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Various toxicities: case report A 56-year-old woman developed cardiotoxicity and acute and isolated right ventricular (RV) failure following overdose of methadone in a suicide attempt. Additionally, she exhibited lack of efficacy during treatment with naloxone for methadone overdose. The woman had a significant medical history of seizure disorder on levetiracetam, chronic hepatitis C infection, chronic obstructive pulmonary disease and major depression. She had been receiving methadone 60 mg/day maintenance therapy for chronic back pain and opiate addiction. She ingested a total of 2.4g of methadone in a suicidal attempt, which was witnessed by her husband at her home. As the paramedics arrived roughly 30 minutes following the witnessed overdose, she was unresponsive, her pupils were pinpoint, heart rate was 96 beats per minute, Glasgow Coma Scale Score was 7, respiratory rate was 12 breaths per minute, BP was 101/69mm Hg, blood glucose level was 157 mg/dL and oxygen saturation was 96%. The woman was treated with a total of 3 doses of naloxone, 1mg each, without any response. For airway protection, she underwent endotracheal intubation. On arrival to the emergency department, her body temperature was 36.1°C, BP was 79/46mm Hg, heart rate was 120 beats per minute, oxygen saturation was 97% and respiratory rate was 16 breaths per minute. On physical examination, she was unresponsive. Her skin was mottled and cold, and her jugular venous pressure was elevated 15cm H2O above the sternal angle level. Her peripheral pulses were regular but weak. The laboratory values were remarkable for elevated high-sensitivity troponin I and B- type natriuretic peptide. Urine and serum drug screen was found to be positive for methadone, but negative for ethyl alcohol, other opiates and cocaine. Arterial blood gas revealed mild metabolic acidosis. CT angiography (CTA) scan of the chest revealed mild dilatation of the right ventricle. Serial ECGs revealed prolonged corrected QT (QTc) intervals and sinus tachycardia, but no significant ischaemic changes. The initial transthoracic echocardiography (TTE) revealed dilated RV with severe systolic dysfunction and relative preservation of contractility at the apex compared with the basal segments. The tricuspid regurgitation doppler waveform was incomplete and not sufficient for the estimation of the RV systolic pressure. A TTE, which was performed 3 months prior to this presentation, for evaluation of atypical chest pain, did not reveal any RV or LV dilation or dysfunction or any evidence of elevated pulmonary artery pressure. She presented with acute RV dysfunction, altered mental status an haemodynamic instability (i.e. shock). The differential diagnoses included acute respiratory failure, acute myocardial infarction, acute intracranial pathology, acute pulmonary embolism, drug toxicity and sepsis. Concerning acute coronary syndrome (ACS) being a possible diagnosis because of elevated cardiac enzymes, a new onset isolated, severe RV dysfunction and haemodynamic instability, she did not