Case report
Diagnosis and management of posterior reversible encephalopathy syndrome in systemic lupus erythematosus. Case report
Diagnóstico y manejo de síndrome de encefalopatía posterior reversible asociado a lupus eritematoso sistémico. Reporte de caso clínico
Michelle Fuseau Herreraa,
, Mariela Villagómez Estradaa, David Garrido Salazarb, Diego Noboa Torresa, Líder Escudero Abada, Beatriz Narváez Castilloc
Corresponding author
a Servicio de Reumatología, Hospital de Especialidades de las Fuerzas Armadas N.° 1, Quito, Ecuador
b Servicio de Medicina General, Centro de Salud N.° 1, Ministerio de Salud Pública del Ecuador, Ibarra, Ecuador
c Servicio de Neurología, Hospital de Especialidades de las Fuerzas Armadas N.° 1, Quito, Ecuador
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Reporte de caso clínico" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1464 "Ancho" => 1355 "Tamanyo" => 150557 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Diagnostic algorithm for posterior reversible encephalopathy syndrome.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Posterior reversible encephalopathy syndrome (PRES) is a rare complication of various clinical entities. Its incidence is unknown, having been reported in a wide range of ages from 14 to 78 years, with an average age of 44 years and a male/female ratio of 0.8/1.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">1</span></a> Although the prognosis is usually favorable, mortality rates of up to 15% have been reported.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">2</span></a> It is determined by typical clinical–radiological manifestations, usually transient.<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">3</span></a> Either in an acute or subacute form, in descending order of frequency it occurs with encephalopathy, seizures, headache, visual disturbances and focal neurological deficit.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">4</span></a> Several pathophysiological theories have been postulated, with two being the most accepted. The first one suggests that the sudden increase in blood pressure exceeds the self-regulation of cerebral blood flow, causing vasodilation and hyperperfusion, with rupture of the blood–brain barrier (BBB) and vasogenic edema.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">5</span></a> Thus, it has been classically associated with eclampsia and hypertensive encephalopathy; however, 20–30% of patients are normotensive, suggesting a second theory of direct endothelial toxicity caused by inflammatory mediators, more correlated to patients with immunosuppressive treatment, renal failure, connective tissue disorders or sepsis.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">6</span></a> It occurs in <1% of patients with systemic lupus erythematosus (SLE), with a higher incidence in young people, with a Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) ≥6 and associated comorbidities.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">7</span></a> Magnetic resonance imaging (MRI) of the brain is determinant for the diagnosis, showing vasogenic edema, usually in the posterior cerebral territory, bilateral and symmetrical.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">8</span></a> Since the diagnosis of PRES requires a high clinical and imaging suspicion, with the subsequent establishment of early treatment for a favorable prognosis; the objective of this work is to provide information for the recognition and management of this unusual syndrome associated with SLE.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Description of the case</span><p id="par0010" class="elsevierStylePara elsevierViewall">A 25-year-old mestizo woman, from Quito, Ecuador, with personal pathological antecedents of hypothyroidism and SLE, diagnosed in December 2012, at the age of 21 years. In December 2016, 4 years after the diagnosis of SLE, she presented an exacerbation triggered by acute diarrheal disease; with musculoskeletal (arthritis, myalgias) and mucocutaneous (oral ulcers) manifestations, serositis (right pleural effusion), bicytopenia (anemia, thrombocytopenia), renal involvement (hematuria, proteinuria, acute renal failure, Acute Kidney Injury Network [AKIN] classification III) and arterial hypertension (AHT); all of which conferred her a high SLEDAI (value: 23). The renal biopsy reported focal proliferative lupus glomerulonephritis class II, not corresponding with intense lupus activity; without changes attributable to antiphospholipid syndrome, as well as negativity of these antibodies. Due to the multi-organ involvement, she received pulses of 1<span class="elsevierStyleHsp" style=""></span>g of methylprednisolone intravenous for 3 days, replacement of blood products, 6 sessions of plasmapheresis, hemodyalisis, amlodipine 10<span class="elsevierStyleHsp" style=""></span>mg/day, atenolol 50<span class="elsevierStyleHsp" style=""></span>mg/day and mycophenolate mofetil 1<span class="elsevierStyleHsp" style=""></span>g/12<span class="elsevierStyleHsp" style=""></span>h orally, since she presented gastrointestinal intolerance to higher doses. Three weeks after admission she presented acceptable analytical and clinical improvement with the treatment, and therefore, her hospital discharge was indicated. Twenty-four hours later, the patient re-enters with a convulsive status. In emergencies they initiated airway management, intravenous anticonvulsants with diazepam 10<span class="elsevierStyleHsp" style=""></span>mg, midazolam 3<span class="elsevierStyleHsp" style=""></span>mg, phenytoin 1<span class="elsevierStyleHsp" style=""></span>g and transferred her to the intensive care unit.</p><p id="par0015" class="elsevierStylePara elsevierViewall">It was requested a cranial tomography, which did not show signs of ischemia or bleeding; a right occipital hypodensity without mass effect was observed, and for this reason the order of exams was broadened to identify its etiology. Metabolic, infectious and pharmacological causes were excluded. Due to AHT difficult to control (up to 190/100<span class="elsevierStyleHsp" style=""></span>mmHg with mean arterial pressure [MAP] of 130<span class="elsevierStyleHsp" style=""></span>mmHg), the patient required up to 6 antihypertensive drugs; atenolol 50<span class="elsevierStyleHsp" style=""></span>mg/12<span class="elsevierStyleHsp" style=""></span>h, losartan 100<span class="elsevierStyleHsp" style=""></span>mg/day, amlodipine 10<span class="elsevierStyleHsp" style=""></span>mg/day, doxazosin 2<span class="elsevierStyleHsp" style=""></span>mg/6<span class="elsevierStyleHsp" style=""></span>h via nasogastric tube, and intravenous nitroprusside 50<span class="elsevierStyleHsp" style=""></span>mg/day and furosemide 20<span class="elsevierStyleHsp" style=""></span>mg/6<span class="elsevierStyleHsp" style=""></span>h. Due to severe lupus activity (SLEDAI 21: seizures, hematuria, proteinuria, hypocomplementemia, anti-DNA, thrombocytopenia), she received again treatment with methylprednisolone 1<span class="elsevierStyleHsp" style=""></span>g/3 days. The electroencephalogram did not show epileptiform activity. It was requested a cerebral angioresonance in which findings consistent with vasculitis or thrombosis of the central nervous system were not found. The MRI of the brain showed typical images of PRES (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>), whose development would be related to the exacerbated SLE, severe AHT, lupus glomerulonephritis and use of immunosuppressants, so oral nimodipine 60<span class="elsevierStyleHsp" style=""></span>mg/6<span class="elsevierStyleHsp" style=""></span>h was added and the trigger factors were controlled. Due to the risk of drug-induced lupus, phenytoin was gradually withdrawn, with progressive increase of levetiracetam up to 1<span class="elsevierStyleHsp" style=""></span>g/12<span class="elsevierStyleHsp" style=""></span>h via nasogastric tube. <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a> details the relevant complementary studies. During the follow-up, she did not present new convulsive events, the renal function remained stationary, the blood pressure values improved (MAP 85–90<span class="elsevierStyleHsp" style=""></span>mmHg), and the lupus activity decreased (SLEDAI 13: hematuria, proteinuria, hypocomplementemia, anti-DNA, thrombocytopenia). The MRI of the brain of control evidenced involution of the previous lesions (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0020" class="elsevierStylePara elsevierViewall">Since the first description of the PRES, made in 1996 by Hinchey et al., the knowledge of several aspects of this entity has been broadened. Its original name of reversible posterior leukoencephalopathy syndrome resulted inappropriate, since the imaging changes are not always limited to the cerebral white matter and its clinical manifestations are not always reversible.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">9</span></a> The first 15 cases reported occurred in patients with hypertensive encephalopathy, eclampsia or under immunosuppressive treatment.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">10</span></a> It has also been observed as a complication of other entities such as sepsis, renal failure and connective tissue disorders; therefore, it is currently known that the risk factors that cause endothelial dysfunction are key for the development of PRES.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">11</span></a> The global incidence is not known, but data of retrospective studies indicate that it is more frequent in individuals between 39 and 47 years, generally women, with comorbidities such as hypertensive, renal or autoimmune disorders.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">12</span></a> In patients with SLE, many autoantibodies are directed against the endothelium; producing its activation, expression of adhesion molecules (E-selectin, VCAM-1, ICAM-1) and exposure to proinflammatory cytokines such as IL-1β, TNFα and IL-6, causing disruption of the BBB and appearance of neurological complications.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">13</span></a> It has been reported that in people diagnosed with SLE, the PRES occurs in the context of moderate to severe lupus activity, as well as associated with renal failure and poorly controlled hypertension.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">14</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Regarding the clinical manifestations of the PRES, it is characterized by variable degrees of encephalopathy, from confusion to stupor (50–80%), seizures (60–75%), headache (50%) and visual disturbances ranging from blurred vision to cortical blindness (33%); being unusual the focal neurological deficit (10–15%) and the status epileptic (5–15%).<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">15</span></a> For the initial assessment of the neurological compromise in these patients, a cranial computed axial tomography (CT) scan is usually requested, which is often normal or can show cortical–subcortical hypodensities, predominantly in posterior brain regions.<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">16</span></a> The MRI of the brain determines the diagnosis, showing vasogenic edema, usually in the white matter of the occipital and parietal lobes (territory of the posterior cerebral circulation), visualized as hyperintense lesions in T2 and FLAIR, bilateral and symmetrical.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">17</span></a> The preferential involvement of the white matter is due to its structure of myelinated fibers, arterioles and capillaries which confers it greater laxity. Similarly, the vessels of the anterior cerebral circulation, having greater sympathetic innervation, can adequately respond by vasoconstriction to the sudden increase in cerebral blood flow secondary to hypertension; a protective mechanism less developed in the vertebrobasilar system.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">18</span></a> Less frequently, the gray matter and other lobes may be affected. The images with diffusion sequences allow to distinguish between the vasogenic edema, typical of the PRES, and the cytotoxic edema that may occur atypically and can progress to infarction.<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">19</span></a> The electroencephalogram does not always correlate with the neurological affectation, but it may reveal encephalopathy by the presence of focal sharp waves. In patients with seizures associated with PRES, the main electroencephalographic alteration is the general slowing in theta/delta frequencies.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">20</span></a> The analysis of the cerebrospinal fluid shows nonspecific changes such as a slight increase in cellularity and proteins, and therefore it is useful when it is convenient to rule out an infection in the central nervous system.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">21</span></a> In addition to the aforementioned tests, those that are considered necessary for the differential diagnosis, mainly with neurolupus, metabolic and parainfectious encephalopathy, encephalitis, infarction of the posterior cerebral artery and demyelinating disorders must be performed.<a class="elsevierStyleCrossRefs" href="#bib0250"><span class="elsevierStyleSup">22,23</span></a> Based on the foregoing, <a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a> shows the algorithm proposed by Fugate et al. for the diagnosis of PRES, which aims to identify even atypical cases.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">15</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">In our patient, given the clinical presentation along with the multiple risk factors, imaging findings and exclusion of other etiologies, the diagnosis of PRES was concluded. Symptomatic treatment with anticonvulsant medication and anti-cerebral edema was instituted in a timely manner, together with the control of the causative factors: severe hypertension, SLE with severe activity, lupus glomerulonephritis, immunosuppressive drugs; ratifying the diagnosis during the follow-up with the resolution of the clinical and imaging alterations. With respect to the management of the PRES, the blood pressure should be reduced, the seizures should be treated and the trigger should be controlled. The rapid decrease in blood pressure could cause cerebral ischemia, which is why a goal of a mean blood pressure between 105 and 125<span class="elsevierStyleHsp" style=""></span>mmHg is suggested, without exceeding 25% of this reduction in the first hour. The first-line drugs are calcium channel blockers (nicardipine or nimodipine of choice, that also prevents cerebral vasospasm) or beta-blockers (for example, labetalol). Sodium nitroprusside or hydralazine can be used as second-line drugs. Nitroglycerin should be avoided due to its vasodilator effect, which would increase the cerebral edema.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">24</span></a> The treatment of the seizures is similar to that of other epileptic seizures. Benzodiazepines such as lorazepam or diazepam are used as the first-line therapy. As second-line, phenytoin or valproate, especially in status epilepticus, or phenobarbital. Magnesium sulfate can be used in pregnant women. In refractory seizures, we can give propofol o pentobarbital.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">25</span></a> Drugs that could cause drug-induced lupus, such as hydralazine, methyldopa, captopril, phenytoin, valproate and carbamazepine, should be avoided in patients with SLE. There is controversy about the management of immunosuppressive drugs in the treatment of PRES in patients with SLE.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">26</span></a> After the resolution of the PRES, seizures are infrequent, and therefore, it should be considered to discontinue anticonvulsants as long as there is an adequate control of the risk factors.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">27</span></a> With a timely and adequate treatment, the majority of patients with PRES evolve satisfactorily with remission of the symptoms and imaging lesions in a few days or weeks, although complications, specially hemorrhagic, have been observed in 9–33% of cases, so this case highlights the importance of its recognition and management, which is often a challenge.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">28</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusions</span><p id="par0035" class="elsevierStylePara elsevierViewall">The diagnosis of PRES requires a high clinical and imaging suspicion. Timely treatment with control of the symptoms and the underlying cause ratifies the diagnosis during follow-up, with the resolution of clinical and imaging alterations; otherwise, it may cause neurological sequelae or death.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors declare they do not have any conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:3 [ "identificador" => "xres1205839" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1123365" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1205840" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1123366" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Description of the case" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Conclusions" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Conflict of interest" ] 9 => array:2 [ "identificador" => "xack411929" "titulo" => "Acknowledgments" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2017-08-10" "fechaAceptado" => "2017-10-12" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1123365" "palabras" => array:3 [ 0 => "Posterior reversible encephalopathy syndrome" 1 => "Hypertensive encephalopathy" 2 => "Systemic lupus erythematosus" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1123366" "palabras" => array:3 [ 0 => "Síndrome de encefalopatía posterior reversible" 1 => "Encefalopatía hipertensiva" 2 => "Lupus eritematoso sistémico" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Posterior reversible encephalopathy syndrome (PRES) is a clinical–radiological disorder that may include encephalopathy, seizures, headache, and visual disturbances. It is associated with conditions that induce endothelial damage, causing vasogenic cerebral edema that can be observed in magnetic resonance scans. It occurs in <1% of patients with systemic lupus erythematosus (SLE). It is usually resolved with timely treatment, but delays may lead to neurological sequelae or death. A case of PRES is presented in a patient with SLE with severe activity, a hypertensive emergency, and lupus glomerulonephritis debuting with epileptic status. The outcome was satisfactory with anticonvulsants, as well as treatment for her cerebral edema and hypertension, along with control of other causal factors.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">El síndrome de encefalopatía posterior reversible (PRES) es un trastorno clínico-radiológico caracterizado por encefalopatía, convulsiones, cefalea y alteraciones visuales. Se asocia a entidades que ocasionan daño endotelial, causando edema cerebral vasogénico evidente en resonancia magnética. En pacientes con lupus eritematoso sistémico (LES) se presenta en <1%. Con tratamiento oportuno usualmente resuelve; caso contrario puede producir secuelas neurológicas o muerte. Se reporta el caso de PRES en una paciente con LES con actividad severa, emergencia hipertensiva y glomerulonefritis lúpica que comienza con estatus epiléptico. Evolucionó satisfactoriamente con tratamiento anticonvulsivante, antiedema cerebral, antihipertensivo y control de los demás factores causales.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Fuseau Herrera M, Villagómez Estrada M, Garrido Salazar D, Noboa Torres D, Escudero Abad L, Narváez Castillo B. Diagnóstico y manejo de síndrome de encefalopatía posterior reversible asociado a lupus eritematoso sistémico. Reporte de caso clínico. Rev Colomb Reumatol. 2019;26:74–79.</p>" ] ] "multimedia" => array:4 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 945 "Ancho" => 3000 "Tamanyo" => 204987 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Simple<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>diffusion nuclear magnetic resonance imaging of the brain at admission: bilateral, symmetric, hyperintense lesions in FLAIR sequence in white matter of occipital and parietal lobes.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 943 "Ancho" => 3000 "Tamanyo" => 221570 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Simple<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>diffusion nuclear magnetic resonance imaging of the brain, of control (3 weeks later): previous lesions in resolution.</p>" ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1464 "Ancho" => 1355 "Tamanyo" => 150557 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Diagnostic algorithm for posterior reversible encephalopathy syndrome.</p>" ] ] 3 => 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="spar0035" class="elsevierStyleSimplePara elsevierViewall">Anti-dsDNA: anti-double stranded DNA; HB: hematic biometry; MU: microscopic urinalysis; ISN/RPS: International Society of Nephrology/Renal Pathology Society; SLE: systemic lupus erythematosus; eGFR CKD-EPI: glomerular filtration rate estimated using the equation of the Chronic Kidney Disease-Epidemiology Collaboration.</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="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Date \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="center" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Clinical tests \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Exacerbation of SLE 4 years after diagnosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">HB: hemoglobin 7<span class="elsevierStyleHsp" style=""></span>mg/dl; hematocrit 22.2%; platelets 75,000/μlC-reactive protein: 2.52<span class="elsevierStyleHsp" style=""></span>mg/dl; procalcitonin 0.348<span class="elsevierStyleHsp" style=""></span>ng/mlCreatinine 5.7<span class="elsevierStyleHsp" style=""></span>mg/dl (eGFR CKD-EPI: 9.6<span class="elsevierStyleHsp" style=""></span>ml/min/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>); urea 187<span class="elsevierStyleHsp" style=""></span>mg/dlCreatine kinase: 18<span class="elsevierStyleHsp" style=""></span>U/l; lactate dehydrogenase: 237<span class="elsevierStyleHsp" style=""></span>U/lMU: proteins 150<span class="elsevierStyleHsp" style=""></span>mg/dl; red blood cells 40.8/field; proteinuria: 1452<span class="elsevierStyleHsp" style=""></span>mg/24<span class="elsevierStyleHsp" style=""></span>hC3: 36<span class="elsevierStyleHsp" style=""></span>mg/dl; C4: 15<span class="elsevierStyleHsp" style=""></span>mg/dl; anti-dsDNA: 200<span class="elsevierStyleHsp" style=""></span>IU/mlLupus anticoagulant, anticardiolipins, beta 2-glycoprotein 1: negativeRenal biopsy; focal lupus proliferative glomerulonephritis class II (ISN/RPS) with a chronicity and activity index of 4 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Readmission \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">HB: hemoglobin 8.90<span class="elsevierStyleHsp" style=""></span>mg/dl; hematocrit 26.3%; platelets 130,000/μlCreatinine 2.77<span class="elsevierStyleHsp" style=""></span>mg/dl (eGFR CKD-EPI: 22.8<span class="elsevierStyleHsp" style=""></span>ml/min/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>); urea 105.1<span class="elsevierStyleHsp" style=""></span>mg/dlLactate dehydrogenase: 527<span class="elsevierStyleHsp" style=""></span>U/l; γ-glutamyl transferase 79<span class="elsevierStyleHsp" style=""></span>U/l; alkaline phosphatase: 138<span class="elsevierStyleHsp" style=""></span>U/l; total bilirubin: 1.23<span class="elsevierStyleHsp" style=""></span>mg/dl; direct: 0.50<span class="elsevierStyleHsp" style=""></span>mg/dl; indirect: 0.73<span class="elsevierStyleHsp" style=""></span>mg/dlMU: proteins 300<span class="elsevierStyleHsp" style=""></span>mg/dl; red blood cells 44/field; proteinuria 1974<span class="elsevierStyleHsp" style=""></span>mg/24<span class="elsevierStyleHsp" style=""></span>hSimple cranial tomography: right occipital hypodensity, without mass effect. No signs of ischemia or bleeding Electroencephalogram: background brain activity at 4<span class="elsevierStyleHsp" style=""></span>Hz in low voltage theta rhythm. Presence of vertex sharp waves with posterior delta rhythms with interhemispheric symmetry, without paroxysmal epileptiform activityMagnetic resonance angiography of the brain in arterial and venous phases: without vascular alterations \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2058208.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Relevant complementary studies of the case.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:28 [ 0 => array:3 [ "identificador" => "bib0145" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Clinical spectrum of reversible posterior leukoencephalopathy syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "V. Lee" 1 => "E. 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Caminero" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Neurologia" "fecha" => "2005" "volumen" => "20" "paginaInicial" => "327" "paginaFinal" => "331" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16163575" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0160" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Clinical predictors and differential diagnosis of posterior reversible encephalopathy syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "L. Faille" 1 => "S. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 October | 105 | 6 | 111 |
| 2024 September | 199 | 16 | 215 |
| 2024 August | 166 | 10 | 176 |
| 2024 July | 268 | 23 | 291 |
| 2024 June | 161 | 17 | 178 |
| 2024 May | 227 | 19 | 246 |
| 2024 April | 218 | 7 | 225 |
| 2024 March | 353 | 14 | 367 |
| 2024 February | 422 | 18 | 440 |
| 2024 January | 643 | 30 | 673 |
| 2023 December | 423 | 17 | 440 |
| 2023 November | 465 | 29 | 494 |
| 2023 October | 460 | 41 | 501 |
| 2023 September | 358 | 14 | 372 |
| 2023 August | 288 | 16 | 304 |
| 2023 July | 365 | 9 | 374 |
| 2023 June | 355 | 30 | 385 |
| 2023 May | 371 | 19 | 390 |
| 2023 April | 329 | 9 | 338 |
| 2023 March | 354 | 19 | 373 |
| 2023 February | 314 | 29 | 343 |
| 2023 January | 246 | 15 | 261 |
| 2022 December | 233 | 12 | 245 |
| 2022 November | 273 | 19 | 292 |
| 2022 October | 238 | 20 | 258 |
| 2022 September | 258 | 9 | 267 |
| 2022 August | 238 | 25 | 263 |
| 2022 July | 223 | 24 | 247 |
| 2022 June | 242 | 31 | 273 |
| 2022 May | 280 | 29 | 309 |
| 2022 April | 323 | 30 | 353 |
| 2022 March | 322 | 29 | 351 |
| 2022 February | 377 | 42 | 419 |
| 2022 January | 354 | 36 | 390 |
| 2021 December | 310 | 46 | 356 |
| 2021 November | 351 | 30 | 381 |
| 2021 October | 391 | 59 | 450 |
| 2021 September | 472 | 54 | 526 |
| 2021 August | 380 | 34 | 414 |
| 2021 July | 482 | 32 | 514 |
| 2021 June | 302 | 24 | 326 |
| 2021 May | 337 | 34 | 371 |
| 2021 April | 784 | 27 | 811 |
| 2021 March | 673 | 33 | 706 |
| 2021 February | 414 | 38 | 452 |
| 2021 January | 377 | 51 | 428 |
| 2020 December | 374 | 28 | 402 |
| 2020 November | 321 | 27 | 348 |
| 2020 October | 259 | 29 | 288 |
| 2020 September | 329 | 47 | 376 |
| 2020 August | 398 | 43 | 441 |
| 2020 July | 387 | 20 | 407 |
| 2020 June | 367 | 55 | 422 |
| 2020 May | 358 | 44 | 402 |
| 2020 April | 386 | 47 | 433 |
| 2020 March | 342 | 20 | 362 |
| 2020 February | 394 | 49 | 443 |
| 2020 January | 311 | 33 | 344 |
| 2019 December | 263 | 26 | 289 |
| 2019 November | 146 | 20 | 166 |
| 2019 October | 112 | 12 | 124 |
| 2019 September | 37 | 6 | 43 |
| 2019 August | 24 | 2 | 26 |
| 2019 July | 24 | 14 | 38 |
| 2019 June | 8 | 15 | 23 |
| 2019 May | 3 | 5 | 8 |
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