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"apellidos" => "Almeida" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2341192918300787" "doi" => "10.1016/j.redare.2017.12.016" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2341192918300787?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935618300045?idApp=UINPBA00004N" "url" => "/00349356/0000006500000006/v1_201805300407/S0034935618300045/v1_201805300407/es/main.assets" ] ] "itemSiguiente" => array:19 [ "pii" => "S2341192918300714" "issn" => "23411929" "doi" => "10.1016/j.redare.2017.12.015" "estado" => "S300" "fechaPublicacion" => "2018-06-01" "aid" => "898" "copyright" => "Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor" "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "cor" "cita" => "Revista Española de Anestesiología y Reanimación (English Version). 2018;65:356-8" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 1 "PDF" => 1 ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letter to the Editor</span>" "titulo" => "Updated Guideline of the Canadian Pain Society for the pharmacological management of chronic neuropathic pain: Does it bring something new?" 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Granell Gil, P. Solís Albamonte, C. Córdova Hernández, I. Cobo, R. Guijarro, J.A. de Andrés Ibañez" "autores" => array:6 [ 0 => array:2 [ "nombre" => "M." "apellidos" => "Granell Gil" ] 1 => array:2 [ "nombre" => "P." "apellidos" => "Solís Albamonte" ] 2 => array:2 [ "nombre" => "C." "apellidos" => "Córdova Hernández" ] 3 => array:2 [ "nombre" => "I." "apellidos" => "Cobo" ] 4 => array:2 [ "nombre" => "R." "apellidos" => "Guijarro" ] 5 => array:2 [ "nombre" => "J.A." 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Mota, C. Filipe, A.L. Almeida" "autores" => array:3 [ 0 => array:4 [ "nombre" => "S." "apellidos" => "Mota" "email" => array:1 [ 0 => "jordana_mota_717@hotmail.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "C." "apellidos" => "Filipe" ] 2 => array:2 [ "nombre" => "A.L." "apellidos" => "Almeida" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Departamento de Anestesiología, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Síndrome urémico hemolítico atípico: una complicación postoperatoria infrecuente" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 965 "Ancho" => 2083 "Tamanyo" => 112396 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Differential diagnosis of microangiopathic haemolytic anaemia (MAHA). <span class="elsevierStyleItalic">Abbreviations</span>: aHUS, atypical haemolytic uremic syndrome; CFH, complement factor H; TTP, thrombotic thrombocytopenic purpura.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uremic syndrome (aHUS) are acute, rare, life threatening thrombotic microangiopathies that require rapid diagnosis and treatment. These conditions are defined by erythrocyte fragmentation and elevated levels of lactate dehydrogenase (LDH) and thrombocytopenia, with renal involvement primarily present in aHUS and neurological and cardiological sequelae in TTP.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The cornerstones of prompt treatment for most cases of TTP and aHUS are plasma exchange (PEX) and monoclonal therapy.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1–4</span></a> HUS is a rare disease with an overall incidence of 1–2 cases per 100,000<span class="elsevierStyleHsp" style=""></span><a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a>; it can be subdivided into typical and atypical forms. Typical HUS is a syndrome of thrombocytopenia, renal dysfunction, and microangiopathic haemolytic anaemia (MAHA) associated with Shiga toxin-producing <span class="elsevierStyleItalic">Escherichia coli</span>. The atypical form is not related to Shiga toxins and accounts for around 5–10% of all cases of HUS.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2–5</span></a> AHUS has a poorer prognosis, with death rates as high as 25% and progression to end-stage renal disease in half of all patients. In the typical form, in contrast, 3% of patients develop end-stage renal disease, and 25% present reduced renal function.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3,4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">AHUS is currently thought to be a consequence of dysregulation of the complement system associated with mutations causing excessive complement activation on the surface of the renal microvasculature. However, further environmental and possible genetic triggers are needed for disease presentation.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,5–7</span></a> Approximately 60% of individuals with aHUS also have an inherited and/or acquired abnormality affecting components of the complement pathway. These include mutations of genes encoding complement regulators (factor H, factor I, CD46 and thrombomodulin) and/or complement activators (C3 and factor B).<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,5,7</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">We present the case of a patient presenting with MAHA, and describe the differential diagnosis, its therapeutic implications, and follow-up.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Clinical case</span><p id="par0025" class="elsevierStylePara elsevierViewall">A 46-year-old female, ASA II, with a history of vertical sleeve gastrectomy without complications, and trazodone 50<span class="elsevierStyleHsp" style=""></span>mg and alprazolam 0.25<span class="elsevierStyleHsp" style=""></span>mg for depression, was scheduled for pericystectomy for hydatid cyst of the liver. The preoperative analytical workup was unremarkable, except for slight normocytic normochromic anaemia (haemoglobin 10.2<span class="elsevierStyleHsp" style=""></span>g/dL). This was not considered relevant for the present surgical indication, and a study of its aetiology was postponed for after surgery.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Surgery lasted for 4<span class="elsevierStyleHsp" style=""></span>h and 30<span class="elsevierStyleHsp" style=""></span>min, with no intraoperative complications or observations of note, and the patient was transferred to the post-anaesthesia care unit.</p><p id="par0035" class="elsevierStylePara elsevierViewall">In the immediate postoperative period, she became oliguric, with decreased urinary output in the following hours, and dark urine. She was calm, cooperative, hemodynamically stable, and with no clinical signs of haemorrhage. Seven hours later, we noticed a progressive fall in haemoglobin levels (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). Fluid therapy and blood transfusion were initiated. Although the patient remained asymptomatic, haemoglobin levels continued to decline. When haemoglobin had fallen to below 7<span class="elsevierStyleHsp" style=""></span>g/dL, 1 unit of packed red cells (PRCs) was administered (between 7 and 8<span class="elsevierStyleHsp" style=""></span>h after surgery). Given the persistent decline of haemoglobin (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>), 3 more units were administered over a 17-h period from the end of surgery (total 4 units). No vasoactive drugs were needed. Blood panels showed decreased platelet count, increased creatinine values, increased LDH, and increased total bilirubin (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). Coagulation studies were unremarkable. Urine analysis showed bilirubinuria, haemoglobinuria and proteinuria. Peripheral blood smear showed schizocytes, considered indicative of MAHA. Abdominal and renal ultrasound were unremarkable. The patient was asymptomatic, in other words, with no current or recent history of diarrhoea.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">The surgical team denied intraoperative rupture of the hydatid cyst.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Given the coexistence of MAHA, thrombocytopenia and acute renal failure, aHUS was suspected, and PEX was initiated as soon as possible (within the first 24<span class="elsevierStyleHsp" style=""></span>h after surgery).</p><p id="par0050" class="elsevierStylePara elsevierViewall">After PEX was started, there was no further need for PCRs. Kidney function initially improved, albeit only slightly, in response to therapy, but serum creatinine values remained high (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). She was admitted for continuing haemodialysis and PEX for 2 weeks.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Further studies of genetic mutations and immunological causes of MAHA were requested. ADAMTS13 activity was normal. Anti-ADAMTS13 antibody, direct Coombs test, anti-ds-DNA antibody, anti-ANA antibody and anti-Scl70 antibody were negative, all but ruling out a TTP or immunological cause (<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>). HIV testing was negative.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0060" class="elsevierStylePara elsevierViewall">Mutations in complement factor H (CFH) associated with factor H deficiency were detected: c.3172T>C (p.Tyr1058His) and c.3178G>C (p.Val1060Leu), and polymorphisms (p.Gln1076Glu).</p><p id="par0065" class="elsevierStylePara elsevierViewall">Creatinine values gradually decreased over the course of 30 days (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). The patient was followed up by the nephrologist, and after 6 months creatinine levels had normalised, without returning to baseline values (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). After 3 years, there was no worsening of renal function and no other complications were observed.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Discussion</span><p id="par0070" class="elsevierStylePara elsevierViewall">AHUS appears to be a “two-hit” disease, involving a presumed “trigger” that leads to inflammation and is thought to increase complement activation, and a “second hit” that may involve an autoantibody or a genetic modifier. Genetic mutations play a role in the pathogenesis of aHUS, and more than 50% of patients with aHUS have causative mutations in complement genes.<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">5–8</span></a> The pathogenesis appears to involve 3 stages: a triggering event (e.g. transplantation, pregnancy, etc.); activation of the complement cascade and/or coagulation pathway, leading to thrombus formation; and a dysregulation loop, with complement overactivation, which leads to thrombi formation. Altered function of the coagulation pathway may be caused by genetic variants in coagulation genes, leading to enhanced formation or decreased degradation of thrombi, promoting thrombosis leading to activation of the complement system. Genetic variants in complement genes and/or acquired factors, such as CFH autoantibodies, lead to inadequate/ineffective complement regulation.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">After reviewing several previous case reports, we hypothesize that any surgery could act as a “trigger”. In 2013, a case of aHUS was reported after laparoscopic hemicolectomy. According to the authors, after the case of postoperative HUS in a child reported by Maki in 1968, only posttransplant HUS cases have been reported.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> In 2013, an anaesthetist reported a case of HUS after orthopaedic surgery, but in a patient with a 2-week history of diarrhoea and confusion, which therefore may not exclude “typical” HUS.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> In 2014, a C3 mutation was discovered in a patient who presented aHUS after correction of Fallot tetralogy.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> In 2016, a patient undergoing myomectomy also presented aHUS, which was treated with eculizumab.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">To the best of our knowledge, this is the second case of post-surgery non-transplant aHUS with a reported mutation, in this case, in CFH.</p><p id="par0085" class="elsevierStylePara elsevierViewall">Although it is a rare postoperative complication, aHUS should be considered as a possible cause of MAHA (with haemoglobin <10<span class="elsevierStyleHsp" style=""></span>g/dL, increased LDH, and presence of fragmented red cells in peripheral smear) and acute kidney injury after surgical procedures associated with thrombocytopenia (platelets <150,000/μL).<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,5,7</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">PEX is the first-line treatment for aHUS in adults, and should be started within 24<span class="elsevierStyleHsp" style=""></span>hours of diagnosis, with supportive treatment.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3,4</span></a> The objectives are to replace mutant elements of the complement with normal elements in order to eliminate pro-inflammatory and thrombogenic factors responsible for symptoms, and to preserve renal function.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,4</span></a> Only 1 or 2 plasma volumes should be exchanged per day, or 20–30<span class="elsevierStyleHsp" style=""></span>ml/kg of body weight can be infused once a day in the first week and then progressively tapered from 5 to 3 sessions per week.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3,4</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">Some patients who respond to PEX may need long-term therapy to maintain remission. Some of these together with non-responders have been selected for clinical trials, for instance, with monoclonal therapy (eculizumab – anti-C5 monoclonal antibody).<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a> Some authors claim that this could be the new gold standard therapy.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2,4</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Patients with a pathogenic complement gene mutation are potentially at risk of disease recurrence.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">After 3 years of follow-up, end-stage renal disease or death occurs in >50% of aHUS patients, with or without plasma-based therapy.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a></p><p id="par0110" class="elsevierStylePara elsevierViewall">In our patient, presumptive diagnosis of aHUS was made, and PEX was initiated before the genetic defect was found. PEX was suspended on the 15th postoperative day, and the patient was clinically and analytically monitored. The patient has been kept under observation, with no specific therapy, for 3 years to date, with normal (but not baseline) creatinine levels.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Conflicts of interest</span><p id="par0115" class="elsevierStylePara elsevierViewall">None declared.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:9 [ 0 => array:3 [ "identificador" => "xres1042064" "titulo" => "Abstract" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0005" "titulo" => "Introduction and objectives" ] 1 => array:2 [ "identificador" => "abst0010" "titulo" => "Clinical case" ] 2 => array:2 [ "identificador" => "abst0015" "titulo" => "Conclusion" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec994824" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1042065" "titulo" => "Resumen" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0020" "titulo" => "Introducción y objetivos" ] 1 => array:2 [ "identificador" => "abst0025" "titulo" => "Caso clínico" ] 2 => array:2 [ "identificador" => "abst0030" "titulo" => "Conclusión" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec994823" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Clinical case" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Conflicts of interest" ] 8 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2017-10-17" "fechaAceptado" => "2017-12-19" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec994824" "palabras" => array:4 [ 0 => "Atypical haemolytic uremic syndrome" 1 => "Complement factor H" 2 => "Postoperative period" 3 => "Plasma exchange" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec994823" "palabras" => array:4 [ 0 => "Síndrome urémico hemolítico atípico" 1 => "Factor H del complemento" 2 => "Periodo postoperatorio" 3 => "Intercambio de plasma" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:3 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introduction and objectives</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Thrombotic thrombocytopenic purpura and atypical haemolytic uremic syndrome (aHUS) are acute, rare, life-threatening thrombotic microangiopathies that require swift management. We report a case of acute microangiopathic haemolytic anaemia (MAHA) presenting in perioperative setting.</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Clinical case</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">After hepatic pericystectomy for hydatid cyst, a 46-year-old female developed MAHA, thrombocytopenia and acute renal failure in the immediate postoperative period. “aHUS” was considered and immediate plasma exchange was initiated. Plasma exchange was performed for 2 weeks with remission of renal dysfunction. Further evaluation of genetic mutations and immunological causes for MAHA were sought. Mutations in complement factor H associated with factor H deficiency were identified, which are associated with increased risk of aHUS.</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Conclusion</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">MAHA is a rare postoperative condition, requiring rapid differential diagnosis and treatment. Anaesthetists should bear in mind aHUS as a possible cause of MAHA, especially concerning immediate care for these patients.</p></span>" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0005" "titulo" => "Introduction and objectives" ] 1 => array:2 [ "identificador" => "abst0010" "titulo" => "Clinical case" ] 2 => array:2 [ "identificador" => "abst0015" "titulo" => "Conclusion" ] ] ] "es" => array:3 [ "titulo" => "Resumen" "resumen" => "<span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Introducción y objetivos</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La púrpura trombocitopénica trombótica y el síndrome urémico hemolítico atípico (SHUa) son microangiopatías trombóticas agudas, infrecuentes y potencialmente fatales que requieren una gestión rápida. Reportamos un caso de anemia hemolítica microangiopática aguda (MAHA) que se presentó en el entorno perioperatorio.</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Caso clínico</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Tras la realización de periquistectomía hepática debida a quiste hidatídico, una mujer de 46 años desarrolló MAHA, trombocitopenia e insuficiencia renal aguda durante el periodo postoperatorio inmediato. Se consideró la posibilidad de SHUa, iniciándose intercambio de plasma inmediato. Se realizó intercambio de plasma durante 2 semanas, con remisión de la disfunción renal. Posteriormente se evaluaron las mutaciones genéticas y las causas inmunológicas de MAHA. Se identificaron mutaciones en el factor H del complemento asociadas a deficiencia del factor H, que están asociadas a un incremento del riesgo de SHUa.</p></span> <span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusión</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">MAHA constituye una situación postoperatoria infrecuente, que requiere un rápido diagnóstico diferencial y tratamiento. Los anestesiólogos deberán considerar el SHUa como causa posible de MAHA, especialmente en lo referente al cuidado inmediato de estos pacientes.</p></span>" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0020" "titulo" => "Introducción y objetivos" ] 1 => array:2 [ "identificador" => "abst0025" "titulo" => "Caso clínico" ] 2 => array:2 [ "identificador" => "abst0030" "titulo" => "Conclusión" ] ] ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Mota S, Filipe C, Almeida AL. Síndrome urémico hemolítico atípico: una complicación postoperatoria infrecuente. Rev Esp Anestesiol Reanim. 2018;65:351–355.</p>" ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 965 "Ancho" => 2083 "Tamanyo" => 112396 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Differential diagnosis of microangiopathic haemolytic anaemia (MAHA). <span class="elsevierStyleItalic">Abbreviations</span>: aHUS, atypical haemolytic uremic syndrome; CFH, complement factor H; TTP, thrombotic thrombocytopenic purpura.</p>" ] ] 1 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">BUN: Blood urea nitrogen; LDH: lactic dehydrogenase.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head " align="" valign="top" scope="col"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " colspan="12" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Time</th></tr><tr title="table-row"><th class="td" title="table-head " align="" valign="top" scope="col"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col">Preoperative \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " colspan="11" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Postoperative</th></tr><tr title="table-row"><th class="td" title="table-head " align="" valign="top" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="" valign="top" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Immediate \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">7<span class="elsevierStyleHsp" style=""></span>h \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">9<span class="elsevierStyleHsp" style=""></span>h \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">17<span class="elsevierStyleHsp" style=""></span>h \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">7 days \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">15 days \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">1 month \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">3 months \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">6 months \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">1 year \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">3 years \t\t\t\t\t\t\n \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry " colspan="13" align="left" valign="top"><span class="elsevierStyleItalic">Blood panels</span></td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Haemoglobin (12–15<span class="elsevierStyleHsp" style=""></span>g/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">10.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">8.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">7.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">6.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">7.7 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">9.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">10.4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">11.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">11.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">12.3 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">12.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">11.0 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Haematocrit (36–46%) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">31.3 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">25.0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">22.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">19.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">22.9 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">27.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">31.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">33.1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">32.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">35.9 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">35.8 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">32.9 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Platelets (150–400<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>/L) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">362 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">271 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">115 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">84 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">100 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">234 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">366 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">313 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">224 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">214 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">202 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">210 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>BUN (7.9–20.9<span class="elsevierStyleHsp" style=""></span>mg/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">13.7 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">15 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">22 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">26 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">35 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">61 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">27.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">16.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">13.4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">14.4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">14.3 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">10.7 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Creatinine (0.55–1.02<span class="elsevierStyleHsp" style=""></span>mg/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.69 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.97 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1.53 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1.80 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2.47 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">7.99 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">4.65 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1.24 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.89 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.85 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.76 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.82 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>LDH (<247<span class="elsevierStyleHsp" style=""></span>U/L) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">181 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">527 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2395 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2203 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2534 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">336 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">307 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">187 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">130 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">140 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">143 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">172 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>Total bilirubin (0.3–1.2<span class="elsevierStyleHsp" style=""></span>mg/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.3 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2.7 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1.8 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1.9 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.5 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0.3 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1770394.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Blood samples.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "How I treat thrombotic thrombocytopenic purpura and atypical haemolytic uraemic syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "M. 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