Severe peripheral artery disease (PAD) is the predominant cause of ischemic ulcerations involving the lower extremities. PAD-associated ulcerations are typically distally located involving the feet, toes, and sometimes the calves. In contradistinction, atypical ischemic ulcerations of the lower extremity are often non-atherosclerotic in etiology, involve the proximal leg (thigh/buttocks), can evolve despite palpable distal pulses, and may coexist with other cutaneous aberrations (e.g. macules, purpura, nodules, and livedo reticularis). A differential diagnosis of atypical ischemic ulcerations involving the legs is presented.
1 Second European consensus document on chronic critical leg ischemia.Circulation1991; 84(4 suppl): IV1–I26.
2.
2 Raines JKDarling RCButh J. Vascular laboratory criteria for the management of peripheral vascular disease of the lower extremities.Surgery1976; 79: 21–29.
3.
3 Carter SATate RB. Value of toe pulse waves in addition to systolic pressure in the assessment of the severity of peripheral arterial disease and critical limb ischemia.J Vasc Surg1996; 24: 258–265.
6 DiFrancesco LMBurkart PHoehn JG. A cutaneous manifestation of the antiphospholipid antibody syndrome.Ann Plast Surg2003; 51: 517–521.
7.
7 Creamer DHunt BBlack M. Widespread cutaneous necrosis occurring in association with the antiphospholipid syndrome: a report of two cases.Br J Dermatol2000; 142: 1199–1203.
8.
8 Wilson WAGharavi AEKoike T. International consensus statement on preliminary classification criteria for definite antiphospholipid antibody syndrome: report of an international workshop.Arthritis Rheum1999; 42: 1309–1311.
9.
9 Budisavlijevic MNCheek DPloth DW. Calciphylaxis in chronic renal failure.J Am Soc Nephrol1996; 7: 978–982.
10.
10 Kant KSGlueck HICoots MC. Protein S deficiency and skin necrosis associated with continuous ambulatory peritoneal dialysis.Am J Kidney Dis1992; 19: 264–271.
11.
11 Mehta RLScott GSloand JAFrancis CW. Skin necrosis associated with acquired protein C deficiency in patients with renal failure and calciphylaxis.Am J Med1990; 88: 252–257.
12.
12 Goli AKGoli SAShah LS. Calciphylaxis: a rare association with alcoholic cirrhosis – are deficiencies in protein C and S the cause?South Med J2005; 98: 736–739.
13.
13 Fine AZacharias J. Calciphylaxis is usually non-ulcerating: risk factors, outcome and therapy.Kidney Int2002; 61: 2210–2217.
14.
14 Chertow GMRaggi PMcCarthy JT. The effects of sevelamer and calcium acetate on proxies of atherosclerotic and arteriosclerotic vascular disease in hemodialysis patients.Am J Nephrol2003; 23: 307–314.
15.
15 Dean SMWerman H. Calciphylaxis: a favorable outcome with hyperbaric oxygen.Vasc Med1998; 3: 115–120.
16.
16 Podymow TWherrett CBurns KD. Hyperbaric oxygen in the treatment of calciphylaxis case series.Nephrol Dial Transplant2001; 16: 2176–2180.
18 Cicone JSPetronis JBEmbert CDSpector DA. Successful treatment of calciphylaxis with intravenous sodium thiosulfate.Am J Kidney Dis2004; 43: 1104–1108.
19.
19 Monney PNguyen Q-VPerroud HDescombes E. Rapid improvement of calciphylaxis after intravenous pamidronate therapy in a patient with chronic renal failure.Nephrol Dial Transplant2004; 19: 2130–2132.
21 Sallah SAbdallah JMGagnon GA. Recurrent warfarin-induced skin necrosis in kindreds with protein S deficiency.Haemostasis1998; 28: 25–30.
22.
22 Srinivasan AFRice LBartholomew JR. Warfarin-induced skin necrosis and venous limb gangrene in the setting of heparin-induced thrombocytopenia.Arch Intern Med2004; 164: 66–70.
23.
23 Zauber NPStark MW. Successful warfarin anticoagulant despite protein C deficiency and a history of warfarin necrosis.Ann Intern Med1986; 104: 659–660.
25 Denton MDMauiyyedi SBazari H. Heparin-induced skin necrosis in a patient with end-stage renal failure and functional protein S deficiency.Am J Nephrol2001; 21: 289–293.
28 Cabili STeachman IGoor Y. Reversal of gangrenous lesions in the blue toe syndrome with lovastatin – a case report.Angiology1993; 44: 821–825.
29.
29 Matsumura TMatsumoto AOhno M. A case of cholesterol embolism confirmed by skin biopsy and successfully treated with statins and steroids.Am J Med Sci2006; 331: 280–283.
30.
30 Radauceanu AAvignon ARibstein IMonnier L. Use of a prostacyclin analogue in cholesterol crystal embolism.Diabet Med1998; 15: 262–263.
31.
31 Elinav EChajek-Shaul TStern M. Improvement in cholesterol emboli syndrome after iloprost therapy.BMJ2002; 324: 268–269.
32.
32 Motegi SAbe MShimizu A. Cholesterol crystal embolization: skin manifestation, gastrointestinal and central nervous symptom treated with corticosteroid.J Dermatol2005; 32: 295–298.
33.
33 Stabellini NCerretani DRusso G. [Renal atheroembolic disease: evaluation of the efficacy of corticosteroid therapy]. G Ital Nefrol2002; 19: 18–21.
34.
34 Funabiki KMasuoka HShimizu H. Cholesterol crystal embolization [CCE] after cardiac catheterization.Jpn Heart J2003; 44: 767–774.
35.
35 Isbister GKWhite JCurrie BJ. Spider bites: addressing mythology and poor evidence.Am J Trop Med Hyg2005; 72: 361–367.
36.
36 Dyachenko PZiv MRozenman D. Epidemiological and clinical manifestations of patients hospitalized with brown recluse spider bite.J Eur Acad Dermatol Venereol2006; 20: 1121–1125.
37.
37 Diaz JH. The global epidemiology, syndromic classification, management, and prevention of spider bites.Am J Trop Med Hyg2004; 71: 239–250.
38.
38 Merchant MLHinton JFGeren CR. Effect of hyperbaric oxygen on sphinogmyelinase D activity of brown recluse spider (Loxosceles reclusa) venom as studied by 31P nuclear magnetic resonance spectroscopy.Am J Trop Med Hyg1997; 56: 335–338.
