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"note_text": "Paciente de 17 años, sexo masculino; consulta por presentar reiterados accesos dolorosos caracterizados por hemicrania pulsátil, dolor urente de tipo neurálgico en área frontal y retroorbitaria y fenómenos productivos autonómicos homolaterales (rinorrea y lagrimeo). Los episodios eran de corta duración (de 45 segundos a 5 minutos), reiterados, subintrantes, postraban al paciente y deterioraban sensiblemente su actividad diaria y su vigilia. Ocasionalmente se acompañaban de vómitos. Este cuadro presentaba, al momento del ingreso en nuestro servicio, 6 semanas de evolución; el tratamiento analgésico y antimigrañoso había sido totalmente ineficaz. Examen neurológico intercrítico normal. Valoración oftalmológica y otorrinolaringológica normales. Psicodiagnóstico y perfil de personalidad sin elementos remarcables. Se efectuaron neuroimágenes (RMN/RMN angiográfica), que fueron normales. Se empleó indometacina, con muy pobres resultados. Los indicadores de calidad de vida y el calendario de cefaleas mostraban un importante deterioro.\n \n Se decidió usar entonces alguno de los fármacos que cumplen un rol de estabilizadores de membrana, como el grupo de drogas antiepilépticas (DAE) relativamente nuevas, entre las cuales se eligió el topiramato (TPM). Tal decisión tuvo en cuenta informes sobre indicios de eficacia en el tratamiento del SUNCT8 y su mejor perfil de bioseguridad, respecto de los otros agentes (gabapentín, lamotrigina). Se comenzó con 25 mg/d en una sola toma nocturna hasta llegar a 75 mg/d con idéntica posología. La introducción del TPM en el esquema redundó en una reducción parcial importante (50-75%, no completa) de los episodios, con una evidente mejoría de la calidad de vida del paciente documentada por el MIDAS, instrumento que si bien no fue desarrollado específicamente para el seguimiento de este cuadro permite valorar, mediante una escala global, el compromiso diario del paciente afectado.\n \n",
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"note_text": "Presentamos un recién nacido de 12 días de vida que acudió al servicio de urgencias por fiebre de 38,5ºC de una hora de evolución y rechazo de la alimentación. Como antecedentes se destacaban un embarazo controlado y normal; serologías negativas para virus de la hepatitis B y C, virus de la inmunodeficiencia humana, sífilis y toxoplasma; frotis vaginal negativo para Streptococcus grupo B; ruptura espontánea de membranas intraparto, parto instrumental con fórceps a las 41 semanas de gestación y peso al nacimiento de 3880 g. La prueba de Apgar fue al minuto de 8 y a los 5 minutos de 9, sin requerir reanimación. Comenzó su esquema de inmunización. Alimentación con lactancia materna exclusiva. Respecto a los antecedentes familiares, los padres refirieron haber padecido amigdalitis los días previos. La exploración física mostró decaimiento y regular perfusión periférica con constantes vitales normales, sin que se objetivasen signos de foco. La analítica inicial mostró una determinación de proteína C reactiva cuantitativa (PC-R) 133,4 mg/L, con un hemograma coagulado y un sedimento de orina normal. La punción lumbar resultó hemorrágica. Ingresó con diagnóstico de síndrome febril sin foco y se inició antibioterapia empírica con ampicilina y cefotaxima intravenosas tras la toma de cultivos. En el hemograma repetido se observaron 5800 leucocitos/mm3, con fórmula normal, 13,4 g/dl de hemoglobina, 32 000 plaquetas/mm3. A las 18 h del ingreso empeoró su estado general y presentó crisis convulsivas generalizadas que requirieron tratamiento con fenobarbital y perfusión de midazolam. En la evolución desarrolló afectación sistémica con hipotensión arterial, acidosis metabólica, hiponatremia, oliguria y plaquetopenia grave; requirió ventilación mecánica convencional, transfusión de hemoderivados, soporte inotrópico con dopamina y diurético con furosemida. El tercer día del ingreso se informó el aislamiento en el hemocultivo de Streptococcus pyogenes sensible a penicilina, por lo que se suspendió la ampicilina y se mantuvo el tratamiento con cefotaxima intravenosa. Tras su estabilización presentó mejoría clínica y analítica, que permitió suspender el tratamiento inotrópico a las 48 h y realizar extubación al cuarto día. No se repitieron las crisis clínicas y el electroencefalograma fue normal, por lo cual se suspendió el tratamiento anticomicial. Se repitió la punción lumbar sin éxito. La ecografía cerebral y la angiorresonancia iniciales mostraron hemorragia intraventricular con discreta ventriculomegalia y lesiones hemisféricas cortico-subcorticales bilaterales, compatibles con meningoencefalitis. No superó el tamizaje auditivo realizado durante el ingreso mediante la técnica de exploración de potenciales provocados auditivos de tronco cerebral automatizados (PEATC-A > 40 dB). En las ecografías cerebrales de control presentó buena evolución sin aumento de la dilatación ventricular.\n \n A los 34 días de vida, después de completar 21 días de tratamiento con cefotaxima, se otorgó el alta hospitalaria con una exploración neurológica normal, excepto una leve hipotonía de eje. Se realizó seguimiento por especialistas de las unidades de rehabilitación, otorrinolaringología y neurología; al año de vida, no presentaba patología auditiva ni neurológica residual.\n",
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"note_text": "Paciente de 16 años de edad, de sexo masculino, sin antecedentes patológicos de importancia, que comienza hace un mes con cuadro de astenia, adinamia y pérdida de peso, al que se agrega 48 h atrás erección peneana persistente, con dolor moderado, por lo que consulta en el hospital zonal, donde le indican analgésicos y medios físicos citándose a las 24 h para control. Al día siguiente concurre a dicho hospital, donde por continuar con erección peneana y palidez generalizada deciden realizar estudios de laboratorio que muestran: plaquetopenia (plaquetas 60 000/mm3), anemia (hematócrito 12%) e hiperleucocitosis (glóbulos blancos 312 000/mm3) y LDH 2056 UI/ml, por lo que se decide su internación y se solicita su derivación a un centro de mayor complejidad. A su ingreso al Hospital Posadas se constata paciente en regular estado general, palidez cutáneomucosa, fiebre y equimosis en miembros inferiores. Se palpa esplenomegalia. Se observa pene erecto con cambios en la coloración de la piel del cuerpo, palidez y leve cianosis del glande. Se realiza interconsulta con urología, quien realiza drenaje de cuerpos cavernosos con solución fisiológica y adrenalina; el procedimiento arroja sangre oscura y coagulada. Por presentar registro febril, se realizan hemocultivos x 2 y se decide iniciar tratamiento empírico con ceftazidima-amikacina y transfundir glóbulos rojos desplasmatizados. El paciente evoluciona en mal estado general, con dificultad respiratoria creciente, por lo cual se lo traslada a terapia intensiva. Se realiza diagnóstico de leucemia mieloide crónica por biopsia de medula ósea y presencia de blastos en sangre periférica. Se descartan otros diagnósticos, como la anemia de células falciforme, por no presentar depranocitos en frotis de sangre periférica; causa medicamentosa, por no presentar ingesta de medicamentos; causa traumática, por falta de traumatismos previos en el pene; asimismo, se descartan tumores sólidos genitourinarios y enfermedades neurológicas e infecciosas. Actualmente, el paciente se encuentra con disfunción eréctil secundaria a priapismo y permanece en tratamiento oncológico por su patología de base.\n",
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"note_text": "Una niña de 9 años de edad con cirrosis fue derivada a nuestro centro para evaluación de trasplante hepático. Se presentó con un cuadro referido como de reciente comienzo, aunque por el examen físico y los resultados de estudios se trataba de una hepatopatía crónica. Presentaba estigmas de cronicidad como eritema palmar, telangiectasias, circulación colateral en pared abdominal y esplenomegalia. En la ecografía abdominal se constató un hígado de pequeño tamaño con heterogeneidad y bazo con diámetro longitudinal aumentado. No recibía medicación antes de la admisión en nuestro hospital. En un contexto social complejo y con poca percepción de la enfermedad, la familia no había consultado previamente. Tampoco tenía seguimiento periódico en salud. Al ingreso, el puntaje de gravedad PELD (Pediatric End-Stage Liver Disease, hepatopatía terminal pediátrica) era de 24, con bilirrubina de 15 mg/dl, un valor de relación internacional normalizada (RIN) de 2,5, albúmina de 2,5 g/dl; su peso y talla eran de 30 kg y 127 cm, respectivamente. Mientras esperaba en lista de trasplante hepático, desarrolló encefalopatía hepática espontánea, de tipo C, grado II-III1 con períodos de conducta inapropiada que alternaban con confusión y excitación. Previamente, no había presentado episodios de encefalopatía. Su amonio sérico aumentó de 139 µg% a 324 µg% (valor normal de referencia 19-82 µg%). Se descartaron factores precipitantes conocidos de encefalopatía hepática, como medicaciones, sangrado gastrointestinal, infecciones bacterianas, constipación, fallo renal, desequilibrios electrolíticos, hipovolemia o hipoxemia. La paciente no tenía antecedentes de ascitis y una ecografía no mostró líquido libre abdominal. Se indicó una dieta con restricción de proteínas (0,8 g/kg/día) y lactulosa por vía oral (40 ml/día, divididos en 4 tomas), logrando 3-4 deposiciones blandas por día. A pesar de estas medidas, el estado neurológico no mejoró luego de 4 días. Sobre la base de experiencias en pacientes adultos, se decidió agregar rifaximina (20 mg/kg/día, por vía oral, divididos en dos tomas), con previa firma del consentimiento informado por parte de los padres. La paciente mostró mejoría clínica en 3 días, sin confusión ni excitación y con ritmo sueño/ vigilia normal. La concentración de amonio descendió gradualmente (236 µg% y 162 µg%, 4 y 10 días luego de iniciado el tratamiento, respectivamente). No presentó cefaleas, dolor abdominal, náuseas ni vómitos relacionados con el tratamiento con rifaximina. Finalmente, la paciente recibió trasplante hepático pasado un mes del tratamiento con rifaximina, sin complicaciones.\n",
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"note_text": "Varón de 51 años que acudió al servicio de urgencias por disminución de agudeza visual de su ojo izquierdo de cinco días de evolución.\n Como antecedentes personales el paciente presentaba diabetes mellitus no insulino dependiente de seis años de evolución, así como haber padecido un traumatismo contuso en el mismo ojo 15 años antes.\n Refería un cuadro de pérdida de visión asintomático de cinco días de evolución de su ojo izquierdo. La agudeza visual (AV) tomada mediante el test de Snellen era 1 para su ojo derecho y 0,5 para su ojo izquierdo, mejorando este último a 1 con una corrección esférica de +1,5D.\n Tanto la motilidad ocular intrínseca como extrínseca, biomicroscopía anterior y tonometría del paciente eran normales.\n La funduscopia del ojo a estudio presentaba una masa yuxtapapilar de color rojo-anaranjado brillante, sobreelevada, bien delimitada. También se apreció una alteración del epitelio pigmentario en región macular así como una alteración de la capa de fibras nerviosas superiores e inferiores. La exploración oftalmoscópica del ojo adelfo presentaba asimismo una leve alteración de epitelio pigmentario. Se realizó una angiografía fluoresceínica que demostró el relleno de un árbol vascular intratumoral compuesto de finos capilares con exudación en tiempos tardíos, confirmando la primera sospecha de hemangioma capilar yuxtapapilar. Se observaron puntos de fuga en polo posterior de ambos ojos, sugestivos de retinopatía central serosa.\n Se realizó un campo visual SITA- Standard 24-2 (Zeiss-Humphrey Instruments, Dublin, CA) con visión corregida, estímulo III, hallándose un defecto infero-nasal del ojo izquierdo.\n Cuatro semanas más tarde, la visión del ojo izquierdo era de 0,6 corregida (+0.5 esf + 1 x 48 cil) 1; mientras que la visión del ojo derecho fue de 0,4 corregida (+0.5 esf +0.25 x 170 cil) 0,6. Una nueva angiografía fluoresceínica demostró que la disminución de agudeza visual del ojo derecho se debía a retinopatía central serosa.\n Ocho semanas después del inicio del cuadro se encontró una regresión espontánea tanto del hemangioma capilar yuxtapapilar como de la retinopatía central serosa bilateral, regresando la AV a la 1 difícil en ambos ojos.\n \n",
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"note_text": "Se presenta el caso de un paciente de 78 años de edad, fáquico, diagnosticado de degeneración macular asociada a la edad exudativa (DMAE) en ojo derecho al que se le realiza terapia fotodinámica (TFD). 48 horas después se le inyecta en cámara vítrea 20 mg en 0,1 ml de acetato de triamcinolona obtenida mediante la técnica de sedimentación.\n La operación se realizó en el quirófano bajo medidas asépticas. La inyección se hizo con aguja de 27 G a 4 mm del limbo en el cuadrante temporo-inferior ayudado de un blefarostato. Durante el procedimiento, y coincidiendo con un intento de cierre forzado de los párpados, se observó con el microscopio cómo parte de la sustancia lechosa pasaba a cámara anterior.\n Se decidió actuar de forma expectante instilando colirio de ciprofloxacino y observando el pulso arterial espontáneo. Al día siguiente el paciente presentaba la triamcinolona precipitada en cámara anterior y en cámara vítrea sin otros signos inflamatorios. La PIO era de 25 mm Hg, por lo que se prescribió maleato de timolol al 0,5% en colirio cada 12 horas.\n \n Se le realizaron controles periódicos en los que se detectó un descenso de la PIO hasta valores normales, una reabsorción progresiva de la triamcinolona y la córnea transparente sin reacción inflamatoria. A los dos meses quedaban escasos restos de la sustancia, la PIO era de 17 mm Hg sin tratamiento y la biomicroscopía endotelial resultó un recuento celular normal e igual que en el ojo contralateral.\n \n",
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"note_id": "S0365-66912008000700007-1",
"note_text": "Varón de 34 años diagnosticado de Síndrome de Sturge-Weber en la infancia, que presentó un glaucoma agudo secundario a luxación de cristalino a cámara anterior y bloqueo pupilar, por lo que fue intervenido de urgencia.\n En la exploración se evidenciaba una mancha en «vino de Oporto» hemifacial izquierda, en el territorio de la primera y segunda ramas trigeminales, exoftalmos severo con rechazo ínfero-temporal del globo ocular e ingurgitación marcada de vasos epiesclerales inferiores «en cabeza de Medusa».\n En la exploración con lámpara de hendidura se observaba una catarata madura totalmente luxada a la cámara anterior en contacto con el endotelio corneal con bloqueo pupilar y presión intraocular de 60 mm Hg, la ecografía mostraba un desprendimiento de retina en el polo posterior junto con una lesión subyacente hiperecogénica.\n \n Tras un infructuoso tratamiento médico hipotensor, se decide la intervención, realizándose extracción intracapsular de cristalino. El fondo de ojo confirmó la sospecha de una lesión coroidea peripapilar nasal superior con desprendimiento de retina exudativo asociado.\n Se realizó una resonancia magnética nuclear (RMN) que mostró lesiones hiperintensas en T1 y T2 en leptomeninges de región frontoparietal izquierda con calcificaciones y atrofia del lóbulo frontal. Una lesión coroidea y dos lesiones orbitarias extraconales en cuadrante nasal superior y temporal superior, bien delimitadas, asociadas a dilatación de vena oftálmica superior. Todas las lesiones eran compatibles con hemangiomas cavernosos.\n \n La presión intraocular tras la cirugía se mantuvo entre 10 y 16 mm Hg sin necesidad de tratamiento antihipertensivo y la agudeza visual final fue menor de 20/200 (visión de bultos). En la actualidad las lesiones coroideas y orbitarias siguen estables, por lo que no precisan tratamiento.\n \n",
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"note_text": "Mujer de 38 años que presentó cefalea y dolor periorbitario izquierdo de una semana de evolución y diplopía las últimas 24 horas. La exploración motora reveló una paresia de los músculos recto superior e interno y ptosis moderada en el ojo izquierdo. No hubo otros hallazgos oculares o neurológicos. La resonancia nuclear magnética (RNM) craneal fue normal. Se diagnosticó un síndrome de Tolosa-Hunt y se inició tratamiento con corticoides. Dos días después, la oftalmoplejía dolorosa persistía y la paciente comenzó a referir disminución de agudeza visual próxima. En la exploración de la paciente se observó midriasis izquierda. Se realizó RNM orbitaria que mostró en T2 un aneurisma de la carótida interna-comunicante posterior (CI-CP) parcialmente trombosado. La angio-tomografía axial computerizada (angio-TAC) mostró un aneurisma CI-CP izquierdo multilobulado de 10x5 mm. Se realizaron angiografía cerebral y embolización, siendo rellenado completamente el aneurisma con Hydrocoil (MicroVention, Aliso Viejo, CA) Cerecyte® (Micrus, Sunnyvale, CA). El tamaño pupilar se normalizó y la ptosis y la adducción mejoraron completamente dos semanas después de la embolización. Ocho meses tras el tratamiento persistía un ligero déficit en la elevación, sin que la paciente refiriese diplopía.\n \n",
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"note_text": "Varón de 36 años que tras traumatismo craneoencefálico presenta, 8 meses después, un síndrome medular incompleto sensitivo motor y par VI de ojo izquierdo (OI) que produce diplopía en todas las posiciones de la mirada. En la exploración motora se observa limitación de la abducción de -3, tortícolis cara izquierda de 10o, endotropía de 45 r en posición primaria de la mirada con ojo derecho (OD) fijador. En la exploración sensorial, la prueba de Worth muestra supresión intermitente de OI. La agudeza visual (AV) es de OD 1 y de OI 1. El resto de la exploración oftalmológica es normal.\n Se realizó tratamiento con dos inyecciones de toxina botulínica 5 UI en recto medio del OI, con lo que disminuyó la endotropía a 30 r sin mejorar la abducción.\n A los 6 meses se realiza TRV con fijación escleral en OI con anestesia general. En el postoperatorio inmediato se observó exotropía consecutiva de 45 r, inversión del tortícolis, limitación de la aducción de -1 y de la abducción de -1 del ojo afectado y diplopía.\n A los 15 días se inyectan 5 U de toxina botulínica en recto lateral del OI sin que se modificase el resultado, por lo que a los 2 meses se decide retirar la fijación escleral, lo que fue técnicamente imposible por las adherencias encontradas. Se reinterviene al paciente realizando una resección del recto medio de OI de 7 mm y se inyectan 5 U de toxina botulínica en recto lateral del OI intraoperatoriamente. El paciente quedó con tortícolis en la cara derecha de 10o, limitación de la abducción de -1, exotropía de 10-15 r en posición primaria de la mirada (PPM) sin diplopía. A los 2 años vuelve a presentar diplopía, exotropÍa de 20-30 r en PPM, limitación de la abducción de -1, limitación de la aducción de -1 y tortícolis en la cara derecha de 20o.\n Se decide realizar una nueva resección del recto medio del OI de 6 mm.\n Un año después de la última cirugía presenta: limitación de la abducción de -1, tortícolis en la cara derecha de 5o, exotropía de 10-15 r en PPM sin diplopía. El paciente está satisfecho con el resultado.\n \n",
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"note_text": "Recién nacido hijo de madre primigesta de 18 años, con embarazo de 36 semanas, con control prenatal irregular, quien presentó parto vaginal y líquido amniótico con meconio. Pesó al nacer 1.240 g (< p 3), midió 41 cm (< p 3), con apgar de 7 y 9. Presentó dificultad respiratoria temprana que requirió soporte ventilatorio y surfactante pulmonar, con adecuada respuesta. Se logró extubación a CPAP, pero presentó taquicardia y taquipnea persistente, por lo cual se realizó ecocardiograma sugestivo de coartación de aorta por lo que fue derivado a un centro de mayor complejidad, a los 13 días de vida.\n A su ingreso a la institución se tomó presión arterial en cuatro extremidades: Miembros superiores derecho e izquierdo 88/49 presión arterial media (PAM) 62 y 90/52 PAM 63, miembros inferiores derecho e izquierdo 86/43 PAM 61, 78/44 PAM 53, frecuencia cardíaca 180 y respiratoria 65 x min. Al examen segmentario destacaba hepatomegalia, frialdad distal, taquicardia, soplo en foco pulmonar II/VI, pulsos femorales presentes, retracción subcostal, temblor distal fino, exoftalmo marcado y precordio hiperdinámico.\n \n Se realizó Ecocardiograma que descartó coartación aórtica, pero mostró disfunción miocárdica que requirió soporte inotrópico. Ecografía transfontanelar y abdominal normales. En los exámenes de laboratorio iníciales destacaron alteraciones de función hepática, bilirrubina de 6,8 mg% (directa de 5,3 mg%).\n Al evaluar a la madre se observó fenotipo sugestivo de hipertiroidismo, con delgadez marcada y exoftalmo, por lo que se sospechó enfermedad tiroidea no tratada. Debido a sospecha de hipertiroidismo neonatal, se realizó perfil tiroideo, que mostró TSH 0,01 uUI/ml y T4 Libre de 7,7 (valores de referencia 0,71-1,85 ng/dl). Se realizaron además anticuerpos antimicrosomales, los cuales fueron negativos, pero no se pudo realizar anticuerpos estimulantes del receptor de tirotropina (TRAab).\n \n Al reevaluar al paciente se observó bocio difuso que se confirmó con ecografía. Se inició metimazol 1 mg/kg/día dividido en 3 dosis, propanolol a dosis de 1 mg/kg/día dividido en 2 dosis, logrando mejoría de la taquicardia. Sin embargo, se notó poca ganancia de peso en los primeros días de manejo, situación revertida después de una semana de tratamiento. Se logró retiro de oxígeno, resolución de hepatomegalia y después de 1 semana de tratamiento la T4 Libre descendió hasta 3,1 mg/dl, persistiendo con supresión de la TSH (0,015 uUI/ml) al momento de su egreso.\n \n En la semana 13 de evolución se normalizaron las pruebas de función tiroidea, retirándose la medicación antitiroidea. Durante el seguimiento, el lactante permaneció en condición eutiroidea, sin alteraciones cardiovasculares ni del neurodesarrollo. La madre fue referida a endocrinología para manejo y asesoría para futuros embarazos.\n",
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"note_text": "Primera hija de padres sanos no consanguíneos, sin antecedentes de epilepsia en familiares de primer grado, debutó a los 2 meses de edad, con CF hemiclónica derecha, de 15 min de duración, con paresia de Todd posterior. Las recurrencias fueron frecuentes, del tipo focal compleja y hemiclónicas de más de 10 min con al menos 5 SE febriles entre el 3 y 6 mes, con un examen normal post crisis.\n La RM cerebral3 fueron normal, al igual que múltiples EEG standard, la cuantificación de aminoácidos en sangre, líquido cefalorraquídeo, ácidos orgánicos y ultramicroscopía de piel. A los 6 meses se solicitó estudio molecular del gen SCN1A confirmándose mutación c.5347G>A (p.Ala1783Thr) en estado heterocigoto en el exón 26 del gen. El estudio molecular de ambos padres fue normal.\n El uso de fenobarbital, clobazam, levetiracetam y topiramato, no logró control de crisis. A los 9 meses se inició stiripentol dosis 50 mg kp día, asociado a topiramato y ácido valproico sin resultados. Entre los 12-18 meses los múltiples SE y crisis frecuentes deterioraron su desarrollo perdiendo marcha, control de tronco y control cefálico. Se inició dieta cetogénica la que se asoció a una pancreatitis grave por lo que se discontinuó.\n La certificación de alteración deglución y cuadros respiratorios recurrentes febriles que precipitaban los SE plantearon gastrostomía lo que logró disminución de episodios febriles y mejor manejo de las crisis.\n Posterior a una serie de adecuaciones de fármacos antiepilépticos el tratamiento triasociado con clobazam, topiramato y lacosamida permitió un control parcial de crisis, sin SE en 18 meses, con crisis de corta duración (segundos) 3-5 por semana que no requerían uso diazepam ni provocaban alteración en actividades de vida diaria.\n",
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"note_text": "Tercera hija, embarazo y parto normal, sin antecedentes de epilepsia en familiares de primer grado. Inició CF a los 6 meses, prolongadas, focales, clonías de hemicara y SE febriles con mulitples EEG standard normales. A los 10 meses se le agregan crisis afebriles pero gatilladas por cuadros infecciosos. Posterior al año persistió con múltiples crisis afebriles hemigeneralizadas, mioclónicas, ausencias atípicas y tónicas clónicas generalizadas precipitadas por foto estimulación. Entre el primer y segundo año presentó 7 SE que requirieron ingreso a Unidad de cuidados intensivos y 10 hospitalizaciones por crisis prolongadas. La triasociación de fenobarbital, ácido valproico y levetiracetam no logró control de crisis. La RM cerebral y estudios metabólicos fueron normales.\n Evolucionó con retraso de lenguaje, compromiso motor de menor cuantía y microcefalia. A la edad de 3 años se solicitó estudio molecular del gen SCN1A que confirmó la mutación c.3311C>A (p.Ser1104X) exón 16 en estado heterocigoto para el gen. El estudio molecular de ambos padres fue normal. El tratamiento con topiramato, clobazam y Levetiracetam permitió controlar crisis prolongadas. Sin SE desde 9 meses pero ha persistido con 5-7 crisis semanales de corta duración que no requieren uso de benzodiacepinas.\n",
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"note_text": "Paciente femenino, previamente sano, con antecedentes de embarazo controlado, nacido a término 38 semanas, pequeña para la edad gestacional (2.670 kg). Consultó a los 47 días de vida por cuadro de 20 días de evolución caracterizado por ictericia progresiva y coluria, con buen incremento de peso, siendo derivada al hospital regional para estudio.\n Exámenes con patrón colestásico, en los cuales destacaba aumento de bilirrubina total (BT), a expensas de la bilirrubina directa (BD) (12,75 mg/dl-10,18 mg/dl) y pruebas hepáticas elevadas, sobre todo la gamma glutamil transpeptidasa (GGT) y la fosfatasa alcalina (FA).\n En Hospital regional se sospechó hepatitis viral, y se tomó serología para hepatitis A, B y C que resultaron negativas. Evolucionó favorablemente pero se constataron deposiciones acólicas. Se derivó a gastroenterología previos exámenes de control que mantenían patrón colestásico con elevación de la BD y de las transaminasas: BT 10,58, BD 7,88, GOT 204, GPT 109, GGT 550.\n A los 52 días de vida se le realizó una ecografía abdominal que mostró dilatación arrosariada de vía biliar intrahepática y vesícula biliar presente pero colapsada a pesar del ayuno.\n Por la presencia de la vesícula y la gran dilatación de vía biliar intrahepática, se decidió diferir la biopsia hepática y se realizó una colangio-resonancia. Esta mostró un hígado normal con parénquima conservado, leve dilatación de ductos biliares intrahepáticos hasta nivel de su confluencia, hacia distal no se logró visualizar vía biliar extrahepática.\n Con el resultado de la colangio-resonancia se sospechó atresia de vía biliar y se decidió cirugía de derivación bilio-digestiva (Kasai). Llamaba la atención que en exámenes seriados la bilirrubina había ido en disminución al igual que la ictericia. Por presencia de deposiciones acólicas se decidió exploración quirúrgica.\n Durante la cirugía se visualizó superficie hepática lisa, hígado congestivo (confirmado por biopsia), vesícula biliar presente, con lumen y bilis en su interior. Se realizó colangiografía intraoperatoria donde se visualizó una zona estenótica crítica a nivel del conducto hepático común logrando paso de contraste hacia proximal y distal (intra y extra hepático), con vía biliar intrahepática dilatada.\n Se realizó colecistectomía y disección de conducto hepático común demostrando una estenosis a nivel de éste, causado por un anillo vascular proveniente de arteria hepática derecha. Se seccionó la vía biliar a nivel proximal de la estenosis realizando una hepático-duodeno anastomosis. Se dejó drenaje abdominal y sonda nasogástrica instalada.\n \n La paciente evolucionó favorablemente, con débito en disminución por el drenaje retirándose al 6 día y alimentándose a los 4 días. Se dio de alta a los 8 días post operatorio con pruebas hepáticas en disminución (BT 3,98, BD 3,46, GOT 266, GPT 134, FA 431, GGT 586). En controles ambulatorios la paciente se encontraba asintomática, con buena tolerancia oral, deposiciones teñidas y exámenes hepáticos y generales normalizados.\n \n",
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"note_text": "Recién nacido masculino de 33 semanas de edad gestacional, nacido vía cesárea por sepsis materna. Madre de 19 años de edad falleció en el puerperio inme diato por sepsis grave, sin antecedentes de consanguinidad, el embarazo fue controlado, el reporte de tres ultrasonidos durante la gestación no mostró signos de hidrops (derrame pleural, derrame pericárdico o asci tis). El peso al nacimiento fue de 2090g, APGAR fue de 6 al minuto y 6 a los 5 minutos. El examen clínico no mostró fenotipo que sugiera síndrome genético. Dos horas después del nacimiento presentó taquipnea y cianosis con dificultad respiratoria grave. Fue tratado con surfactante exógeno de rescate por la presencia de signos y síntomas de síndrome de dificultad respiratoria, catecolaminas, antibióticos y ventilación mecánica por 22 días; la ventilación convencional con presión media de la vía aérea máxima de 16 cm H2O, seguida de VAFO por acidosis respiratoria e hipoxemia refrac taria (pCO2 75 mmHg y pO2 45 mmHg).\n La radiografía de tórax mostró infiltración reticular en ambos pulmones y sobre distención pulmonar sin consolidaciones. La TAC de tórax describió cambios reticulares en todas las zonas, engrosamiento intersticial, múltiples bullas y atrapamiento de aire en pulmón izquierdo, así como neumonía derecha (Fi gura 2). Se descartó la presencia de linfangiectasia en otros órganos por TAC abdominal. Se realizó biopsia pulmonar y por indicación de cirugía pediátrica lobectomía inferior izquierda. En el estudio histopatológico se observó dilatación quística de los canales linfáti cos broncovasculares,. Por ecocardiografía se diagnosticó comunicación interauricular (CIA) y persistencia de conducto arterioso (PCA) y fueron corregidas quirúrgicamente a los 30 días de vida extra uterina. La evolución fue satisfactoria, el seguimiento pediátrico a los 19 meses de edad reportó peso y talla adecuados para su edad, desarrollo psicomotor nor mal, sin cuadros infecciosos de la vía respiratoria in ferior, no requirió oxigeno suplementario; la TAC de tórax de control informó con engrosamiento intersti cial, bullas enfisematosas difusas pequeñas y mejoría con respecto a la TAC inicial,.\n",
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"note_id": "S0376-78922006000100006-1",
"note_text": "Se presenta el caso de una joven de 17 años de edad que consultó a nuestro Servicio para lograr una mejoría estético funcional de su dedo pulgar de la mano izquierda. Había nacido con un dedo pulgar pequeño y sin función, unido al resto de la mano a través de un pequeño y delgado tubo de piel; durante la lactancia, había sido tratada en el Hospital Infantil donde le habían únicamente extirpado el área cutánea del pequeño tubo de unión a fin de lograr la implantación directa del apéndice pulgar en la mano.\n Cuando acude a nuestra consulta presenta un pulgar con implantación distal a nivel de la articulación metacarpofalangica del índice, con un primer espacio estrecho, sin capacidad motora de oposición ni flexo-extensión, pero con buena sensibilidad en ambos bordes del mismo. No presentaba eminencia tenar y no se palpaba el primer metacarpiano; además tenía ausencia de pulso radial pero sí se palpaba adecuadamente el pulso cubital. La parte funcional compensatoria la realizaba con alguna dificultad mediante una pinza dígito-digital lateral entre el índice y el medio. Se solicitaron estudios radiológicos que evidenciaron hipoplasia y fusión de las falanges, agenesia del primer metacarpiano, atrofia del trapecio y resto de huesos del carpo, así como también atrofia del radio; el estudio con doppler color revelo ausencia de la arteria radial con dilatación compensatoria de la arteria ulnar. Con este examen clínico se diagnosticó un típico pulgar flotante izquierdo parcialmente tratado.\n En su mano derecha dominante presentaba en el pulgar las siguientes anomalías: primer espacio estrecho, ausencia de los pliegues de flexión, ausencia de la eminencia tenar, imposibilidad para flexionar la articulación metacarpofalángica pero con buena movilidad pasiva de la misma, anquílosis de la articulación interfalángica; a pesar de todo esto había buena función del mismo. El estudio radiológico y con doppler color no evidenciaron anomalías óseas o vasculares. Con estos hallazgos podríamos clasificar el pulgar derecho en el grupo I de Blauth.\n No se detectaron otras anomalías corporales congénitas.\n Tratamiento y resultados\n Al reconstruir un pulgar se deben tener bien claros algunos objetivos generales que ayudarán a la funcionabilidad del mismo, como son lograr estabilidad, oposición, sensibilidad, darle una longitud adecuada, darle movilidad en lo posible y un buen aspecto estético.\n En la reconstrucción de un pulgar flotante existen dos conductas básicamente opuestas, que deben discutirse ampliamente con los padres y con el paciente si éste se encuentra en una edad de comprender.\n Desde el punto de vista práctico se trata de decidir entre una de las siguientes actitudes terapéuticas:\n Amputación y reconstrucción:\n La amputación del pulgar flotante conducirá a una aplasia que necesitará una reconstrucción con técnicas microquirúrgicas tales como pulgarización del índice que se realiza con buenos resultados desde 1964 ( 3,4), o la transferencia de un ortejo, técnica que conlleva muchos riesgos sobre todo cuando no se tiene un buen entrenamiento en microcirugía (5,6) o no se cuenta con la infraestructura idonea. En teoría, son las técnicas que mejor resultado estético-funcional producen.\n Conservación y estabilización:\n Son posibles tres tipos de conducta dependiendo del tipo de patología según la clasificación de Blauth\n -Estabilización de la articulación metacarpofalángica. -Estabilización de la metacarpofalángica más una transferencia de oposición. - Reconstrucción del metacarpiano con una transferencia ósea vascularizada o no.\n En nuestra paciente, una vez hecho el diagnóstico e identificados los problemas, se plantearon a la madre y a la paciente las conductas quirúrgicas presentadas anteriormente, pero en definitiva fue sumamente difícil convencerlas de amputar el pulgar vestigial y reconstruirlo con una pulgarización del índice, por lo que se tomó la decisión de reconstrucción y estabilización del metacarpiano.\n Debido a que la posibilidad de efectuar, por ejemplo, una transferencia con colgajo óseo del tercio distal del radio nutrido por la rama perforante superior de la arteria ínterósea anterior a flujo retrogrado (7), no era viable por las anomalías vasculares observadas con el doppler, se optó por la toma de un injerto óseo convencional a pesar del riesgo de reabsorción que puede presentarse a largo plazo. Para no cambiar de campo operatorio se cosechó el injerto óseo del olécranon ipsilateral; después se estabilizó a nivel del trapecio vestigial con una miniplaca y a nivel de las falanges con alambre, logrando darle al neo-pulgar orientación en oposición. Para mantener estable esta posición y evitar futuros desplazamientos se decidió efectuar la transferencia del músculo abductor del meñique para fijarlo al neo-metacarpiano y reforzar o estabilizar la oposición del pulgar, así como para tratar de aumentar el volumen y por ende la estética del área tenar. La cirugía se efectuó con un bloqueo regional bajo torniquete neumático.\n No se presentaron complicaciones postoperatorias\n La paciente fue remitida al Servicio de Fisioterapia para el diseño de una ortesis funcional y posteriormente, para el inicio de reeducación funcional.\n Psicológicamente la paciente ha respondido de forma positiva ya que ha logrado darle utilidad a su nuevo pulgar y éste ha mejorado en su aspecto estético, aunque no es el aspecto que sus expectativas, normales o no, le hicieron desear.\n",
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"segment": "Cuando acude a nuestra consulta presenta un pulgar con implantación distal a nivel de la articulación metacarpofalangica del índice, con un primer espacio estrecho, sin capacidad motora de oposición ni flexo-extensión, pero con buena sensibilidad en ambos bordes del mismo. No presentaba eminencia tenar y no se palpaba el primer metacarpiano; además tenía ausencia de pulso radial pero sí se palpaba adecuadamente el pulso cubital. La parte funcional compensatoria la realizaba con alguna dificultad mediante una pinza dígito-digital lateral entre el índice y el medio. Se solicitaron estudios radiológicos que evidenciaron hipoplasia y fusión de las falanges, agenesia del primer metacarpiano, atrofia del trapecio y resto de huesos del carpo, así como también atrofia del radio; el estudio con doppler color revelo ausencia de la arteria radial con dilatación compensatoria de la arteria ulnar. Con este examen clínico se diagnosticó un típico pulgar flotante izquierdo parcialmente tratado.\n En su mano derecha dominante presentaba en el pulgar las siguientes anomalías: primer espacio estrecho, ausencia de los pliegues de flexión, ausencia de la eminencia tenar, imposibilidad para flexionar la articulación metacarpofalángica pero con buena movilidad pasiva de la misma, anquílosis de la articulación interfalángica; a pesar de todo esto había buena función del mismo. El estudio radiológico y con doppler color no evidenciaron anomalías óseas o vasculares. Con estos hallazgos podríamos clasificar el pulgar derecho en el grupo I de Blauth.\n No se detectaron otras anomalías corporales congénitas.\n ",
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"note_text": "Presentamos el caso de un varón de 56 años de edad con historia de 35 años de abuso de alcohol y sin otra patología asociada. El paciente acudió a nuestro Servicio de Cirugía Plástica y Reparadora del Hospital Carlos Haya de Málaga (España) presentando masas en hombros, mamas y flancos que habían aumentado de tamaño de forma progresiva y rápida durante los últimos dos años y medio, que le dificultaban la movilidad y por tanto su actividad laboral.\n El examen físico reveló masas no dolorosas de consistencia blanda, sin bordes bien definidos, localizadas en ambos hombros, mamas, fosas lumbares y flancos sin afectación cervical (Collar de Madelung).\n \n En el estudio radiológico mediante secuencias axiales de Tomografía Axial Computerizada (TAC) se apreciaba un exceso de depósito graso de distribución homogénea no encapsulada (difusa) sobre los hombros, mamas y cintura abdominal, sin afectación de las estructuras profundas. Asimismo, no se encontraron depósitos grasos de localización mesentérica o mediastínica, ni a nivel cervical anterior o posterior. Dado que el paciente había sido intervenido de hernia inguinal y eventración se realizó una Resonancia Magnética Nuclear (RMN) abdominal para valorar la integridad de la pared abdominal. Se realizaron cortes en los tres planos del espacio con secuencias potenciadas en SE T1, TSE T2 y Stir, visualizándose una correcta disposición de la musculatura abdominal, un importante aumento difuso del tejido celular subcutáneo adiposo abdominal y ausencia de grasa intrabdominal.\n \n El estudio histopatológico informó de depósitos grasos no encapsulados con adipocitos no patológicos.\n Tras completar estos datos con la anamnesis y la exploración física, el diagnóstico definitivo fue de Enfermedad de Madelung o Lipomatosis Simétrica Benigna tipo II.\n El tratamiento quirúrgico propuesto fue la liposucción de los cúmulos grasos localizados en abdomen, área lumbar y hombros y la dermolipectomía en ambas mamas. El paciente rehusó ambos procedimientos, por lo que se le aconsejó entonces la pérdida de peso y la abstinencia alcohólica, aún conociendo sus limitados beneficios.\n",
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"note_text": "Presentamos el caso de una paciente de 41 años de edad, fumadora, con antecedentes de mielomelingocele congénito y paraplejia secundaria y con una nefrostomía en la infancia. Había sido operada 3 años antes en nuestro Servicio por presentar una úlcera sacra, realizándose un colgajo glúteo. Desde entonces no había presentado ninguna recidiva debido a su buena higiene postural domiciliaria.\n Seis meses antes de acudir de nuevo a nuestro Servicio, sufrió una fractura de fémur, por lo que tuvo que portar una férula pelvi-pédica de yeso. La imposibilidad de movilización y de cambios posturales que la paciente realizaba habitualmente en su domicilio, le ocasionaron la aparición de una gran úlcera en la región sacra, motivo por el cual fue remitida a nuestra consulta para valoración. Presentaba en ese momento una gran úlcera isquiotroncantéreo-sacra de unos 20 x 25 cm, con trayecto fistuloso hacia pala iliaca y que en algunas zonas profundizaba hasta plano óseo con exposición del sacro. Se recomendó ingreso hospitalario que la paciente rechazó por motivos personales, acudiendo de nuevo a las 3 semanas, momento en que la úlcera medía ya 24 x 30 cm.\n Durante el ingreso y debido a la gran úlcera que presentaba se le realizó una colostomía. La paciente tenía un mal estado general, con alteraciones analíticas importantes tanto en las cifras de hematocrito como en las de proteínas totales, por lo que se tuvo que iniciar nutrición parenteral para remontar su estado general.\n Para cerrar el gran defecto que presentaba fue intervenida y se le realizó un colgajo póstero-medial de muslo, para lo cual procedimos a desbridar la úlcera y cubrirla posteriormente mediante el colgajo anteriormente descrito como alternativa a la desarticulación de la cadera.\n La intervención duró unas 5 horas y se desarrolló sin contratiempos. La zona donante del colgajo se cerró directamente en su mayor parte, teniendo que cubrir solo la porción distal con un injerto de piel parcial tomado del muslo contralateral. Durante el postoperatorio la paciente permaneció en la UCI 2 días para control de su situación metabólica, tras lo que fue trasladada de nuevo a planta hospitalaria.\n \n A los 15 días, el colgajo presentaba buen estado, con adecuado relleno capilar. A pesar de ello, el estado general de la paciente empezó a deteriorarse. Comenzó con una insuficiencia hepato-renal progresiva que tras un diagnóstico exhaustivo por el Servicio de Medicina Interna se catalogó como secundaria a alteraciones biliopancreáticas derivadas de la nutrición parenteral. Tras valoración por el Servicio de Nefrología, se inició tratamiento con diálisis, que mejoró las cifras de creatinina aunque se manifestó una hipoproteinemia severa que no se consiguió remontar. A la cuarta semana de postoperatorio, la paciente presentó fiebre alta de origen desconocido que evolucionó a sepsis y fracaso multiorgánico que provocaron el fallecimiento.\n",
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"note_text": "Varón de 55 años y sin antecedentes previos de interés. Diez meses antes de la consulta comenzó con inflamación progresiva pero indolora en el cuarto dedo de la mano derecha. La inflamación dio lugar a un déficit funcional, con imposibilidad para realizar la flexoextensión del dedo afectado. El estudio radiográfico mostró una pérdida de definición de la cortical anterior en la base de la falange proximal del cuarto dedo, junto con un aumento de partes blandas que parecía presentar una incipiente calcificación que se extendía distalmente por la cara palmar de la falange; no se vio lesión intramedular.\n \n Se practicó biopsia incisional, cuyo diagnóstico anatomopatológico fue de periostitis reactiva florida.\n El paciente fue remitido a nuestro Servicio en donde se comprobó la existencia de una masa en la falange proximal del cuarto dedo con inflamación y tumefacción. No se encontraron signos locorregionales de infección. La movilidad en todas las articulaciones del dedo estaba afectada, existiendo una impotencia funcional absoluta. El paciente refería dolor con parestesias en el territorio del nervio colateral cubital.\n El estudio radiográfico mostró un estadio evolutivo de la lesión con respecto al primer estudio, en el que la calcificación de las partes blandas de la zona palmar de falange proximal se había hecho más ostensible, extendiéndose a lo largo de la falange. Aparecía una clara reacción perióstica en la base de la falange que parecía conectar con la calcificación pero que además, se extendía al lado opuesto. Es interesante señalar también que se apreciaba una reacción perióstica sólida de borde irregular en la falange media.\n En el estudio radiográfico preoperatorio la calcificación en la base de la falange media se volvió más definida y grande, abarcando toda la extensión de la falange.\n \n El estudio mediante Resonancia Magnética (RM) permitió apreciar una lesión de partes blandas que englobaba los tendones flexores y contactaba con el periostio de la falange proximal. Era hipointensa en T1, hiperintensa en T2 y realzaba de forma homogénea con Gadolinio. En su margen palmar presentaba un reborde hipointenso que pudiera representar calcificación. No se apreciaron vacíos de señal internos, por lo que el patrón de calcificación debería ir unido a una matriz celular (lo que sugiere tumor o psedotumor). En los márgenes laterales de la falange se visualizaron levantamientos periostios, así como un componente de partes blandas que desplazaba al tendón extensor. En los cortes sagitales se evidenció que la medular ósea estaba respetada y que la cortical anterior no estaba infiltrada pero si mostraba un ligero festoneado en su superficie externa.\n \n La lesión fue extirpada realizando una amputación estética del 4º radio de la mano derecha por el déficit funcional del dedo.\n \n El estudio anatomopatológico de la pieza de amputación señaló la existencia entre el tendón flexor y la superficie de la primera falange, de hueso maduro con intensos fenómenos de remodelación. En el centro del mencionado hueso existía una proliferación fibroblástica con casi total ausencia de mitosis, que diferenciaba pequeñas cantidades de osteoide. Al comparar esta biopsia con la previa o diagnóstica, se observó una mayor celularidad, con discreta atipia celular y mayor actividad mitótica.\n \n La evolución del paciente fue satisfactoria y la lesión no ha recidivado tras 8 años de seguimiento, conservando en la actualidad una buena función de la mano.\n \n",
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"note_text": "Mujer de 27 años de edad que se queja por el aspecto inestético de su labio superior que comenzó a notar a los 18 años. Refiere gran dificultad para la relación social, así como para la relación de pareja.\n La historia clínica familiar no reveló la existencia de casos semejantes.\n Presentaba un aumento pronunciado del labio superior, que se hacía mucho más evidente cuando sonreía, junto con la presencia de una retracción central.\n \n El tratamiento quirúrgico se realizó bajo bloqueo anestésico de ambos nervios infraorbitarios. Marcamos la zona quirúrgica con azul de metileno en forma de dos elipses tranversas con una \"z\" central. Resecamos el exceso de tejido mucoso y submucoso labial con excisiones elípticas y la brida central se corrigió con una z-plastia de acuerdo con el marcaje realizado. La cirugía finalizó con el cierre mediante suturas simples con hilo sintético reabsorbible de poliglactin 6-0.\n \n La herida quirúrgica evolucionó con edema local que se resolvió al final de la segunda semana de postoperatorio. Dos meses después, en revisión en consulta ambulatoria, la paciente estaba plenamente satisfecha con el resultado obtenido, contando incluso que había vuelto a frecuentar relaciones sociales en compañía de su pareja. Tras 18 meses de seguimiento, no hay señales de recidiva o complicaciones tardías.\n \n",
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"note_text": "Paciente pediátrica de 15 meses de edad diagnosticada de púrpura fulminans secundaria a infección meningocóccica grave complicada con fallo multiorgánico, shock séptico, edema agudo de pulmón complicado con neumonía nosocomial que requirió soporte ventilatorio y grave necrosis isquémica por CID en las extremidades inferiores.\n A los 4 días de su ingreso en Unidad de Cuidados Intensivos (UCI) pediátrica, se pide consulta a nuestro Servicio para valoración de las lesiones cutáneas. Apreciamos flictenas y signos de sufrimiento cutáneo en miembro superior derecho (MSD) y principalmente, en miembros inferiores (MMII), acompañados de lesiones purpúricas y necrosis irreversibles de los dedos de ambos pies. Dada la evolución tórpida y la extensión de las lesiones, se decide la intervención quirúrgica 17 días después.\n \n Realizamos desbridamiento superficial para demarcar la zona de necrosis profunda y colocamos Biobrane® (Biobrane, Smith & Nephew B.V., Barcelona, España). Las zonas intervenidas se curaron con sulfadiazina argéntica antes y después de la cirugía.\n \n Ante la mala evolución de las heridas, contactamos con el Servicio de Traumatología para nueva valoración. Se realizaron 2 gammagrafías óseas en un intervalo de 15 días para valorar el estado de ambos MMII y ambas informaron de la existencia de tejido óseo sin captación desde aproximadamente el 1/3 proximal de la tibia. Dada la gangrena establecida, con necrosis irreversible evidente y mal olor, los traumatólogos pediátricos deciden, de acuerdo con la familia, proceder a practicar amputación infrarrotuliana bilateral para conservar la máxima movilidad ulterior de la paciente.\n El resultado anatomopatológico diferido informó de trombosis vascular múltiple y necrosis abscesificante en piel y tejidos blandos.\n Durante el postoperatorio, se delimitó aún más la necrosis de tejidos blandos en la zona de cobertura de ambos muñones de amputación, lo que produjo una exposición de los segmentos tibial y peroneo de ambas extremidades. Debido a la corta longitud de los muñones, no se podía proceder a una nueva amputación de los segmentos y cobertura con tejido proximal, pues no garantizaría la posible colocación en el futuro de las prótesis. Por tanto, optamos por iniciar terapia de presión negativa con sistema VAC® para favorecer el crecimiento tisular y la eliminación del exudado de las heridas.\n \n Procedimos en primer lugar a lavar las extremidades con una solución de clorhexidina jabonosa al 0,4% y suero fisiológico. Luego colocamos los apósitos VAC-Granufoam ® según la guía clínica de la terapia VAC®. Al principio utilizamos los apósitos medianos según el modelo Pitta-VAC® (10,11), dividiendo en dos mitades el apósito, de manera que cada una de ellas es separada parcialmente para ser colocada sobre la zona a tratar, como si fuera un guante. Esta técnica está descrita como rápida en su diseño y en su ejecución. No obstante, en zonas en las que la necrosis es parcheada, hemos notado que este sistema macera la piel sana si ésta entra en contacto directo con el apósito de poliuretano reticulado, por lo que es necesario colocar apósitos hidrocoloides recortados bajo la esponja para evitarlo, lo cual hace más engorrosa la cura. Decidimos por tanto volver a la colocación clásica de los apósitos: pequeños fragmentos recortados sobre las pérdidas de sustancia conectados entre sí mediante íntimo contacto en alguna de sus partes. La presión utilizada fue de -125 mmHg y en modo continuo. La granulación en el lecho y la mejoría fueron evidentes.\n \n Tras 40 días de terapia, conseguimos el recubrimiento de los segmentos óseos expuestos y tras la colocación de láminas regeneradoras dérmicas Integra® (Integra, San Priest, Francia) durante 1 mes, logramos la cobertura definitiva mediante injertos de piel parcial mallados 1:1,5 tomados del muslo izquierdo.\n \n La evolución fue satisfactoria, con epitelización completa de los muñones de amputación, procediéndose al alta hospitalaria de la paciente tras exactamente 4 meses de ingreso hospitalario. Mantuvimos seguimiento ambulatorio durante 3 semanas más. Tras 2 años del suceso, la paciente se encuentra en proceso de rehabilitación de sus secuelas neurológicas, control del tronco y adaptación a prótesis infracondíleas.\n \n",
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"note_text": "Mujer de 36 años de edad sin antecedentes patológicos de interés y madre de un hijo de 5 años de edad, que consulta para valorar aumento mamario bilateral. Presenta atrofia mamaria moderada con ptosis muy leve. La piel es de buena calidad, hidratada y sin estrías. No se palpan nódulos mamarios y la paciente no refiere ningún antecedente patológico mamario de relevancia. En las mamografías recientes no se detectó ninguna patología.\n Tras la consulta y exploración clínica se decide llevar a cabo una cirugía de aumento mamario bilateral por vía periareolar inferior, con disección de bolsillo subpectoral y colocación de prótesis anatómicas de gel de silicona (McGhan® Style 140 MM de 320 cc.).\n La intervención se realizó bajo anestesia general y transcurrió sin incidencias; la paciente fue dada de alta al día siguiente. A los 7 días de postoperatorio se encuentra bien, el aspecto de las mamas es normal, la simetría es adecuada y las molestias son de escasa relevancia. La paciente refiere que nota tensión en las mamas, pero sin dolor a la palpación. La cicatrización es correcta.\n \n A los 15 días de postoperatorio acude a la consulta presentando aumento simétrico del volumen mamario y drenaje espontáneo de material líquido de coloración blanquecina a través de una pequeña dehiscencia de la herida periareolar derecha. No ha presentado fiebre y las mamas no muestran signos inflamatorios. En el margen lateral de la cicatriz se aprecia un pequeño de fecto de 2 mm. por el que drena material, que al exprimir la mama aumenta su caudal. Sospechando la existencia de un absceso retroareolar y decidimos dilatar dicho defecto usando una pinza de hemostasia, momento en el que se produce el drenaje espontáneo de una gran cantidad del citado material. Al proceder a la expresión de la mama se aprecia igualmente que el material drena por el pezón y al hacer la misma maniobra en la mama izquierda, se aprecia también este drenaje por el pezón. Tomamos muestra para cultivo, siendo el resultado negativo. Ante estos hallazgos pensamos que la tumefacción de las mamas se debe a la producción de leche.\n \n Recomendamos a la paciente realizar una analítica para estudiar los niveles de prolactina (PRL) y se realiza consulta con Ginecología que recomienda una ecografía mamaria bilateral, TAC craneal y análisis de hormonas tiroideas y suprarrenales. Los resultados de todas estas pruebas no mostraron signos patológicos. La ecografía mamaria reveló un aumento de la densidad del tejido mamario y no se apreció líquido en el bolsillo que alojaba la prótesis. Aún así se decide instaurar tratamiento con bromocriptina por vía oral de forma empírica, a una dosis inicial de 1,25 mg., 3 veces al día. Después de una semana de tratamiento y al no obtener respuesta, se aumentó la dosis hasta 2,5 mg. 3 veces al día. El tratamiento se mantendría hasta 2 semanas después del cese de la secreción.\n A pesar del tratamiento la evolución fue tórpida y el cuadro de galactorrea no cesó, continuando el drenaje de leche a través de la herida de la mama derecha. Ambas mamas continuaban turgentes. Se mantiene a la paciente con vendajes moderadamente compresivos considerando que el drenaje continuo de leche por la fístula de la herida puede ser un estímulo mantenido para la lactancia, así como para sellar posibles espacios muertos en el bolsillo o en el tejido mamario.\n Al cabo de 2 meses en los que la paciente fue sometida a revisiones y curas semanales, el cuadro de galactorrea cesó, deteniéndose el drenaje de leche a través de la herida y disminuyendo la turgencia en ambas mamas.\n Sin embargo, 2 semanas después la paciente acude de nuevo presentando en esta ocasión aumento de volumen mamario unilateral derecho. Se realiza nueva ecografía mamaria que revela la existencia de un seroma intracapsular derecho. Se procede al drenaje del mismo bajo condiciones de asepsia y éste se resuelve en 7 días; pero la morfología de la mama comienza a verse afectada de tal forma que el trayecto a través del cual drenaba la leche se retrae deformando la areola. Se constata también que la mama desarrolla un grado incipiente de contractura capsular. Optamos por llevar a cabo revisión quirúrgica debido sobre todo a la deformidad provocada por la fístula areolar.\n \n La paciente es intervenida procediendo a la revisión del bolsillo en el que no se aprecia la existencia de ninguna colección líquida, tan solo escasos depósitos blanquecinos que se analizan Practicamos capsulotomías, recolocación de la prótesis que permanecía intacta y sin depósitos en su superficie y reparación de la retracción areolar. El informe anatomopatológico de los depósitos blanquecinos hallados describe la existencia de fibrosis hialinizada con infiltración crónica granulomatosa e infiltrado de histiocitos.\n \n Durante este segundo postoperatorio la paciente no desarrolla galactorrea y se recupera sin incidencias. Sin embargo, después de 1 año la mama derecha desarrolla contractura capsular grado III por lo que se decide reintervenir nuevamente, realizando capsulectomía parcial debido a que los tegumentos se han adelgazado y se considera el riesgo de afectar la integridad de la piel durante la realización de una capsulectomia total, y capsulorrafia medial por ser esta la zona en la que el adelgazamiento de los tejidos es mayor. Cambiamos la prótesis por otra de idénticas carácterísticas. En el postoperatorio de esta nueva intervención detectamos como única complicación un síndrome de Mondor en la mama derecha.\n \n Al cabo de 2 años de postoperatorio la paciente presenta nuevamente signos compatibles con contractura capsular recidivada en la mama derecha, con notable afectación estética y de aparición más lenta en la mama izquierda. El tratamiento quirúrgico que podría plantearse en esta ocasión sería: en la mama derecha nueva capsulectomía, si los tegumentos lo permiten, pudiendo precisar de refuerzo mediante malla de material sintético o biológico en la región ínferomedial, y en la mama izquierda capsulectomía y recambio de prótesis. No se descarta la necesidad de añadir procedimientos de mastopexia para corregir la posición del complejo teloareolar.\n \n",
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"note_text": "Presentamos el caso de un paciente varón de 39 años de edad que presentó aumento de región maseterina bilateral de varios años de evolución, siendo de mayor tamaño el músculo masetero del lado izquierdo, lo que motivó la consulta. En su historia clínica el paciente refiere estar asintomático, sin patologías agregadas, con malos hábitos dietéticos y bruxismo diurno y nocturno. Se realizó estudio en marzo del 2008 mediante Tomografía Axial Computerizada (TAC) simple y contrastada para descartar patología de tejidos blandos y duros tipo neoplasia, proceso infeccioso crónico o crecimiento óseo. Se diagnosticó finalmente como hipertrofia del músculo masetero bilateral, mayor en el lado izquierdo.\n \n Tomamos medidas de los músculos maseteros en los cortes tomográficos, de anterior a posterior de ambos músculos maseteros y en su diámetro transverso con los siguientes resultados: 1.40 cm, 1.60 cm y 0.95 cm en masetero derecho; 1.83 cm, 1.53 y 1.13 cm en músculo masetero izquierdo, ambos mayores de lo normal. Iniciamos tratamiento a base de guarda oclusal nocturna y aplicación de toxina botulínica en noviembre del 2009, de acuerdo al protocolo seleccionado.\n \n Se propuso la aplicación de toxina botulínica. La Primera aplicación a dosis de 50 U, 25 de las cuales se aplicaron en la zona de mayor hipertrofia (zona IV descrita por Da-Hye Kim), 15 U en dirección al borde inferior mandibular y 10 U por encima de la aplicación previa (correspondiente a zona V de Da-Hye Kim). Con esta distribución de aplicación en los puntos propuestos por Nam-Ho Kim que mejoran el contorno mandibular, se realizó marcaje sobre la piel a nivel de ambos músculos maseteros (5). Para la preparación del producto se utilizó una aguja gruesa (18G) con el fin de evitar la formación de turbulencias. El alcohol, usado ya sea en el tapón del vial o bien en la piel del paciente, debe evaporarse completamente antes de aplicar la toxina dado que también puede inactivarla. A pesar de que el vial puede reconstituirse a una dilución de 8 cc/100 U, preferimos la dilución en 4 cc. a fin de conseguir una dosificación de 2.5 U/0.1 cc. El obtener de esta forma un volumen menor, limitará la posibilidad de que la toxina difunda hacia las zonas adyacentes. Es importante recordar que una vez realizada la reconstitución, el producto deberá utilizarse en el plazo de las 4 horas siguientes para evitar pérdida de eficacia, aunque algunos autores señalan que se puede utilizar sin disminuir su eficacia dentro de los 3 a 7 días posteriores.\n Para disminuir las molestias y que la aplicación sea segura utilizamos una aguja fina (30G). Es importante insistir en que el paciente no debe tomar medicamentos que interfieran con la coagulación de 10 a 14 días antes de la inyección para evitar equímosis. También solicitamos al paciente la correspondiente autorización para llevar a cabo el procedimiento mediante un consentimiento informado específico, tal y como habitualmente hacemos con cualquier procedimiento invasivo.\n Para las aplicaciones posteriores citamos al paciente cada 12 semanas (3 meses), utilizando la misma técnica y completando hasta un total de 4 aplicaciones. Se sabe que al utilizar toxina botulínica de forma repetitiva se causa atrofia en los grupos musculares infiltrados, lo que hace que el paciente presente mejoría clínica. También se indicó continuar con el uso de la guarda oclusal nocturna para controlar el bruxismo.\n \n",
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"note_id": "S0376-78922013000400009-1",
"note_text": "Varón de 37 años, sin antecedentes personales de interés, remitido desde el Servicio de Urgencias de nuestro hospital por presentar una masa en el compartimento posterior del miembro inferior izquierdo de años de evolución, no dolorosa hasta las 3 últimas semanas cuando comienza con dolor, aumento de la velocidad de crecimiento, impotencia funcional y parestesias.\n A la exploración física el paciente presentaba una gran masa en la región posterior de la pierna izquierda de aproximadamente 15 cm de diámetro, con distensión de los compartimentos posteriores y laterales. Asimismo, refería parestesias discontinuas en la extremidad afecta e hiperestesia en el pulpejo del primer dedo del pie y en la región peronea. La vascularización del miembro estaba indemne, presentando pulsos poplíteos, tibial posterior y pedio conservados. No obstante, constatamos una mayor frialdad en el pie izquierdo con respecto al contralateral.\n \n Realizamos Trucut de la masa con resultado anatomopatológico de sarcoma fusocelular de alto grado (sarcoma sinovial). La resonancia magnética nuclear (RMN) informó de la presencia de una gran masa en la pierna izquierda que afectaba a todo el espesor del músculo sóleo, marcadamente heterogénea, multinodular y polilobulada, de 14x10x7 cm de diámetro máximo, con signos de sangrado reciente. En la parte posterior, la lesión comprime y desplaza los vientres musculares de los gemelos interno y externo, con los que contacta sin planos grasos, y en la parte anterior con el poplíteo, tibial posterior y flexor común de los dedos. Anterocaudalmente, la masa infiltra el polo superior del flexor del primer dedo.\n Con respecto a las estructuras óseas observamos una estrecha relación con la diáfisis de la tibia y, aunque se mantienen los planos grasos, el espesor del tejido interpuesto entre ambas estructuras es inferior a 1cm. En cuanto al peroné, el tumor lo engloba semicircularmente en una extensión de unos 12 cm. A pesar de la estrecha relación del tumor con la tibia y el peroné, no observamos signos sugestivos de infiltración ósea. En relación a las estructuras vasculares, apreciamos cómo el polo superior del tumor llega a contactar con la arteria poplítea a nivel de su bifurcación de la salida del tronco tibial anterior, pasando a englobar distalmente al tronco tibio-peroneo con repermeabilización distal de los vasos peroneos.\n En resumen, se trata de una tumoración en la musculatura sólea izquierda de 14 cm de diámetro máximo sugerente de sarcoma con signos de infiltración vascular y de la musculatura adyacente.\n \n El paciente fue intervenido bajo anestesia general y la intervención fue realizada por un único equipo quirúrgico que practicó tanto la resección tumoral como la posterior reconstrucción.\n Comenzamos con el colgajo plantar disecando un colgajo fileteado B3 de Künstcher (6) y posteriormente con la amputación infracondilea incluyendo la cortical posterior de la tibia. Realizamos anastomosis términoterminales (T-T) a la arteria poplítea y a ambas safenas y neurorrafia entre ciático poplíteo externo y tibial posterior.\n \n En el postoperatorio inmediato el paciente no presentó alteración hemodinámica alguna y el colgajo evolucionó de forma favorable sin necesidad de revisión microquirúrgica del mismo en los días posteriores a la intervención.\n El resultado anatomopatológico de la pieza extirpada resultó ser de sarcoma sinovial bifásico de alto grado de 15 cm de diámetro máximo en el espesor del tejido muscular, con bordes quirúrgicos respetados (tumor a 1,5 cm del borde quirúrgico proximal de partes blandas). No se evidenció infiltración del tejido óseo.\n El paciente siguió un postoperatorio favorable, siendo dado de alta a su domicilio a los 30 días de la intervención. Llevamos a cabo un seguimiento semanal del mismo hasta obtener una cicatrización óptima para comenzar con el tratamiento ortopédico. A los 60 días el paciente deambulaba con prótesis transtibial tipo PTB (patellartendon-bearing prosthesis) con sistema endoesquelético y pie dinámico con sensibilidad completa en el muñón de amputación. El seguimiento total por nuestra parte fue de 7 meses tras la cirugía. Dos años después de la intervención, continúa en seguimiento por parte de los Servicios de Oncología y Rehabilitación de nuestro hospital, que procederán al recambio protésico según su protocolo cada 2 años. Hasta la fecha, no se han encontrado evidencias de recurrencia local.\n \n",
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"note_id": "S0376-78922014000100014-1",
"note_text": "Paciente de 41 años de edad con el único antecedente médico de hepatitis A en la infancia, remitido a nuestra consulta por una tumoración premaxilar izquierda, blanda, móvil y no adherida a planos profundos en la exploración, de unos 4cm. de diámetro y 6 meses de evolución, sin otra sintomatología asociada, y que ha presentado crecimiento lento durante este tiempo. A simple vista impresiona de lesión quística o lipoma, pero en la exploración su localización y su consistencia blanda, elástica y móvil hacen sospechar que pueda tratarse de otro tipo de lesión.\n \n El paciente aporta resonancia magnética nuclear (RMN) realizada en otro centro, con informe de nódulo de 25mm. en tejido celular subcutáneo que no afecta a hueso maxilar y de naturaleza inespecífica, para descartar posibilidad de tumor fibroso o hematoma, a pesar de no existir antecedentes de traumatismo facial.\n Ante esta sospecha diagnóstica programamos al paciente para la realización de biopsia en quirófano, bajo anestesia local, durante la cual encontramos una gran friabilidad y sangrado en sábana del tumor que impresiona de lesión de naturaleza vascular, lo que posteriormente se confirma con el informe anatomopatológico que refiere: tumoración mesenquimal vascular cuya morfología y perfil inmunohistoquímico es compatible con el patrón observado en el hemangiopericitoma. El estudio inmunohistoquímico de la biopsia informa de resultado: positivo para CD99 (difuso), BCL2, Betacatenina (focal intracitoplasmática) y CD34 (focal citoplasmática), y negativo para S100, GLUT-1, WT1, AE1, CD31 y Factor VIII. El índice de proliferación celular Ki 67 es de un 5%.\n Tras la confirmación diagnóstica y al haberse realizado la RMN inicial en otro centro, el Servicio de Radiología de nuestro hospital nos recomienda realizar un estudio de imagen adicional con tomografía axial computarizada (TAC) para descartar con mayor certeza la afectación ósea de cara a la cirugía; este estudio informa de la existencia de una tumoración hipervascular en partes blandas de la región premaxilar izquierda, con afectación del tejido celular subcutáneo y extensión en profundidad hacia planos musculares, sin datos de afectación de estructuras óseas vecinas..\n \n Bajo ese diagnóstico final, intervenimos quirúrgicamente bajo anestesia general empleando visión de aumento con gafas lupa (x4.3); realizamos extirpación de la tumoración en bloque con margen de seguridad de aproximadamente 2,5cm. e incluyendo la musculatura afectada: porción orbitaria del músculo orbicular mayor inferior izquierdo y parcialmente el músculo cigomático menor y el elevador del labio superior, incluidos en el tumor. Identificamos la rama angular de la arteria facial, que se introduce en el seno de la tumoración, y que ligamos, así como las ramas cigomáticas del nervio facial que quedan en el lecho quirúrgico y que se preservan en su totalidad.\n \n Realizamos la reconstrucción del defecto quirúrgico con un colgajo de avance de mejilla de base ínfero-lateral.\n \n La evolución postoperatoria fue favorable, y el paciente fue dado de alta a los 2 días de la cirugía sin complicaciones.\n El informe anatomopatológico final de la pieza fue de hemangiopericitoma que respeta los bordes quirúrgicos de resección, con inflamación gigantocelular de cuerpo extraño acompañante. El estudio inmunohistoquímico definitivo de la pieza de resección fue positivo para CD34 difuso, CD99 focal, y negativo para S-100, CD31 y factor VIII, con un índice de proliferación celular Ki-67 del 5%.\n \n Presentamos el caso en el Comité de Tumores del hospital, donde en función de los resultados postoperatorios, se decidió que no era necesario realizar ningún tratamiento complementario, solo un seguimiento periódico del paciente. Tras 2 años de postoperatorio, el paciente presenta una evolución favorable, con buen resultado estético y funcional, y sin datos de recurrencia ni clínica ni radiológica en los controles postoperatorios realizados hasta la fecha.\n \n",
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"note_text": "Niña de 2 años de edad que es traída a Urgencias por presentar una deformidad del 2o dedo de la mano derecha. La familia refiere que 1 año antes sufrió caída desde una altura de 20 cm. y antecedente de aplastamiento 6 meses antes.\n Como antecedentes personales destaca un estudio de cariotipo con resultado normal en el contexto de alteraciones electroencefalográficas y plagiocefalia parietooccipital resueltas.\n En la exploración realizada en Urgencias observamos ensanchamiento de la base de la falange media del 2o dedo de la mano derecha y alteración en la flexión de la articulación interfalángica proximal, que alcanza los 50 grados de flexión máxima. La exploración neurovascular no determinó hallazgos patológicos de interés. Efectuamos también exploraciones radiológicas del 2o dedo en proyecciones anteroposterior y de perfil, que determinan la existencia de un aumento de la base de la falange media de dicho dedo a nivel volar.\n \n La paciente fue diagnosticada de subluxación y remitida a consultas de Traumatología Infantil con control radiográfico. Allí se objetiva a la exploración un aumento macroscópico de la base de la falange media del 2o dedo de la mano derecha, y limitación de la flexión interfalángica proximal, con un máximo de 50 grados. Acude con radiografía control.\n \n En la radiografía se observa un aumento de la porción palmar de la base de la falange media con borramiento del cartílago de crecimiento a ese nivel; en la proyección anteroposterior se evidencia superposición ósea. Se postula como posible diagnóstico la existencia de una fractura antigua de falange media con callo de fractura prominente y epifisiodesis. La paciente es remitida Unidad de mano de Cirugía Plástica y Reparadora para valoración de secuela de fractura.\n En la primera consulta en el Servicio de Cirugía Plástica y Reparadora no se aprecian cambios en la exploración respecto a los descritos por Traumatología Infantil. La paciente no aporta las radiografías que le habían sido entregadas en mano en Urgencias y Traumatología Infantil por lo que se le cita nuevamente para radiografía de control y se insiste en la necesidad de que aporte las radiografías previas. Osteocondroma gigante de falange en paciente pediátrico Cirugía\n La paciente no acude a la cita en los 2 años siguientes. Pasado este tiempo, solicita nuevamente cita en consulta de Cirugía Plástica y Reparadora por aumento de la deformidad del dedo. A la exploración se observa un notable aumento de la base de la falange media del 2o dedo de la mano derecha (macrodactilia). La alteración de la flexión es mayor, alcanzando los 20 grados de flexión máxima. Solicitamos radiografía de control.\n \n Observamos en las radiografías, en proyección de perfil, la existencia de una masa de aspecto lobulado, con distintas densidades, que parece provenir del tercio inferior de la falange media del 2o dedo. La masa alcanza el tercio superior de partes blandas de la falange proximal. Asimismo destaca la presencia de una muesca en su porción superior. En la proyección anteroposterior apreciamos que la masa sobrepasa la extensión de anchura de la segunda falange.\n Ante la sospecha de osteocondroma/encondroma solicitamos RM que informa de la existencia de una exóstosis lobulada de 12 mm de espesor, con base de 20x20 mm, que se extiende proximalmente afectando a la placa volar de inserción del sistema flexor superficial, con desplazamiento del tendón flexor profundo y del sistema de anclaje de poleas, compatible con osteocondroma.\n \n Estadiamos el tumor empleando la clasificación de Enneking y determinamos que se trataba de un estadio III, lesión benigna agresiva: lesión benigna de baja agresividad (G0), con afectación de la inserción perióstica del extensor superficial (extracompartimental) (T2) y sin metástasis (M0).\n Dada la alteración funcional que presentaba la paciente y el tamaño de la masa tumoral, decidimos llevar a cabo tratamiento de la lesión.\n En la cirugía efectuamos acceso a la lesión mediante técnica de Brunner en zig-zag evitando así la sección transversal de los pliegues palmares que pudiera generar futuras retracciones. Localizamos el tendón flexor superficial y colocamos la articulación metacarpofalángica del 2o dedo, así como la muñeca, en flexión máxima para alcanzar la porción más proximal del tendón flexor superficial. Lo seccionamos, elegiendo realizar dicha sección a nivel proximal para prevenir la aparición del fenómeno conocido como Cuádriga de Verdán, entendido como alteración de la flexión de la articulación metacarpofalángica por adhesión en una articulación del cabo proximal de un tendón tras su sección. Mediante escoplo, escindimos la porción de la tumoración que sobresalía de la falange sana y una porción de la cortical adyacente. Seguidamente practicamos curetaje mediante cucharilla de la médula y del tejido óseo de la superficie dorsal.\n \n Para la reconstrucción: de la cavidad generada empleamos material osteoconductor (Actifuse Abx Silicated Calcium Phosphate®, BioSurgery, EE.UU). Efectuamos inmovilización mediante férula dorsal de yeso desde tercio proximal del antebrazo hasta final de los dedos, con muñeca en 40o de flexión palmar, articulaciones metacarpofalángicas en 90o y articulaciones interfalángicas en extensión. Mantuvimos la inmovilización durante 3 semanas, tras las cuales no fue necesaria la rehabilitación dada la edad de la paciente y la buena movilidad postoperatoria que presentaba.\n Practicamos radiografía de control anual sin evidencias de recidiva y con movilidad completa tras 3 años y 8 meses de seguimiento postoperatorio.\n \n",
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"note_text": "Mujer de 49 años de edad con antecedentes personales de asma bronquial. En revisión ginecológica periódica se le diagnostica carcinoma ductal infiltrante de mama izquierda y es sometida a mastectomía radical modificada con vaciamiento axilar por el Servicio de Cirugía General, recibiendo tratamiento adyuvante con radioterapia y quimioterapia. El estudio de extensión resultó negativo para adenopatías locorregionales y metástasis a distancia (pT3pN0M0). Al finalizar el tratamiento la paciente solicita reconstrucción mamaria, por lo que es remitida al Servicio de Cirugía Plástica.\n A los 4 años de la mastectomía se procedió a la reconstrucción mamaria con diversos procedimientos que describimos a continuación. En primer lugar reconstrucción de mama izquierda con colgajo miocutáneo de recto abdominal transverso (TRAM), sufriendo pérdida parcial del mismo que se resolvió con desbridamiento y cierre directo. Dos años después se colocó prótesis expansora de Becker subTRAM y finalmente, se realizó recambio del expansor por prótesis mamaria definitiva y mastopexia simetrizadora de mama contralateral, quedando pendiente de completar la reconstrucción del complejo areola pezón (CAP). En el postoperatorio de la última intervención comienza la aparición en la zona periareolar de la mama derecha y en el centro del colgajo de la mama izquierda de pequeñas lesiones pustulosas con posterior desarrollo de úlceras dolorosas de borde violáceo y fondo con tejido de granulación,.\n \n Con el presunto diagnóstico de dehiscencia de herida quirúrgica se realiza biopsia que informa de tejido de granulación, por lo que la paciente es sometida a curas con desbridamiento durante más de 12 meses. Dada la mala evolución, se decide interconsulta al Servicio de Dermatología, donde ante la sospecha inicial de pioderma gangrenoso, se realiza estudio exhaustivo para descartar otros procesos. Se solicitaron las siguientes pruebas:\n - Analítica, incluyendo estudio de autoinmunidad (ANAs y ENAs) y proteinograma: sin alteraciones patológicas.\n - Serología luética, virus hepatitis B y C, VIH: negativa.\n - Mantoux: negativo.\n - Radiografía de tórax: engrosamiento difuso de las paredes bronquiales; cambios quirúrgicos en mama izquierda con grapas en región axilar.\n - Biopsia con técnicas de PAS, Grocott y Ziehl- Neelsen: ulceración epidérmica focal con abscesificación dérmica y folicular, inflamación crónica linfohistiocitaria y plasmocitaria adyacente y de distribución perivascular en dermis superficial y profunda. Hallazgos histopatológicos compatibles con la sospecha clínica de pioderma gangrenoso clásico o ulcerado.\n \n - Cultivo biopsia (aerobio, anaerobio, hongos y micobacterias): negativo.\n Tras el diagnóstico de exclusión de pioderma gangrenoso clásico, iniciamos tratamiento con prednisona oral a dosis de 60 mg/día asociando propionato de clobetasol 0,05% tópico durante 3 meses. Al reducir la pauta esteroidea a 30 mg/día la paciente comenzó con un rebrote de las lesiones, por lo que decidimos asociar tratamiento con ciclosporina a dosis de 4 mg/Kg de peso, sustituir los corticoides tópicos por tacrolimus 0,1% tópico y reducir también paulatinamente la prednisona hasta su suspensión durante un periodo de mes y medio.\n Inicialmente, la paciente experimenta una evolución favorable salvo hipertensión controlada con un diurético tiazídico y se consigue una buena reepitelización de las lesiones; pero tras 2 meses de tratamiento con ciclosporina comienza con efectos secundarios muy molestos: hiperplasia gingival, hipertricosis, hirsutismo y disestesias que nos obligan a la reducción progresiva de este tratamiento, lo que tiene como consecuencia un nuevo rebrote de pequeñas lesiones pustulosas que infiltramos con triamcinolona a la vez que retiramos el tacrolimus tópico. La intolerancia de la paciente a los efectos secundarios de la ciclosporina, nos obligó a su suspensión completa tras 4 meses de tratamiento.\n \n Finalmente, ante la aparición de nuevas lesiones y la mala tolerancia a los tratamientos previos, optamos por iniciar tratamiento con infliximab (agente anti-TNF), comenzando con una terapia de inducción de 5 mg/kg a las 0, 2 y 6 semanas similar a la empleada en la enfermedad inflamatoria intestinal o en la psoriasis, continuando con infusiones de mantenimiento cada 8 semanas. La paciente evolucionó de forma satisfactoria con reepitelización completa a los 2 meses del nuevo tratamiento, por lo que decidimos mantener el tratamiento de forma similar al de otras dermatosis inflamatorias hasta objetivar estabilización de la enfermedad, tras lo cual nos plantearemos reducir, con espaciamiento progresivo de las dosis.\n \n",
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]
},
"note_id": "S0376-78922016000300005-3",
"note_text": "Paciente varón recién nacido a las 40 semanas de gestación, sin antecedentes de interés, que es remitido a nuestro servicio desde Pediatría de nuestro hospital por presentar malformación linfática microquística cérvicoescápulo- humeral.\n \n A los 7 días de vida se le realiza la punción y evacuación del linfangioma con posterior instilación de polidocanol y etanol. Se repitió el tratamiento 5 días después. De los 7 drenajes colocados, 1 de localización axilar fue retirado a los 3 días por aparente sufrimiento cutáneo.\n Tras la segunda infiltración observamos herida superficial de 3x10 cm de diámetro, que afecta a la región humeral y a la superficie anterior del tórax, secundaria a extravasación por punta del catéter de instilación de polidocanol. La lesión fue tratada con curas con apósitos de hidrocoloide. Una semana después, procedimos a la colocación de un sistema de terapia de vacío (Renasys®, Smith&Nephew®, Londres, Reino Unido) a 100 mmHg, en modo continuo, con la finalidad de acelerar el cierre de la herida y controlar la linforrea. Los cambios de apósitos se realizaron cada 72 horas y la terapia de vacío se utilizó durante 21 días.\n \n El paciente permaneció hospitalizado hasta los 2 meses de vida y fue dado de alta con curas domiciliarias con Aquacel® Ag (ConvaTec®, Reino Unido), hasta lograr el cierre total y estable de la herida de manera ambulatoria.\n A los 11 meses de vida presenta una masa persistente, fundamentalmente a expensas de hipertrofia del tejido celular subcutáneo, con lesiones quísticas residuales de predominio microquístico en la superficie medial del brazo y en la pared torácica. Dado que el paciente está asintomático, tras consultar con la familia decidimos mantener un tratamiento conservador y valorar su evolución con la edad.\n \n",
"section_annotation": {
"gold": [
{
"end_offset": 60,
"label": "PRESENT_ILLNESS",
"segment": "Paciente varón recién nacido a las 40 semanas de gestación, ",
"start_offset": 0
},
{
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"label": "PAST_MEDICAL_HISTORY",
"segment": "sin antecedentes de interés, ",
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},
{
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"label": "DERIVED_FROM/TO",
"segment": "que es remitido a nuestro servicio desde Pediatría de nuestro hospital por presentar malformación linfática microquística cérvicoescápulo- humeral.\n \n ",
"start_offset": 89
},
{
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"label": "TREATMENT",
"segment": "A los 7 días de vida se le realiza la punción y evacuación del linfangioma con posterior instilación de polidocanol y etanol. Se repitió el tratamiento 5 días después. De los 7 drenajes colocados, 1 de localización axilar fue retirado a los 3 días por aparente sufrimiento cutáneo.\n ",
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},
{
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"label": "EVOLUTION",
"segment": "Tras la segunda infiltración observamos herida superficial de 3x10 cm de diámetro, que afecta a la región humeral y a la superficie anterior del tórax, secundaria a extravasación por punta del catéter de instilación de polidocanol. ",
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},
{
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"label": "TREATMENT",
"segment": "La lesión fue tratada con curas con apósitos de hidrocoloide. Una semana después, procedimos a la colocación de un sistema de terapia de vacío (Renasys®, Smith&Nephew®, Londres, Reino Unido) a 100 mmHg, en modo continuo, con la finalidad de acelerar el cierre de la herida y controlar la linforrea. Los cambios de apósitos se realizaron cada 72 horas y la terapia de vacío se utilizó durante 21 días.\n \n ",
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},
{
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"label": "EVOLUTION",
"segment": "El paciente permaneció hospitalizado hasta los 2 meses de vida y fue dado de alta ",
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},
{
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"label": "TREATMENT",
"segment": "con curas domiciliarias con Aquacel® Ag (ConvaTec®, Reino Unido), hasta lograr el cierre total y estable de la herida de manera ambulatoria.\n ",
"start_offset": 1241
},
{
"end_offset": 1631,
"label": "EVOLUTION",
"segment": "A los 11 meses de vida presenta una masa persistente, fundamentalmente a expensas de hipertrofia del tejido celular subcutáneo, con lesiones quísticas residuales de predominio microquístico en la superficie medial del brazo y en la pared torácica. ",
"start_offset": 1383
},
{
"end_offset": 1785,
"label": "TREATMENT",
"segment": "Dado que el paciente está asintomático, tras consultar con la familia decidimos mantener un tratamiento conservador y valorar su evolución con la edad.\n \n",
"start_offset": 1631
}
]
}
} |
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