Case Presentation: A 44-year-old female with a past medical history of systemic lupus erythematosus (SLE) and severe peripheral artery disease (PAD) presented to the emergency department with worsening pain, numbness, and discoloration of right hand digits, predominantly involving the index finger. Symptoms persisted despite outpatient vasodilator therapy for suspected Raynaud’s phenomenon. Examination showed a cool, cyanotic fingertip with decreased sensation but intact radial pulse. Laboratory studies revealed elevated double-stranded DNA (10,131) and low complement levels, consistent with SLE flare. Arterial duplex ultrasound showed markedly reduced radial and ulnar signals with monophasic waveforms, suggesting significant arterial disease. Patient was started on heparin and vasodilators. Angiography was done and demonstrated patent brachial, radial, and ulnar arteries without obstruction, but poor opacification of the digital arteries. The discrepancy between arterial duplex and angiography raised concern for small-vessel SLE vasculopathy rather than progression of PAD. The patient received pulse-dose steroids followed by a prednisone taper. Symptoms stabilized without tissue loss, and the patient was discharged home with close rheumatology follow-up.
Discussion: This case highlights the challenge of evaluating digital ischemia in a patient with overlapping SLE and advanced PAD. Although arterial duplex ultrasound suggested severe large-vessel disease, angiography showed preserved patency of major arteries, consistent with reports that arterial duplex may appear abnormal in the setting of vasospasm or microvascular inflammation. Literature also describes that angiography frequently fails to visualize distal digital vessels affected by lupus vasculitis, thus normal large-vessel imaging does not exclude clinically significant ischemia. The patient’s serological findings suggestive of SLE flare, combined with imaging discrepancies, supported small-vessel involvement rather than atherosclerotic progression. Recognizing this distinction is critical because treatment differs substantially. PAD-related ischemia would not improve with immunosuppression, whereas SLE-associated vasculopathy may rapidly worsen without it. Early initiation of corticosteroids likely prevented digital necrosis, which has been reported in untreated lupus vasculitis. This case demonstrates how anchoring on PAD could have delayed the correct diagnosis and appropriate therapy.
Conclusions: Digital ischemia in SLE requires a broad, integrated diagnostic approach. Discrepancies in vascular studies should prompt consideration of small-vessel disease, especially during a lupus flare. Awareness of the limitations of duplex ultrasound and angiography is essential to avoid misdiagnosis. Timely recognition and treatment of lupus-related microvascular disease can prevent irreversible tissue loss, even in patients with severe coexisting PAD.
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