Cholesterol microembolization syndrome: a complication of anticoagulant therapy

Abstract

A n elderly man with a history of hypertension and atrial flutter was referred to an internal medicine outpatient clinic because of purple-tinged and painful toes for over a year. His medications were candesartan, lercanidipine and warfarin. One and a half years earlier he had been given warfarin for paroxysmal atrial flutter. After six months on warfarin, the patient had been examined for the same symptoms in his toes by a vascular surgeon. At that time, computed tomography (CT) of the aorta, Doppler ultrasonography of the arteries of the legs and ankle pressure measurements had been performed, but no substantial abnormalities had been found. Only slightly elevated serum creatinine levels of 130-140 (normal 60-100) µmol/L had been observed.At his visit to the outpatient clinic, the patient reported that the pain in his toes occurred with walking or putting socks on. On examination, his toes were purple with plaques ( Figure 1) and tender on palpation. Distal pulses were present. No discoloration of fingers or skin elsewhere was detected. Except for the presence of atrial flutter, the rest of his physical examination was normal. Conventional and transesophageal echocardiographic examinations were performed, along with CT of the aorta and ultrasonography of the abdomen. Echocardiography showed minor mitral and aortic valve insufficiencies, but no signs of bacterial vegetations were evident. Computed tomographic investigation showed small plaques in the aortic wall. Ultrasonography of the abdomen showed no abnormalities. As found previously, the patient's serum creatinine level was slightly elevated (134 µmol/L), but no kidney abnormalities were observed on the CT scan. Results of laboratory tests, including urinalysis, were normal, except for an international normalized ratio that was above 2.0 because of the warfarin therapy.Based on these findings, ischemia of the large vessels could be excluded as a cause of the patient's discoloured and painful toes. Vasculitis was also unlikely, because typical clinical findings and a suggestive pattern of laboratory parameters were lacking. The findings of echocardiographic examinations and laboratory tests excluded the possibility of infective endocarditis and bacterial emboli. Instead, the presence of atherosclerotic plaques in the aortic wall and continuous warfarin therapy launched the suspicion of cholesterol

Adverse Drug Reactions and Cutaneous Manifestations Associated With Anticoagulation

“…The embolus causes vessel occlusion and ischemia. 42,45,46 The evidence for this is supported by skin biopsies of the affected region, which show the presence of cholesterol emboli occluding the dermal arteries, resulting in ischemia of the epidermis. 42 The risk factors of WIPTS include (a) male sex, (b) advanced age, and (c) patients with atherosclerosis on long-term anticoagulation.…”

“…42 The risk factors of WIPTS include (a) male sex, (b) advanced age, and (c) patients with atherosclerosis on long-term anticoagulation. 44,45…”

“…42 The risk factors of WIPTS include (a) male sex, (b) advanced age, and (c) patients with atherosclerosis on long-term anticoagulation. 44,45 Treatment involves warfarin cessation, and improvement can often be seen within 1 to 7 weeks. 44 Patients with WIPTS who require long-term anticoagulation should be switched to FXa inhibitors such as fondaparinux or apixaban.…”

Renal cholesterol crystal embolism in the setting of warfarin use

“…Two types of emboli can originate from these plaques, thromboemboli and atheroemboli. There have been a few case reports in the literature involving AERD and warfarin use 5 6. There are no randomised clinical trials with cholesterol embolism due to warfarin use as the primary outcome 7…”

Treatment of "Blue toe" syndrome with Hyperbaric oxygen therapy: Case study

“…Po registrovanju sindroma plavih prstiju, pristupa se pažljivom uzimanju anamnestičkih podataka, fizikalnom pregledu, a potom vizuelizacionim procedurama (Doppler pregled krvnih sudova, ultrazvuk abdomena i srca, CT ili MRI angiografija, odnosno klasična kontrastna angiografija), sa ciljem detekcije potencijalnog ishodišta embolusa. Istovremeno, sprovodi se diferencijalna dijagnostika okluzije distalne mikrocirkulacije (vazospazam, vaskulitis, hiperviskozni sindromi, stanja hiperkoagulabilnosti, kalcifilaksa, embolizacija, toksini, upotreba glikokortikoida, paraneoplastični sindrom) [11][12][13]. Iako savremen pristup tretmanu sindroma plavih prstiju uključuje suportivnu terapiju i sekundarnu prevenciju uperenu protiv potencijalnih ponavljanih epizoda embolizacije [14], otkrivanje i uklanjanje izvora embolusa je krucijalno [6,15].…”