oalib

Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99

Submit

Any time

2019 ( 173 )

2018 ( 1009 )

2017 ( 906 )

2016 ( 1303 )

Custom range...

Search Results: 1 - 10 of 569078 matches for " María José; Kakarieka W "
All listed articles are free for downloading (OA Articles)
Page 1 /569078
Display every page Item
Cerclaje profiláctico en mujeres con nacimientos prematuros espontáneos previos, asociados con infección bacteriana ascendente
Ovalle S,Alfredo; Valderrama C,Oscar; Rencoret P,Gustavo; Fuentes G,Ariel; del Río V,María José; Kakarieka W,Elena; Martínez T,María Angélica; Pizarro S,Dagoberto;
Revista chilena de obstetricia y ginecología , 2012, DOI: 10.4067/S0717-75262012000200004
Abstract: aims: determine the effectiveness of prophylactic cerclage in women with singleton pregnancies, cervix >25 mm and a history of spontaneous premature deliveries associated to ascending bacterial infection (abi). methods: women with singleton pregnancies and history of preterm births, with no fullterm deliveries, associated to abi. cases with >25 mm cervical length at admission were included. cervical cerclage performed on patients derived before 20 weeks of pregnancy was compared to the expectant management of women submitted at a later gestational stage with sustained cervical length of >25 mm. pregnant women with <25 mm cervix at referral, with cervical shortening <25 mm at expectant management, and women with previous preterm birth without placental histology were excluded. results: 51 patients were included, 23 with cerclage and 28 without cerclage. prophylactic cerclage significantly reduced the frequency of premature birth <37 weeks, 4.3% vs 35.7% and <34 weeks, 4.3 % vs 28.6 % and histologic chorioamnionitis 4.3% vs 32.1% (9/28), or (95%ci) 0.08 (0.09-0.70), 0.11(0.01-0.99) and 0.01 (0.01-0.83), respectively. conclusions: in patients with preterm births associated to abi, singleton pregnancy and cervical length >25 mm, prophylactic cerclage reduces the frequency of premature delivery <37 and <34 weeks as well as histologic chorioamnionitis.
CALCINOSIS TUMORAL EN PEDIATRíA: REPORTE DE UN CASO CLíNICO Y REVISIóN DE LA LITERATURA
Espinoza G,Aníbal; Céspedes V,María José; Kakarieka,Elena;
Revista chilena de radiología , 2008, DOI: 10.4067/S0717-93082008000200010
Abstract: we repon a case oftumoral calcinosis in young girl, a quite infrecuent condition, causee! by a herditary dysfunción of phosphfate regulation. ouraims are to review imaging signs (plain radiography ultrasound, computed tomography and nuclear medicine) and clinical and labortory findigs as well. finally we made a literature search, oriented to help in diagnosing this disease, specially regarding images.
Histiocitosis de células de Langerhans localizada en hueso malar: Presentación de un caso
Castellón Zirpel,María Loreto; Fuenzalida Kakarieka,Carlos; Barrios Tapia,José Ignacio; Uribe Fenner,Francisca;
Revista Espa?ola de Cirugía Oral y Maxilofacial , 2011, DOI: 10.4321/S1130-05582011000300004
Abstract: localized langerhans cell histiocytosis (llch), also known as eosinophilic granuloma, represents 50 to 60% of all cases of langerhans cell histiocytosis. the standard treatment for llch has been lesion curettage or resection. cases treated with intralesional corticosteroid injections combined with curettage have been described. we report the case of a three-year-old patient diagnosed of llch with extensive zygomatic bone involvement, who was treated with corticosteroid infiltrations and subsequent curettage of the lesion. one year after treatment, the patient is asymptomatic with zygomatic reossification evidenced on computed tomography.
CALCINOSIS TUMORAL EN PEDIATRíA: REPORTE DE UN CASO CLíNICO Y REVISIóN DE LA LITERATURA TUMORAL CALCINOSIS IN YOUNG CHILDREN: REPORT OF A CASE AND LITERATURE REVIEW
Aníbal Espinoza G,María José Céspedes V,Elena Kakarieka
Revista Chilena de Radiología , 2008,
Abstract: Presentamos el caso de una ni a preescolar portadora de calcinosis tumoral, entidad infrecuente, causada por una disfunción hereditaria en la regulación de la excreción de fosfatos. Damos a conocer los hallazgos radiológicos (radiografía simple, ultra-sonografía, tomografia computada y cintigrafía ósea), así como también hallazgos clínicos y laboratorio del caso, además de revisar la literatura para una breve actualización de esta condición, especialmente en lo que respecta al diagnóstico y las imágenes. We repon a case oftumoral calcinosis in young girl, a quite infrecuent condition, causee! by a herditary dysfunción of phosphfate regulation. Ouraims are to review imaging signs (plain radiography ultrasound, Computed Tomography and nuclear medicine) and clinical and labortory findigs as well. Finally we made a literature search, oriented to help in diagnosing this disease, specially regarding images.
Histiocitosis de células de Langerhans localizada en hueso malar: Presentación de un caso Localized langerhans cell histiocytosis of the zygomatic bone: A case report
María Loreto Castellón Zirpel,Carlos Fuenzalida Kakarieka,José Ignacio Barrios Tapia,Francisca Uribe Fenner
Revista Espa?ola de Cirugía Oral y Maxilofacial , 2011,
Abstract: La histiocitosis de células de Langerhans localizada (HCLL), conocida como granuloma eosinófilo, representa entre el 50 y el 60% de todos los casos de histiocitosis de células de Langerhans. El tratamiento clásico para la HCLL ha sido el curetaje o la resección de las lesiones óseas. Hay publicaciones de casos tratados con inyección intralesional de corticosteroides, combinado con curetaje. Se presenta un caso clínico de un paciente de tres a os de edad con diagnóstico de HCLL que compromete en su extensión el hueso malar, tratado con infiltraciones de corticosteroides y posterior curetaje de la lesión. A un a o de realizado el tratamiento, el paciente se encuentra asintomático y con una regeneración ósea del hueso malar, evidenciable en la tomografía axial computarizada. Localized Langerhans cell histiocytosis (LLCH), also known as eosinophilic granuloma, represents 50 to 60% of all cases of Langerhans cell histiocytosis. The standard treatment for LLCH has been lesion curettage or resection. Cases treated with intralesional corticosteroid injections combined with curettage have been described. We report the case of a three-year-old patient diagnosed of LLCH with extensive zygomatic bone involvement, who was treated with corticosteroid infiltrations and subsequent curettage of the lesion. One year after treatment, the patient is asymptomatic with zygomatic reossification evidenced on computed tomography.
ESTUDIO ANáTOMO-CLíNICO DE LAS CAUSAS DE MUERTE FETAL
Alfredo Ovalle S.,Elena Kakarieka W.,ángel Correa P.,María Teresa Vial P.
Revista Chilena de Obstetricia y Ginecología , 2005,
Abstract: Objetivo: Conocer la causa de muerte fetal, mediante antecedentes clínicos maternos, análisis de los hallazgos de la autopsia fetal y estudio de la placenta. Material y Método: Se analizaron retrospectivamente 299 muertes fetales ocurridas entre las 22 y 42 semanas de gestación en un período de 5 a os. Se incluyeron 279 casos con estudio histopatológico de la placenta y autopsia fetal. Se hizo la siguiente clasificación de causas primarias de muerte fetal: 1) Hipoxia fetal extrínseca, incluye asfixia aguda y shock: a) patologías placentarias, b) patologías del cordón umbilical, c) enfermedades maternas, d) causas no determinadas. 2) Anomalías congénitas. 3) Infecciones ascendentes. 4) Traumatismo del parto. 5) Hidrops fetal. No se clasificaron fetos macerados o placentas con alteraciones involutivas. Se establecieron tres grupos según la edad gestacional en que ocurrió la muerte fetal: 22-29 semanas, 30-36 semanas y 37-42 semanas. Resultados: Se conoció la causa de muerte fetal en 79,2% de los casos. Las causas más frecuentes fueron hipoxia fetal extrínseca 43,5%: insuficiencia placentaria 9,0%, hipertensión arterial 8,6%, desprendimiento placentario 6,1%, infarto placentario 5,7% y patología del cordón umbilical 4,3%. Anomalías congénitas 16,5%, infección bacteriana ascendente 16,1%, traumatismo del parto 2,2% e hidrops fetal 1,4%. Causa desconocida 20,8%. En gestaciones < de 30 semanas las principales causas fueron: infección ascendente 33,3%, patología placentaria 17,7% y anomalías congénitas 15,6%. Entre las 30 y 36 semanas de gestación las principales causas fueron: patología placentaria 34,8%, anomalías congénitas 24,1% e hipertensión arterial 10,7%. En gestaciones entre 37 y 42 semanas las principales causas fueron: patología placentaria 19,7%, embarazo postérmino (causa no determinada de hipoxia fetal) 15,5%, patología de cordón 11,3% y diabetes 8,5%. Conclusiones: el análisis de los hallazgos de la autopsia fetal, del estudio de la placenta y de los antecedentes clínicos maternos, permiten aclarar la causa de la mayoría de las muertes fetales y planificar el manejo de un futuro embarazo Objective: To know cause of fetal death through clinical maternal history, autopsy finding of the stillborn fetus and histological examination of the placenta. Method: There were analysed retrospectively 299 cases of fetal death between 22 and 42 week gestation in a 5 year period. There were included 279 cases with histopathological examination of the placenta and fetal tissue from autopsy. The following classification was made for primary fetal death: 1) Extrins
HISTOPATOLOGIA DEL ABORTO ESPONTANEO ENTRE 12 Y 22 SEMANAS
Alfredo Ovalle S,Elena Kakarieka W,María Teresa Vial P,Reinaldo González R
Revista Chilena de Obstetricia y Ginecología , 2003,
Abstract: Objetivos: Analizar los resultados histopatológicos encontrados en el aborto espontáneo entre 12 y 22 semanas de gestación y su relación con los correspondientes antecedentes obstétricos y clínicos, para determinar los factores causantes. Métodos: Se estudiaron retrospectivamente cuatrocientas seis pacientes con aborto espontáneo entre 12 y 22 semanas de gestación ocurridos durante 1 a o. Se incluyeron cientonueve casos con estudio histopatológico de los anexos ovulares y/o del feto. El aborto se clasificó: a) según ultrasonografía en: aborto con feto vivo, aborto con muerte fetal y restos de aborto y b) según edad gestacional (semanas) en tres grupos: A) entre 12 y 14,6, B) entre 15 y 18,6 y C) entre 19 y 22. Se analizaron antecedentes ginecoobstétricos: aborto recurrente (pérdida reproductiva recurrente consecutiva), embarazo con dispositivo intrauterino y antecedentes clínicos del aborto: deprendimiento placentario, infección ovular y huevo roto. Los hallazgos histopatológicos se clasificaron en: 1) lesiones inflamatorias, 2) lesiones placentarias no inflamatorias, 3) síndromes malformativos, 4) hidrops fetal y 5) alteraciones placentarias involutivas. Resultados: Las cientonueve pacientes tuvieron las siguientes lesiones histológicas: Inflamatorias 56% (corioamnionitis 53,2%), funisitis 24,8%, perivellositis 21,1%, vellositis 3,7%, deciduitis 8,3% y síndrome de infección del saco amniótico: 13,9%). Síndromes malformativos: 11%. Placentarias no inflamatorias: 7,3%. Hidrops fetal: 4,6%. Existieron alteraciones involutivas en el 14,7% de los abortos y no se encontraron lesiones en el 10,1% de los casos. Se identificaron lesiones en el 75,2% de los abortos. Más frecuentes en los abortos con feto vivo 83,6%, en comparación con los restos de aborto 68,4% y con el aborto con muerte fetal 65,7%, p< 0,05. Lesiones encontradas. Según edad gestacional: en el grupo A (corioamnionitis 29,7%, perivellositis 18,9%, síndromes malformativos 13,5%), en el grupo B (corioamnionitis 63,9%, funisitis 33,3%, perivellositis 22,2%) y en el grupo C (corioamnionitis 66,7%, funisitis 33,3%, síndrome de infección del saco amniótico 25%). Según ultrasonografía: con feto vivo (inflamatorias preferentemente), con feto muerto (inflamatorias, placentarias no inflamatorias, síndromes malformativos). Según antecedentes obstétricos y clínicos: aborto recurrente (inflamatorias 21,4%, placentarias no inflamatorias 21,4% y síndromes malformativos 14,3%), aborto con DIU (inflamatorias 66,7% y síndromes malformativos 13,3%), desprendimiento placentario (inflamatorias 54,5%, placentarias no i
Factores asociados con el parto prematuro entre 22 y 34 semanas en un hospital público de Santiago
Ovalle,Alfredo; Kakarieka,Elena; Rencoret,Gustavo; Fuentes,Ariel; del Río,María José; Morong,Carla; Benítez,Pablo;
Revista médica de Chile , 2012, DOI: 10.4067/S0034-98872012000100003
Abstract: background: preterm births are responsible for 75 to 80% of perinatal mortality. aim: to determine the factors associated with preterm births, using maternal clinical data, laboratory results and pathological placental findings. patients and methods: retrospective study of 642 preterm single births at 22-34 weeks' gestation. four hundred and seven cases with pathological placental studies were included. births were subdivided into preterm births as a consequence of a medical indication and spontaneous births with or without premature rupture of membranes (prom). risk factors for preterm births were classified as maternal, fetal, placental, indeterminable and unclassifiable. results: the proportions of preterm births were spontaneous 69% (with prom 27% and with intact membranes 42%) and medically indicated births 31%. a risk factor associated with prematurity was identified in 98 and 85% of medically indicated and spontaneous births, respectively. ascending bacterial infection (abi) was the most frequently associated factor with spontaneous preterm delivery in 51% of women (142/280, p < 0.01) and with preterm births of less than 30 weeks in 52% of women (82/157, p < 0.01). vaginal or urinary infection with group b streptococcus, was the most common clinical condition associated with abi related deliveries. hypertension was present in 94 of 127 medically indicated preterm deliveries (preeclampsia in 62% and chronic hypertension in 12%), and in 29% (preeclampsia 24%) of preterm births of more than 30 weeks. congenital anomalies were mainly associated with a maternal age over 35 years in 15% (14/92) of women. the frequency of placental diseases was higher in spontaneous preterm deliveries (14%) and in pregnancies of more than 30 weeks in (14%). conclusions: abi was the most common factor associated with spontaneous preterm births at 2234 weeks, while preeclampsia is the most common factor associated with medically indicated preterm births.
ESTUDIO ANáTOMO-CLíNICO DE LAS CAUSAS DE MUERTE FETAL
Ovalle S.,Alfredo; Kakarieka W.,Elena; Correa P.,ángel; Vial P.,María Teresa; Aspillaga M.,Carlos;
Revista chilena de obstetricia y ginecología , 2005, DOI: 10.4067/S0717-75262005000500005
Abstract: objective: to know cause of fetal death through clinical maternal history, autopsy finding of the stillborn fetus and histological examination of the placenta. method: there were analysed retrospectively 299 cases of fetal death between 22 and 42 week gestation in a 5 year period. there were included 279 cases with histopathological examination of the placenta and fetal tissue from autopsy. the following classification was made for primary fetal death: 1) extrinsic fetal hypoxia, including acute asphyxia and shock: a) placental pathology, b) umbilical cord pathology, c) maternal disease, d) non determined cause. 2) congenital anomalies, 3) ascending infection, 4) birth trauma, 5) fetal hydrops. cases with macerated fetus or placental involutive changes were not included. three groups were established, using gestational age for fetal death: 22-29 weeks, 30-36 weeks, 37-42 weeks. results: it could be know cause of fetal death in 79.2% of the cases. the most frequent were extrinsic fetal hypoxia 43.5%: placental insufficiency 9%, maternal hypertensive disease 8.6%, abruptio placentae 6.1%, placental infarcts 5.7% and umbilical cord pathologies 4.3%. congenital anomalies 16.5%, ascending infections 16.1%, birth trauma 2.2% and fetal hydrops 1.4%. in 20.8% of cases the cause of fetal death could not be know. in gestations of less than 30 weeks main causes were: ascending infections 33.3%, placental pathology 17.7% and congenital anomalies 15.6%. between 30 and 36 weeks gestations main causes were placental pathology 34.8%. between 37 and 42 weeks gestation main causes were placental pathology 19.7%, post term pregnancy (not determined cause of fetal hypoxia) 15.5%, umbilical cord pathology 11.3% and maternal diabetes 8.5%. conclusions: the analysis of findings obtained from fetal autopsy, placental histopathological examination and maternal clinical history allows clarifying most causes of fetal death and planified future pregnancies
HISTOPATOLOGIA DEL ABORTO ESPONTANEO ENTRE 12 Y 22 SEMANAS
Ovalle S,Alfredo; Kakarieka W,Elena; Vial P,María Teresa; González R,Reinaldo; Correa P,Angel; Sukni G,Mohamed; Figueroa P,Jorge;
Revista chilena de obstetricia y ginecología , 2003, DOI: 10.4067/S0717-75262003000500002
Abstract: objectives: to analyze the histophatological results found in the spontaneous abortion between 12 and 22 weeks of gestation and their relationship with the corresponding obstetrical and clinical data for determining their ethiology. methods: four hundred and six patients with spontaneous abortion between 12 and 22 weeks of gestation, during the course of one year, were studied retrospectively. of these, one hundred and nine cases with histopathological study of the placenta and umbilical cord, and/or the fetus, were included in the study. the abortions were classified: a) according to ultrasonography of abortion with live fetus, abortion with fetal death and abortion remnants, and b) according to the gestational age (weeks), in thrree groups: a) between 12 and 14.6; b) between 15 and 18.6, and c) between 19 and 22. gyneco-obstetrical data were analized: recurrent abortion (consecutive recurrent loss of reproductive capacity), pregnancy with intrauterine dispositive, and clinical data of the abortion: placental abruption, clinical chorioamnionitis and ovum with rupture of membranes. histophatological findings were classified as: 1) inflammatory lesions; 2) non-inflammatory placental lesions, 3) malformation syndromes; 4) fetal hydrops; 5) involutive placental alterations. results: the one hundred and nine patients presented the following histological lesions: inflammatory, 56% (choroamninitis, 53.2%; funisitis, 24.8%; perivellositis, 21.1%; vellitis, 3.7%; deciduitis, 8.3% and amniotic sac infection syndrome, 13.9%. malformation syndromes, 11%. non-inflamatory placental, 7.3%. fetal hydrops, 4.6%. there were involutive alterations in 14.7% of the abortions and no lesions were found in a 10.1% of the cases. lesions were identified in a 75.2% of the abortion, more frequently in the abortions with a live fetus (83.6%) as compared to those with abortion remnants (68.4%) and to abortions with fetal death (65.7%, p< 0,05). lesions found: according to gestational age: in gr
Page 1 /569078
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.