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"note_text": "En Mayo de 1997, una mujer de 29 años de edad fue intervenida, en otro centro, de un carcinoma de la glándula suprarrenal izquierda clínicamente no funcionante que se manifestó clínicamente como molestias en el flanco izquierdo, poco específicas, en el postparto inmediato; la ecografía y la tomografía axial computerizada abdominales mostraron una masa suprarrenal izquierda de 10 cmts., sólida y con áreas de calcificación y necrosis en su interior, siendo la radiografía de tórax y la gammagrafía ósea normales. En los análisis, presentaba ligero aumento de la cortisoluria (284.5 mcgr./24h.) y de 17-OH-esteroides en orina (12.7 mcg./24h.), sin síntomas de hipercortisolismo sistémico. Se realizó resección completa de la tumoración, con el diagnóstico histológico de carcinoma suprarrenal de 10 x 7 x 5 cmts. (215 grs.) bien encapsulado, aunque con invasión vascular, amplias zonas de necrosis y un índice mitótico de 5.8/50; el estudio histoquímico fue (+) para Vimentina y (-) para Citoqueratina, EMA, Cromogranina y Sm- 100. Se etiquetó como Estadio II y Grado II. Treinta meses después, la paciente presentó en los estudios radiológicos de seguimiento una masa en el lecho de resección previo de 7 cmts., en contacto con el hilio renal izquierdo y técnicamente resecable; se reintervino y se llevó a cabo una resección de la recidiva asociada a nefrectomía izquierda, esplenectomía y pancreatectomía distal (radical completa y con márgenes libres). Posteriormente, recibió tratamiento quimioterápico sistémico adyuvante con 6 ciclos completos de cisplatino (CDDP) y etopósido (VP-16) en régimen adyuvante.\n Cuatro años y once meses tras el tratamiento inicial, se detecta en el seguimiento radiológico la presencia de varios nódulos hepáticos sugerentes de metástasis. Se sometió de nuevo a cirugía abdominal realizándose, previo control con ecografía hepática intraoperatoria, una bisegmentectomía IV-B y V y una resección limitada del segmento VIII; el análisis de anatomía-patológica informó de la presencia de 7 nódulos (de tamaño variable entre 0.5 y 1.5 cmts.) compatibles con metástasis de carcinoma suprarrenal.\n Diez meses después, se detecta una nueva recidiva tumoral a nivel subdiafragmático izquierdo (de 6 x 4 cmts. según la TAC) y en la raiz del mesenterio, esta última de 4 x 3 cmts. y localizada a nivel de la salida de la arteria mesentérica superior (AMS). Dada la difícil resecabilidad de la nueva recidiva se decide tratamiento quimioterápico con intención neoadyuvante ( 5 ciclos completos de CDDP y VP-16), decidiéndose por regresión parcial de las lesiones una nueva exploración quirúrgica. Se realizó la resección de las dos masas tumorales, la primera incluyendo el pilar izquierdo del diafragma y una pastilla de 5 cmts. de dicho músculo, y la segunda disecando en su origen el tronco celíaco y la AMS y resecando todo el tejido tumoral entre ambos vasos. La anatomía patológica confirmó la recidiva, estando los bordes de resección no afectos. La evolución postoperatoria fue satisfactoria.\n La paciente se encuentra, tras 7 años y 3 meses del diagnóstico del tumor primario, libre de enfermedad y con una calidad de vida aceptable, mínimamente limitada por las deposiciones diarreicas secundarias a la denervación simpática celíaca.\n",
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"note_text": "Paciente varón de 61 años sin antecedentes patológicos acudió a nuestro servicio por presentar tumoración escrotal derecha aparecida desde hace unos tres años, que ha ido creciendo de tamaño muy lentamente sin dolor y por la presencia de hernia inguinal izquierda. En la exploración física el testículo derecho parecía situarse hacia la raíz escrotal, se apreciaba una masa móvil de consistencia elástica y suave de unos 15 cm que ocupaba todo el hemiescroto. El diagnóstico clínico fue de lipoma escrotal.\n Los exámenes de sangre y de orina, la radiografía de tórax y el electrocardiograma fueron todos normales. No se realizó la ecografía escrotal y se decidió la intervención.\n Durante la operación, en primer lugar, se procedió a la reparación de la hernia inguinal izquierda con malla de prolene y después se realizó la exploración del hemiescroto derecho.\n A través de una primera incisión cutánea escrotal derecha intentamos aislar una voluminosa masa blanquecina. Sin embargo, por la dificultad que teníamos en separar la neoformación de los tejidos circundantes y encontrar el testículo derecho, que estaba envuelto por la masa, decidimos eligir otra vía.\n Se realizó una segunda incisión inguinoescrotál a través de la cual, mediante disección roma fue más fácil aislar la neoformación, que se extendía superiormente hasta la altura del anillo inguinal externo. Una vez que fue aislado el cordón espermático conseguimos traer fuera el testículo, que tenía aspecto hipotrófico pero no resultaba afectado. También la resección de la masa resultaba más facil y segura. Los márgenes de la lesión estaban bien delimitados y fáciles de separarse a excepción de una zona del fondo de la bolsa escrotal, donde la neoformación tenía más adherencia con el dartos.\n El aspecto macroscópico de la neoformación extirpada era el de una masa de forma alongada de 15 x 7 x 5cm y peso de 140 gr aparentemente encapsulada con superficie externa lisa y regular. Al corte la superficie se presentaba uniforme, de aspecto denso y fibroso, de color blanquecino y de consistencia elástica sin evidencia de degeneración mixoide o necrosis.\n \n El examen microscópico demostró una tumoración constituida por grupos de células fusiformes, onduladas e hipercrómicas, estrechamente interpuestas en haces de fibras de colágeno. Con la inmunohistoquímica se evidenciaba positividad citoplásmica para la proteína S-100. No se documentaron signos de necrosis, mitosis ni atipias nucleares. El diagnóstico histopatológico definitivo fue el de neurofibroma.\n \n Un año después de la intervención no se han revelado signos objetivos de recidiva.\n \n",
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"note_text": "Varón de 62 años de edad, que acude a urgencias por referir dolor testicular izquierdo de 24 horas de evolución, acompañado de fiebre termometrada de 40ºC, junto con escalofríos y síndrome miccional acompañante (disuria, polaquiuria, tenesmo y urgencia miccional), ausencia de dolor lumbar.\n Durante la anamnesis el paciente revela su profesión, veterinario, profesión de riesgo para ciertas patologías infecciosas (brucelosis, triquinosis y algunas parasitosis).\n A la exploración se objetiva un teste derecho de características normales, y, en el teste izquierdo, se visualiza un aumento de tamaño así como eritema y dolor al tacto sin fluctuación de la zona afecta aunque con dolor a la movilización testicular.\n El tacto rectal resulta sin hallazgos patológicos y la exploración abdominal así como la percusión renal también descartó afecciones acompañantes al ser normales.\n Analíticamente destaca leucocitosis de 22.240 con neutrofilia (neutrófilos 90%).\n En la Ecografía testicular realizada previa al ingreso muestra aumentos homogéneos de la ecogenicidad del testículo afecto, sin afectación del epidídimo. Engrosamiento de partes blandas con ausencia de absceso testicular. Imágenes compatibles con orquitis sin afectación del epidídimo.\n Se realiza el diagnóstico de orquitis infecciosa, procediéndose a su ingreso con un tratamiento antibiótico que comprendió Doxiciclina, Imipenem y Teicoplanina, asociando Corticoides y terapia analgésica.\n Dos días tras el ingresse realiza una nueva ecografía, objetivándose aumento de la ecogenicidad homogénea similar al contralateral, afectación epididimaria. Engrosamiento de partes blandas con ausencia de absceso testicular. Se termina de filiar el cuadro sindrómico: Orquiepididimitis infecciosa.\n Para averiguar la causa de la patología que presenta el paciente se hace necesaria la realización de pruebas que permitan conocer el germen causante.\n El urocultivo resulta ser negativo, así como la aglutinación específica de Brucella. Sin embargo la seroaglutinación de Rosa de Bengala resulta positiva, así como los hemocultivos, que son positivos a Brucella spp. (los tres).\n Ante la confirmación del diagnóstico de orquiepididimitis brucelar se decide mantener el tratamiento con Doxiciclina y ciprofloxacino.\n El paciente evoluciona favorablemente con remisión completa de los síntomas.\n \n",
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"note_text": "Presentamos el caso de una mujer de 35 años con antecedentes de cirugía litiásica en otro centro y en ambos riñones. Según se informaba se le había realizado, pielolitotomía derecha hacía 15 años. Dos años después se le practica pielolitotomía izquierda y 10 meses antes de ser atendida en nuestro Servicio (año 2005) nueva nefrolitotomía sobre riñón izquierdo, por litiasis renal compleja.\n La paciente presenta un episodio de infección urinaria complicada con pionefrosis y septicemia, tras lo cual se le coloca cateter doble J que queda mal posicionado, subpiélico, que no resuelve el cuadro séptico, por lo que es preciso realizar nefrostomia percutánea izquierda para drenaje renal, situación, en la cual la paciente es remitida a nuestro centro. En la urografía intravenosa que aporta la enferma, se observa litiasis radiodensa infecciosa, pielolocalicial múltiple compleja, sobre riñón con hidronefrosis grado III-IV por importante esclerosis piélica secundaria a cirugías previas sobre dicha unidad renal. Presenta función renal relativamente conservada. Observamos asimismo, cambios postquirúrgicos con moderada atrofia parenquimatosa de unidad renal derecha. La analítica de la paciente reflejaba cifras de urea y creatinina normales.\n \n Ante los hallazgos urográficos, dada la situación del riñón contralateral y la edad de la paciente, se decide lumbotomía exploradora para intentar cirugía conservadora, consistente en nefrectomía polar inferior con nefrolitotomía y reconstrucción de la vía urinaria superior mediante uréterocalicostomía.\n En el postoperatorio la paciente requiere la trasfusión de dos concentrados de hematíes por anemia persistente. La evolución posterior no presenta mayores complicaciones dándose de alta al séptimo día. La anatomía patológica de la pieza informó de cambios compatibles con pielonefritis crónica postlitiásica y el análisis del cálculo reveló su composición de fosfato amónico magnésico.\n Dos años y medio después de la cirugía, la paciente refiere únicamente molestias leves en flanco izquierdo.\n La urografía de control refleja ausencia de litiasis con cierto retraso nefrográfico izquierdo y vía excretora derecha sin cambios respecto a previos. El renograma muestra una función renal izquierda del 30%, con riñón derecho compensador, 70%. Continúa con cifras de función renal dentro de la normalidad, y solo ha presentado un episodio de ITU que ha cedido con ciprofloxacino. Presencia de pequeños restos litiásicos bilaterales subclínicos según técnicas de imagen.\n \n",
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"note_id": "S0034-98872005001100012-1",
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"note_text": "Mujer de 37 años, procedente de Puerto Aisén, con antecedente de tiroidectomía realizada a los 18 años de edad, a causa de un bocio difuso hipertiroideo. Como consecuencia de la cirugía, la paciente desarrolló un hipoparatiroidismo definitivo. Se indicó suplemento de calcio y vitamina D, tratamiento que la paciente cumplió de forma muy irregular y sin controles de laboratorio.\n Quince años más tarde, en 1999, consultó en nuestro hospital por calambres, parestesias y espasmos faciales, además de signos de Chvostek y Trousseau manifiestos. Se reinició el tratamiento con calcio y vitamina D y se solicitó exámenes de calcemia, T4 y TSH. La paciente no regresó a control.\n Reapareció en noviembre de 2003, sin tratamiento. Presentaba marcado compromiso del estado general, astenia, debilidad muscular, calambres, parestesias y cefalea. Sus menstruaciones eran abundantes. En el examen físico destacaban facies hipotiroidea, cicatriz de la tiroidectomía, pulso regular 70x', presión arterial 110/70 mmHg, palidez y signos de Chvostek y Trousseau; el examen cardiopulmonar y abdominal eran normales.\n Sus exámenes revelaron: calcemia 7,98 mg/dL (probable error de laboratorio, por discordancia con la clínica y calcemias posteriores), fosfemia 6,2 mg/dL, BUN 14 mg/dL, proteína total 6,6 g/dL, albuminemia 3,7 g/dL, hematocrito 27%, hemoglobina 6,7 g/dL, microcitosis e hipocromía, TSH 9,7 µU/ml (vn: 0,4-4,8).\n Con diagnóstico de hipoparatiroidismo e hipotiroidismo postiroidectomía y anemia ferropriva, se indicó tratamiento con Elcal D Forte® (carbonato de calcio 1.125 mg + vitamina D 175 UI) 1, Elcal® (carbonato de calcio 800 mg) 1, levotiroxina 50 µg y sulfato ferroso 400 mg/día.\n Dos semanas después, la paciente se presentó con disnea a mínimos esfuerzos, dolor epigástrico, náuseas y edema de rápida progresión. En el examen físico se encontraba afebril, con frecuencia cardíaca 70x' regular, presión arterial 100/70 mmHg, ortopnea, edema generalizado, ingurgitación yugular, estertores pulmonares, ruidos cardíacos apagados, no se auscultaron soplos, hepatomegalia sensible 4 cm bajo el reborde costal. No presentaba signos de trombosis venosa profunda.\n Se le indicó hospitalización. En sus exámenes de ingreso destacaba: radiografía de tórax: cardiomegalia y congestión pulmonar. ECG: ritmo sinusal, 83x', bajo voltaje generalizado, intervalo QT prolongado y alteraciones inespecíficas de la repolarización ventricular. Ecocardiograma: marcada dilatación, disfunción sistólica y disfunción diastólica de tipo restrictivo del ventrículo izquierdo, severa insuficiencia mitral y tricuspídea, hipertensión pulmonar sistólica moderada, derrame pericárdico moderado y dilatación de aurícula izquierda. Ecotomografía abdominal: hepatomegalia congestiva. Endoscopia digestiva alta: gastritis hiperémica. Calcemia 2,9 mg/dL, parathormona 5,9 ng/l (vn: 10-73), magnesio 1,08 mEq/l (vn: 1,4-2,1), albúmina 3,3 g/dL, sodio 140 mEq/l, potasio 2,3 mEq/l, hematocrito 26%, hemoglobina 7,4 g/dL, proteinuria de 24 h: negativa, bilirrubinemia total 1,3 mg/dL, transaminasas glutámico oxalacéticas 63 U/l (vn: <35), creatinfosfokinasa total 1.260 U/l (vn: <70) (fracción miocárdica 3%), TSH 18,1 µU/ml.\n \n Se planteó el diagnóstico de insuficiencia cardíaca congestiva secundaria a hipocalcemia severa, descompensada por sustitución con hormona tiroidea y agravada por anemia ferropriva.\n Se trató con gluconato de calcio 1 g iv c/12 h, carbonato de calcio 2 g vo, vitamina D 175 µ/día, vitamina D 300.000 UI por una vez, l-tiroxina 100 µg, sulfato ferroso 400 mg, furosemida 40 mg, cloruro de potasio 1,8 g, captopril 12,5 mg y digoxina 0,125 mg/día.\n La paciente evolucionó favorablemente, con diuresis intensa y mejoría de las manifestaciones de insuficiencia cardíaca, desaparición del edema y la hepatomegalia. Diez días después tenía calcemia de 6 mg/dL, hematocrito de 37% y en ecocardiograma de control, se observó reducción del grado del reflujo mitral y tricuspídeo, disminución de la presión sistólica de la arteria pulmonar de 50 a 33 mmHg (vn: 15-30) y del derrame pericárdico. En controles posteriores, hasta los 18 meses, la paciente cumplía rigurosamente el tratamiento, sólo presentaba disnea a esfuerzos medianos a mayores, su calcemia se mantenía entre 8 y 8,5 mg/dL y en seguimiento ecocardiográfico, se observó, además, una recuperación de la marcada disfunción diastólica inicial -evaluada por el índice E/A: relación entre fase de llene ventricular rápido (E) y la fase de llene relacionada a la contracción auricular (A)-, normalización del tamaño de la aurícula izquierda y desaparición del derrame pericárdico, persistiendo la dilatación y disfunción sistólica del ventrículo izquierdo, en grado similar a la observada en exámenes iniciales.\n \n",
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"note_text": "Familia afectada de la madre.\n \n Estudio molecular y hormonal. El estudio hormonal de la tía y de la madre del probando (sujetos II. 2 y II. 3) incluyó una prueba de ACTH, cuyos valores de 170H Progesterona basal y estimulado fueron normales, no permitiendo aclarar si estos sujetos eran heterocigotos de una mutación del CYP21A2.\n El estudio molecular se realizó en ADN genómi-co extraído de leucocitos y las siete mutaciones más frecuentes del gen CYP21A2 fueron estudiadas con PCR alelo específica (Fardella, 1998). Este estudio demostró en la familia paterna (sujetos II.2, II.4, II.6) la mutación Q318X en el exón 8, que consiste en el cambio de una glutamina por un codón de stop. Este resultado no permitió clasificar a la familia materna y por ende decidir sobre la necesidad del tratamiento prenatal en estas parejas.\n Posteriormente, el gen CYP21A2fue secuenciado en la Universidad de Sao Paulo según las técnicas clásicas (Wedell, 1993). Usando esta metodología, se encontró en uno de los alelos de la familia paterna (sujetos II.2, II.4, II.6) la mutación Q318X junto a la mutación R483W, la que consiste en la sustitución de una arginina por triptofano (CGG>TGG). En la familia materna (sujetos II. 1, II.3, II.5) se encontró un alelo con la mutación R483->frameshift, también conocida como R483delGGinsC, la cuál consiste en el cambio de los nucleótidos GG por C, alterando la lectura del codón. De este modo se certificó que los seis cónyuges poseen mutaciones para HSC perdedora de sal, y por lo tanto, se encuentran en riesgo de tener hijas con ambigüedad genital.\n Consejo genético y manejo de los embarazos. Se procede a dar consejo genético a los tres matrimonios afectados. La tía paterna (sujeto II.2), mujer sana de 34 años, suspende el método anticonceptivo por deseos de fertilidad y logra concepción espontánea en marzo 2005. Se explican los beneficios y riesgos del tratamiento prenatal con corti-coides, los que la paciente entiende y acepta, firmando un consentimiento en que opta por realizar esta terapia. El tratamiento comenzó a las 6 semanas de edad gestacional (EG) con dexametasona en dosis de 20 µg/kg/día.\n A las 13 semanas se realizó el diagnóstico de sexo fetal masculino por ultrasonografía de alta resolución (Voluson 730, General Electric, Austria, transductor transabdominal de 3,5-5 MHz), la cual es capaz de predecir conectamente el sexo fetal con 99% de certeza después de 12+6 semanas EG (Efrat, 2006); la familia no aceptó técnicas invasivas de diagnóstico prenatal. Se disminuyó progresivamente las dosis de esteroides, suspendiéndolo en forma completa a las 22 semanas. Durante el período de tratamiento la paciente presentó edema e hipertensión arterial que requirió tratamiento con ametildo-pa. Los síntomas revirtieron parcialmente con la suspensión de terapia corticoidal, y totalmente posparto. A las 39 semanas se realizó cesárea y se obtuvo recién nacido de sexo masculino, con peso adecuado y examen físico normal. Los niveles de 170HP a los 5 días se muestran en la Figura IB.\n La tía materna (sujeto II.5) de 37 años consultó por embarazo inicial de 5 semanas de EG. Se ofrece nuevamente tratamiento prenatal de HSC, y también se solicitó firma de consentimiento informado. La familia optó nuevamente por seguir este tratamiento. A las 6 semanas de EG se inició dexametasona en dosis de 20 Lig/kg/día. La madre no aceptó las técnicas invasivas de diagnóstico prenatal y se decidió realizar diagnóstico de sexo fetal mediante ecografía precoz. En caso de que se tratara de un feto femenino continuarían el tratamiento hasta el término del embarazo. A las 12 semanas se diagnosticó sexo fetal masculino y se programó suspensión de esteroides. La paciente no presentó efectos adversos a la dexametasona. A las 40 semanas nació niño sano, no afectado.\n",
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"note_text": "Paciente de sexo masculino, de 11 años de edad. Después de un mes de haber presentado varicela, inició dificultad para deglutir en forma progresiva, sin evidencia de síntomas de hipo o hipertiroidismo. Su velocidad de crecimiento pondoestatural durante el último año fue normal (5 cm/año) y su edad ósea fue de 12 años.\n Antecedentes previos. Recién nacido pretérmino de 33 semanas; durante el periodo neonatal cursó con distress respiratorio; requirió ventilación mecánica por cuatro días. Sin antecedentes mórbidos relevantes. Actualmente cursa sexto básico con buen rendimiento escolar.\n Historia familiar Hijo de padres sanos, con antecedente de tiroiditis de Hashimoto en el abuelo y tía materna. Su talla familiar es de l69±5 cm (percentil 13,7).\n Examen físico. Talla: 146,4 cm (percentil 54), índice de Masa Corporal: 18,2 kg/m2 (percentil 62,5); sin desarrollo puberal (vello púbico Tanner I, testículos de 3 ce, simétricos). En la faringe, se visualiza una masa rojiza de aproximadamente 2x2 cm en la base de la lengua, con vasos venosos en su superficie, sin evidencia de hemorragia o ulceración. Sin estridor u odinofagia. En el examen de cuello no se palpó tiroides en la posición pre traqueal.\n Laboratorio. Las pruebas de función tiroidea revelaron TSH elevada 10,79 UI/mL (rango normal =0,7-5,7 UI/mL), con tiroxina normal, pero en su cuartil más bajo, 6,0 Lig/dl (rango normal TT =5,5-11,7 Hg/dl) y triyodotironina baja 57,8 ng/dL (rango normal =84,4-214,3 ng/dL) y anticuerpos antiperoxidasa y antiroglobulina ausentes.\n Estudio de imágenes. La nasofibrolaringoscopia óptica evidenció una masa rojiza, tensa, redondeada, con vasos sanguíneos en la superficie. La tomografía computarizada (TC) de cuello confirmó una masa bien circunscrita en la base de la lengua, de 2,0 x 1,9 x 1,8 cm, hiperdensa en los cortes sin medio de contraste endovenoso, sin nodulos en su interior. El estudio con cinügrafía con Tc-99 mostró captación en la base de la lengua, sin evidencias de tiroides en su localización normal, concordante con una ectopia lingual de la glándula tiroides.\n Seguimiento. Después que el diagnóstico fue realizado, el paciente inició L-Tiroxina en dosis de 75 \\ig/día. Al mes de tratamiento la TSH estaba suprimida (0,11 UI/mL) con tiroxina libre normal alta 1,93 ng/dL (0,8-2,0). El examen físico reveló una disminución gradual en el tamaño de la tiroides lingual y desaparición de la disfagia.\n \n",
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"note_text": "Varón de 47 años con DM diagnosticada hace 9 años, en tratamiento actual con esquema insulínico intensivo (una dosis nocturna de insulina glargina e insulina lispro previo a las comidas). Entre sus antecedentes destacaban gran tabaquismo, dislipidemia mixta en tratamiento irregular con ciprofibrato 100 mg/día y microalbuminuria de 50 mg/12 h, sin hipertensión arterial en tratamiento con enalapril 5 mg/día.\n Consultó en un centro de salud por sensación febril no cuantificada, calofríos, odinofagia, náuseas y vómitos alimentarios de 2 días de evolución. Se constató deshidratación moderada, temperatura axilar de 37,8°C y glicemia capilar mayor de 400 mg/dl. Fue internado, recibiendo solución fisiológica e insulina cristalina en esquema de minidosis. Entre los exámenes de laboratorio obtenidos al ingreso destacaban glicemia 549 mg/dl, creatinina 1,67 mg/dl, pH 6,91, BE -27, HC03 4,6 (en sangre arterial), cetonemia +++, natremia 141,7 mEq/L, kalemia 5,92 mEq/L, cloremia 98 mEq/L, amilasemia 48 U/L, hematocrito 40,5%, leucocitos 9-100 mm3, VHS 38 mm/h y urocultivo negativo. Fue dado de alta con el diagnóstico de cetoacidosis diabética, se le indicó mantener el esquema insulínico intensificado y asistir a control ambulatorio. El paciente se trasladó a la ciudad de Temuco, consultando 10 días después del alta por sensación febril no cuantificada, sudoración nocturna, odinofagia y dolor al movilizar el cuello. Al examen físico destacaba un gran aumento de volumen de la región posterior del cuello, sensible, sin signos inflamatorios ni crepitación, fetor pútrido y faringe congestiva con escaso exudado purulento. Se indicó hospitalización con el diagnóstico de DM descompensada, faringo-amigdalitis pultácea y masa cervical en estudio. Entre los exámenes destacaban glicemia 270 mg/dl, creatinina 0,8 mg/ di, hematocrito 35,7%, leucocitos 18.800 por mm3, VHS 91 mm/hora, PCR 309 mg/L. Se inició hidratación con solución fisiológica e infusión endovenosa continua de insulina, fue evaluado por otorrinolaringólogo con nasofaringoscopia, pesquisándose flegmón faríngeo. Se inició terapia con penicilina sódica EV 20 millones U/día, cloxacilina 12 g EV/ día y ceftriaxona 2 g EV/día. El aumento de volumen cervical fue estudiado con ecotomografía cervical, que mostró una colección en el compartimiento posterior del cuello y tomografía axial computarizada multicorte de cuello en que se apreciaba aumento de volumen del espacio retrofa-ríngeo y de los compartimientos posteriores del cuello de aspecto flegmonoso.\n \n Evaluado en conjunto con otorrinolaringólogo y cirujano de cabeza y cuello, se decidió practicar drenaje quirúrgico de la colección. Al segundo día de hospitalización se realizaron 2 incisiones en la región posterior del cuello, drenando líquido purulento. No se encontró evidencias de necrosis o gas. Se obtuvo cultivo de la secreción, aislándose Streptococcus grupo B, los hemocultivos fueron negativos. Luego de una semana con antibióticos EV, los drenajes Penrose dejaron de entregar secreción y fueron retirados. La exploración de las incisiones fue satisfactoria. Se dio de alta con antibiótico oral hasta completar otra semana (Ampicilina/Sulbactam).\n",
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"note_id": "S0034-98872008000900015-1",
"note_text": "Hombre de 33 años con antecedentes de ser fumador (20 cig/día) y un episodio de urolitiasis a los 27 años. Consultó por cuadro de dolor intenso en flanco derecho, de inicio súbito, sin irradiación, asociado a náuseas y vómito en una ocasión que cede espontáneamente. El cuadro se repitió 5 h después, siendo de similares características al anterior.\n No presentó fiebre y al examen físico destacaba una presión arterial de 140/82 mmHg y dolor a la palpación en fosa ilíaca derecha (FID).\n Dentro de los exámenes de laboratorio se encontró orina completa sin hematuria, hemogra-ma con leucocitosis (17.200 x mm3), creatininemia de 1,2 mg/dl y LDH de 1.457 UI/1.\n Se realizó pieloTC que resultó ser negativa para urolitiasis, prosiguiéndose con TC de abdomen y pelvis, en la cual se observó una extensa área hipodensa de aspecto cuneiforme en la cara posterior del parénquima renal derecho, compatible con infarto parcial renal derecho.\n Se hospitalizó al paciente. Se tomaron exámenes para trombofilia, cuyos resultados fueron normales, previo al inicio de anticoagulación (Fragmin y Neosintrón ). Además se realizó ecocardiografía transesofágica que resultó normal y un angioTC que reveló la presencia de una arteria renal derecha dominante (AD) y otra polar de menor calibre con trayecto normal, e imagen compatible con alteración de la pared arterial con infarto renal.\n \n Se prosiguió con estudio angiográfico, el cual reveló una aortografía normal, alteración en la perfusión del polo superior, cara anterior y posterior del riñon derecho, sin compromiso de la perfusión del polo inferior dado por la arteria polar secundaria. La arteria renal dominante se observó irregular, dilatada a partir de su tercio medio que además presentó un flap de disección que comprometió el origen de las ramas interlobares, limitando así el flujo distal. El flap de disección fue descrito como de alta complejidad sin posibilidades de maniobras endovasculares.\n \n Dos días después presentó nuevo episodio de dolor en flanco derecho. Nuevo angioTC mostró una clara progresión del infarto renal en los 2/3 superiores del riñon derecho.\n \n El paciente evolucionó con presiones arteriales en el rango de 160/100 mmHg y sin deterioro de la función renal (creatininemia 1,2 mg/dl). Fue dado de alta con terapia antihipertensiva (Blox 4 mg/día) en buenas condiciones generales para su manejo ambulatorio. En control ambulatorio a los dos y diecisiete días posterior al alta se encontró al paciente asintomático, normotenso y con el resto del examen físico sin hallazgos patológicos.\n",
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"note_text": "Paciente de sexo masculino de 76 años, quien fue operado de urgencia en 1974 por una lesión ulcerada gástrica sangrante. Se le practicó una gastrectomía subtotal con reconstrucción tipo Billroth II. La evolución postoperatoria fue normal. En la pieza de gastrectomía subtotal se encontró un tumor ulcerado en la cara anterior, distante 15 mm de la sección gástrica y 3 cm del píloro. El tumor medía 3,5 cm en el eje longitudinal y 7 cm en el transversal, comprometiendo la curvatura menor y extendiéndose 2,5 cm a la cara posterior. Al corte, estaba constituido por tejido rosado pálido lobulado, liso y brillante, que reemplazaba las túnicas submucosa, muscular propia y subserosa, abombando levemente la serosa. El examen histopatológico demostró un linfoma no Hodgkin mixto linfo-histiocítico de la clasificación de Rappaport de 1966, vigente hasta que se formularon las clasificaciones de Kiel (1974) y de Lukes y Collins (1974). No se encontró compromiso de los ganglios linfáticos por linfoma. El enfermo recibió radioterapia adyuvante y fue seguido con endoscopias anuales por 23 años. No se observaron nuevas lesiones gástricas ni se demostró la presencia de Helicobacter pylori. Durante este período, el paciente desarrolló hipertensión arterial, tumores de Warthin de ambas glándulas parótidas, de los cuales sólo se resecó el derecho y un cáncer de piel de tipo epidermoide en la extremidad inferior derecha.\n \n En septiembre de 2006, 32 años después de la operación gástrica, consultó por síntomas de anemia. En el examen físico se observó palidez, sin masas abdominales. El hematocrito fue de 34,5% y una endoscopia digestiva alta mostró una lesión proliferativa y ulcerada en el muñón gástrico que obstruía parcialmente la anastomosis gastroyeyunal. El estudio anatomopatológico mostró que la mucosa gástrica se encontraba infiltrada por un adenocarcinoma tubular moderadamente diferenciado. No se comprobó la presencia de Helicobacter pylori. La tomografía computada de tórax, abdomen y pelvis fueron normales.\n \n El paciente fue operado y se le realizó una gastrectomía total con disección ganglionar. La recuperación postoperatoria fue normal. El estudio anatomopatológico de la pieza quirúrgica mostró una lesión tumoral ulcerada en el muñón gástrico con infiltración de la anastomosis gastroyeyunal. El estudio microscópico demostró un adenocarcinoma tubular moderadamente diferenciado con compromiso de la subserosa de la pared gástrica, metástasis en 10 linfonodos de 16 resecados y permeaciones vasculares linfáticas (T2bN2M0, Etapa IIIB).\n \n",
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"note_text": "En septiembre de 2006 acudió al Servicio Dento-Máxilo-Facial del Hospital Clínico de la Universidad de Chile, una paciente de 17 años, estudiante, derivada por Servicio de Hematología por presentar lesiones blanquecinas en mucosa bucal.\n La paciente tenía el antecedente de anemia aplásica severa diagnosticada en 2005, la que se atribuyó a un derivado fenotiacínico y por lo cual fue sometida a trasplante de médula ósea (TMO) alogénico. Presentó las primeras manifestaciones de EICH agudo, con compromiso predominante cutáneo el día +42, manifestado como lesión máculo-pápulo eritematosa de tronco y extremidades con biopsia compatible con EICH agudo, momento en que se administró asociación de corticoides (prednisona 20 mg/dia) con ciclosporina, reemplazándose luego la ciclosporina por tacrolimus, 3 mg/dia vía oral, debido a toxicidad neurológica de la primera. Las lesiones de la mucosa oral aparecieron en forma más tardía y su primera descripción aparece en la evolución del día +310.\n En el momento del examen clínico, las lesiones bucales comprometían casi la totalidad de la mucosa, pero se manifestaban mayormente en cara interna de labios, cara interna de mejilla y cara ventral de lengua. Las lesiones eran de color blanquecino, con aspecto reticular y no se desprendían al raspado. La paciente no refería síntomas asociados.\n \n Con la hipótesis diagnóstica de compromiso de mucosa oral por enfermedad de injerto contra huésped se procedió a realizar biopsia incisional de mucosa de cara interna de labio inferior, lugar en el cual las lesiones eran manifiestas.\n El informe histopatológico fue compatible con EIVH. Se describió un epitelio de revestimiento plano pluriestratificado hiperparaqueratinizado y con hiperplasia agujiforme. Un estrato basal con desorganización celular y en el corion inmediatamente subyacente infiltración linfocitaria junto con vasos de neoformación y proliferación fibroblástica. También se describió leve infiltrado linfocitario periductal en glándula salival menor vecina.\n \n Se indicaron medidas locales para disminuir el riesgo de infecciones y mantener adecuada humectación del medio bucal; clorhexidina al 0,12% dos veces al día, sustituto de saliva de uso diario, además de instrucción de higiene oral.\n Seis meses después la paciente fue controlada manifestando dolor en algunas zonas de la mucosa bucal, evidenciándose lesiones erosivas en el examen clínico. Se decidió incorporar en el esquema de tratamiento local, el uso de betametasona al 0,1% en plastibase, reforzando las medidas de higiene bucal. Sin embargo, las lesiones permanecieron y el dolor aumentó, por lo cual se cambió por tacrolimus 0,1% en aplicación tópica 3 veces al día, agregándose además miconazol 2% (Daktarin Gel) de aplicación tópica, 3 veces al día. Además se sustituyó la clorhexidina al 0,12% por una concentración más baja, 0,05%, dado que la paciente le costaba tolerar la primera por provocarle ardor al momento de usarla. Después de una semana las lesiones remitieron y la paciente no presentaba dolor ni dificultades para alimentarse.\n",
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"note_text": "Mujer de 36 años, sin antecedentes patológicos de importancia, hospitalizada por peritonitis de origen no precisado. Consultó por dolor abdominal de 7 días de evolución asociado a distensión abdominal, náuseas y vómitos. La presión arterial fue 131/76, frecuencia cardiaca de 126 x' y 38,9eC de temperatura rectal. El abdomen estaba distendido, mate a la palpación y ausencia de ruidos intestinales a la auscultación. La evaluación ginecológica fue normal y la ecografía reveló líquido libre intraperitoneal y una estructura quística adyacente al intestino delgado. La tomografía computarizada abdominal (TAC), demostró algunas asas de intestino delgado rodeando una estructura tubular quística y líquido libre peritoneal. Los exámenes de laboratorio revelaron leucocitosis de 25.700 x mm3 y proteína C reactiva de 356,06 mg/dl. Con el diagnóstico de tumor quístico intestinal complicado la paciente fue operada. La cavidad abdominal se encontró llena de líquido seroso del cual se tomaron muestras para citología y cultivo. La exploración reveló múltiples implantes tumorales en el peritoneo parietal y visceral, e infiltración extensa del epiplón mayor, se tomaron muestras de estos implantes para biopsia. En el mesenterio del íleon se encontró un tumor quístico tubular blanquecino rodeado de asas intestinales, que medía 12 cm de diámetro por 15 cm de longitud. Se abrió el tumor aspirándose un líquido oscuro y espeso que fue enviado a citología. Se resecó la mayor cantidad posible de pared tumoral quedando una parte adherida al mesenterio, la resección completa del tumor no fue posible por la diseminación peritoneal y su localización en el mesenterio del íleon. La recuperación postoperatoria fue satisfactoria y sin complicaciones. Sin embargo, treinta y cuatro días después la paciente falleció. La muestras citológicas tomadas del líquido peritoneal y del contenido tumoral fueron positivas para células neoplásicas. La histopatología del tumor demostró la presencia de arquitectura típica de pared intestinal, en la cual se reconocían capas de músculo liso circular y longitudinal bien organizadas, identificándose plexos nerviosos mientéricos entre ambas capas musculares. La superficie interna estaba revestida por un adeno carcinoma mucosecretor moderadamente diferenciado que infiltraba todo el espesor de la pared en varias partes y que se extendió superficialmente por la serosa. Los hallazgos intraoperatorios y el informe histopatológico confirmaron el diagnóstico de adenocarcinoma en una duplicación intestinal de una paciente adulta.\n \n",
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"note_text": "Paciente indio de 44 años, hipertenso sin tratamiento por 10 años, fumador ocasional, quien se levantó en la mañana previa al ingreso con debilidad en el hemicuerpo derecho, así como pérdida de sensibilidad en la hemicara derecha, cuadro que progresó en las siguientes 24 horas en forma de imposibilidad para la marcha, por lo que hubo de ingresar una vez que fue llevado al departamento de emergencias, donde se le constató una presión arterial de 165/105 mmHg, pulso de 92 latidos x' y 16 de frecuencia respiratoria x'. El examen neurológico mostró una hipoestesia en la rama maxilar del trigémino derecho como único trastorno objetivo de la sensibilidad. La fuerza muscular y el tono estaba conservados a todos los niveles, pero se encontró una hiperreflexia osteotendinosa en el hemicuerpo derecho con Babinski ipsilateral. Elementos de disfunción cerebelosa se evidenciaron al existir disdiadococinesia, dismetría y discronometría al movilizar las extremidades derechas. La marcha era imposible por la tendencia a caer hacia la derecha al tratar de hacerla sin apoyo. La analítica sanguínea mostró hemoglobina, conteo diferencial de leucocitos y electrolitos dentro de límites normales. Se constató una hiperlipidemia dada por un incremento del colesterol total (7,42 mm/1). El electrocardiograma y el ecocardiograma transtorácico resultaron normales. La resonancia magnética (RMN) identificó un área de infarto isquémico subagudo que comprendía el núcleo lenticular y la cápsula interna izquierdos.\n \n El tratamiento consistió en anti-agregantes plaquetarios, estatinas y fisioterapia. El paciente fue egresado una semana después con evidente mejoría.\n",
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"note_text": "Paciente chileno, masculino, de 59 años, que de viaje en el Cuzco, Perú, inicia súbitamente un cuadro de disnea en reposo al que se agrega dolor abdominal epigástrico intenso, sensación de distensión abdominal y compromiso del estado general. Se diagnostica mal de altura agudo, recibiendo furosemida, acetazolamida, dexametasona, ranitidina y ceftriaxona.\n En Chile, 6 días después consultó por persistir con idéntica sintomatología y fue derivado al Servicio de Urgencia del Hospital Clínico Universidad de Chile por sospecha de tromboembolismo pulmonar. Ingresó afebril, disneico, con tope inspiratorio y distensión abdominal. Tenía antecedentes de síndrome de apnea-hipopnea del sueño, trastorno bipolar manejado con ácido valproico, rinitis alérgica, várices en miembros inferiores, apendicectomizado, tabáquico de 10 paquetes-año, bebedor de 2 copas de vino diarias por 30 años.\n Signos vitales: Pulso 81, ventilación 18 por minuto, presión arterial 102-67 mmHg, temperatura axilar 36°C. Al examen: en decúbito dorsal, consciente, hidratado, bien perfundido, piel blanca, pálida. Destacaba abdomen doloroso en hipocondrio izquierdo, con bazo aumentado de tamaño, várices en extremidades inferiores. El resto del examen era normal.\n Exámenes de laboratorio: hemograma con hematocrito 27,1%, hemoglobina 8,7 g/dl, VCM y CHCM normales, leucocitos 10.100/uL, VHS 28 mm/hr, tiempo de protrombina y TTPK normales. Dímero D 4.683 ng/ml (normal < 500), LDH en sangre 1.247 (rango: 313-618), proBNP, CK, CK-MB y troponinas normales. Angio-TAC pulmonar descartó tromboembolismo y demostró un hematoma periesplénico, subcapsular de 17 cm, El paciente fue ingresado a cuidados intermedios con diagnóstico probable de infarto esplénico con transformación hemorrágica.\n \n Hemogramas seriados no mostraron cambios, se realizó ecocardiografía que resultó normal y una tomografía de control que reveló crecimiento del hematoma esplénico a 19 cm de diámetro. Ante estabilidad clínica fue trasladado a sala en cirugía.\n La clínica y el laboratorio no sugerían etiologías infecciosas de su hematoma esplénico, y no había elementos sospechosos de síndromes mieloproliferativos, linfoproliferativos u otra neoplasia en los estudios de tomografía y bioquímicos. Hemogramas previos a este evento eran normales. Ante el cuadro de síndrome esplénico, pese a ser una causa rara, fue estudiado para un posible rasgo falciforme con una prueba de inducción de drepanocitos con metabisulfito de sodio al 2%, que fue positiva. Dada la evolución intrahospitalaria favorable, acompañado de laboratorio general y estudios radiológicos sin progresión, se decidió no intervenir quirúrgicamente y el paciente fue dado de alta.\n \n En control ambulatorio por hematología se solicitó electroforesis de hemoglobina en medio alcalino que reveló hemoglobina normal A 54,8% y 41,8% de fracción 3, compatible con hemoglobina S y se diagnosticó rasgo falciforme.\n",
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"note_text": "Paciente de sexo masculino de 14 años, sin antecedentes mórbidos, quien consultó luego de sufrir trauma de baja intensidad (pelotazo) en zona genital.\n Al examen físico presentaba dolor que dificultaba la palpación, evidenciándose un aumento de volumen asimétrico testicular izquierdo, sin otras lesiones asociadas. Se solicitó ecotomografía testicular presentándose a control luego de transcurridos 5 meses, constatándose clínicamente una masa indurada en testículo izquierdo de aproximadamente 2 cm de diámetro mayor, no dolorosa y sin compromiso escrotal; testículo derecho y pene sin alteraciones. La ultrasonografía demostró en el espesor del testículo izquierdo un nódulo de 18 x 19 x 15 mm, bien delimitado, de paredes hiperecogénicas con sombra acústica posterior. El testículo derecho, epidídimos y cordones espermáticos no presentan alteraciones de su ecoestructura. El estudio serológico para marcadores tumorales (α-feto proteína y hormona gonadotropina coriónica sub-unidad β) fueron normales. Se complementó estudio con tomografía computada (TC) de pelvis, abdomen y tórax las que no demostraron lesiones secundarias.\n \n Se efectuó enucleación del tumor y biopsia intra-operatoria. Se examinó un fragmento de tejido testicular de 5 g de 35 x 17 x 15 mm presentando en la superficie de corte una lesión subcapsular redondeada, bien delimitada, amarillenta, de consistencia firme de 22 mm de diámetro mayor, con áreas grumosas de aspecto arenoso. El corte histológico por congelación y diferido demostró una lesión que presentaba nidos y cordones conformados por células ovales a poligonales de núcleos grandes, excéntricos y con nucléolo prominente, el citoplasma es eosinófilo y abundante, apreciándose infiltrado inflamatorio polimorfonuclear neutrófilo en la región central del tumor y linfocitos en la periferia en partes formando agregados linfoides. El estroma es en partes hialino con áreas de degeneración mixoide y abundantes calcificaciones dispuestas a nivel intersticial y en el lumen de los nidos tumorales, concluyéndose en la biopsia contemporánea un tumor de células de Sertoli calcificado. No se observó extensión tumoral intratubular, figuras mitóticas, necrosis, acentuada atipía citológica ni extensión tumoral extra-testicular. El estudio inmunohistoquímico demostró intensa positividad para α-inhibina, S-100 y vimentina; con un índice de proliferación (Ki-67) bajo (< 1%).\n \n Se completó la cirugía realizándose orquiectomía radical. No se registraron complicaciones post-operatorias. A los 8 meses post-cirugía, el paciente se encuentra sano, sin evidencia de enfermedad en TC de tórax-abdomen y pelvis; descartándose en este paciente la asociación con complejo de Carney y síndrome de Peutz-Jeghers.\n",
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"note_text": "Un hombre de 34 años de edad, ingeniero, previamente sano, presentó en el curso de 24 horas, fiebre, retención urinaria, debilidad de las extremidades inferiores y déficits sensoriales irregulares en el tórax y abdomen. Como único antecedente, comunicó una tos leve los últimos 4-5 días antes de admisión a la clínica. Una evaluación urológica descartó uropatía obstructiva. Al examen neurológico estaba alerta, febril (38°C), sin déficits en nervios craneales. La fuerza en los miembros superiores era normal, pero se observó una debilidad moderada en las extremidades inferiores con incapacidad para levantarse desde una posición sentada. Los reflejos plantares eran extensores, había déficit sensorial en la parte posterior del cuello y a nivel del dermatoma D6. Los exámenes de rutina: hemograma, velocidad de sedimentación, proteína C reactiva, hemocultivos y urocultivos fueron negativos El análisis del LCR mostró 35 glóbulos blancos por mm3, con predominio de células mononucleares. La proteínorraquia fue 75 mg/dl. No se detectaron bandas oligoclonales. La detección de ARN viral por técnica de PCR-Microarray (Entherpex®, Genomica, España), fue positiva en el LCR sólo para VHH-7. Los herpes virus VHS-1, VHS-2, VHH-6, Epstein-Barr, VVZ, citomegalovirus y también anterovirus fueron negativos. El test para VIH y HTLV-1 fue negativo, así como pruebas inmunológicas para vasculitis y test serológico para Mycoplasma pneumoniae. La resonancia magnética (RNM) cerebral fue normal y la RNM de médula evidenció lesiones inflamatorias, difusas, extensas en los segmentos cervical, y dorsal de la médula (ver Figuras 1 y 2).\n \n Se inició metilprednisolona 1 g al día durante 3 días y ganciclovir iv 300 mg al día. A las 48 h el paciente recuperó la fuerza en extremidades por completo; la retención urinaria persistió por 1 mes para resolverse por completo en el segundo mes de seguimiento.\n El control de LCR a los 10 días mostró una PCR negativa para virus de la familia Herpesviridae. Se observaron 15 células con proteinas en rango normal. La repetición de la PCR en la muestra inicial de LCR, tomada al ingreso, también fue negativa. El diagnóstico de alta fue mielitis viral asociada a HHV-7.\n Los controles posteriores a los 6 meses de evolución evidenciaron un paciente sano, sin signos de haber desarrollado inmunodeficiencia.\n \n",
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"note_text": "Paciente masculino de 2 años de edad, originario de Tamaulipas, México, evaluado por xerosis generalizada, así como fiebre de origen incierto. Producto del segundo embarazo de una pareja sin antecedentes aparentes de consanguineidad, se caracteriza por presentar intolerancia al calor y ausencia de la sudoración desde el nacimiento. No refierían antecedentes heredofamiliares de importancia. En la exploración física destacaba la frenteprominente, hipoplasia del puente nasal, dos incisivos únicos en forma de cono, pigmentación periorbitaria, pelo escaso, fino, disperso y frágil así como cejas y pestañas. El paciente presentaba una dermatosis diseminada a cabeza, tronco y principalmente en extremidades superiores e inferiores, constituida por pápulas puntiformes eritematosas, con eritema difuso en una piel xerótica.\n \n La biopsia de piel de la palma de la mano izquierda demostró la ausencia parcial de las glándulas sudoríparas y sebáceas. Después de obtener el consentimiento informado, obtuvimos sangre periférica para realizar el estudio de cariotipo reportándose normal y a la vez, obtuvimos sangre no coagulada en tubos de EDTA (ácido etilendiaminotetraacético) de todos los miembros de la familia siguiendo los Principios de la Declaración de Helsinki. Se extrajo ADN de las muestras sanguíneas utilizando el equipo PUREGENER (Systema Gentra). Para el estudio de las mutaciones todos los exones así como las secuencias de los uniones de los intrones-exones fueron amplificados por medio de PCR (reacción en cadena de la polimerasa) del gen EDA-A1 en condiciones reportadas previamente. Las condiciones para la amplificación de cada PCR fueron de 94 °C por 2 minutos, seguido por 35 ciclos de 94°C durante 30 segundos, 55°C por 30 segundos y 72°C por 30 segundos con una extensión final a 72°C durante 7 minutos. Los productos de PCR fueron colocados en un gel de agarosa al 1% y posteriormente fueron analizados por la Secuenciadora Automática Directa ABI Prism 310, utilizando el equipo de Reacción \"ABI PRISM® BigDye™ Terminator Cycle Sequencing' (PE Biosystem) 8.\n Debido a que comúnmente la displasia ectodérmica hipohidrótica se encuentra ligada a X, se decidió obtener ADN genómico, logrando identificar la mutación sinsentido Ala349Thr en el gen EDA, se realiza la correlación clínico-patológica, concluyendo así con el diagnóstico de displasia ectodérmica hipohidrótica..\n",
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"note_id": "S0034-98872012000200011-1",
"note_text": "Paciente hombre de 23 años sin antecedentes mórbidos que presentó cefalea ictal y compromiso de conciencia cuantitativo progresivo. Consultó inicialmente en otro hospital donde se diagnosticó mediante tomografía computarizada (TC) de encéfalo un hematoma intraparenquimatoso parietal derecho de 42 ml, asociado a hidrocefalia aguda. En pabellón y de forma urgente, se instaló un drenaje ventricular externo (DVE). Se registróuna presión intracraneana (PIC) inicial de 45 cm de H2O. Se conectó a ventilación mecánica (VM) y se indicó sedación profunda. Inicialmente, la hipertensión intracraneana se trató con drenaje de líquido cefalorraquídeo y sodio hipertónico intravenoso en bolos, según necesidad. Se trasladó a nuestro servicio tres días más tarde.\n Ingresó intubado y conectado a VM, sedado con propofol 0,71 mg/kg/h, y hemodinamia apoyada con noradrenalina a 0,06 μg/kg/min, PIC de 6 cm de H2O y presión de perfusión cerebral (PPC) de 80 mmHg. En el examen neurológico se encontraba en coma, con midriasis fija a derecha, reflejos corneales abolidos, reflejos oculocefálicos esbozados, tono y reflejos osteotendíneos disminuidos, reflejos plantares indiferentes bilaterales.\n Exámenes generales de ingreso: Na+ 146 mEq/L, K+ 3,5 mEq/L, hematocrito 31%, lactato 1,4 mmol/L, leucocitos 9.600 por mm3 y proteína C reactiva 11,4 mg/dl.\n La angiografía cerebral de 6 vasos mostró una malformación arteriovenosa (MAV) parietal mesial derecha con signos de rotura reciente, asociada a tres aneurismas paranidales. Se realizó una embolización con N-butil-cianocrilato (Histoacryl®, Braun, Alemania), logrando reducir el nido de la MAV y excluir sus aneurismas. Después del procedimiento, la TC de encéfalo mostró el Histoacryl® correctamente situado. Sin embargo, se observó un incremento del hematoma con acentuado efecto de masa y presencia de edema cerebral difuso con obliteración de los surcos de la convexidad, además de herniaciones subfalcina y uncal con desviación de la línea media de 10 mm, a nivel de la glándula pineal. Se realizó la evacuación del hematoma y una craniectomía descompresiva frontoparietoccipital derecha extensa de 10,2 x 9,3 cm. La TC de encéfalo de control al día siguiente mostró una reducción del hematoma a 11 ml, pero aún se mantenía un importante efecto de masa, con desviación de la línea media de 5 mm.\n \n A pesar de la craniectomía evolucionó con PIC mayores a 20 cm H2O (23 ± 5 cm H2O; media ± DS). Se instauró un manejo médico escalonado de la HEC, con sedación profunda (fentanilo 2,86 μg/kg/h, midazolam 0,11 mg/kg/h y propofol 1,43 mg/kg/h), bloqueo neuromuscular (vecuronio 0,09 mg/kg/h), además del uso frecuente de bolos de sodio hipertónico frente a cifras de PIC > 30 cm H2O. Se descartó actividad epiléptica no convulsiva mediante un electroencefalograma y la TC de encéfalo 48 h post craniectomía no mostró cambios significativos. Debido a la persistencia de cifras de PIC > a 20 cm H2O, se decidió iniciar hipotermia terapéutica.\n Se empleó hipotermia moderada, con temperatura objetivo de 33°C, mediante técnica intravascular (Alsius, Zoll, Chelmsford, Massachusetts, EEUU). Se midió la temperatura central con catéter intravesical. Una vez conseguida la hipotermia (~12 h desde el diagnóstico de HEC refractaria), se logró un rápido control de la PIC con cifras entre 9 a 12 cm H2O (~3 desde el inicio del procedimiento). El bloqueo neuromuscular se mantuvo en infusión continua los primeros dos días de hipotermia, para evitar los calofríos.\n Luego de 48 h en hipotermia, se realizaron intentos programados de recalentamiento a una tasa de 0,5°C/h. Sin embargo, todos ellos fueron interrumpidos por rebote de la PIC. A partir del día 20 de evolución del cuadro clínico y coincidiendo con una disminución del edema cerebral en las neuroimágenes, se logró el control definitivo de la PIC. Completó ~13 días en hipotermia moderada, sin evidenciarse arritmias, trastornos de la coagulación o electrolíticos. Presentó una traqueobronquitis asociada a ventilación mecánica, resuelta satisfactoriamente con antibioticoterapia.\n Se suspendió progresivamente la sedación, el paciente adquirió vigilia y se objetivó una hemiparesia leve con heminegligencia y hemianopsia homónima izquierda. Una vez extubado se constató lenguaje apropiado. Se inició neurorrehabilitación y finalmente, luego de 40 días de hospitalización, fue dado de alta. Dos años después se encuentraen Rankin 2, con hemiparesia izquierda espástica leve y completando sus estudios universitarios.\n \n",
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"note_text": "Un varón de 29 años, natural de Brasil, con antecedentes personales de dermatitis seborreica y lupus cutáneo subagudo, fue remitido a nuestra consulta por el desarrollo de un cuadro cutáneo abrupto de una semana de evolución localizado en región centrofacial y torácica anterior.\n El paciente se había aplicado un corticoide tópico (mometasona furoato al 0,1%) dos veces al día durante 1 mes para intentar controlar las lesiones. Reseñaba el antecedente de lesiones pustulosas aisladas en cara ocasionales y episodios de enrojecimiento facial con calor y alcohol.\n Clínicamente mostraba, eritema facial y lesiones pápulo-pustulosas localizadas en frente, mejillas, región perioral y tórax. Además presentaba ausencia de comedones y padecía afectación ocular con inyección conjuntival acompañado de fotofobia y lagrimeo. No presentaba fiebre ni otra clínica sistémica. La analítica con bioquímica general y hemograma resultaron normales.\n Con el juicio clínico de rosácea fulminans con afectación ocular inició tratamiento oral con prednisona 40 mg/día, metronidazol 500 mg/12 horas, isotretinoína 50 mg/día (0,7 mg/kg/día), y lágrimas artificiales. El metronidazol y la prednisona se suspendieron tras un mes de tratamiento (la última en pauta descendente). Por último, la isotretinoína oral se retiró tras tres meses de tratamiento realizando descenso progresivo de la dosis. El paciente evolucionó favorablemente con mejoría importante de las lesiones hasta la desaparición completa tras los tres meses de tratamiento. El paciente no ha presentado recaídas de la enfermedad en los posteriores seis meses.\n",
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"note_text": "Varón de 48 años, oriundo de Marchigüe, VI Región de Chile, quien durante su vida laboral trabajó como faenador de corderos. Tenía antecedentes de hipertensión arterial, dislipidemia y un quiste hidatídico pulmonar operado en 1996. Quince años después, presentó un accidente vascular encefálico, sin referir otro tipo de sintomatología cardiovascular. Dentro del estudio etiológico se realizó un ecocardiograma y una tomografía computarizada de tórax (TAC) donde se evidenció una masa quística de 4 x 3 cm en el ventrículo izquierdo, sin signos de ruptura. Se realizó además una ecotomografía abdominal que descartó la presencia de quistes hepáticos. Tampoco tenía antecedentes o síntomas previos sugerentes de anafilaxia.\n Posteriormente, evolucionó con dolor precordial opresivo sin irradiación, de intensidad EVA 6/10. Evaluado por cardiología en su hospital base se indicó anticoagulación oral siendo derivado al Instituto Nacional del Tórax con la sospecha de hidatidosis cardiaca.\n El paciente ingresó en buenas condiciones generales, afebril y sin alteraciones hemodinámicas, con presión arterial de 130/85 mmHg y 90 latidos por min. Al examen físico no presentaba ingurgitación yugular, roces ni soplos cardiacos (que fueron exhaustivamente buscados) ni tampoco signos de insuficiencia cardiaca. El examen pulmonar fue normal.\n El hemograma reveló una eosinofilia de 21%, sin leucocitosis. El perfil bioquímico fue normal. La determinación de anticuerpos IgG anti-Echinococcus granulosus no fue realizada.\n La radiografía de tórax era normal y el electrocardiograma presentaba ritmo sinusal, ondas T negativas en DII y alteraciones inespecíficas en la repolarización.\n La ecocardiografía realizada en nuestro servicio evidenció una imagen poliquística, ovalada y adherida al macizo de músculos papilares anterolaterales, de contornos bien delimitados en pared libre del ventrículo izquierdo que medía 4,5 x 3,2 x 2,7 cm, sin derrame pericárdico. Estos hallazgos fueron confirmados por resonancia magnética (RNM). El estudio preoperatorio fue completado con una coronariografía, que fue normal.\n \n La cirugía se realizó bajo esternotomía media y circulación extracorpórea, poniendo principal atención en la manipulación cardiaca para no lesionar el quiste. Una vez puesto el clamp aórtico, se disecó la superficie del quiste, se aisló el campo con compresas embebidas en cloruro de sodio al 10% y se puncionó el quiste vaciándolo parcialmente e inyectando solución salina hipertónica al 30%. Posteriormente, se abrió el quiste hacia la cara anterior del ventrículo izquierdo y se vació, retirando las membranas y vesículas hijas. Se completó el aseo de la cavidad con sodio hipertónico y posteriormente se realizó quistectomía parcial y cierre por capitonaje del remanente. El paciente no presentó complicaciones intraoperatorias y la evolución posterior fue favorable. En control ambulatorio post-quirúrgico, el paciente se ha mantenido asintomático, sin evidencias de complicaciones o recidivas y se controlará semestralmente con ecocardiografía y serología para E. granulosus.\n \n",
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"note_text": "La paciente índice (PAF19) de sexo femenino consultó a los 41 años (2004) por un síndrome anémico. Como parte de su estudio se realizó una endoscopia digestiva alta que no mostró hallazgos patológicos y una colonoscopia completa que demostró la presencia de múltiples pólipos sésiles (más de 100) y pediculados (más de 15), desde el margen anal hasta el ciego. A nivel cecal se evidenció una lesión proliferativa de aproximadamente 2,5 cm de diámetro mayor, cuya biopsia confirmó un adenocarcinoma tubular moderadamente diferenciado. El diagnóstico preliminar fue de una PAF asociada a un adenocarcinoma cecal. El estudio de etapificación con TAC (tomografía abdominal computarizada) de abdomen y pelvis no mostró signos de diseminación tumoral, realizándose una colectomía total con íleorrectoanastomosis. El estudio anatomopatológico de la pieza quirúrgica mostró una lesión tumoral de 3 cm de diámetro con invasión hasta la subserosa y compromiso linfonodal. La mucosa del resto de la pieza resecada presentaba un centenar de pólipos sésiles y pediculados, abollonados y lisos de 0,2 a 2 cm de diámetro mayor. Por tratarse de una paciente en etapa III se realizó un tratamiento con quimioterapia adyuvante en base a 5-fluorouracilo y leucovorina. Hasta la fecha la paciente ha completado 70 meses de seguimiento sin evidencia de enfermedad.\n Debido a su historia clínica (poliposis colónica y CCR a edad temprana), la paciente fue derivada al registro de tumores hereditarios para definir el estudio genético apropiado. Este registro incorpora a pacientes con sospecha de enfermedades hereditarias (poliposis adenomatosa familiar, síndrome de Lynch, síndrome de Peutz-Jeghers, entre otros) con la finalidad de educar a los pacientes y familiares respecto a su enfermedad, predisposición de desarrollarla y transmitirla a su descendencia, y de este modo prevenir el desarrollo del CCR en aquellos familiares asintomáticos.\n El análisis de la genealogía de la paciente índice demostró consanguinidad de los padres, sin historia de poliposis o CCR en ellos. Además permitió identificar a una hermana (de un total de 12 hermanos) que presentó CCR, a la que identificamos como PAF585. Ella presentó un cáncer de colon derecho con invasión hasta la subserosa y compromiso linfonodal a los 53 años que fue tratado con cirugía y quimioterapia adyuvante. Un año después, la colonoscopia de control mostró dos nuevos tumores sincrónicos, uno en colon sigmoides a 35 cm del margen anal y otro cáncer en recto inferior (adenocarcinoma tubular invasor). Cabe destacar que el informe médico de la paciente no registra la presencia de poliposis adenomatosa colónica. La paciente evolucionó tórpidamente falleciendo a los 4 meses posterior a la cirugía debido a un cuadro séptico secundario.\n \n Con respecto a los demás hermanos, cinco de ellos fallecieron en la infancia por accidentes y enfermedades no relacionadas al cáncer. En los cinco hermanos vivos, la paciente índice no declara más casos afectados de poliposis o CCR, sin embargo, desconocemos si ellos se han realizado estudios colonoscópicos.\n Estudio genético\n Obtención del ADN genómico desde sangre periférica: el ADN genómico fue aislado a partir de 10 ml de sangre venosa periférica, utilizando el protocolo descrito por Lahiri y Nurnberger (1991 )9.\n Este ADN fue previamente estudiado en el análisis molecular del gen APC, el cual resultó negativo8.\n Análisis mutacional del gen MUTYH: Los 16 exones del gen MUTYH fueron amplificados mediante la técnica de PCR (reacción en cadena de la polimerasa) usando los partidores descritos por Kim y colaboradores, en 200610. Reacciones de PCR fueron realizadas en un volumen total de 50 Ql que contiene 100 ng de ADN genómico, 25 pmoles de cada partidor, 0,2 mM de cada uno de los dNTPs, 1,5 mM MgCl2 1X del amortiguador suministrado por la enzima y 1U de la enzima Platinum Taq ADN polimerasa (Invitrogen, Sao Paulo, Brasil). La amplificación fue realizada con el siguiente protocolo: una desnaturación inicial de 1 min a 95°C, seguido por 30 ciclos de 30 seg a 95°C, 30 seg a una temperatura de apareamiento de los partidores (rango 50-58°C), 30 seg a 72°C, y un paso de extensión final de 10 min a 72°C. Los productos amplificados fueron posteriormente analizados mediante dos técnicas de alta sensibilidad para la detección de alteraciones en la secuencia del ADN, que incluye la técnica de SSCP (single strand conformation polymorphism) y secuenciación de ADN. Brevemente, los productos de PCR fueron desnaturados a 95°C por 5 min, enfriados en hielo por 5 min, y resueltos por electroforesis en geles de poliacrilamida MDE 0,5X\n (FMC Bioproducts), aplicando una corriente de 3 W a 18°C por 12 h. Después de la electroforesis, los geles fueron teñidos con nitrato de plata con el fin de visualizar las bandas de ADN. Los productos de PCR que presentaron una migración anormal en relación al control, fueron secuenciados. Las mutaciones fueron analizadas y confirmadas por dos reacciones de PCR independientes y por secuenciación de las dos hebras de ADN. La mutación se nombró de acuerdo a la nomenclatura propuesta por la Human Genome Variation Society (www. hgvs.org/mutnomen/).\n",
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"note_text": "Mujer de 70 años que consultó en servicio de Urgencias de nuestro hospital por cuadro de dolor retroesternal opresivo, intensidad 10/10, irradiado a epigastrio, de aproximadamente 15 min de duración, asociado a sudoración profusa y palpitaciones.\n Refería haber presentado episodio de similares características dos días antes, lo que motivó consulta en otro servicio de urgencias, donde fue evaluada con electrocardiograma (ECG) y enzimas cardiacas; no impresionando cuadro de origen coronario, por lo que se derivó a su domicilio. Dentro de sus antecedentes destacaba historia de hipertensión arterial de data no precisada, en tratamiento con atenolol 50 mg al día, y cáncer de mama tratado 20 años antes con cirugía y radioterapia. La paciente no era fumadora ni tenía antecedentes familiares de cardiopatía coronaria.\n Al ingreso, la paciente se encontraba sudorosa, pero sin dolor. La presión arterial era 100/60 mmHg y su frecuencia cardiaca 87 lpm. Al examen físico destacaban yugulares colapsables en inspiración, la auscultación cardiaca no reveló soplos ni galope y había sensibilidad a la palpación epigástrica. El resto del examen no era destacable. Al interrogatorio, la paciente refería historia de episodios similares durante los últimos 6 meses, sin clara relación con esfuerzos físicos, que en un principio eran esporádicos pero que durante la última semana se hicieron más frecuentes, casi diarios. El ECG mostró un discreto supradesnivel del segmento ST (SDST) anteroseptal con inversión de la onda T de V1 a V3, que ya era evidente en ECG tomado 2 días antes y que no fue evolutivo.\n \n La radiografía de tórax mostró una silueta cardiaca de tamaño normal y no se observaban signos de congestión pulmonar. La paciente fue admitida a la unidad coronaria, con terapia de síndrome coronario agudo sin SDST. La troponina I de ingreso fue de 0,07 pg/ml (valor normal < 0,05) y la CK total fue de 117 U/L con una fracción MB de 25.\n A las pocas horas de ingreso la paciente evolucionó con crisis de angor intenso, 10/10, asociado a disnea, palpitaciones, cefalea, sudoración y enrojecimiento facial. Se constató alza de presión arterial hasta 260/130 mmHg y al monitor se evidenció taquicardia sinusal con extrasistolía supraventricular y ventricular frecuentes, y conducción aberrante con morfología de bloqueo completo de rama derecha de aproximadamente 5 min de duración. No hubo episodios de hipotensión ni síncope. Dado las características del episodio se sospechó el diagnóstico de feocromocitoma. Se suspendió heparina, se aportó solución fisiológica y se inició doxazosina en dosis de 1 mg cada 12 h. Se midió durante la crisis catecolaminas plasmáticas y metanefrinas urinarias (previo al inicio de doxazosina), que fueron marcadamente elevadas.\n \n Se solicitó una resonancia magnética de abdomen, que confirmó el diagnóstico, evidenciando una masa suprarrenal derecha de 6 cm de diámetro.\n \n El cintigrama con 123-I-metaiodobencilguanidina (MIBG) confirmó la captación en la masa descrita y no mostró metástasis.\n \n Adicionalmente se realizó un ecocardiograma transtorácico, que mostró hipertrofia ventricular izquierda leve y compromiso leve de la función sistólica global, con una fracción de eyección (FE) estimada por Simpson de 42%, y una coronariografía sin incidentes durante el procedimiento, que descartó la presencia de enfermedad coronaria. La disfunción ventricular fue asumida en contexto de daño miocárdico por catecolaminas.\n La paciente se preparó para la intervención quirúrgica con bloqueo α y β-adrenérgico escalonado con doxazosina y, luego de 2 días, propanolol. La cirugía se realizó 11 días después, sin complicaciones hemodinámicas significativas y cursó con un postoperatorio favorable. La paciente fue dada de alta a los 4 días en buenas condiciones. Desde el punto de vista clínico, cursó con buena evolución posterior con disminución progresiva en la dosis de antihipertensivos y normalización de la función ventricular en ecocardiografía de control.\n",
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"note_id": "S0034-98872014000500015-1",
"note_text": "Mujer de 46 años que consultó por debilidad progresiva y mialgias intensas de una semana de evolución que le impedían deambular. Destacaba entre sus antecedentes la presencia de hipotiroidismo en tratamiento con T4 50 mcg/día y bypass intestinal por obesidad mórbida 5 años antes, con adelgazamiento de más de 70 Kg desde ese entonces. Desde la cirugía presentaba 4 a 5 deposiciones pastosas diarias. Al ingreso se encontraba vigil, eupneica y apirética. Presentaba adelgazamiento con índice de masa corporal (IMC) de 19. Tenía buen estado de hidratación y sus cifras de presión arterial (TA) eran 120/70 mmHg. La evaluación neuromuscular mostró hipotonía generalizada, paresia de cuatro miembros sin fasciculaciones y reflejos osteotendinosos presentes. Presentaba un potasio plasmático (K+pl) de 1,1 mEq/L y elevación de la CK. La dosificación de TSH se encontraba dentro de rango normal. Se inició reposición hidroelectrolítica con mejoría de la paresia muscular, disminución progresiva de las mialgias y normalización de los valores de K+pl y CK. La hipopotasemia se atribuyó a las pérdidas de origen digestivo, secundarias al procedimiento quirúrgico. Si bien la severidad de la misma puede ser causa de las manifestaciones neuromusculares, el hallazgo de niveles elevados de CK confirmó la sospecha de RM asociada.\n \n",
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}
} |
Subsets and Splits