluconate is diluted in 50-500 ml of 5% dextrose and administered intravenously slowly over 10 minutes. An infusion of 10mg of the solution over 4-6 hours will serum calcium by 1.2-2mg/dl (0.3-0.5 mmol/l). Oral calcium supplementation should be given concurrently and 1 microgram/day of calcitriol is given if parathyroid is deficient.

Adjust the rate every 4 hours as required if symptoms persist or recur.

Complete Diagnostic Approach

Physical Examination

• Patient who develop gradual hypocalcemia may be completely asymptomatic while in those patient who has acute hypocalcemia can develop any of these following symptoms.

Characterize the symptoms: ❑ Neuromuscular excitability ❑ Muscle twitching. ❑ Tingling. ❑ Numbness. ❑ Muscle spasms. ❑ Tetany. ❑ Carpopedal spam. ❑ Seizures. ❑ Paresthesia. ❑ Perioral numbness. ❑ Laryngospasm. ❑ Neuropsychiatric symptoms. ❑ Cataract formation. ❑ Raised intracranial pressure. ❑ Prolonged QT intervals. ❑ Cardiac dyasarhythmia. ❑ Heart failure.

Obtain a detailed history: ❑ Age. ❑ Congenital defects of growth, mental retardation or hearing loss. ❑ Previous surgical history of neck surgery. ❑ List of medications. ❑ Family history of hypocalcemia.

Examine the patient: Vital signs ❑ Blood pressure ❑ Heart rate ❑ Tachycardia (suggestive of heart failure) ❑ Bradycardia (suggestive of heart block or bradyarrhythmias) Pulses ❑ Strength ❑ Bruits Skin ❑ Surgical marks on neck. Heart ❑ Heart sounds ❑ S3 (suggestive of heart failure) ❑ S4 (associated with conditions that increase the stiffness of the ventricle) Musculoskeletal system ❑ Chvostek sign ❑ Tapping on the cheek 2cm anterior to the earlobe, below the zygomatic process, overlying the facial nerve produces twitching of the upper lip. ❑ Trousseau sign ❑ Application of the inflated blood pressure cuff over the systolic pressure for 3 minutes produces carpopedal spasm

Order labs and tests: ❑ Basic Investigations ❑ Serum calcium (Corrected for albumin) ❑ Magnesium. ❑ Phosphate. ❑ Electrolytes. ❑ Alkaline phosphatase. ❑ Creatinine. ❑ Parathyroid hormone. ❑ 25-hydroxy vitamin D. ❑ Complete blood count. ❑ Serum pH. ❑ Further Investigations. ❑ 24-hour urinary phosphate, calcium, Magnesium and creatinine. ❑ Ionized calcium. ❑ Renal ultrasonography to asses for nephrolithiasis. ❑ 1,25-dihydroxyvitamin D. ❑ DNA sequencing to exclude genetic mutations. ❑ Biochemistry in first degree family members.

Low calcium, high phosphate and low parathyroid hormone indicate hypoparathyroidism. Goal of treatment is raise calcium levels and remove the symptoms. 1 to 1.5 g of elemental calcium is given orally as calcium carbonate or calcium citrate. 0.25 mcg of calcitriol is also given as twice daily with weekly increments to achieve low- normal serum calcium.

Family history of hypocalcemia can indicate the autosomal dominant hypocalcemia. Asymptomatic patients require no treatment.

Low calcium, low phosphate and low vitamin D levels may be due to vitamin D deficiency. 50,000 international units of vitamin D2 or D3 is given weekly for 6-8 weeks.

Symptomatic hypocalcemia with high blood urea nitrogen and serum creatinine indicates chronic kidney disease. Treatment includes oral calcium and active form of vitamin D

Hypercatabollic state(trauma, tumor lysis syndrome) requires the correction of phosphate levels before you correct the calcium level. Symptomatic hypocalcemia requires hemodialysis.

Pseudohypoparathyroidism requires 0.25 mcg of calcitriol for twice daily.

Treatment

Treatment of Acute Hypocalcemia ❑ Intravenous calcium (1 to 2 g of calcium gluconate is infused over 10-20minutes) is indicated for acute symptomatic hypocalcemia or asymptomatic hypocalcemia with corrected calcium less than 7.5mg/dl. It is continued until the patient is receiving oral calcium or vitamin D. ❑ For corrected calcium greater than 7.mg/dl, oral calcium is administered. ❑ For vitamin D deficiency or hypoparathyroidism, long term management include addition of vitamin D. ❑ If concurrent hypomagnesemia is there, 2 g of Magnesium sulphate is infused over 10-20 minutes as 10 percent solution. It should be followed by 1g in 100 ml of fluid per hour. It is continued as long as serum magnesium level is below 0.8mEq/l. Treatment of mild or chronic hypocalcemia ❑ Oral calcium ❑ Vitamin D analog ❑ Calcitriol

Dos

• Serum calcium concentrations should be measured frequently during pregnancy and lactation.
• In patients with hyper or hypoalbuminemia, the serum calcium measured must be corrected for the standard units and abnormality in albumin.
• In patients with asymptomatic hypocalcemia, repeated measurement of the ionized calcium or total serum calcium corrected for albumin must be done to determine whether there is a true decrease in calcium.
• As concentrated calcium can cause vein irritation, calcium should be diluted in water or dextrose and saline before IV administration in acute symptomatic hypocalcemia.
• For hypoparathyroidism, urinary and serum calcium and serum phosphate are measured weekly until stable levels are achieved.
• For hypoparathyroidism induced hypocalcemia, urinary calcium excretion is measured periodically to check for hypercalciuria and dose of calcium and vitamin D is reduced if needed.

Don'ts

• Do not administer IV calcium gluconate for mild or chronic hypocalcemia.
• Don't take the total serum calcium with high or low serum albumin as an estimate of hypocalcemia.
• IV calcium gluconate should not contain phosphate or bicarbonate as it can form insoluble calcium salts. If they are needed, they must be administered through separate limbs.
• Acute hypocalcemia and hyperphosphatemia induced by hypercatabolic states (such as tumor lysis syndrome or massive trauma) should not be treated with calcium until the hyperphosphatemia is corrected to prevent the precipitation of calcium phosphate.

References