Non–injection‐site necrotic skin lesions complicating postoperative heparin thromboprophylaxis

Abstract

A 75-year-old African-American man with Type II diabetes, hypertension, and hyperlipidemia was admitted with a painful right leg secondary to bilateral iliac artery obstruction. Admission hemoglobin level was 14.4 g/dL, white blood count was 11.9 3 10 9 /L (neutrophils, 10.4 3 10 9 /L), and the platelet count was 366 3 10 9 /L. Unfractionated heparin 5,000 IU thrice daily by subcutaneous injection was given for 5 days. Aortobifemoral bypass surgery was performed with full-dose intravenous heparin followed by daily subcutaneous unfractionated heparin thromboprophylaxis. After an initial decline, the platelet count rose to 480 3 10 9 /L on postoperative Day 4 (Day 10 after start of preoperative course of heparin), at which time the patient developed a swollen right leg. Vascular duplex revealed a gastrocnemius vein clot of indeterminate age, which was not treated.This patient was found to have a gastrocnemius vein thrombosis on Day 4 after surgery. Controversy exists over whether to anticoagulate deep muscular vein thromboses. No large randomized trials have been done, and some smaller studies show similar resolution with or without anticoagulation [1,2]. Thus, the decision to continue subcutaneous (SC) prophylactic-dose heparin was reasonable.On postoperative Day 5, a right leg patchy retiform purpuric skin rash developed (Fig. 1A). Arterial duplex showed improved but still poor arterial flow to the right leg. Skin biopsy (right medial thigh) showed intravascular thrombus in a mid-dermal vessel and partial epidermal necrosis, without vasculitis (Fig. 1B,C). Laboratory investigations, including complete blood count, measurement of antithrombin, protein C, protein S, ANCA, cryoglobulins, homocysteine, viral hepatitis serology, complement, and antiphospholipid antibodies, were normal/ negative. The necrotic skin rash was considered secondary to "transient ischemia" during the preceding vascular surgery. The patient was discharged to a rehabilitation facility off heparin.The patient's right lower limb rash included multiple discrete lesions extending from the thigh to the ankle with blisters, SC hemorrhage, and necrosis in an angulated branched configuration described as "retiform purpura." These lesions have a broad differential, including vasculitis, hypercoagulable state, purpura fulminans, cholesterol embolism, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, warfarin-induced skin necrosis, heparin-induced skin necrosis, cryoglobulinemia, and calciphylaxis [3][4][5]. The biopsy finding of epidermal necrosis and intravascular thrombus without vasculitis, calcification, or inflammatory cell infiltrate, plus the negative hypercoagulability testing, lack of infection, renal failure, hemolysis, and absence of warfarin therapy, rules out most of these entities. Additionally, skin necrosis from low blood flow alone can be seen in livedo racemosa, but this entity is accompanied by a perilesional violaceous reticulated skin discoloration, which was not seen [3,4].Our patient had received SC inj...

Endotracheal tube fastening device-related pressure necrosis of the upper lip

“…Failure to detect early signs of the injury prevented initiation of earlier treatment of the pressure-induced wound and allowed progression to an advanced stage. Prolonged administrations of vasoactive medications and thrombogenic heparin-induced thrombocytopenia were also possible contributing factors 1 2. This patient eventually underwent upper lip reconstruction with bilateral reverse Karapandzic flap (figure 2).…”

A career in solving clinical‐pathological conundrums: Heyde syndrome, anti‐platelet factor 4 disorders, and microvascular limb ischemic necrosis

“…The availability of a high-quality test for HIT antibodies-the SRA [11][12][13] -along with supportive ELISA data-permitted identification of numerous HIT presentations in diverse clinical settings. We were able to show that HIT was associated with: deep-vein thrombosis (DVT-including bilateral DVT) 33,35 ; upper-extremity DVT (almost invariably intravascular catheter-associated) 40 ; post-intravenous bolus heparin acute anaphylactoid reactions (also called "acute systemic reactions") 34,37,41 ; necrotizing skin lesions (usually at heparin injection sites, 42 but occasionally distinct from heparin injections 43 ); unilateral or bilateral adrenal hemorrhagic necrosis 42,44 ; cerebral venous sinus thrombosis, 45 and so forth. A truism of HIT: the more unusual the thrombotic event is, the more likely it is that HIT is the underlying explanation.…”

Clinical picture of heparin-induced thrombocytopenia (HIT) and its differentiation from non-HIT thrombocytopenia

“…Other complications of HIT include anaphylactoid reactions (e. g. fever/chills, dyspnea, transient global amnesia, cardiopulmonary arrest) that occur 5-30 minutes post-intravenous heparin bolus (2,42,43) or up to 2 h post-subcutaneous injection of LMWH (44), necrotising skin lesions at heparin injection sites (26) and, rarely, skin necrosis at non-injection sites (45).…”