Hypo/hypercalcemia

1. Description of the problem

What every clinician needs to know

Calcium regulation is critical for normal cell function, neural transmission, membrane stability, bone structure, blood coagulation and intracellular signaling. In the blood, about half of all calcium is bound to proteins such as albumin, but it is the unbound, or ionized, calcium that the body regulates. If a person has abnormal levels of blood proteins, then the plasma calcium may be inaccurate. The ionized calcium level is considered more clinically accurate in this case. Only 5-10 minutes of direct sunlight on hands and face meet daily Vitamin D requirement.

Severe hypocalcemia can rarely present as laryngospasm (stridor).
Hypomagnesemia causes this by causing end organ unresponsiveness to PTH.
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GNR sepsis thought to cause macrophage activation that produce cytokines that impair Vitamin D and PTH effectiveness (or the lasix you’re giving them to help with volume overload).
No IV calcium for digoxin toxicity.
Corrected Serum Calcium (to account for hypoalbuminemia)
corrected Ca = measured Ca + [ (4- albumin concentration) x 0.8]
In setting of hypoventilation: for every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. Hypocalcemia related to alkalosis is partially responsible for the cerebral vasoconstriction that produces lightheadedness and paresthesias or tetany.

Clinical features

Hypocalcemia

1. Perioral paresthesia, tingling of fingers and toes, spontaneous tetany, elicited tetany (Chovstek and Trousseau-as below), seizures, laryngospasm, arrhythmias.

Trousseau sign: eliciting carpal spasm by inflating a blood pressure cuff and maintaining the cuff pressure above systolic
Chvostek sign: tapping of the inferior portion of the zygoma will produce facial spasms.

Hypercalcemia

Symptoms: lethargy, weakness, vomiting, anorexia, constipation, HTN.

Most common associated feature is dehydration (excess Calcium impairs kidney’s response to ADH resulting in loss of free water.

Key management points

Evaluate airway, breathing, circulation: evaluate for evidence of abnormal rhythm or laryngospasm.
Draw baseline labs including albumin, ionized calcium, phosphorus, and PTH.
Consult endocrinology.
Admit to floor vs. PICU depending on severity.

2. Emergency Management

Symptomatic hypocalcemia

Laryngospasm and cardiac arrhythmias are two major life threatening conditions.

Treat with IV calcium – calcium gluconate diluted out if given through peripheral IV. If central access available, administer calcium chloride.

These are preferred routes. If one form is not readily available will need to replete with alternative form.

If underlying condition is chronic then rapid push of calcium can be fatal, given the body has acclimated to lower baseline level overtime.

If persistently symptomatic start a calcium drip preferably through central venous line.

Check magnesium level: important co-factor for parathyroid hormone release and for calcium reabsorption in the kidney.

Check phosphorus: if high could be binding calcium peripherally (calcium phosphorus product).

Symptomatic hypercalcemia

a) NS 10-20 cc/kg IV over 1 hour and keep urine output ~ 2-3 cc/kg/hr (Na excretion causes Ca excretion).

b) Lasix 0.5-1 mg/kg IV q 2-4 hours for diuresis (once hydrated).

c) Hydrocortisone 1-2 mg/kg IV QD and taper if sarcoidosis, vitamin A and D intoxication, leukemia.

d) Mithramycin 25 mcg/kg/day IV over 3-4 days.

e) Calcitonin 4 units/kg IM/SQ q12; may increase up to 8 units/kg q12 to max of q6 hrs (common tachyphylaxis limits utility).

f) Etidronate 7.5 mg/kg/day IV over 2 hours for 3-7 days.

g) Gallium nitrate 200 mg/m² per liter NS over 5 days.

h) Consider dialysis

3. Diagnosis

Hypocalcemia diagnosis:

Obtain serum calcium level, albumin, phosphorus, and PTH level simultaneously

Guiding rule: If phosphorus is up then deficient PTH effect; if phosphorus is low then excess PTH.

Hypocalcemia differential diagnosis

a. Early neonatal hypocalcemia (< 72 hrs of life):

i. prematurity, birth asphyxia (lots of cell death causing massive phosphorus release prompting fall in Ca ~ similar pathophysiology to tumor lysis syndrome)

ii. infants of diabetic mothers (parathyroid impairment)

b. Late neonatal hypocalcemia (5-10 days of life)

i. often related to phosphorus load or hypomagnesemia (used to be a problem due to old types of formula or cow’s milk with high phosphorus)

c. Childhood

i. PTH deficiency, vitamin D Deficiency, vitamin D resistance

ii. Vitamin D deficiency is being linked as a contributing factor to many disorders from asthma to sepsis. Its relationship to cathelcidin, a component of innate immunity, has generated further interest.

Hypercalcemia diagnosis

Hypercalcemia is defined as a free ionized calcium level greater than 6.0 mg/dl (normal level 4-6 mg/dl), or a serum calcium concentration less than 10.5 mg/dl (normal level 8.5-10.5 mg/dl).

Differential diagnosis of hypercalcemia includes

Williams Syndrome – elfin facies, supravalvar aortic stenosis.
Familial hypocalciuric-hypercalcemia – excess PTH due to defect in calcium-sensing receptor (normally inactivates PTH)
Hyperparathyroidism
Malignancy
Hypervitaminosis D – treatment = glucocorticoids b/c impair action of Vitamin D on bone and gut
Hypervitaminosis A – increases bone resorption
Immobilization (common after leg injuries, SCI, and burns)
Adrenal insufficiency
Hyperthyroidism

4. Specific Treatment

Hypocalcemia treatment

1. In general, treat serum levels less than 7.5 in neonate or less than 8 in older child to prevent development of tetany

2. Symptomatic: (beware IV calcium can cause arrhythmia and is caustic).

a. Ca gluconate 20 mg/kg elemental calcium

b. Ca chloride 20 mg/kg (use this in codes because gluconate can’t be metabolized by liver).

3. Asymptomatic:

a. Young child: calcium glubionate (tastes good) 100 mg/kg/day divided Q6.

b. Older child: Oral Tums 50 mg/kg/day div TID-QID.

4. Treatment will vary based on clinical setting:

a. i.e. cardiogenic shock will aim to keep iCa greater than 4.5/5.

5. Therapy:

a. Calcium gluconate 10% 60-100 mg/kg IV over 1 hour (Ca⁺²may potentiate digoxin).

b. CaCl₂10%: 20 mg/kg over 15-20 minutes; ü for Mg⁺²and ¯K⁺.

c. Calcium gluceptate: 200-500 mg/kg/day IV divided every 6 hours.

Hypercalcemia treatment

Refractory cases: consider continuous veno-venous hemofiltration for hypercalcemia until underlying etiology can be controlled.

Hypercalcemic crisis due to hyperparathyroidism: somnolence, coma, and renal failure may require emergent removal of parathyroid gland.

5. Disease monitoring, follow-up and disposition

Serum calcium levels should be evaluated serially. Endocrinology consultation is important for evidence of underlying chronic abnormalities.

Pathophysiology

Pathophysiologic etiology of hypocalcemia and hypercalcemia is based on the underlying condition as noted in the section above on differential diagnosis.

Epidemiology

Good epidemiologic data does not exist defining incidence of this particular electrolyte disorder.

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