Oxycodone
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Hypercarbia and hypoxia manifested as PRES: case report A 62-year-old woman developed hypercarbia and hypoxia manifested as PRES following treatment with oxycodone [route and indication not stated]. The woman who had a history of chronic obstructive pulmonary disease (COPD) presented with severe shortness of breath and decreased level of consciousness following an upper respiratory tract infection. Considering her clinical presentation as an acute exacerbation of COPD (AECOPD), she was intubated, treated with unspecified inhalers, prednisone and an IV course of antibiotics. Thereafter, for further care, she was transferred to the ICU. She had a evident medical history of hypertension, dyslipidaemia, anaemia, upper gastrointestinal bleed, coronary artery disease, depression and a metatarsal fracture. At that time, she was receiving oxycodone 5mg four times per day as needed, montelukast, ezetimibe and various other home medications. Upon admission, her vitals were as follows: body temperature of 37.5°C, BP of 139/61mm Hg, HR of 83 and RR of 16. She was drowsy, not responsive to voice and was unable to follow simple commands. Glasgow coma scale (GCS) was 7T (E2VTM5). Cranial nerve exam showed pupils that were 5mm bilaterally and reactive to light. Plantar responses were equivocal bilaterally. Sensory examination showed withdrawal in all four limbs to pain. Her lab investigations were as follows: haemoglobin of 108 g/L, elevated WBC count and creatinine 63 mmol/L. Chest radiography showed patchy subsegmental consolidation in left lower lobe in keeping with pneumonia. Arterial blood gas showed acidosis with a pH of 7.08, partial pressure of oxygen (pO2) of 43mm Hg and severe hypercarbia with a partial pressure of carbon dioxide (pCO2) of >150mm Hg. Total CO2 was 48 on blood chemistries. Her earlier baseline pCO2 was between 60 and 70mm Hg. During her first night in hospital, she developed a focal seizure. After treatment with IV lorazepam and diazepam, the woman’s seizure terminated. An electroencephalography (EEG) showed independent bi-temporal sharp wave discharges, more prominent over right than left temporal regions. MRI showed multifocal, predominantly white matter T2/FLAIR hyperintensities involving bilateral frontoparietal and right occipital lobes, bilateral thalami and less prominent patchy involvement of the cerebellar hemispheres. These MRI changes were indicative of posterior reversible encephalopathy syndrome (PRES). Based on the clinical and radiological findings, hypercarbia was considered as aetiology of PRES. Her oxycodone therapy, presence of a pneumonia were considered as contributing factors for the hypercarbia and hypoxia. Following phenytoin treatment, she remained seizure-free. During re-examination, she was alert, oriented, fluent and able to follow complex commands. Facial strength and sensation were normal. At 3-month follow-up, she remained asymptomatic with a normal neurological examination [time to reactions onset not stated]. Gupta H, et al. Posterior Reversible Encephalopathy Syndrom
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