sustained release verapamil
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2007 ◽  
Vol 16 (5) ◽  
pp. 520-518 ◽  
Author(s):  
Nirav P. Patel ◽  
Meredith E. Pugh ◽  
Steven Goldberg ◽  
Glenn Eiger

A 49-year-old woman was brought to the emergency department because of an intentional overdose of sustained-release verapamil along with captopril and glyburide. The estimated interval between ingestion and the time she was found was several hours. Initial findings were blood pressure 72/39 mm Hg, heart rate 32/min, and a score of 9 on the Glasgow Coma Scale. She was intubated and given intravenous fluid and vasopressor support. Decontamination with activated charcoal was instituted. Administration of dopamine and norepinephrine, atropine, sodium bicarbonate, and calcium chloride did not yield significant clinical improvement. Hyperinsulinemic euglycemia therapy was started: a bolus of regular insulin then infusions of insulin and 10% dextrose. After 24 hours of therapy, the bradycardia resolved and the patient’s hemodynamic condition stabilized with normalization of cardiac indices. On day 5 the patient was transferred to the medical unit, and on day 8 she was discharged to psychiatric care.


2003 ◽  
Vol 22 (9) ◽  
pp. 515-521 ◽  
Author(s):  
A Tracqui ◽  
C Tournoud ◽  
P Kintz ◽  
M Villain ◽  
C Kummerlen ◽  
...  

A fatality involving verapamil, a calcium channel blocker agent, is presented. A 51-year old male ingested 7200 mg of sustained-release (SR) verapamil at T0 and died 40 hours later of refractory, mixed shock and multiorgan failure. The symptoms displayed during hospitalization were quite typical and involved altered consciousness, hypotension, bradycardia, atrioventricular block, metabolic acidosis and renal failure. Verapamil and its primary metabolite, norverapamil, were assayed on eight plasma and two urine samples, successively taken between the admission to the ICU (T0-4 hours) and time of death, using an original high-performance liquid chromatography/mass spectrometry (HPLC/MS) procedure with verapamil-d3 as internal standard. Plasma verapamil and norverapamil levels on admission were 0.94 and 1.36 mg/mL, respectively, then verapamil remained practically unchanged throughout the hospitalization (0.85 mg/mL at T0-40 hours). The discussion focuses on the detrimental role of SR formulations in overdose, with special emphasis on the risk of pharmacobezoar development already reported with SR-verapamil. To our knowledge, this is the first report of a verapamil fatality documented by repeated plasma measurements of the drug during the antemortem period.


1997 ◽  
Vol 31 (5) ◽  
pp. 593-595 ◽  
Author(s):  
Liubov Ben-Noun

OBJECTIVE: TO describe a patient with asymptomatic bronchial asthma and hypertension who developed an acute asthma attack after receiving sustained-release verapamil. CASE SUMMARY: A 66-year-old white woman with a 10-year history of hypertension and bronchial asthma was switched from immediate-release verapamil hydrocloride 40 mg tid to sustained-release verapamil 240 mg/d po for better hypertension control. After taking the first tablet, she developed dyspnea, cough, and wheezing. Antiasthmatic medications were prescribed, but the asthma symptoms did not improve. She continued taking verapamil for 6 months, then, on her own, stopped all medications including the sustained-release verapamil, and her asthma symptoms disappeared. On rechallenge she developed severe dyspnea, cough, and wheezing 20 minutes after administration. The asthma resolved within 24 hours following three albuterol inhalations. The next day similar symptoms developed with rechallenge of the same brand of sustained-release verapamil in a 120-mg formulation, and verapamil was discontinued. Six months later she was again prescribed sustained-release verapamil 240 mg in another clinic where the physician was unaware of her previous reaction. Once again, severe dyspnea, cough, and wheezing developed. DISCUSSION: On four separate occasions the patient was challenged, advertently or inadvertently, with sustained-release verapamil. Similar symptoms developed after each challenge and resolved after discontinuing this preparation. Although dyspnea associated with verapamil administration has been reported, this is the first report of an elderly asymptomatic asthmatic patient with hypertension who developed an acute asthma attack following sustained-release verapamil administration. CONCLUSIONS: Sustained-release verapamil is thought to be the cause of the asthma attack in this patient because she was not taking any other preparations; the symptoms started with the administration of sustained-release verapamil and were relieved after its discontinuation.


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