A 48-year-old male patient with a long-term smoking history and no other significant disorders was admitted to the clinic in May 2016. His major symptoms included a 2-year history of damage to the skin and nail of the hallux of the right foot, often complicated by secondary bacterial superinfection. He complained of chronic rest pain in the big toe and swelling of the right foot but denied the typical intermittent claudication. There was no direct injury to the right foot preceding the symptoms. However, in the past the patient used to play football.
Physical examination revealed trophic changes involving the right foot, particularly advanced in the big toe and less severe in the second and third toe. The skin there was thickened with hyperkeratosis and peeling. There was also partial necrosis of the big toe. His right hallux, foot, and calf appeared swollen, with local tenderness of the great toe. The hallux nail plate was deformed, thickened, and brittle with hyperkeratosis and yellow discoloration (Figures 1  and 2). There were easily palpable symmetric pulses in both lower and upper extremities.
The only laboratory test finding was mildly elevated CRP (21 mg/l). Kidney, liver, and lipid parameters and electrolytes were all normal. Antibody tests (ANA, cANCA, pANCA, anti-CCP, RF, LA, anti-cardiolipin, and anti-beta 2 glycoprotein I antibodies) were negative. Viral tests for HBV, HCV, and HIV were negative. An oral glucose tolerance test and glycated hemoglobin assay (HbA1c 4.9%) excluded glucose metabolism disorders.
Standard imaging tests (chest X-ray, ECG, abdominal ultrasound) were normal.
X-ray of the right foot did not show any signs of destruction or inflammation involving the bones. There was no calcification in the projection of the vessels. The ankle-brachial index was normal (1.11 on the right side, 1.15 on the left). Doppler ultrasonography of the lower extremity arteries showed normal symmetrical high resistance flows. The walls of the vessels were normal. Aneurysms, which could be a potential source of peripheral embolism, were excluded. However, a slight dilatation of the right posterior tibial artery was detected. CT angiography revealed a rare vascular anomaly in the right lower extremity: hypoplasia of the distal segment of the anterior tibial artery, a slightly dilatated and tortuous posterior tibial artery, that fed the arteriovenous malformation (AVM) in the big toe with increased venous flow in the lower limb (Figures 3, 4, 5). There were no changes typical of Buerger's disease.
The decision was taken to amputate the distal phalanx of the right hallux, because of the location of the lesion, the lack of remedial possibilities, and the significantly intensified symptoms.
Histopathological examination of the removed tissues excluded neoplasm, but confirmed the features of vascular anomaly. Additionally, thickened stratum corneum with chronic inflammatory infiltration and dilated stromal vessels were described.
After the amputation, the wound healed normally, the right lower limb edema resolved, and CRP decreased in laboratory test results. At 3-year follow-up, no recurrence of skin lesions in the lower extremities was observed.