Rivaroxaban
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Acute haemopericardium: case report An 82-year-old woman developed fatal acute haemopericardium during treatment with rivaroxaban for paroxysmal atrial fibrillation. The woman with paroxysmal atrial fibrillation, had been receiving treatment with rivaroxaban 15mg once daily [route not stated] along with flecainide and denosumab. She presented to the emergency department (ED) with chest pain. In the ED, she experienced an intermittent, dull, aching chest pain. Examinations revealed a clear chest and heart sounds, with no added sounds, her BP was 180/74mm Hg and HR was irregular at 80 bpm. A subsequent review of the ECG showed new lateral T-wave and ST-segment changes. Due to potential new ECG changes and severity of her chest pain, she remained under observation. Laboratory investigations revealed Troponin I level of 126.6 ng/L (after 4 hours, repeat Troponin I level was 91.4 ng/L), increased creatine, WBC count of 9.4 × 109/L and increased CRP. Coagulation panel revealed an increased prothrombin time associated with rivaroxaban therapy. Her urea level was 14 mmol/L. A chest X-ray revealed overt cardiomegaly. The woman received paracetamol for pain, as required. A cardiology team noted that her ECG findings had variations as compared to ECGs from the last month, which were static, and her troponin level increased 10% of the peak from the prior month at 126 ng/L and declining, which made a further cardiac event unlikely. Despite clinical stability, her early warning score (EWS) was consistently 1 due to an RR between 14–20 bpm. Her creatinine level increased to 217 µmol/L and during this time her HR was 80 bpm and BP was 118/56mm Hg. Digital rectal examination showed faecal loading, and her oral intake reduced. It was suspected that her acute kidney injury was pre-renal due to dehydration, resulting in constipation. Therefore, on the third day, she was treated with IV fluids which helped on both fronts. A repeat laboratory investigation showed troponin level of 71 ng/L. The symptoms progressed to nausea and vomiting. Her urine output decreased dramatically. No interval changes were observed on the chest X-ray. Cardiomegaly was noted on both - the chest Xray from the prior admission and the re-admission films. She developed an asystole cardiac arrest. She died of cardiac arrest after unsuccessful resuscitation attempts. A post mortem exam revealed pericardial distension with 700mL of fresh blood. No ventricular rupture and no overt characteristics of established recent myocardial infarction were noted. Moderately severe focal coronary artery atherosclerosis was observed without significant stenosis or thrombi. Histopathological investigation of ventricles revealed florid fibrinous pericarditis with features of early organisation without significant abnormality of the endocardium or myocardium. These findings of post-mortem examination suggested that the cause of death was acute spontaneous haemopericardium, associated with rivaroxaban therapy [duration of treatment to reaction onset not stated]. Author comment:
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