Aspirin/clopidogrel
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Cholesterol embolisation syndrome: case report A 75-year-old man developed cholesterol embolisation syndrome during treatment with aspirin and clopidogrel as dual antiplatelet therapy. The man had presented to an outpatient clinic with slurred speech and cognitive impairment. He had a significant medical history of smoking and had hypertension for ~16 years, which was properly controlled with regular treatment. He was diagnosed with severe left internal carotid artery (ICA) stenosis with diffuse atherosclerosis. For further evaluation, he was transferred to the hospital (current presentation) 1 month later and underwent left ICA stenting by using local anaesthesia. The surgery was completed with no immediate complications. On postoperative day (POD) seven, he was discharged with no focal deficits and continued receiving dual antiplatelet therapy with clopidogrel 75mg daily and aspirin 100mg daily [routes not stated]. Additionally, he was receiving various concomitant medications. At 3 weeks following the surgery, he was brought in as an emergency case with an episode of generalised tonic-clonic seizures, followed by continuous drowsiness on POD 20. On clinical examination, he was conscious, disoriented, pale, anicteric, afebrile and had regular tachycardia. His BP was 100/72mm Hg. He showed mild pitting bilateral pedal oedema and the toes on both feet were blue. The neurological examination results showed him to be disoriented. He showed leukocytosis (once detected having eosinophilia), an increased C-reactive protein (CRP) level and an increased erythrocyte sedimentation rate. Also, renal dysfunction, neurological dysfunction and transaminitis were noted. A non-contrast CT on admission revealed left high parietal lobar haemorrhage with a hypodense area in the basal ganglia, periventricular white matter and insular cortex on the left side. An emergency MRI scan revealed hyperintense lesions in the bilateral thalamus (left greater than right), the left frontoparietotemporal region, bilateral basal ganglia (left greater than right), cerebellar hemisphere and brainstem and a haematoma in the left high parietal region. A skin biopsy taken from a blue toe on the right foot revealed thrombotic occlusion of multiple arterioles and cholesterol crystal emboli (cholesterol embolisation syndrome) [duration of treatment to reaction onset not stated]. The man was initiated on haemodialysis. He was prescribed beraprost [beraprost sodium] and an unspecified PCSK9 inhibitor. Therapy with clopidogrel and aspirin were discontinued. Also, methylprednisolone was administered for 3 days, followed by prednisolone, which was tapered with a plan to discontinue prednisolone in 2 weeks. Additionally, he received supportive treatment in the form of adequate hydration and nutrition. His right hemiparesis and sensorium ameliorated gradually. An MRI performed 2 days following admission (POD 22) revealed some regression of the lesions and a newly formed asymptomatic ischaemic area in the left posterior temporal lobe. At the end of the first
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