A 25 year-old man presented with one month of progressively painful, bruised, and swollen bilateral calves. Symptoms started as bilateral feet and ankle pain followed by the development of bruising over the posterior aspects of his calves. The pain was described as “hard, tight” and constant, worsening with weight bearing. He was prescribed a five day course of steroids with no improvement. Afterwards, the bruising extended to the lower posterior thighs bilaterally. The pain progressed to the point that he was only able to ambulate by walking on his tip toes. He denied fevers, nausea, gum bleeding, hemoptysis, hematuria, or hematochezia. He denied arthralgias, myalgias, or rash other than the bruising on his legs. He did complain of numbness and tingling in his lower legs. His diet consists mainly of pizzas and fast food with little to no fruits or vegetables. He denied any alcohol or IV drug use. There is no family history of connective tissue disease or blood disorder. Except for mild tachycardia, vital signs were within normal limits. He had poor dentition with gingivitis but no cheliosis. There were no joint deformities. Bilateral posterior calves had diffuse ecchymosis, tenderness to palpation, coiled hairs, and swelling without pitting edema. There were non-palpable perifollicular hemorrhages on the posterior thighs and shins. Lower extremity sensation was intact to light touch; strength was 4/5 bilaterally, limited by pain. Laboratory analysis revealed a normal basic metabolic panel, hepatic panel, white blood count, and platelet count. Hemoglobin was 9.2 mg/dL. INR was 1.1. CTA of the lower extremities revealed normal bilateral arterial runoff without evidence of bleeding. Vitamin B12 and K levels were within normal limits. Vitamin C level returned undetectable.
In the United States, vitamin C deficiency is typically seen in patients with severe nutritional deficiencies (namely diets void of fruits and vegetables) and alcoholics. Its deficiency leads to impaired collagen synthesis and disorders of connective tissue. Common symptoms include ecchymoses, gingival hemorrhage, impaired wound healing, coiled hair, and hyperkeratosis with perifollicular hemorrhage. This last finding can mimic palpable purpura and can lead to an incorrect diagnosis of vasculitis. Cutaneous manifestations of vasculitis can include petechiae, palpable purpura, bullae, urticaria, splinter hemorrhages, and ulcers in non-dependent areas. The distinguishing feature of scurvy related hemorrhage is the perifollicular lesions with coiled hair.
While hospitalists are typically well-versed in recognizing vasculitis, they should be cognizant of processes which mimic vasculitis. Pattern recognition is important in determining etiology and guiding evaluation. This case demonstrates how the recognition of perifollicular hemorrhages and coiled hair helped to expediently diagnose a rarely seen deficiency in the United States.
To cite this abstract:Pedram K, Syed H, Bradley M, Zahirovic S, Raja M. This Is Not Vasculitis, Do You C? [abstract]. Journal of Hospital Medicine. 2015; 10 (suppl 2). http://www.shmabstracts.com/abstract/this-is-not-vasculitis-do-you-c/. Accessed April 26, 2017.
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