Clonazepam/verapamil overdose
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Various toxicities: case report A 44-year-old woman developed hypotension, bradycardia, slurred speech, altered mental status, increase in aspartate aminotransferase levels, mitral valve regurgitation and acute respiratory distress syndrome (ARDS) secondary to drug intoxication following an overdose of verapamil with the intent to commit suicide. Additionally, an overdose of clonazepam also contributed in the development of these reactions. The woman previously ambulatory and healthy presented to the emergency department following an overdose of extendedrelease verapamil 125mg (60 tablets) and clonazepam 0.25mg (90 tablets) [routes not stated] with the intent to commit suicide. It was reported that, she had been receiving clonazepam for restless leg syndrome (RLS) and verapamil for migraine prevention. The number of pills she took was provided via self-report. At presentation, she was bradycardic and hypotensive with altered mental state and slurred speech. Physical examination revealed that she was sedated with heart rate (HR) of 46, BP of 80/40, Glasgow coma score (GCS) of 12/15 (E3, V4, M5) and respiratory rate of 16. Her pulse was regular and slow with no S3 or S4 gallop. Systemic examination of her cardiorespiratory system was unremarkable with lungs clear to auscultation and no new/changed murmurs. For airway protection, she was emergently sedated and intubated. After the consultation with poison control, the woman underwent aggressive fluid resuscitation followed by treatment with calcium gluconate, calcium chloride and atropine. To combat calcium channel blocker overdose, she also received an additional treatment with lipid emulsion therapy, dextrose, insulin and glucagon. Her vasopressor support consisted of norepinephrine, epinephrine and dopamine. Due to unstable bradycardia, a temporary pacemaker was placed. Thereafter, she was started on mechanical ventilation with permissive hypercapnia and low tidal volume ventilation. After ventilation (with 100% fraction of inspired oxygen), her blood gas analysis revealed partial pressure of carbon dioxide (PCO2) of 32, partial pressure of oxygen (PO2) of 169 and pH of 7.37. Her initial laboratory tests revealed creatinine of 1.05, blood glucose of 156 mg/dL and an estimated glomerular filtration rate of 57 mL/min. Her urine drug screen was positive for benzodiazepines and negative for the other drugs. Liver function test revealed mild elevation in aspartate aminotransferase levels. Her initial chest x-ray demonstrated left basilar atelectasis. Chest xray performed on day 3 of the hospitalisation showed extensive and patchy geographic regions of airspace opacities in the majority of her lungs with sparing of apices, which was indicative of ARDS. ECG showed a prolonged QRS of 122ms and junctional rhythm with rates of 42, indicative of sinus rhythm with atrioventricular dissociation and wide QRS rhythm. Transthoracic 2D echocardiography showed normal systolic function of both the right and the left ventricle and normal morphology with an ejection fraction of 6
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