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It presents an overall incidence of 0.2–5%, although it is variable and depends on the type of heparin, prior heparin exposure and the administration context. HIT is caused by the formation of IgG antibodies against the heparin/platelet factor 4 (PF4) antigenic complex, resulting in platelet activation and thrombin generation.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of a man who developed thrombocytopenia after 7 days of treatment with UFH, associating aortoiliac thrombosis which was treated with argatroban, confirming the presence of antiheparin/PF4 antibodies.</p><p id="par0015" class="elsevierStylePara elsevierViewall">We report the case of a 62-year-old male with a history of hypertension, dyslipidaemia, obesity, atrial flutter treated with ablation, ex-smoker and COPD. A femorofemoral <span class="elsevierStyleItalic">bypass</span> was performed from right to left due to a grade <span class="elsevierStyleSmallCaps">ii</span>b chronic ischemia of the left lower limb (LLL) with occlusion of the left iliac axis. It required immediate thrombectomy and <span class="elsevierStyleItalic">bypass</span> reimplantation due to LLL ischemia. The clinical course during his stay in postoperative care was torpid. The following conditions stood out as main complications: LLL compartment syndrome, requiring fasciotomy, respiratory distress syndrome secondary to septic <span class="elsevierStyleItalic">shock</span>, oligoanuric multifactorial renal failure requiring continuous veno-venous hemofiltration, and cardiovascular dysfunction with arrhythmias treated with electrical cardioversion. In the ninth postoperative day, the patient developed cyanosis and lividity of the operated limb, detecting on the emergency CT angiography a massive thrombosis from the infrarenal aorta to the iliofemoral axis of the operated limb. UFH infusion was maintained for anticoagulant range right from the immediate postoperative period, observing a progressive decrease in platelet count, from 177<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/L on the sixth postoperative day to 28<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/L at that time. Given the context of UFH infusion 7 days before the decrease in platelets, a history of major vascular surgery and the new massive acute thrombotic episode, the diagnosis of HIT was suspected with a <span class="elsevierStyleItalic">4T Score</span> (Thrombocytopenia<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>Thrombosis<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>Time relative to the use of heparin<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>Other causes of thrombocytopenia) of high probability. UFH infusion was immediately suspended and detection of antiheparin/PF4 antibodies was requested. An emergency axillobifemoral <span class="elsevierStyleItalic">bypass</span> was performed with argatroban 1<span class="elsevierStyleHsp" style=""></span>μg/kg/min due to intraoperative thrombosis, with coagulation controls through lab tests and thromboelastometry (ROTEM). In ROTEM, a prolonged clotting time of EXTEM and INTEM was observed, without HEPTEM correction (discarding a residual effect of UFH), and a decrease in maximum clot amplitude, alterations possibly due to thrombocytopenia, decrease hepatic synthesis factors and argatroban. Lab results confirmed a thrombocytopenia of 47<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/L, INR 5.4, APTT<span class="elsevierStyleHsp" style=""></span>><span class="elsevierStyleHsp" style=""></span>120 and fibrinogen impossible to calculate, so argatroban infusion was suspended. Despite this hypocoagulability situation maintained for 24<span class="elsevierStyleHsp" style=""></span>h, possibly due to consumption and impaired synthesis coagulopathy, the patient presented a new episode of thrombosis requiring thrombectomy. He died hours later from multiple organ failure. Lab results confirmed the presence of antiheparin/PF4 antibodies by ELISA.</p><p id="par0020" class="elsevierStylePara elsevierViewall">This case reflects the severity of HIT and the importance of early diagnosis and treatment. The diagnosis is clinical in cases of thrombocytopenia after heparin administration. Laboratory diagnosis based on demonstrating the presence of antiheparin/PF4 antibodies, helps to confirm the clinical diagnosis and should not delay treatment. Heparin must be suspended immediately, establishing an alternative anticoagulant therapy to prevent or treat thromboembolic complications, with thrombin inhibitors being the indicated drugs: lepidurin, bivalirudin and argatroban. The latter, has a short half-life, hepatic metabolism and biliary elimination. The safety and efficacy of thrombosis treatment due to HIT with argatroban has been demonstrated in 2 prospective studies.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">2</span></a> Its monitoring is conducted through APTT, but its effects are also evident using ROTEM. However, no studies are yet available on ROTEM monitoring regarding coagulation disorders caused by the administration of thrombin inhibitors.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Alarcón Pérez L, Rodríguez Huerta AM, Duque González P. Trombocitopenia inducida por heparina con trombosis aortoilíaca tratada con argatrobán. Med Clin (Barc). 2017;148:286–287.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:2 [ 0 => array:3 [ "identificador" => "bib0015" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Trombocitopenia inducida por heparina" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "I. Cruz-González" 1 => "M. Sánchez-Ledesma" 2 => "P.L. Sánchez" 3 => "I.K. 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Mertzlufft" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Biologics" "fecha" => "2007" "volumen" => "1" "paginaInicial" => "105" "paginaFinal" => "112" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/19707320" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000014800000006/v1_201704120030/S2387020617301894/v1_201704120030/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000014800000006/v1_201704120030/S2387020617301894/v1_201704120030/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020617301894?idApp=UINPBA00004N" ]
