Pathophysiology

Metabolic and endocrine emergencies require an understanding of normal physiology.

Calcium regulation is maintained by parathyroid hormone (PTH), vitamin D, and calcitonin through complex feedback loops. These compounds act primarily at bone, renal, and GI sites. Calcium also is affected by magnesium and phosphorus.

History

• The patient may complain of muscle cramping, shortness of breath secondary to bronchospasm, tetanic contractions, distal extremity numbness, and tingling sensations.
• Chronic manifestations include cataracts, dry skin, coarse hair, brittle nails, psoriasis, chronic pruritus, and poor dentition.
• Acute hypocalcemia may lead to syncope, congestive heart failure (CHF), and angina due to the multiple cardiovascular effects.
• The patient's past medical history should be explored for pancreatitis, anxiety disorders, renal or liver failure, gastrointestinal disorders, and hyperthyroidism or hyperparathyroidism.
• The patient may have a recent history of thyroid, parathyroid, or bowel surgeries or recent neck trauma.
• Inquire about recent radiocontrast, estrogen, loop diuretics, bisphosphonates, calcium supplements, antibiotics, and anti-epileptics.
• Evaluate for appropriate dietary intake.

Physical

Neuromuscular and cardiovascular findings predominate. Neural hyperexcitability due to acute hypocalcemia causes smooth and skeletal muscle contractions. The patient should be examined for the following:

• Dry skin and psoriasis (if long-term hypocalcemia)
• Perioral anesthesia, cataracts, papilledema, and laryngeal stridor
• Scars over thyroid region
• Recent trauma or surgery to the neck
• Cardiopulmonary effects

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• Wheezing, dysphagia, stridor, bradycardia, rales, and S₃ may be noted.
• Acute hypocalcemia causes prolongation of the QT interval, which may lead to ventricular dysrhythmias. It also causes decreased myocardial contractility, leading to CHF, hypotension, and angina. Cardiomyopathy and ventricular tachycardia may be reversible with treatment.
• Smooth muscle contraction may lead to laryngeal stridor, dysphagia, and bronchospasm.
• Smooth muscle contraction causes biliary colic, intestinal colic, and dysphagia.
• Diarrhea and/or gluten intolerance (celiac sprue) may result in significant malabsorption and electrolyte abnormalities.
• Preterm labor or detrusor dysfunction may result from smooth muscle contraction.
• Peripheral nervous system findings include tetany, focal numbness, and muscle spasms.
• Classic peripheral neurologic findings include the Chvostek sign and Trousseau sign.

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• Chvostek sign: Tap over the facial nerve about 2 cm anterior to the tragus of the ear. Depending on the calcium level, a graded response will occur: twitching first at the angle of the mouth, then by the nose, the eye, and the facial muscles.
• Trousseau sign: Inflation of a blood pressure cuff above the systolic pressure causes local ulnar and median nerve ischemia, resulting in carpal spasm.
• Irritability, confusion, hallucinations, dementia, extrapyramidal manifestations, and seizures may occur.

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• Calcification of basal ganglia, cerebellum, and cerebrum may occur.
• Seizures often occur in individuals with preexistent epileptic foci when the excitation threshold is lowered.

Causes

The causes of hypocalcemia include hypoalbuminemia, hypomagnesemia, hyperphosphatemia, multifactorial enhanced protein binding and anion chelation, medication effects, surgical effects, PTH deficiency or resistance, and vitamin D deficiency or resistance.

Prehospital Care

Standard advanced cardiac life support (ACLS) procedures should be initiated in the patient whose condition is unstable. No specific therapy, other than supportive care, is recommended.

Emergency Department Care

Most hypocalcemic emergencies are mild and require only supportive treatment and further laboratory evaluation. On occasion, severe hypocalcemia may result in seizures, tetany, refractory hypotension, or arrhythmias that require a more aggressive approach.

• Mild hypocalcemia (when symptoms are not life threatening)

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• Confirm ionized hypocalcemia and check other pertinent laboratory tests.
• If the cause is not obvious, send for a PTH level.
• Depending on the PTH level, the endocrinologist may do further laboratory workup, particularly an evaluation of vitamin D levels.
• Oral repletion may be indicated for outpatient treatment; patients requiring intravenous (IV) repletion should be admitted. (Recommended dose of elemental calcium in healthy adults is 1-3 g/d.)
• Severe hypocalcemia (life-threatening symptoms)

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• Supportive treatment often is required prior to directed treatment of hypocalcemia (ie, IV replacement, oxygen, monitoring). Be aware that severe hypocalcemia often is associated with other life-threatening conditions.
• Check ionized calcium and other pertinent screening laboratory tests.
• IV replacement is recommended in severe cases. Doses of 100-300 mg of elemental calcium (calcium gluconate – 10 mL contains 90 mg elemental calcium; calcium chloride – 10 mL contains 272 mg elemental calcium) should be given over 5-10 minutes. This dosage raises the ionized level to 0.5-1.5 mmol and should last 1-2 hours. Caution should be used when giving CaCl intravenously (see Medication).
• Calcium infusion drips should be started at 0.5 mg/kg/h and increased to 2 mg/kg/h as needed, with an arterial line placed for frequent measurement of ionized calcium.

Consultations

Depending on the clinical situation, multiple consultations may be necessary, including internist, endocrinologist, intensivist, surgeon, oncologist, nephrologist, dietitian, and/or toxicologist.

Date: 2015-01-12; view: 947