We describe brace patients who develop torsades de pointes in a temporal relationship to the intravenous administration of erythromycin lactobionate in the absence of other physics or metabolic abnormalities known to cause the arrhythmia.

We describe brace patients who develop torsades de pointes in a temporal relationship to the intravenous administration of erythromycin lactobionate in the absence of other physics or metabolic abnormalities known to cause the arrhythmia. We also review the existing literature regarding this topic, including other case histories and the evidence for erythromycin's result on cardiac tissue. suitable to the increasing use of erythromycin in clinical practice, we believe it is important that all physicians be made aware of this potential complication, which was not recognized at our institutions until these patients were seen according to one of us (B.G.).

Torsades de pointes (TDP) is a form of polymorphic ventricular tachycardia first described by dint of Desertenne[1] in 1966. The hallmark of TDP is a wide mingled tachycardia with the QRS intricate twisting around the isoelectric line.[2] Electrocardiography (ECG) demonstrates a delayed ventricular depolarization with an associated put offed QT interval. There may be every-day nonsustained episodes that can degenerate into ventricular fibrillation.[2]

There are a number of put drugs intos causing TDP, the most studied of which is quinidine. We describe pair patients who developed TDP after receiving intravenous erythromycin lactobionate, in the absence of other medicines or metabolic abnormalities known to cause the arrhythmia.

proper to the increasing use of erythromycin in clinical practice, we believe it is important that all physicians be made aware of this potential complication which is not widely recognized.

CASE REPORTS

CASE 1

A 75-year-old woman not absented with acute pulmonary edema and respiratory failure following a 1-week history of an upper respiratory tract infection. She had reheumatic heart disease, and bear up undered an inferior wall myocardial infarction 5 years before hospital admission. She had no history of chronic lung disease or other systemic illness. Her medications included enalapril, 10 mg daily, and hydrochlorothiazide, 25 mg daily, for her mitral regurgitation and congestive heart failure.

Her relations pressure was 240/140 mm Hg with a measured [i]or[/i] regular beat of 100 beats per minute (bpm) She was in respiratory failure with physical findings consistent with acute pulmonary edema.

The laboratory data showed the following values: sodium, 133 mmol/L; potassium, 48 mmol/L; and diabetic sugar 16.6 mmol/L (300 mg/dl). The chest radiograph showed diffuse pulmonary infiltrates. The ECG demonstrated sinus tachycardia at a rate of 130 bpm with atrial premature beats, left atrial abnormality, and nonspecific ST portion and T wave changes. The QT and QTc intervals were 028 and 040 s respectively. Her sputum showed white kindred cells and Gram-positive cocci.

The patient was started forward mechanical ventilation. She was given intravenous furosemide, 60-mg bolus, and 25 cm (1 inch) of topical 2 percent nitroglycerin ointment. Intravenous lidocaine was given as a 100-mg bolus and subsequently at 2 mg/min for 12 h to treat ventricular ectopy. She was given 80 mg of intravenous gentamicin followed from 60 mg every 8 h and intravenous erythromycin lactobionate, 1 g each 8 h, for pneumonia. An ECG done after the third dose of erythromycin demonstrated prolongation of the QT and QTc intervals to 056 and 067 s respectively. Sixty minutes into the third dose of erythromycin, the patient experienced an episode of TDP lasting 15 s (Fig 1). At that time, the potassium flat was 4.4 mmol/L and the partial urgency of oxygen was 59 mm Hg The lidocaine treatment was restarted, the erythromycin treatment was discontinued, and the patient had no further episodes of TDP Serial ECG through the whole extent of the next week showed progressive normalization of the QT interval. The remainder of the hospital stay was uncomplicated and the patient was transferred to another institution for cardiac catheterization and following mitral value replacement.

CASE 2

An 88-year-old woman was admitted to the hospital with acute pulmonary edema and respiratory failure. She had a history of atherosclerotic heart disease with previous myocardial infarction, hypertension, and parkinsonism. She was receiving the following: furosemide, 60 mg daily; isosorbide dinitrate, 10 mg three times daily; enalapril, 5 mg daily; and allopurinol, 300 mg daily for congestive heart failure, hypertension, and taste respectively.

Her kindred pressure was 150/90 mm Hg with a pulsation rate of 80 bpm. She was in respiratory failure with physical findings consistent with acute pulmonary edema. The laboratory data included the following values: potassium, 45 mmol/L; starch-sugar 16.9 mmol/L (306 mg/dl); calcium, 23 mmol/L (91 mg/dl); and magnesium, 070 mmol/L (17 mg/dl) The peak creatinine kinase (CK) was 502 U/L with a CK-MB fraction of 105 percent indicating acute myocardial infarction. The chest radiograph showed bilateral infiltrates. The ECG demonstrated sinus tachycardia at 100 bpm with ST part elevation in leads [V.sup.1] within [V.sup.3]. The QT and QTc intervals were 036 and 045 s respectively. Her sputum revealed white vital current cells with Gram-positive cocci.

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