%0 Journal Article
%T Low Molecular Weight Heparin Induced Skin Necrosis without Platelet Fall Revealing Immunoallergic Heparin Induced Thrombocytopenia
%A Thomas Godet
%A S¨¦bastien Perbet
%A Aur¨¦lien Lebreton
%A Guillaume Gayraud
%A Sophie Cayot
%A Aymeric Tremblay
%A Aur¨¦lie Ravinet
%A S¨¦bastien Christophe
%A Renaud Gu¨¦rin
%A Julien Pascal
%A Matthieu Jabaudon
%A Amr Hassan
%A Anne-Fran£¿oise Sapin
%A Jean-Etienne Bazin
%A Jean-Michel Constantin
%J Case Reports in Hematology
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/849168
%X Low molecular weight heparins (LMWH) are commonly used in the ICU setting for thromboprophylaxis as well as curative decoagulation as required during renal replacement therapy (RRT). A rare adverse event revealing immunoallergic LMWH induced thrombopenia (HIT) is skin necrosis at injection sites. We report the case of a patient presenting with skin necrosis witnessing an HIT after RRT, without thrombocytopenia. The mechanism remains unclear. Anti-PF4/heparin antibodies, functional tests (HIPA and/or SRA), and skin biopsy are of great help to evaluate differential diagnosis with a low pretest probability 4T¡¯s score. 1. Introduction Renal failure is a frequent condition observed among ICU patients. Renal replacement therapy (RRT) is often required to treat this affection. Curative anticoagulation with heparin derivatives is mandatory to prevent filter clotting especially during proaggregant conditions such as sepsis. We wish to report a rare complication of heparin treatment with enoxaparin with a low pretest probability 4T¡¯s score [1], due to an immunoallergic heparin induced thrombopenia (HIT): skin necrosis at injection site. 2. Case Report A 57-year-old woman with a history of severe melancholic state was hospitalized in psychiatric ward for 4 months before admission to our hospital. She presented in the emergency department with arterial hypotension and hypothermia due to severe dehydration because of severe feeding troubles with self-induced vomiting, anorexia, and loss of weight. The patient had no history of previous exposition to heparin derivatives. Platelet count was 490£¿G/L. Biological investigations found severe acute kidney injury (creatinine 720£¿¦Ìmol/L and urea 37£¿mmol/L), metabolic acidosis (pH 7.10, HCO3¨C14£¿mmol/L), and mild hyperkaliemia of 5.4£¿mmol/L. Abdominal scanning found no renal or digestive abnormality. First line treatment consisted of important fluid loading with crystalloids (5000£¿mL ringer lactate, 500£¿mL sodium bicarbonate 1,4%, and 500£¿mL sodium bicarbonate 4,2%) and parallel norepinephrine infusion to obtain satisfying hemodynamics. The patient was then transferred to our ICU. The hospitalization course was marked with an acute respiratory distress syndrome due to acute aspiration, cardiac failure with infusion of inotropic agent, and persistent anuric renal failure with the need of RRT (continuous venovenous hemofiltration (CVVHF), using the Aquarius System, Edwards Lifesciences, France, blood flow 200¨C250£¿mL/min, and ultrafiltrate flow 35£¿mL/kg/h, priming with 5000£¿UI unfractionated heparin (UFH) in 2000£¿mL saline
%U http://www.hindawi.com/journals/crihem/2013/849168/