A 12 y/o male presents with new onset acute renal failure.
Q1. What does the EKG show?
Q2. What are potential causes?
A1. Prolonged QT interval (QTc 565 ms)
A2. This patient had hypocalcemia (Ca=5).
There are many other possible causes of prolonged QT including inherited syndromes, hypokalemia, hypomagnesemia, myocarditis, and medications (e.g., procainamide, erythromycin, cyclic antidepressants, phenothiazines, quinidine, organophosphates). Individuals with QTc intervals longer than 0.55 second have a higher risk of sudden death. Prolongation of the QT interval predisposes the individual to ventricular tachycardia, torsades de pointes, and ventricular fibrillation, which is often initiated by a premature ventricular contraction occurring during the prolonged repolarization phase.
Treatment of a prolonged QT interval depends on the cause. Correction of any underlying metabolic disorder and discontinuation of a medication that induced the prolongation of the QT interval are the easiest therapies to implement. Magnesium sulfate is the drug of choice in the treatment of torsades de pointes. Antidysrhythmic agents that also can prolong the QT interval, such as procainamide and amiodarone, should be avoided. Therefore, the safest medication to use in a patient with prolonged QT interval–induced ventricular tachycardia or fibrillation is lidocaine. Beta-blockers have been used to prevent sudden ventricular dysrhythmias in those patients with the familial forms of QT prolongation. Adjunctive treatment in these selected patients also includes the insertion of pacemakers or internal defibrillators. (Horeczko,Inaba.Cardiac Disorders. In Rosen’s Emergency Medicine, 8th ed. Chapter 171, p. 2166-67.)
Although there are many clinical manifestations of hypocalcemia, neuromuscular and cardiovascular findings predominate. Severe, symptomatic hypocalcemia may result in cardiovascular collapse, hypotension, and dysrhythmias. Clinically evident hypocalcemia generally is manifested in milder forms and is usually the result of a chronic disease state. The patient may complain of muscle cramping, perioral or finger paresthesias, shortness of breath secondary to bronchospasm, and tetanic contractions. More severe symptoms include hypotension, QT prolongation, angina, and CHF. Chronic hypocalcemia may be manifested with cataracts, poor dentition, dry skin, coarse hair, and pruritus. Chvostek's sign may be present: when the examiner taps the facial nerve, facial or eye muscle twitching will be elicited. Trousseau's sign may also be present: when the examiner inflates the blood pressure cuff to 20 mmHg above the systolic blood pressure for 3 minutes, carpal spasms will be induced because of local ulnar and median nerve ischemia. Trousseau's sign is relatively specific for hypocalcemia, whereas Chvostek's test is less diagnostic.
Most asymptomatic patients and those with mild symptoms can be treated with oral calcium supplementation, such as calcium carbonate. Intravenous calcium is administered, either as calcium chloride or calcium gluconate, to patients with moderate to severe symptoms; 100 to 300 mg of elemental calcium given during 5 to 30 minutes will raise the ionized calcium level 0.5 to 1.5 mEq. Calcium chloride contains 272 mg of elemental calcium but can be caustic to veins and thus should be given only to critically ill hypocalcemic patients who require calcium urgently. It is best given through a central line. Calcium gluconate contains 92 mg of elemental calcium. Although this is one-third the amount contained in calcium chloride, it is safer to administer and can be given peripherally. Most patients requiring intravenous calcium should be admitted to the hospital for monitoring and treatment of nausea, vomiting, hypertension, and bradycardia.
(Pfennig, Slovis. Electrolyte Disorders. In Rosen’s Emergency Medicine, 8th ed. Chapter 125, p. 1646-7.)