Document Type

Conference Proceeding

Publication Date

5-2-2025

Abstract

Abstract: A 73-year-old male with polyarticular gout, hypertension, and rheumatoid arthritis presented with non-healing necrotic wounds on the distal aspect of his upper extremity digits, most severely affecting the left index finger with eschar. His symptoms had been present for the past six weeks. He also had a history of Raynaud’s phenomenon, which preceded these symptoms. Examination revealed necrotic wounds on the nail beds of seven fingers bilaterally, with significant left index finger necrosis. Despite the severity of his condition, he remained hemodynamically stable throughout hospitalization. Laboratory studies showed positive cardiolipin IgM and beta-2 glycoprotein antibodies on two separate occasions, tested 12 weeks apart. Inflammatory markers were elevated, with an ESR of 28 mm/hr and a CRP of 24.2 mg/L. Arterial duplex ultrasound and CT angiography showed no significant arterial disease, ruling out large-vessel vasculitis. A transthoracic and transesophageal echocardiogram ruled out endocarditis or any thrombi. Blood cultures did not reveal any bacterial or fungal growth. The patient was started on IV heparin and was later transitioned to warfarin with a goal INR of 2–3. He was also administered a pulse dose of Solu-Medrol for three days, followed by a maintenance dose of prednisone. Sildenafil and nifedipine were initiated for Raynaud’s. IV cyclophosphamide was added for suspected vasculitis. Autoimmune workup was negative for lupus, Sjögren’s, scleroderma, small-vessel vasculitis, and other connective tissue diseases. Vascular surgery determined that the etiology was more likely microvascular, with no acute surgical intervention indicated. The patient was discharged initially on prednisone, sildenafil, and nifedipine. Despite aggressive treatment, ischemic wounds worsened, with necrosis spreading up the fingers and involving more nail beds. He was re-evaluated in the hospital three weeks later, and his immunosuppression was intensified, with cyclophosphamide transitioning to rituximab. Discussion: Upper extremity digit ischemia presents a diagnostic challenge due to a broad differential. An extensive workup is warranted, including echocardiogram, computed tomography angiography, thrombophilia panel, and autoimmune panel. In our patient, an extensive workup revealed positive antiphospholipid antibodies, although the underlying etiology could still not be elucidated. While glucocorticoids and anticoagulation typically improve acute digital ischemia in primary antiphospholipid syndrome, his condition worsened despite anticoagulation, steroids, and cyclophosphamide, suggesting a predominant microvascular etiology. Vascular imaging ruled out large-vessel involvement, reinforcing microvascular dysfunction. With no surgical options, management was focused on medical therapy and supportive care. Conclusion: This case highlights the challenges of managing refractory ischemic digital necrosis in autoimmune and hypercoagulable disorders such as antiphospholipid syndrome, emphasizing a multidisciplinary approach. A microvascular etiology must be suspected in ischemic digital necrosis when large-vessel disease is ruled out. Management with anticoagulation and immunosuppression may not always prevent progression, and referral may be warranted for vasodilatory treatment such as intravenous prostaglandins. Multidisciplinary management is crucial for optimizing treatment and monitoring disease progression in these complex vasculopathies.

Comments

American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter Resident and Medical Student Day, May 2, 2025, Troy, MI

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