Noncardiogenic pulmonary edema has not been (to our knowledge) previously reported associated with a verapamil overdose.

Noncardiogenic pulmonary edema has not been (to our knowledge) previously reported associated with a verapamil overdose. We describe a 27-year-old woman who discloseed this complication after an overdose of 15 120-mg verapamil tablets (total of 1800 mg) This report illustrates the possibility of serious pulmonary embarrassment in the course of a verapamil overdose and the ne to avoid excessive crystalloid administration during the hypotensive period.

Verapamil, a strong calcium channel antagonist, possesses various systemic consequences including smooth muscle relaxation, negative dormotropism and inotropism, and decreased insulin release from pancreatic beta cells[1-6] Reported clinical complications of verapamil overdosage have included hypotension, sinus arrest, atrioventricular fill up asystole, decreased cardiac output, and hyperglycemia.[7-11]

In this report, we describe a patient with noncardiogenic pulmonary edema who ingested a toxic amount of verapamil, an association, to our knowledge, not previously reported.

CASE REPORT

A 27-year-old healthy woman was brought to the hospital 5 h after ingesting 15 120-mg verapamil tablets (total of 1800 mg Calan, GD Searle & Company, Chicago), 4 g of ibuprofen, and 10 tablets of a combination of acetaminophen, butalbital, and caffeine (Fioricet, Sandoz Pharmaceuticals Corporation, East Hanover, NJ) She was alert and oriented; the systolic BP was 70 mm Hg; vibration 62 beats per minute; and respirations, 24 breaths through minute. The pupils were equal and responsive, and examination of the chest and cardiac and neurologic evaluations were within normal limits. The ECG revealed junctional rhyme with a rate of 60/min, and was otherwise normal. The arterial family gas values with the patient breathing 3 L of oxygen administered nasally were pH 711; [PCOsub2] 27 mm Hg; and [POsub2] 68 mm Hg (Table 1) The diabetic sugar level was 1,157 mg/dl. In the strait room, 6.5 L of 09 percent normal saline solution and 10 ml of 10 percent calcium chloride was given intravenously. The BP dropp to 52/39 mm Hg and with the use of dopamine it rose to 79/63 mm Hg After 18 h of steady improvement, the arterial life-current gas values were as follows: pH 730; [PCOsub2] 29 mm Hg; and [POsub2] 98 mm Hg She then bring outed progressive dyspnea and repeat arterial posterity gas values revealed pH, 737; [PCOsub2] 33 mm Hg; [POsub2] 51 mm Hg with the patient forward a 100 percent nonrebreathing mask. Diffuse bilateral air space disease was seen onward a chest radiograph (Fig 1) A two-dimensional transthoracic echocardiogram showed normal left ventricular size and function. She was then intubated, and mechanical ventilation was instituted. Right heart hemodynamics showed pulmonary artery press 35/20 mm Hg; pulmonary capillary wedge hurry 9 mm Hg; and thermodilution cardiac output 71 L/min. Broad-spectrum antibiotics were begun because she had a febrile affection (temperature, 38.3 [degrees] C). With continuous ventilatory support and administration of diuretics, the arterial kin gas values and chest radiograph improved, she became afebrile, and was extubated. life-blood sputum, and urine cultures showed no sprouting Drug urine screening was trace-positive for barbiturates and acetaminophen. The serum verapamil of the same height 24 h after admission was 135 ng/ml (therapeutic flat 80 to 300 mg/ml). The chest radiograph taken at the time of discharge was unrestrained of all infiltrates.

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DISCUSSION

This patient demonstrates a caase of noncardiogenic pulmonary edema after massive ingestion of verapamil. Noncardiogenic pulmonary edema was documented on bilateral diffuse pulmonary infiltrates in succession a chest radiograph with normal pulmonary capillary wedge hurry and thermodilution cardiac output. The signs and symptoms of noncardiogenic pulmonary edema resolv with conservative management and assited ventilation for 72 h

There appear to be several potential etiologies of this patient's noncardiogenic pulmonary edema. postponeed hypotension and shock-like state may have contributed to the increase of this syndrome.[12,13] However, there are several reports of verapamil overdose with similar severity of hypotension further without development of overt pulmonary edema.[8,10,14] Additionally, an ibuprofen overdose elicits numerous toxic reactions nevertheless pulmonary edema has not been reported in rather large form into groupss of patients with pure ibuprofen overdose.[15,16] An infectious etiology was rul revealed by the negative culture of the endotracheal aspirate.

the pair cardiogenic and noncardiogenic pulmonary edema have been reported after an overdose of diltiazem and nifedipine,[17,18] and pulmonry congestion has been ascertained at autopsy in a patient who died after an overdose of verapamil.[19] These reports have attributed the pulmonary edema to the negative inotropic issues of these medications or excessive fluid resuscitation during hypotension.[18,20]

Multiple cellular mechanisms appear to be responsible for the progression in a continuously ascending gradation of noncardiogenic pulmonary edema after overdoses of calcium channel blocker First, prostaglandins have been shown to play an important part in maintaining cellular integrity, especially during lung inflation.[21,22] It has been noted that nifedipine inhibits prostacyclin release in answer to high-dose calcium infusion.[23] If prostaglandins normally shelter the cellular membranes, loss of this event with excessive concentrations of calcium channel blocker may lead to a leaky capillary syndrome Secondly calcium channel blocker cause systemic precapillary vasodilation and peripheral edema proper to their effect on vascular flat muscle.[24] This mechanism may be involved in pulmonary capillary transudation and increase of pulmonary edema. Finally, it has been shown that the pulmonary vasodilatory efficiency of calcium antagonists may lead to perfusion-ventilation mismatch and hypoxemia.[25]

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