Generally occurred necessitating debridement and if not

Generally LMWHs are a well-established means of parenteral anticoagulation  and are indicated for treatment of deep vein thrombosis (DVT), pulmonary embolism (PE), reduction of recurrent pregnancy loss,  treatment of thrombosis of prosthetic heart valve, portal vein, cerebral venous sinus, or other veins, coronary artery disease – acute ischemia or during percutaneous coronary intervention and additionally for thromboembolic prophylaxis in patients with  atrial fibrillation, prosthetic heart valves, thrombophilias and other risk factors for thromboembolism.  In certain occasions, LMWHs are preferred to unfractionated heparin (UFH) since they lack the need of close monitoring and are also preferred from oral anticoagulants because of smaller half-life in cases of possible foreseeable intervention. The most common side effect of LMWH includes an increased bleeding risk, which manifests as anemia, major hemorrhage, hematomas etc. Tissue necrosis in the injection site or even to distal parts is a rarer adverse effect although its true incidence is probably underestimated.

The etiology of LMWH –induced tissue necrosis remains unclear with several theories being developed to explain the phenomenon. Some authors suggest heparin-induced thrombocytopenia (HIT) as a possible mechanism, while microthromboses of dermal vessels lead to necrosis. Others implicate a Type III hypersensitivity reaction that causes vasculitis as a possible pathophysiological mechanism, aka Arthus Phenomenon, creating immunocomplex deposits on endothelium. Repeated local trauma is an alternative approach explaining tissue necrosis with local hemorrhage leading to pressure on small cutaneous blood vessels and subsequent ischemia and necrosis of the overlying tissue. The average onset of skin necrosis ranges from 5 to 11 days after initial administration of LMWH beginning as painful, erythematous, edematous, subcutaneous lesions at injection sites or rarely at distal sites; which rapidly progress into purpuric demarcated plaques and finally into necrosis. The size of the necrotic areas varies, with more cases referring at a small and circumscribed zone with a maximum diameter of a few centimeters. There are also a few incidences where extended skin necrosis has occurred necessitating debridement and if not treated leads to life-threatening complications.

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Investigation of factors increasing the risk of skin necrosis is of crucial importance for early diagnosis and cessation of LMWH-administration. The majority of cases reported with LMWH induced skin necrosis revealed HPF-4 Abs and were correlated with HIT. At such cases changing the LMWH-therapy to fondaparinux or vitamin K antagonists exhibited good outcomes. Platelet counts should be monitored to early diagnose heparin-induced thrombocytopenia. A rough control of coagulation parameters including Protein S, C, antithrombin III, activated Partial Thromboplastin Time and prothrombin time is also recommended.

Most published reports regarded an uneventful outcome with conservative treatment, so a first-line pragmatic approach consists of immediately ceasing the patient`s treatment with heparin/ LMWH and replacing it with another anticoagulant. Close assessment of tissue necrosis is suggested for early recognition of possible progression of the lesion needing surgical debridement.    


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