TRASTORNOS BENIGNOS EN GINECOLOGÍA

ATENCIÓN DEL BIENESTAR DE LA MUJER

 ANAMNESIS Y EXPLORACION FISICA:

 Detallada
 Antecedentes familiares y personales
 Primera consulta de atención a la salud reproductiva: entre 13 y 15 años
 Exploración mamaria:
 Inspección mamaria. Autoexploración.

 Valoración de los ganglios linfáticos

 Palpación mamaria.

 Exploración clínica de las mamas: anual a partir de los 40 años

 Exploración pélvica:

 Ganglios linfáticos inguinales e inspección perineal

 Exploración con especulo

 Exploración bimanual

 Exploración recto vaginal

MEDIDAS PREVENTIVOS
 Vacunas
 Detección de enfermedades de transmisión sexual.
 Anticoncepción
 Detección sistemática del cáncer
 Cáncer cervical
 Cáncer mamario. 2da causa de muerte por neoplasia en EE.UU.

 Cáncer de colon. 3ra causa de muerte por neoplasia en EE.UU.

 Cáncer de piel

 Cáncer de pulmón. 1ra causa de muerte por neoplasia en EE.UU.

 Obesidad: Problemas ginecológicos: Anomalías menstruales, Cáncer de endometrio,
Empeoramiento del SOP
 HTA
 Diabetes mellitus
 Enfermedad cardiovascular
 Síndrome metabólico
 Dislipidemia
 Hipertrigliceridemia
 Apoplejia
 Enfermedades de las tiroides
 Salud mental
 Cambios en el estilo de vida:
Tabaquismo: ↓ fecundidad, ↑ complicaciones del embarazo y posoperatorias
ejercicio
ESTUDIOS DE IMAGEN UTILIZADOS EN GINECOLOGÍA
 ECOGRAFIA;
 Se produce por las ondas sonoras reflejadas en la estructura que se examina.
 La frecuencia de ondas ecográficas guarda relación inversa con la longitud de la
inda
 Ecografía transabdominal. FAST valoración focalizada con ecografía para
traumatismos. Identifica líquido libre.
 Ecografía transvaginal. Dolor pélvico, herragia uterina anormal, tumoraciones
pélvicas, infecundidad, embarazo temprano, cancer de ovario y endometrio,
infecundidad
 Ecografias transrectal y transperitoneal: poco usadas. Suelo pélvico
 Tecnología doppler: para determinar el flujo sanguíneo. Color rojo flujo mas
próximo al transductor y el color azul al flujo mas alejado.
 Sonohisterografia o ecografía con solución salina. Evalúa endometrio.
Contraindicada en embarazo, infección, hematómetra.
 Ecografía 3D. Cavidad uterina, tumoración ováricas complejas, reserva de
fecundidad de ovarios, anomalías uterinas y embarazo intersticial
 Radiografía:
 Pielografia intravenosa
 Histerosalpingografia
 Densitometría ósea
 Mamografía

 TAC
 RNM. Complemento excelente para valoración en neoplasias
ginecológicas
INFECCIONES EN GINECOLOGIA
 FLORA VAGINAL NORMAL.
 Los microorganismos anaerobios predominan sobre los aerobios 10:1.
 Algunos microorganismos producen Ácido láctico y peróxido de hidrogeno que
inhiben a los microorganismos que no son parte de la flora normal. Como
protección de sustancias toxicas la vagina secreta inhibidor de proteasa
leucocitica.

 PH VAGINAL:
 Entre 4-4.5
 El glucógeno contenido en la mucosa vaginal sana proporciona nutrientes para
muchas bacterias en el ecosistema vaginal y es metabolizado en ácido láctico
 CAMBIOS EN LA FLORA:
 Dependiente de la edad y el ciclo de la mujer
 PH del esperma 7.2 a 8
 VAGINOSIS BACTERIANA:
 Crecimiento excesivo de: G. Vaginalis, Ureaplasma, Mycoplasma
 Mobiluncus y Prevotella
 Reducción o ausencia de lactobacilos
 Factores de riesgo: Sexo oral, duchas vaginales, raza negra, tabaquismo,
actividad sexual durante la menstruación, DIU, inicio de relaciones sexuales a
edad temprana, promiscuidad, lesbianismo.
 Diagnostico: secreción vaginal fétida no irritante. Cuello uterino y vagina sin
anomalías.
 Prueba de liberación de aminas.
 Presencia de células guía
 Ph mayor a 4.5
 Tto: metronidazol 500mg VO 2 veces al día por 7 días
2gr tinidazol VO cada 24 hs por 2 días. o
300 mg clindamicina via oral c/12 hr por 7 días.
 ULCERAS GENITALES
 Herpes simple:
 Mas prevalente y crónica. Se conocen virus tipo 1 y tipo 2. afecta células
epidérmicas
 Síntomas: eritema y formación de pápulas, vesículas que luego se rompe y queda
una ulcera dolorosa.
 Etapas de la lesión:
1. Vesícula con o sin evolución a pústula (1sem)
2. Ulceración
3. Costra. Se disemina en las primeras dos fases, en gral la primera semana
 Diagnostico: cultivo de tejido. PCR. Examen físico.
 Tratamiento: antivírico, AINES, narcóticos leves, anestésicos tópicos, medidas
locales (Aciclovir 400 mg c/ 8 hs por 7 - 10 días, recurrente: Aciclovir 4 mg c/ 8 hs
por 5 días)
 Sífilis:
 Chancro (sífilis primaria)
 Condilomas planos (sífilis secundaria) erupción maculopapulosa
 Sífilis latente después de 1 año de la secundaria no tratada
 Sífilis terciaria incluso 20 años después de la latencia: CV, músculo, SNC
 Dx: VDRL, FTA-ABS, Tto: Penicilina, doxiciclina
 Chancroide:
 Haemophilus ducreyi
 Pi: 3 – 10 días
 No se acompaña de reacciones generalizadas ni síntomas prodrómicos.
 Bordes de la úlcera dolorosa, irregulares y blando, con linfadenopatia uni o
bilateral dolorosa
 Tratamiento: azitromicina 1 gr como dosis única o ceftriazona 250 mg IM
 Granuloma inguinal:
 Donovanosis… calymmatobactrium granulomatis
 POCO CONTATGIOSA
 Pi: semanas a meses
 Sintomas: nódulos inflamatorios no dolorosos, que se ulrceran y sangran con
faciliadad, cicatrización queloide, no linfadenopatias
 Diagnostico: cuerpos de donovan en estudio microscópico
 Tratamiento: doxiciclina 100 mg c/12 hs por 3 sem o hasta desaparición de
lesiones
 Linfogranuloma venéreo:
 Causado Clamydia tracomatis: Serotipo L1 L2 L3
 Pi: 3 días a 2 semanas
 Sintomas: fases:
1. Vesículas o papulas pequeñas
2. Linfadenopatia inguinal o femoral (síndrome inguinal). Signo del surco
3. Sx anogenitorectal. Prurito secreción mucoide
 Diagnostico: ´prueba positiva para clamydia, biopsia de ganglios
linfáticos, exclusión de otros cuadros
 Tratamiento: doxiciclina 100 gr c/ 12 hs por 21 días.
VAGINITIS INFECCIOSA

 Secreción vaginal anormal con ardor, irritación o prurito vulvar.

 Micosis causada por Cándida albicans, C. troplicalis, C. glabrata
 Mas frecuentes en diabéticas, embarazadas, obesas, inmunodeprimidas,
uso reciente de ATB, se puede transmitir por via sexual
 Sintomas: prurito, dolor, eritema vulvar y edema con excoriaciones,
secreción similar a material cuajado o queso cottage.
 pH normal
 Tratamiento: en las complicadas: tto vaginal + fluconazol a 100 a 200
mg dos a tres veces por semana.
 Tricomoniasis:
 Causada por Tricomona vaginalis con predilección por el epitelio
escamoso. Generalmente los varones permanecen asintomáticos.
ETS no viral mas frecuente. Marcador de conducta sexual de alto
riesgo.
 Pi: 3 dias a 4 sem
 Se ubican en vagina, uretra, endocervix y vejiga.
 Sintomas: secreción vaginal amarillenta o verdosa fétida y liquida,
disuria, dispareunia, prurito vulvar y dolor. En la vagina se
observan las manchas de fresa.
 Diagnostico: cultivo en medio de diamond
 Tto: metronidazol 2 gramos dosis única o 500 mg cada 12 hs por 7
días
CERVICITIS SUPURATIVA
 Neisseria gonorrhoeae:
 En mujeres gralmente. Asintomática, ≤ 24 años, historia de ETS
 Sintomas: cervicitis o vaginitis, secreción vaginal inodora, no irritante
blanco o amarillento. Infecta las glándulas de bartolino, skenne y la
uretra, puede ascender al endometrio y las trompas,
 Diagnostico: frotis y cultivo de secreción endocervical. Orina
 Tratamiento: ceftriazona 200 mg IM + azitromicina 1 g dosis única y la
pareja.

 Chlamydia trachomatis :
 Cuello uterino edematoso e hiperemico, provoca uretritis y disuria
 Dx: frotis y cultivo de endocervix
 Tto: azitromicina 1 gramo via oral dosis única
ENFERMEDAD PÉLVICA INFLAMATORIA
 Es una infección de los órganos del aparato reproductor. Se la
llama también salpingitis aguda.
 La salpingitis típica esta muy relacionada con infecciones de
Neisseria g. y es secundaria a ellas. Otra especie es T vaginalis. La
vaginosis bacteriana no es un factor de riesgo para desarrollo de
EPI. Es facilitada por la menstruación por la perdida de la barrera
endocervical.

 Factores de riesgo: duchas vaginales, soltera,

farmacodependencias, múltiples parejas sexuales, nivel
socioeconómico bajo, edad 10 a 19 años, otras ETS, dx previo de
EPI
 Enf. pélvica inflamatoria asintomática: es el diagnostico final que se
le da a una mujer con esterilidad por factor tubarico que carece de
antecedentes compatibles con infección de la porción superior del aparato
reproductor. En la laparoscopia se observan adherencias en las trompas o
perihepaticas.
 Enf. Pélvica inflamatoria aguda: en mujeres con síntomas, estos
aparecen durante o justo después de la menstruación. Dolor a la
palpación del útero, de los anexos o con la movilización del cuello uterino.
Uno o más de los datos siguientes aumenta el diagnostico: 1-
temperatura bucal mayor a 38.3°C.
2- secreción vaginal o cervicouterina mucopurulenta.
3- abundantes leucocitos en el examen microscópico de las secreciones
cervicouterinas.
4- VSG o PCR elevada.
5- presencia de N. gonorrhoeae o C trachomatis en el cuello uterino.
 SÍNTOMAS:
 dolor en la porción inferior del abdomen, dolor pélvico,

 secreción vaginal amarillenta,

 menorragia

 fiebre, escalofríos, anorexia, nausea, vómito, diarrea, dismenorrea

y dispareunia.
 Puede acompañarse de síntomas urinarios.

 Fondo de saco doloroso, frenkell positivo,

 dolor abdominal.
 diagnostico laparoscópico con hiperemia de la serosa tubárica,
edema en las paredes de las trompas y un exudado purulento
proveniente de las fimbrias.
 A la ecografía: trompas ovoides y distendidas llenas de líquido
anecoico o ecogeno, engrosamiento de las paredes tubaricas,
tabiques incompletos, apariencia de rueda dentada., biopsia
endometrial para diagnosticar endometritis.
 ABSCESO TUBOOVÁRICO: cuando se infectan las trompas de
Falopio inflamadas y supurativas pueden adherirse a los ovarios.
Si la inflamación avanza se pierden los planos volviéndose
inidentificables, entonces se aplica este término. Casi siempre es
unilateral y afecta estructuras adyacentes. El drenaje mas ATB
pueden considerarse como régimen inicial si el absceso es grande.
 ENFERMEDAD PÉLVICA INFLAMATORIA CRÓNICA:
paciente que ha sufrido EPI aguda y padece dolor pélvico crónico.
Un criterio es la presencia de hidrosalpinge, medios histopatológico
(inflamación crónica)
 Tratamiento: oral o parenteral según las indicaciones precisas.
VERRUGAS Y PÁPULAS INFECCIOSAS
 VERRUGAS GENITALES EXTERNAS:
 Causadas por HPV
 Lesiones desde pápulas planas hasta lesiones verrugosas exofiticas
clásicas llamadas condiloma acuminado
 Dx: ex físico.
 Tto: bisturí, crioterapia o ablación laser, fármacos tópicos
 Molusco contagioso:
 Poxvirus DNA por contacto directo entre personas
 PI: 2 a 7 semanas
 Papulas con umbilicación central, únicas o multiples, contagiosas hasta
que las lesiones desaparezcan
 Dx: examen físico
 Tto: crioterapia o coagulación electroquirurgica o raer el centro de la
lesión con aguja
INFESTACIONES PRURIGINOSAS
 Escabiosis

 Pediculosis

INFECCIÓN URINARIA

Cistitis aguda: disuria, polaquiuria, urgencia miccional, hematuria e

incontinencia. ≥ 100.000 UFC en cultivo
Pilonefritis aguda: leve o grave. Leucocitosis alta y fiebre. ATB por
14 días
INFECCIONES POSOPERATORIAS

 Representan un gran porcentaje de las infecciones hospitalarias.

 Los riesgos de experimentarlas son: tabaquismo, hemorragias
excesiva, anemia preoperatoria, nivel socioeconómico bajo,
inmunosupresión, cirugía reciente en el campo quirúrgico,
obesidad, juventud, senectud, procedimiento quirúrgico prolongado,
colocación de cuerpos extraños.

 Clasificación clásica
INFECCIONES ESPECIFICAS.

 Celulitis del muññon vaginal:

 posterior a las histerectomías.
 Celulitis pélvica: infección mas frecuente que ocurre después de
la histerectomía. Cuando los mecanismos de defensa humoral y
celular del hospedador combinados con la profilaxis ATB no pueden
superar el inoculo bacteriano y el proceso inflamatorio en el borde
quirúrgico abdominal. La inflamación se extiende hasta los
parametrios, con dolor y elevación de la temperatura. Al final del
2do día post operatorio. Internación y ATB parenteral 24 a 48 hs.
 Infección de los anexos: poco frecuentes y muy similares a la
celulitis pélvica. Se manifiestan después de una
salpingooforectomia.
 Absceso ovárico: complicación rara pero letal de la histerectomía
vaginal. Evolución hasta 10 días post operatorio con dolor agudo en
alguna de las fosas iliacas que luego se generaliza se agrega
septicemia que la convierte en una urgencia ginecológica. ATB y
laparotomía exploradora inmediata.
 Absceso pélvico o hematoma pélvico infectado: complicación
de la histerectomía. Con disminución de la Hb post operatoria,
aumento de temperatura, dolor, tumoración discernible de
ubicación medial. ATB y drenaje
OTRAS INFECCIONES GINECOLOGICAS

 Absceso vulvar
 Absceso del conducto de Bartholin.

 Infección por Actinomyces

TRASTORNOS BENIGNOS DE LA PORCIÓN INFERIOR DEL
APARATO REPRODUCTOR

 Vulva
 Vagina

 Cuello uterino
LESIONES VULVARES
 La piel de la vulva es mas permeable.
 Manifestaciones clínicas: dolor, prurito, dispareunia, hemorragia y
secreción.
 Consulta inicial: tranquilizar, crear una alianza con la paciente
para la estrategia del tto.
 Diagnostico:
 Anamnesis
 Prurito vulvar.
 Exploración física: iluminación adecuada con lupa o colposcopio, tacto vaginal,
bimanual
 Biopsia vulvar: bordes, y las áreas hiperpigmentadas en su región de mayor

espesor.
 DERMATOSIS VULVARES:
 LIQUEN SIMPLE CRONICO: excoriaciones contra un fondo de piel eritematosa.
La piel reacciona con mecanismos como el engrosamiento denominado
liquenificacion. Los cambios suelen ser bilaterales y simétricos y pueden rebasar
los labios mayores.
 El tto comprende medidas para interrumpir el ciclo de prurito-rascado.
 LIQUEN ESCLEROSO: dermatosis inflamatoria crónica que afecta la piel ano
genital. Postmenopáusicas. El 20-30% tiene otros trastornos inmunitarios. la
mayoría no tiene síntomas y refieren síntomas ano genitales que empeoran por la
noche, creando el circulo vicioso y creando lesiones en la piel. Mayor riesgo de Ca
de vulva.
 Dx: pápulas blanco porcelana que deforman los contornos anatómicos normales.
Regresión de labios menores, ocultamiento del clítoris, obstrucción de la uretra y
estenosis del introito.
 Tto y vigilancia: no existe opción curativa. Control de síntomas y evitar distorcion
anatómica. Clobetazol al 0.05%. Cirugia.
 RECOMENDACIONES PARA EL CUIDADO DE LA VULVA.
 No usar geles, productos perfumados, toallitas humectantes ni
jabones.
 Utilizar cremas acuosas para limpiar la vulva.

 No utilizar paño destinado a la cara o al cuerpo.

 Secar suavemente con suaves golpes.

 No utilizar ropa interior demasiado ajustada. Debe ser de algodón

 No lavar la ropa interior con exceso de detergente o productos

perfumados.
 Dormir sin ropa interior
DERMATOSIS INFLAMATORIAS
 DERMATITIS POR CONTACTO: el trastorno es frecuente y en
casos inexplicables de prurito e inflamación vulvar el 54% son
diagnosticadas con esta patología. Dermatitis irritante por
contacto: Ardor y comezón inmediatas con la exposición al agente
lesivo. Dermatitis alérgica por contacto: prurito de comienzo tardío
evolución intermitente y eritema, edema y vesículas o ampollas
localizadas.
 INTERTRIGO: fricción de dos superficies húmedas cutáneas,
origina este problema crónico. Se complica con infecciones
bacterianas o micoticas. La fase eritematosa evoluciona a
inflamación intensa. Hiperpigmentacion y cambios verrugosos.
Tto: sustancias secantes .
 PSORIASIS: es un trastorno auto inmunitario mediado por los linfocitos
T, que en que las citosinas pro inflamatorias inducen la proliferación de
queratinocitos y células endoteliales. manchas rojas y gruesas con
escamas plateadas. Suele aparecer en el monte de venus o los labios
mayores. Se exacerba con tensiones nerviosas y la menstruación y mejora
en los climas cálidos y el embarazo. tto: corticoesteroides.
 ECCEMA ATOPICO: surge en los primeros 5 años de vida. Prurito
intenso crónico y recurrente. Tto: corticoesteroides e inmunomoduladres
tópicos.
 LIQUEN PLANO: entre los 30-60 años. Autoinmunidad de linfocitos T
dirigidos contra los queratinocitos basales. 3 variantes: 1- erosiva, 2-
papuloescamosa 3- hipertrófica. La erosiva es la mas común.
 Dx: pápulas, con estrías blancas en entramado. Secreción vaginal crónica, prurito,
dolor urente, dispareunia, sangrado post coital.
 Tto: corticoesteroides.
 HIDRADENITIS SUPURATIVA: lesiones papulosas que pueden
culminar en abscesos, formación de fistulas y cicatrices.
Inflamación y obstrucción crónica de folículos cutáneos. Se
desconoce el origen. Tto: ATB y compresas calientes. Laser y
fototerapia.
 ULCERAS AFTOSAS: dolorosas y desaparecen en unos meses. Se
desconoce su origen. Tto: corticoesteroides tópicos.
MANIFESTACIONES VULVARES DE ENFERMEDAD
SISTÉMICA

 ACANTOSIS NIGRICANS
 ENFERMEDAD DE CROHN

 ENFERMEDAD DE BEHCET
DISCROMÍAS
 NEVO
 VITILIGO
TUMORES VULVARES SOLIDOS
 ACROCORDON: lesión fibroepitelial polipoide benigna varia de 1-
6mm. Masa suave y sésil o pediculada casi siempre del mismo color
de la piel y sin vello. Tto: extirpación quirúrgica
 QUERATOSIS SEBORREICA: lesiones circunscriptas que
sobresalen ligeramente con una superficie apera y grasienta.
 QUERATOACANTOMA

 SIRINGOMA

 LEIOMIOMA

 FIBROMA

 LIPOMA

 TEJIDO MAMARIO ECTOPICO

QUISTES VULVARES
 QUISTES Y ABSCESOS DE LA GLANDULA DE
BARTHOLIN.por E. coli
 QUISTES Y ABSCESOS DE LA GLANDULA DE SKENE

 DIVERTICULO URETRAL

 QUISTES EPIDERMOIDES
VULVODINIA
 Molestias vulvares que la paciente suele describir con
manifestaciones como dolor ardoroso que aparece sin que haya
signos visibles o algún trastorno neurológico especifico.
 Molestia vulvar que tiene 3 a 6 meses de duración y no muestra
causa identificable. Prevalencia de 3-11%. Causas: pueden ser
múltiples, uso de ACO, infecciones. Se describe como un dolor
ardoroso en carne viva, pruriginoso o cortante
TRASTORNOS VAGINALES

 Cuerpos extraños
 Vaginitis inflamatoria descamativa

 Anomalias inducidas por dietilestilbestrol

 Quiste del conducto de gartner

CERVICOUTERINAS

 Eversión:el tejido endocervical en algunas mujeres migra y

ocasiona el cuadro llamado eversión o ectropión, es un dato normal.
 Quiste de Naboth: células cilíndricas secretoras de moco recubren
el conducto endocervical. Es benigno, no necesitan tratamiento o se
pueden drenar con una pinza.
 Pólipo endocervical: neoplasia benigna mas frecuente del cuello
uterino es la protuberancia hiperplasica de los pliegues
endocervicales. Rara ve son malignos pero deben biopsiarse.
 Estenosis cervicouterina: congénita o adquirida. Causa
dismenorrea, infertilidad, amenorrea, hematómetra, hidrorrea. Tto
dilatación del cuello.
 MÉTODOS ANTICONCEPTIVOS Y ESTERILIZACION
❖ METODOS REVERSIBLES.
➢ NATURALES.
▪ RITMO CALENDARIO
▪ TEMPERATURA BASAL
▪ MOCO CERVICAL
▪ COITO INTERRUMPIDO.
▪ SINTOTERMICO
▪ LACTANCIA PROLONGADA
➢ BARRERA.
▪ CONDÓN
▪ DIAFRAGMA
▪ QUÍMICOS: ESPERMICIDAS
➢ MECÁNICOS.
▪ DISPOSITIVO INTRAUTERINO.
➢ HORMONALES.
▪ ANTICONCEPTIVOS ORALES.
▪ Anticoncepción Oral de Emergencia (AOE)
 MÉTODOS DE PLANIFICACIÓN FAMILIAR

❖ METODOS IRREVERSIBLES.
➢ LIGADURA DE TROMPAS
➢ VASECTOMÍA
CLASIFICACIÓN SEGÚN SU NIVEL DE EFICACIA
 Primer tipo: eficacia máxima. DIU(con levonogestrel, T de cobre),
implantes de levonogestrel, esterilización de la mujer y el varón.

 Segundo tipo: muy eficaces. Píldoras combinadas, anillo vaginal,

parche, DMPA, píldora con progestágeno solo. Lactancia

 Tercer tipo: eficaces. Preservativo masculino y femenino, diafragma con

espermicidas, conocimientos de los días de fecundidad, sintomas térmicos

 Cuarto tipo: eficacia mínima. Espermicidas, esponjas

 Sin categoría: coito interrumpido, ningún MAC

DISPOSITIVO CON LEVONORGESTREL (MIRENA).
 Libera levonorgestrel constante de
20 µg/día.
 Es una estructura de polietileno
con forma de T cuyo tallo está
envuelto con una muestra cilíndrica
de
polidimetilsiloxano/levonogestrel.
T DE COBRE (PARAGARD T 380A).
 Esta hecho de polietileno y sulfato de
bario .
 Es el más utilizado en nuestro país.

 El tallo se encuentra cubierto por un

alambre fino de cobre de 33 mm2, lo
que suma un total de 380 mm2 de
cobre. Además, dos hilos se extienden
desde la base del tallo.
CGenerales
ONTRAINDICACIONES
- Embarazo o sospecha de embarazo
- Anormalidades del útero que originan distorsión de la cavidad uterina
- EPI aguda o antecedentes de EP
- Endometriosis posparto o aborto infectado en los últimos tres meses
- Ca uterino o cervical conocido o sospechoso, incluyendo un papanicolau anormal sin
tratamiento
- Hemorragia genital de causa desconocida
-Cervicitis o vaginitis aguda sin tratamiento, así como vaginosis bacteriana, hasta
eliminar la infección
- La paciente o su pareja tienen varias parejas sexuales
- Situaciones que aumentan la predisposición a padecer infecciones, SIDA o
fármacodependencia
- Actinomicosis genital
- Presencia de un DIU previo que no se ha extraído
CONTRAINDICACIONES
Específicas
El ParaGard T 380ª se contraindica cuando existen una o más de las
situaciones siguientes (por su contenido de cobre):
- Enfermedad de wilson
- Alergia al cobre

La inserción de Mirena se contraindica cuando existe una o más de las

situaciones siguientes:
- Hipersensibilidad a cualquiera de los componentes de este producto
- Carcinoma mamario conocido o sospechoso
- Antecedente de embarazo ectópico o situación que predisponga a un
embarazo ectópico.
- Hepatopatía aguda o tumor en el hígado
 ESTERILIZACION FEMENINA

Es una cirugía que se realiza con el fin de unir las trompas de Falopio de una mujer, lo
que produce esterilidad permanente ya que se evita el paso del ovulo hacia el útero
y se obstruye el paso de los espermatozoides hacia la trompa y hasta el ovario que
esta ovulando, en el cual se lleva acabo la fertilización.
 Esterilización tubaria puerperal

 Esterilización tubaria no puerperal

 Oclusión mecánica de las trompas: sistema ESSURE. Introducción de dispositivo

(espiral de acero inoxidable) en la zona proximal de las trompas con histeroscopio.

 Oclusion tubaria con sustancias quimicas: quinacrina

Técnica de Irving

Técnica de Pomeroy

Técnica de parkland

Otra técnicas Madlener, finbriectomia de Kroener

 Índice de fracaso

 La salpingoclasia puerperal fracaza por dos motivos

1- errores quirúrgicos que comprenden la ligadura del ligamento redondo, en lugar del
oviducto.
2- formación de un trayecto fistuloso entre los muñones seccionados de las trompas o
reanastomosis espontánea.
ESTERILIZACIÓN MASCULINA
 La vasectomía es un método de planificación familiar

.Es un procedimiento quirúrgico, que consiste en la ligadura de los conductos deferentes

del hombre (conductos que van desde los testículos a la próstata). Esto impide que
haya espermatozoides en el semen. Es uno de los métodos más efectivos de control de
la natalidad.
Técnica en consultorio, con analgesia local, 20 min para realizarlo.
 Desventajas de la vasectomía
1- la esterilidad no es inmediata
2- tarda de 3meses a 20 eyaculaciones
3- se debe analizar en semen hasta que dos cuentas espermáticas a cero
4- debe utilizar otro método anticonceptivo antes de la azoospermia
5- la razón del fracaso es el coito sin protección des pues de la vasectomía
ANTICONCEPTIVOS ORALES

Los anticonceptivos orales son una combinación de estrógenos y progestágenos (la

píldora) o constan únicamente de progestágenos (minipíldora).

Los anticonceptivos orales constan de una combinación de un estrógeno y un

progestágeno que se ingiere diariamente durante tres semanas y luego se omite
durante una semana, que es cuando se produce una hemorragia uterina por
supresión.
Mecanismo de acción.
SEGURIDAD.

Se ha comprobado que los anticonceptivos orales son muy seguros en la

mayoría de las mujeres. Cuando se usa correcta y sistemáticamente
teniendo una tasa de embarazo accidental al primer año de uso de
menos del 1%. (Tasa teórica).
 BENEFICIOS
1.- Es un método anticonceptivo reversible y
efectivo
2.- Reducen el riesgo de embarazo ectópico
3.- Reduce la hemorragia menstrual y la anemia
4.- Mejoran la dismenorrea por endometriosis
5.- Menos molestias premenstruales
6.-Reducen el riesgo de cáncer endometrial y ovárico
7.- Reducen varios trastornos benignos de la mama
8.-Reducen la frecuencia y gravedad de la salpingitis aguda
9.-Aumenta la densidad ósea
10.- Mejoran el acné y la artritis reumatoide
11.- Previenen la aterogénesis
12.- Aumenta la densidad ósea.
EFECTOS SECUNDARIOS
- Algunas mujeres pueden presentar:
- Cefalea
- Náusea
- Mareo
- Sensibilidad mamaria anormal

- Irregularidades menstruales

- Cambios del estado de ánimo

 CONTRAINDICACIONES
-Tromboflebitis o alteraciones tromboembólicas
- Vasculopatías cardíacas trombógenas
- Arritmias cardíacas trombógenas
- Diabetes con lesiones vasculares
- Hipertensión descontrolada
- Carcinoma mamario y endometrial
- Hemorragia genital anormal sin diagnóstico
- Embarazo conocido o sospechado
EFICACIA
 Depende básicamente de las alteraciones que produce en el moco
cervical y sus efectos en el miometrio. Los cambios del moco no
duran más de 24 horas, de manera que la minipíldora se debe
tomar a la misma hora todos los días para aumentar su eficacia.
 VENTAJAS DESVENTAJAS

99% de eficacia Requiere uso diario

Son de efecto reversible y se pueden Requiere de continuidad y

discontinuar fácilmente responsabilidad en la ingesta

No interfieren con el acto sexual No protege contra las Infecciones de

Transmisión sexual
USO CORRECTO
 Tomar una píldora por día.
 Establecer un horario de ingesta y procurar que éste se cumpla todos los días.

 En caso de olvido, debes tomarte la píldora apenas la recuerdes y luego tomar

la que corresponde en el horario establecido.
 Procura no tener vómitos ni diarrea dentro de las primeras 4 hs. después de la
ingesta.
ANTICONCEPTIVOS HORMONALES
INYECTABLES

25
DEFINICIÓN

Los anticonceptivos hormonales inyectables son métodos que

contienen solamente una progestina sintética

• Acetatode Medroxiprogesterona (DMPA)

• Enantato de Noristerona (NET-EN)

27
 ACETATO DE MEDROXIPROGESTERONA.

 Suspensión
sintética de microcristales de un prostágeno sintético.
 Aprobado como anticonceptivo en 1992

 Son de larga duración, se aplican cada 2 ó 3 meses, según el tipo

de inyectable.
 Tasas de embarazo de 0.3 por 100 mujeres.

 La administración de fármacos no reduce la eficacia del

prostágeno.
 No depende del peso de la paciente.
MECANISMO DE ACCION

•Inhibición de la ovulación

•Espesamiento del moco cervical

28
DURACIÓN DEL EFECTO ANTICONCEPTIVO

• Acetato de Medroxiprogesterona (DMPA)

Se extiende hasta por lo menos 90 días después de su aplicación

• Enantato de Noristerona (NET-EN)

Se extiende por lo menos a 60 días después de su aplicación
 INICIO DEL MÉTODO
• En cualquier momento del ciclo menstrual en que se esté razonablemente seguro que
la mujer no está embarazada.
• Preferentemente durante los primeros 7 días del ciclo menstrual.
• Si el método se inicia después del 7° día del ciclo, debe usarse un método de
respaldo, como condones y abstinencia durante 7 días.
• En el postparto, en mujeres lactantes, se debe iniciar después de la sexta semana.
• En las mujeres no lactantes y en el postaborto se pueden iniciar inmediatamente
después del evento.

31
MODO DE USO Y FORMA DE ADMINISTRACIÓN

Enantato de noretisterona (NET-EN): 1 ampolla inyectable profunda cada 8

semanas (2 meses); no debe darse masaje en el sitio de aplicación.

En caso necesario, puede administrarse 2 semanas antes y hasta 1 semana

después de la fecha indicada.

33
Acetato de medroxiprogesterona (DMPA): 1 ampolla
inyectable profunda cada 12 semanas (3 meses). En caso
Necesario puede administrarse 4 semanas antes y de
2 a 4 semanas después de la fecha indicada.
 RETORNO DE LA FERTILIDAD

Es más tardío que con los otros métodos hormonales

La posibilidad de embarazo durante el primer año de uso del método

es menor entre usuarias de DMPA que entre usuarias de otros métodos.

70% de las usuarias: a los 12 meses

90% lo han hecho en el plazo de 24 meses.

30
BENEFICIOS
 Disminución de trastornos: anemia, embarazo ectópico y cáncer endometrial.
 No se relaciona con el cáncer de ovarios

ni cáncer cervicouterino
 Cáncer de mamario… riesgo en los primeros 4 años.

 Reducción del colesterol total y de los triglicéridos.

 No se relaciona con infarto de miocardio.

 No se relacionado con crisis trombóticas en mujeres en edad de reproducirse.

 No se acompaña de teragenocidad.

 Seguro para la lactancia.

 No trastornos afectivos
 EFECTOS SECUNDARIOS
• Las usuarias de DMPA a largo plazo pueden tener menor densidad ósea. Pero no ha habido incremento
de las fracturas.

• El sangrado profuso es poco común, puede controlarse administrando dosis mayores de AOC o estrógeno;
si el sangrado continúa, debe descartarse una patología de base y tratarse según corresponda.

• Ligera reducción del colesterol HDL con ligero incremento del LDL.

• Pequeño aumento de la glucosa

•Trombosis en mujeres ancianas con cáncer avanzado que se trataron con DMPA.

•Aumento de peso de 1 a 1.5 kg durante varios años.

•Trastornos de ciclos menstruales. Al principio manchado de ropa interior y hemorragia a intervalos

irregulares.

•Casi todas las usuarias presentan

412 amenorrea total; 50% en un año, 80% a los 3 años.
 ANILLO VAGINAL
Libera etinilestradiol y etonogestrel

Ineficacia: embarazos por 100

mujeres/año

Se introduce en los primeros 5 días

luego de la menstruación y se extrae
luego de 3 semanas. Se espera 1
semana y se introduce uno nuevo

Si hay molestias durante el coite se

puede extraer y colocar al culminar,
 CONDÓN MASCULINO
 Efectividad: 97-98%

 Funda delgada de látex o

poliuretano

 Aumenta efectividad con

espermicidas
 Ventajas
Efectivo si se utiliza correctamente.
De los métodos anticonceptivos que brinda
protección contra las ETS.
Fácil de conseguir.
Sin efectos secundarios (exceptuando alergia al
látex, lo cual es bastante raro)
No afecta la lactancia.
No interviene en procesos hormonales.
Económicamente accesibles.
Desventajas
Su colocación puede interrumpir el acto sexual.
Ocasionalmente puede ocurrir ardor y comezón
como reacción alérgica al material del condón.
El látex puede romperse, si el condón no se
manipula con cuidado.
Se requiere de motivación y educación para usarlo
de forma consistente y sistemática en cada relación
sexual.
En algunas personas la sensibilidad sexual puede
verse afectada.
 CONDÓN FEMENINO

 Efectividad: 72-95%

 Tubo flexible de 17 cm de largo

 Poliuretano
 DIAFRAGMA O CAPUCHÓN CERVICAL
 Efectividad:
80-94% con
espermicidas

 Cúpulacircular de hule de
diámetro variable

 Se coloca varias horas antes del

coito
 ESPERMICIDAS
 Efectividad: 75-80%

 Jaleas,
supositorios, películas,
espumas

 Elingrediente activo es el
nonoxinol-9 ó el otoxinol-9
 ESPONJA ANTICONCEPTIVA
 Efectividad: 80%, con condón del
98%

 Discode poliuretano impregnado

con nonoxinol-9

 Se coloca 24 horas antes del coito

 Gracias!
ABORTO
DEFINICIÓN
 Es
la interrupción del embarazo
antes de las 22 semanas de
gestación y cuyo embrión pesa
<500 gr
FRECUENCIA

 Difícil
establecer
Malos registros
Diferencias entre países.
Diferencias de definiciones
Desconocimiento o encubrimiento
Abortos provocados extra hospitalarios
 CONCEPTOS.
NOMENCLATURAS
Aborto espontaneo: perdida involuntaria
antes de las 20 semanas.
Aborto provocado ( legal o ilegal):
interrupción artificial, por utilización de
diferentes métodos.
Aborto precoz: antes de las 12 semanas
(80%)
Aborto tardío: 13- 20 semanas.
Missed abortium (retenido):interrupción no
seguido de expulsión.
Embarazo anembrionado: saco sin embrión,
sin síntomas. Dx por Ecografía
ABORTO HABITUAL
 Repetición de 3 o mas abortos seguidos, o 5
alternantes
ETIOLOGÍA

Causas maternas orgánicas

 Generales: toxoplasmosis, lúes, TBC

 Locales : infecciones genitales, tumores,

malformaciones
Funcionales :
DBT, endocrinopatías, alteraciones
funcionales del ovario, trofoblasto (déficit
de progesterona)
Inmunológicas:
Sx Ac Anti fosfolípidos, Incompatibilidad
ABO, trombofilias.
Desconocidas:
50% alteraciones genéticas
35% alteraciones endocrinas
15 % otras causas.
CLASIFICACIÓN CLÍNICA
Connato o Amenaza de aborto
Aborto inminente
Aborto diferido
Aborto
En curso
Incompleto
Completo
Infectado
ABORTO ESPONTANEO

10 – 20 %
El 80% < 12 semanas
CONNATO O AMENAZA DE ABORTO
Síntomas:
✓Hemorragia genital
leve
✓ dolor tipo cólico.
✓Cuello sin
modificación
AMENAZA O CONNATO DE ABORTO
Diagnostico:
Cuadro clínico
Ecografías : confirmar vitalidad

Diagnostico Diferencial:
Pólipos cervicales
Cervicitis
Procesos neoplasicos cervicales

Tratamiento : reposo, antiespasmódicos,

uteroinhibidores ( isoxuprine), tratar la
causa probable, Progesterona(VO, VV)
ABORTO INMINENTE

Exageración de los síntomas

Hemorragias mas abundantes,

coágulos
 ABORTO INEVITABLE
Diagnostico: sangrado, dolor.
ABORTO EN CURSO
 ABORTO DIFERIDO, RETENIDO
HUEVO MUERTO Y RETENIDO
 El útero no se contrae, cuello no se dilata para
expulsar el “cuerpo extraño” ( missed abortium)
 PRONOSTICO

 El 10% de los embarazos ABORTO

 EN EL 50% LAS CAUSAS SON: genéticas

Huevo Abortivo
 En el otro 50%: desconocidas
TRATAMIENTO
 TRATAMIENTO
ABORTO INCOMPLETO
MEDIDAS GENERALES ANTES
INTERVENCIÓN
SEGÚN LA HISTORIA CLÍNICA
ABORTO INFECTADO
ABORTO INFECTADO
Muchas gracias
Definición
Alteración biológica en la Salud
Reproductiva de la mujer y se
caracteriza por una implantación o
nidación anómala de un huevo
fecundado como consecuencia de
factores que alteran tanto la
migración ovular, como también el de
su ubicación topográfica final
Clasificación:
I) INTRAUTERINOS
Cornuales.
Cervicales
II) EXTRAUTERINOS
Tubaricos
Ováricos
Abdominales
Ubicaciones mas frecuentes
Causas
Extra ovulares:

Obstructivas mecánicas
Procesos inflamatorios: gonococcia,
sepsis, Clamydias, TBC (raro).
Endometriosis
Procesos adherenciales
Cirugías previas
Causas
Extra ovulares:
Alteraciones genéticas
Modificaciones biológicas del
trofoblasto.
Evolución
Reabsorción precoz
Aborto tubarico (60%)
Rotura cataclismica (40%)
A Termino ( emb. Abdominal)
Regresión :
Maceración
Momificación
Calcificación o litopedium
Infección
Evolución Clínica
I) Sub aguda: aborto tubarico

II) Aguda : rotura cataclismica.

III) Crónica: hematocele pelviano

Modificaciones del Endometrio
Existe correlación entre el endometrio y
el embarazo ectópico.

REACCION DECIDUAL SIN EVIDENCIA

INTRAUTERINA DE NIDACION O
IMPLANTACION
1- reacción pseudo decidual
2-presencia de hormonas trofoblasticas
3-Ausencia vellosidades coriales
4-Reacción endometrial focal (complejo de
Arias- Stella):

Núcleos voluminosos
N. hipercromaticos, perdida de polaridad
Abundante mitosis
Macrocitosis
Vacuolas
Formación adenomatosa glandular
Frecuencia de los E.E. según
ubicación
 Extrauterino tubarico: 95%
Ampular 80%
Istmico 10%
Infundibular 7%
Intersticial 3%
 Extrauterino Ovárico:
 características
Trompa separada del
ovario e integra.
SG ocupa posición del Ov.
SG unido al útero por Lig.
Útero ovárico.
Tejido ovárico en paredes
Del SG
Extrauterino Abdominal:
Primario: raro
Secundario : por aborto tubarico.
Ubicación:
F.S.D. (Mas frecuente)
Fosita ovárica
Mesocolon
Mesosalpinx
Epiplón
Hígado .
Cuadro clínico
no complicados:
silenciosos
asintomáticos
retraso menstrual
turgencia mamaria/ calostro
nauseas
molestias en FII o FID
Complicados :
dolor abdomino/pelviano constante
signo Blumberg/ grito del Douglas
metrorragia: sangrado escaso,
achocolatado. Borra de café
hemorragia interna
SHOCK
DIAGNOSTICO
Historia clínica
Examen físico e instrumental
Laboratorio
Punción del Douglas
Ecografía
Laparoscopia/ culdoscopia
Legrado uterino ( Imagen Arias/Stella)
Laparotomía exploradora ( ante dudas)
Diagnósticos diferenciales
1- aborto incompleto
2-anexitis aguda. EPI.
3- apendicitis aguda
4- quiste de ovario complicado
5- rotura folicular o cuerpo lúteo
 Pronostico
Antiguamente ALTA MORTALIDAD
Actualmente: métodos de diagnósticos
precoces.
 Tratamiento
Tener en cuenta
Edad de la paciente
Antecedentes patologicos
Deseo de gestacion.
No complicados:
 Tratamiento medico: METHOTREXATE
Control ecográfico o endoscópico y
laboratorial de la evolución.
Tratamiento quirúrgico
Gest. Extrauterinas Tubaricas:
anexectomia
Otros tratamientos invasivos s/
zona de implantacion
Aspiracion endotubarica
Video laparoscopia
Histeroscopia ( en variedades corneal
o cervical).
Microcirugías
Histeroscopia
Culdoscopia
Video laparoscopia
seguimiento
recidivas
adherencias
Infecciones
utilización DIU
alteraciones de org. Vecinos
controles ecográficos periódicos
 Gracias.
GINECOLOGIA Y OBSTETRICIA II

HEMORRAGIA UTERINA
ANORMAL
HEMORRAGIA UTERINA ANORMAL
• Relación perfectamente cronometrada entre el endometrio y los factores
que lo regulan.

• Menorragia: menstruación duradera y profusa, mas de 7 días o 80 ml de

sangre.

• Metrorragia o H. intermestrual: perdida sanguínea intermestrual.

• Hipomenorrea: disminución del volumen o la duración.

• Oligomenorrea: intervalo mayor a 35 días

• NORMAL ES CADA 28 DÍAS ± 7 DIAS

• Afecta del 10-30% de las mujeres.

• Diagnostico:
– Exploración física
– Lab: BHCG y hmg
– Fcsv
– Estudio de cuello uterino
– Biopsia de endometrio
– Ecografía tv
– Histeroscopia
 Etiología
FIGO propone acrónimo PALM-COEIN

• P: Pólipos
• A: Adenomiosis
• L: Leiomiomas
• M: neoplasias Malignas

• C: Coagulopatías
• O: trastornos Ovulatorios
• E: disfunción Endometrial
• I: situaciones Iatrógenas
• N: trastornos No clasificados
 Etiología y opciones terapéuticas
• Anormalidades estructurales
• POLIPOS ENDOMETRIALES: neo formaciones uterinas
carneas y blandas formadas por glándulas endometriales y
estroma fibrotico cubiertas por epitelio superficial.
Prevalencia del 8%. Fac de riesgo: edad, obesidad, y uso de
tamoxifeno. Dx y tto: eco tv (antes del día 10 del ciclo),
Histeroscopia.
• POLIPO ENDOCERVICAL: masas de estroma endocervical
benigno cubiertas de epitelio, masas únicas, rojas, lisas y
elongadas que se extienden desde el conducto endocervical.
• DEFECTOS DEL CONDUCTO DE MULLER
• MALFORMACION ARTERIOVENOSA
• CAUSAS EXTERNAS
– DIU
– SIU- LVN
– ACO
– TERAPIA DE REMPLAZO HORMONAL
– TAMOXIFENO
• INFECCION. Endometritis: Mycoplasma, Neisseria, Chlamydia
• CAUSAS SITEMICAS
– NEFROPATIA
– HEPATOPATIA
– ENF DE LA TIROIDES
– COAGULOPATIA: enfermedad de Von Willebrand
Proliferaciones epiteliales con diverso tejido conectivo,
glandular y fibromuscular.

Pueden estar presentes en la cavidad

endometrial o en el canal cervical.

Se clasifican como presentes o

ausentes.

Síntomas:

• HUA
• Sangrado poscoital
• Infertilidad.
 Dx. Postmenopausia (sintomáticos).

1 o una combinación de ecografía de

contraste (SIS) e histeroscopia
diagnóstica (con o sin
histopatología).

La incidencia aumenta con la edad

(FIBROMAS).
Tradicionalmente Dx histopatología
de la profundidad del tejido
“endometrial” por debajo de la
interfase endometrio-miometral de
las muestras de histerectomía.

SÍNTOMAS:
Dismenorrea.

Dx: imagen del útero

• se propone criterios sonográficos

Se asocia con el aumento de la edad y puede coexistir con fibromas.
Puede ser tanto focal como difusa y puede ser más difícil establecer el
diagnóstico si los fibromas también están presentes.
Se asocian con subfertilidad, aborto
espontáneo, parto prematuro.

En tamaños más grandes, pueden causar la

compresión del tracto renal (función renal
alterada) y la vasculatura pélvica
(tromboembolismo venoso).

Asintomáticas / HUA y anemia ferropenica.

Sintomas:

• HUA.
• Dolor pélvico.
• Dismenorrea.
• Esterilidad y aborto
La relación entre la AUB y los fibromas
permanece incompleta.

• Fibromas →sangrado normales.

• Fibroma→ SUA

Superficie endometrial
Vasculatura fragil y congestionada

Cambios celulares y moleculares,

angiogénesis, alt. Sust vasoactivos - FG y
una alt. en la coagulación.

• MMP 2 y 11 aumentados,
• VEGF, bFGF, PDGF, PTHrP y prolactina
Asintomáticos, su
presencia no es la
causa de queja de
HUA.
Poco comunes en las mujeres en edad
reproductiva.

La hiperplasia atípica y la malignidad son

importantes causas potenciales.

Factores predisponentes.

Se subclasificaría por la OMS o el sistema

FIGO
Englobar el espectro de trastornos
sistémicos de la hemostasia.

13%→ Enf. Von Willebrand.

90% pacientes con estas

anormalidades puede identificarse
por una historia estructurada.
 Tiempo de sangrado y una cantidad variable de
flujo → HMA

Ausencia de producción cíclica y

predecible de progesterona.

Endocrinopatías.

Iatrogénico→ uso de esteroides

gonadales o medicamentos.
 Menstruaciones predecibles y cíclicas
(ovulación normal) y ausencia de otras
causas→ TRAST. 1° DE ENDOMETRIO

• Producción local de vasoconstrictores

• Lisis acelerada del coágulo endometrial.
• Producción de sustancias
vasodilatadoras.

Sangrado intermenstrual → TRAST. 1°

DE MEC. DE REPARACIÓN ENDOMETRIAL

Se determina por exclusión de otras

anormalidades que parecen tener un
función ovulatoria normal.
Intervenciones médicas o dispositivos.

Sangrado endometrial a destiempo

durante el uso de esteroides gonadales
exógenos → “sangrado de avanzada”.

Sistema intrauterino liberador de

levonorgestrel→ sangrado de avanzada
(6m).

Anticoagulantes (C) o agentes

sistemicos que contribuyen a trast. de
ovulación (O)
Afecciones → se han definido de
forma deficiente, se evaluaron de
forma inadecuada o raras.

• Malformaciones arteriovenosas.
• Hipertrofia miometrial.

Trast. no identificados que se

definiran solo por ensayos
bioquímicos o de biología molecular.
 METRORRAGIA DISFUNCIONAL
• UNA VEZ DESCARTADO CAUSAS ORGANICAS.
• Trastornos de la ovulación
• Anovulatorio: si no es liberado el ovulo no se produce
progesterona y persiste el endometrio proliferativo.
Degradación del estroma, disminución del nro de
arteriolas espirales y dilatación e inestabilidad de los
capilares venosos. Disminuyen las prostaglandinas y el
acido araquidonico
• Ovulatorios: depende en primera instancia solo de
dilación vascular.
• Tto: hormonal. AINES. Progestagenos orales, legrados,
histeroscopia: ablación del endometrio. Histerectomia.
Endometriosis
 Endometriosis
• Enfermedad benigna con presencia de glándulas
endometriales y estroma fuera de la ubicación
normal.
• Peritoneo pélvico, ovarios, LIGAMENTOS, tabique
rectovaginal, uréteres, vejiga, pericardio, y pleura.
• Dependiente de hormonas.
• Dolor pélvico, infertilidad o subfecundidad o ser
asintomáticas.
• Método principal de diagnostico es la
laparoscopia y la biopsia, aunque esta ultima no
es necesaria para hacer el diagnostico.
• ETIOLOGIA: se desconoce aun la causa
definitiva pero se plantean algunas teorías:

– MESTRUACION RETROGRADA
– DISEMINACION LINFATICA O VASCULAR
– METAPLASIA CELOMICA
– TEORIA DE LA INDUCCION
– TEORIA DE LAS CELULAS MADRE
La endometriosis es una enfermedad inflamatoria crónica dependiente
de estrógeno, en que hay proliferación aberrante de tejido
endometrial ectópico. Resistencia a la progesterona en un ambiente
estrogénico.

La prostaglandina E2 constituye el inductor mas potente de la

actividad de la aromatasa en células del estroma endometrial.
Estimulando a la cox-2 en células del endotelio uterino.

Disfunción del sistema inmunitario los macrófagos actúan como

fagocitos y estimulan la actividad del tejido endometriosico.
Disminuye la citotoxicidad de los NK contra el endometrio.
FACTORES DE RIESGO:
• Predisposición familiar
• Mutaciones genéticas y polimorfismos
• Defectos anatómicos
• Toxinas ambientales
• SISTEMA DE CLASIFICACION DE LA
ENDOMETRIOSIS
– Visualización de las lesiones por medio de
laparoscopia.
– Blancas , rojas o negras
– Superficial o profunda.
• Etapa I: mínima
• Etapa II: leve
• Etapa III: moderada
• Etapa IV: intensa o grave
• SINTOMATOLOGIA:
– Dolor pélvico crónico:
• Dismenorrea. 24 a 48 hr antes de la menstruación
• Dispareunia
• Dolor no cíclico
– Disuria
– Disquesia (dolor con la defecación)
– Infecundidad. 20 a 30%
– Obstrucción intestinal y ureteral
– Dolor cíclico en tórax o en hombro. Hemoptisis o
hemotórax
• DIAGNOSTICO:
– Exploración física: tacto bimanual.
– CA 125. mayor sensibilidad Grados III/IV
– ECOGRAFIA TV (vidrio esmerilado)
– TAC
– RNM
– LAPAROSCOPIA DIAGNOSTICA. Método primario
– ANALISIS HISTOPATOLOGICO
• TRATAMIENTO:
• CONSERVADOR: síntomas leves o asintomáticas.
Se especta.
• TRATAMIENTO MEDICO DEL DOLOR: inhibidores
de la cox-2, ACOS combinados.
• ACOS: progestagenos
• TRATAMIENTO QUIRURGICO DEL DOLOR:
eliminación de las lesiones y de las adherencias.
Resección de endometriomas, neurectomia
presacra. Histerectomía con
salpingoovariectomia.
 Dolor pélvico
• Somático: se origina en fibras aferente
nerviosas del sistema somático que inervan al
peritoneo parietal, piel, músculos y tejido
subcutáneo. Agudo, localizado.
• Visceral: proviene de fibras aferentes del
sistema nervioso autónomo. Sordo y
generalizado.
• Dolor inflamatorio.
• Dolor neuropático
• Dolor agudo: menor a 7 días. Anamnesis,
exploración física. Rx, ecografía, TAC, RNM,
laparoscopia.

• Dolor crónico: dolor no cíclico que persiste mas

de 6 meses, se localiza en la pelvis anatómica,
pared anterior del abdomen, zona infra umbilical
o lumbosacra y glúteos, con una intensidad
suficiente para ocasionar una discapacidad
funcional o culminar en una intervención médica.

• Dx: anamnesis, exploración física, Rx y

endoscopia.
• Tto: dependiendo de la causa.
• AINEs
• Paracetamol
• Opioides
• Estrógeno
• Antidepresivos y anticonvulsivos. Amitriptilina
• Cirugía: neurectomia, ablación nerviosa,
Histerecotomia con Salpingooferectomia bilateral
 Dismenorrea
• Dolor cíclico con la menstruación
• Cólico, lumbar, nauseas, vomito, cefalea,
diarrea
• Primaria: sin alteracion identificable, poco
despues de la menarca
• Secundaria: por alguna complicación.
Endometriosis, leiomiomas, adenomiosis, etc
• Tto: AINEs, ACO, agonistas GnRH, andrógenos
Gracias.
 Trastornos
Hipertensivos del
Embarazo
 Los trastornos hipertensivos complican 5 a 10% de todos
los
embarazos.

 Constituyen uno de los miembros de la tríada letal,

junto con la hemorragia y la infección.

 16% de las muertes maternas se debe a trastornos

hipertensivos (Khan, 2006).

 En Estados Unidos, Berg et al. (2010) publicaron que de

1998 a 2005, el 12.3% de 4 693 muertes maternas
relacionadas con el embarazo se debía a preeclampsia o
eclampsia.
Durante los últimos 20 años, en Estados Unidos
la hipertensión en el embarazo se consideró con
el uso de la terminología y la clasificación
propuestas por el Working Group of the
National High Blood Pressure Education
Program (NHBPEP) (2000).

El Presidente del American College

of Obstetricians and Gynecologists (2013b), estableció un
grupo que generara recomendaciones basadas en la
evidencia para la práctica clínica. Se conservó la
clasificación básica, que describe cuatro tipos de
enfermedad hipertensiva
 Hipertensión gestacional (evidencia de preeclampsia que no
aparece y la hipertensión desaparece a las 12 semanas
despuésdel parto).

 Síndrome de preeclampsia y eclampsia.

Hipertensión crónica de alguna causa.

Preeclampsia superpuesta a hipertensión crónica

 Diagnóstico de los trastornos
hipertensivos
❖ La hipertensión se diagnostica de forma empírica cuando la
medición correcta de la presión arterial sistólica es >140 mmHg o la
diastólica es >90 mmHg.

❖ En el pasado, se usaban incrementos

de 30 mmHg de la sistólica o de 15 mmHg en la diastólica en los
valores de la presión arterial en la parte intermedia del embarazo
como criterios diagnósticos.

❖ Estas pacientes deben vigilarse más de cerca, porque algunas de

estas mujeres cuya presión se mantiene <140/90 mmHg han tenido
convulsiones eclámpticas.

Williams OBSTETRICIA
24ªEDICIÓN
 Hipertensión gestacional

El diagnóstico de hipertensión gestacional se establece en

mujeres cuya presión arterial alcanza 140/90 mmHg o más por
vez primera después de la mitad del embarazo, pero en quienes
no se identifica proteinuria .
 Hipertensión gestacional

Casi 50% de estas pacientes presenta después preeclampsia, que

incluye signos como cefalea o dolor epigástrico, proteinuria y
trombocitopenia.

 10% de las convulsiones eclámpticas ocurre antes

que haya proteinuria detectable.

▪ Hay quienes han reclasificado la

hipertensión gestacional como hipertensión transitoria si no
aparece evidencia de preeclampsia y la presión arterial normal se
recupera hacia las 12 semanas del puerperio.
 Preeclampsia

Con características no Graves:

▪ PA >o igual 140/90mmHg después de 20 sem de gestación.
▪ Proteinuria >o igual300mg/24h, o >o igual 1+ con tira reactiva
 Preeclampsia

➢ Con características Graves:

▪ PA >o igual 160/110mmHg.
▪ Proteinuria de 2.0g/24 h, o >o igual 2+ con tira reactiva.
▪ Creatinina sérica >1.2mg/dl.
▪ Plaquetas <100 000 microlitros.
▪ Hemolisis microangiopatica, aumento de la DHL.
▪ Aumento de transaminasa sérica: AST o ALT.
▪ Cefalea persistente u otro trastorno cerebral o visual.
▪ Dolor epigástrico persistente.
 Eclampsia

➢ Complicación de la pre eclampsia con convulsiones tipo

tonicoclónicas generalizadas
➢ Aumenta en gran proporción el riesgo para la madre y el feto.
 Preeclampsia superpuesta
a hipertensión crónica

▪ Proteinuria de inicio reciente >o igual 300mg/24h en

mujeres hipertensas, pero sin proteinuria antes de las 20 sem
de gestación.
▪ Aumento súbito de proteinuria o presión arterial, o
recuento plaquetario <100 000 microlitros.
 Hipertensión Crónica:

▪ PA > o igual 140/90mmHg antes del embarazo o

diagnosticada antes de las 20 sem de gestación, no
atribuible a enfermedad trofoblastica gestacional.
▪ o
▪ Hipertensión diagnosticada después de las 20 sem de gest.
Y persistente 12 sem después delparto.
 INCIDENCIA Y FACTORES DE RIESGO

▪ Las mujeres jóvenes y nulíparas son vulnerables en particular a

padecer preeclampsia

▪ Las pacientes mayores tienen riesgo aumentado de hipertensión crónica con preeclampsia
agregada.

▪ La incidencia depende en buena medida de la

raza y el grupo étnico y, por tanto, de la predisposición
genética.
 INCIDENCIA Y FACTORES DE RIESGO

▪ La incidencia de preeclampsia fue de 5% en mujeres

caucásicas, de 9% entre las hispanas y de 11% entre las
afroamericanas

▪ Hay varios factores de riesgo más relacionados con la

preeclampsia, los cuales incluyen obesidad, embarazo
múltiple, edad materna y síndrome metabólico

▪ Las mujeres con preeclampsia en el primer embarazo

tienen mayor riesgo en un segundo embarazo,
 El tabaquismo durante el embarazo tiene varios
resultados
adversos, pero resulta irónico que se ha observado
una relación constante con un menor riesgo de
hipertensión durante el embarazo (Bainbrigde,
2005; Zhang, 1999). Kraus et al. (2013) proponen
que esto se debe a que el tabaquismo incrementa la
expresión de adrenomedulina (nuevo peptido
vasoactivo: efecto vasodilatador) placentaria, lo
cual regula la homeostasis del volumen.
 Etiología

1. Implantación placentaria con invasión trofoblástica anormal

de vasos uterinos.

2. Tolerancia inmunitaria mal adaptada entre tejidos maternos,

paternos (placentarios) y fetales.

3. Mala adaptación de la madre a los cambios cardiovasculares

o inflamatorios del embarazo normal.

4. Factores genéticos, incluidos genes predisponentes heredados e

influencias epigenéticas.
• La preeclampsia tiene una expresión fenotípica clínica muy
variable. Hay al menos dos subtipos principales diferenciados
por la remodelación defectuosa o no de las arteriolas espirales
uterinas por invasión trofoblástica endovascular. Este concepto
dio origen a la teoría del “trastorno en dos etapas” para la
etiopatogenia de la preeclampsia.

• Consideran que el trastorno en dos etapas :

o la etapa 1 se debe a la remodelación trofoblástica endovascular

alterada que origina después síndrome clínico de la etapa 2.

o La etapa 2 es susceptible a la modificación por los trastornos

maternos preexistentes que se manifiestan por activación o
inflamación de las células endoteliales.
Invasión trofoblástica anormal
 Disfunción endotelial:

• Aumento de la concentración de agentes

vasopresores y agregantes plaquetarios (endotelina 1
y TBX A2), y una disminución de las sustancias vaso
dilatadoras y antiagregantes plaquetarias. (NOy
PG2).

• Determinan un estado de vasoconstricción con

aumento de la resistencia vascular periférica y así un
aumento de la presión arterial.
 Inflamación Sistémica:

❖ El embarazo normal se caracteriza por un estado de

inflamación sistémica, con activación de monocitos,
granulocitos y plaquetas.
❖ En la preeclampsia existe una respuesta
inflamatoria sistémica exagerada (RIS)por lo que
los distintos marcadores de actividad
proinflamatoria ( TNF ∞,IL1B, IL 6) se encuentran
elevados.
• Se distinguen dos etapas una asintomática con
estado Hipóxico de la placenta y una segunda
etapa sintomática caracterizada por una RIS
(Respuesta Inflamatoria Sistémica) exagerada y
disfunción endotelial.
• Entre ambas etapas hay mediadores (moléculas o
sustancias producidas por la placenta capaces de
difundir este daño placentario y traducirlo en
compromiso sistémico):
1. Estrés Oxidativo.
2. Apoptosis (fragmentos de sincitiotrofoblasto)
 Estrés Oxidativo:

❑ Corresponde al desbalance entre la producción de

radicales libres y sustancias antioxidantes.El
incremento de las concentraciones de peróxidos
lipídicos, junto con el descenso de la actividad
antioxidante, dio lugar a la posibilidad de que los
marcadores de estrés oxidativo permitan predecir la
preeclampsia.

❑ El daño en la preeclampsia sería a través de la

transferencia de este estrés oxidativo placentario a
la circulación materna vía lipoperóxido
(Peroxidacion Lipídica).
❑ Éstos a su vez generan radicales muy tóxicos
que lesionan a las células endoteliales,
modifican su producción de óxido nítrico e
interfieren con el equilibrio de prostaglandinas.
❖ Otras consecuencias del estrés oxidativo son:

• Activación de la coagulación microvascular, que se

manifiesta como trombocitopenia y aumento de la
permeabilidad capilar, que se expresa como edema
y proteinuria.

24a Edicion WilliamsObstetricia

 Apoptosis :

Proceso que ocurre normalmente en todos los tejidos

que están en permanente renovación, incluyendo el
trofoblasto pero que necesita un tiempo prudencial
(entre 4 a 6 semanas).
En la preeclampsia este proceso de degradación
subcelular esta sobre exigido, de esta manera
parcialmente digerido entra a la circulación
materna, lo que se conoce como microfragmentos
de sincitiotrofoblasto.(STBM)
Estos STBM, alteran el comportamiento de
macrófagos y producen activación de neutrófilos,
disrupción de células endoteliales y disminución de
la relajación endotelial.
 Factores genéticos :

La predisposición hereditaria a la preeclampsia es el resultado

de interacciones de cientos de genes heredados, tanto maternos
como paterno.
 Prediccion :

❖ Velocimetría Doppler de la arteria uterina (IP medio)

❖ Proteina A asociada al embarazo (PAPP-A)(niveles

reducidos de PAPP-A en el primer y segundo trimestre se
asocian a un riesgo incrementado de preeclampsia)
❖ Proteina 13 placentaria (PP13)(Varios estudios han
confirmado valores significativamente inferiores de PP13
en gestaciones que posteriormente desarrollan PE)
❖ Hemoglobina fetal y alfa 1 microglobulina (incremento en
l
os niveles de dichas moléculas en gestantes con PE)
 Prevención :

❖ Dieta hiposódica
❖ Calcio complementario
❖ Ejercicio.
❖ Antihipertensores
❖ Antioxidantes
❖ Ácido acetilsalicílico en dosis bajas
(En dosis orales de 50 a
150 mg cada 24 h, el ácido acetilsalicílico inhibe de manera eficaz
la biosíntesis del tromboxano A2 plaquetario, con efectos mínimos
sobre la producción de prostaciclina vascular).
 Complicaciones :

▪ Parto prematuro

▪ RCIU

▪ Desprendimiento de placenta

▪ Edema pulmonar materno

▪ Eclampsia
 SINDROME DE HELLP

Hemolisis, Elevated Liver enzymes, Low

Platelets
Criterios de Diagnóstico
 Clasificación:

➢ TIPO I. Cuenta plaquetaria ↓ 50,000 mm3

➢ TIPO II. Cuenta plaquetaria entre 50,000 y 100,000 mm3

➢ TIPO III. Cuenta plaquetaria entre 100,000 y 150,000

mm3
Tratamiento Farmacológico:
 Agentes antihipertensivos utilizados para el control urgente de la presión arterial en el embarazo
Droga Dosis
Labetalol 10-20 mg IV, a
continuación, 20-80 mg
cada 20-30 min a una
dosis máxima de 300 mg o
constante infusión de 1-2
mg / min IV
Hydralazine 5 mg IV o IM, luego 5-10
mg IV cada 20-40 minutos
o Infusión constante 0.5-
10 mg / h
Nifedipine 10-20 mg por vía oral,
repita en 30 minutos si es
necesario; luego 10-20 mg
cada 2-6 horas
Considerado un agente de
primera línea La
taquicardia es menos
común y tiene menos
efectos adversos.
Contraindicado en
pacientes con asma,
enfermedad cardíaca o
insuficiencia cardíaca
congestiva
Una dosificación más alta
o más frecuente asociada
con hipotensión materna,
dolores de cabeza y
sufrimiento fetal puede ser
más común que otras
Puede observarse
taquicardia refleja y
dolores de cabeza
 Agentes antihipertensivos orales comunes en el embarazo

Labetalol 200-2,400 mg / d por vía Bien tolerado

oral en dos a tres dosis Posibles efectos
divididas broncoconstrictores
Evitar en pacientes con
asma y
insuficiencia cardíaca
congestiva
Nifedipine 30-120 mg / d por vía oral , No use forma sublingual
de liberación lenta

Methyldopa 0.5-3 g / d por vía oral en Datos de seguridad infantil

dos a tres dosis divididas hasta los 7 años de edad
Puede no ser tan eficaz en
el control de graves
hipertensión
En casos de Eclampsia:
 Sulfato de magnesio para controlar las
convulsiones

Es un anticonvulsivo eficaz que evita la

depresión del sistema nervioso central,
tanto de la madre como del feto

Puede administrarse por vía

intravenosa en infusión continua o
intramuscular por inyección
intermitente
El sulfato de magnesio no se administra para tratar la hipertensión.
24a Edicion WilliamsObstetricia
En caso de Intoxicación por Sulfato
de Magnesio disponer 1 Amp de
Gluconato de Calcio al 10% diluirla
hasta 20ml luego pasar EV lento
Las mujeres con preeclampsia de caracteristicas grave
tratadas con un mínimo de 8 horas de sulfato de
magnesio antes del parto no se benefician al continuar
el sulfato de magnesio durante las 24 horas posteriores
al parto.
Task Force del American College of Obstetricians and Gynecologists (2013b)
 Recomendaciones

➢ La Task Force de 2013 recomendó el uso de dosis bajas de

ácido acetilsalicílico en pacientes con riesgo alto de
preeclampsia o antecedente para disminuir el riesgo de
preeclampsia.
➢ No se debe indicar reposo en cama o restricción de otra
actividad física para la prevención primaria de la
preeclampsia.
➢ Sesugiere que no se haga restricción de sal en las mujeres
embarazadas para prevenir la preeclampsia
➢ Monitoreo estricto en mujerescon hipertensión
gestacional o preeclampsia sin características de
severidad, con valoración seriada de síntomas maternos y
movimientos fetales (diariamente por la mujer), medidas
seriadas de la presión sanguínea (dos veces por semana) y
valoración del conteo de plaquetas y enzimas hepáticas
 Recomendaciones

➢ La importancia de IP Medio de las Arterias Uterinas en

el primer trimestre como predictor.
➢ Cuando se evidencia crecimiento fetal restringido en
una mujer con preeclampsia la vigilancia feto
placentaria debe incluir velocimétria Doppler de la
Arteria Umbilical y ACM.
➢ En mujeres con hipertensión gestacional o
preeclampsia sin características de severidad y sin
indicación de interrupción antes de las 37 semanas,
se sugiere el manejo expectante, con monitorización
materna fetal.
➢ En mujeres con preeclampsia con caracteristicas de
severidad mas allá de las 34 semanas de gestación y
con condiciones maternas y fetales inestables, se
sugiere la interrupción del embarazo
independientemente de la edad gestación, tan
pronto se estabilicen las condiciones maternas.
 Recomendaciones

➢ En mujeres con preeclampsia con caracteristicas de

severidad de menos de 34 semanas de gestación
traslado a lugares con cuidados intensivos maternos
y neonatales.
➢ La administración de corticoesteroides, para la
maduraciónpulmonar fetal.
➢ Se recomienda la administración de sulfato de
magnesio en mujeres con eclampsia
➢ Toda mujer con embarazo evidente con
convulsiones es una Eclampsia hasta demostrar lo
contrario.
GRACIAS
 Visual summary Manejo de Hipertensión en el Embarazo
Resumen visual de las guías NICE 2019
Los médicos generales y especialistas, además de los obstetras, juegan un rol vital en la identificación de la hipertensión durante el
embarazo, tratamiento de primera línea y referencia al especialista. Este gráfico muestra un resumen de las recomendaciones
actualizadas del Instituto Nacional para la Excelencia Clínica (NICE) del Reino Unido acerca del diagnóstico y manejo de la hipertensión
en el embarazo. Las recomendaciones de manejo son iguales para mujeres con hipertensión crónica y gestacional. La elección de
tratamiento farmacológico es la misma para las mujeres con cualquier tipo de hipertensión en el embarazo.

VÍA DE HIPERTENSIÓN VÍA DE PREECLAMPSIA

HIPERTENSIÓN HIPERTENSIÓN SEVERA HIPERTENSIÓN HIPERTENSIÓN SEVERA
Presión arterial 140/90 a 159/109 mmHg 160/110 mmHg o más 140/90 a 159/109 mmHg 160/110 mmHg o más
Admisión si existe
No admitir preocupación clínica
Admisión hospitalaria Admisión Admisión
rutinariamente (ver más adelante)
Administrar tratamiento farmacológico a todas las pacientes con presión arterial arriba de 140/90 mmHg
Manejo inicial
Primera opción: Segunda opción: Tercera opción: Objetivo: presión arterial
LAB NIF MET
Labetalol Nifedipino Metildopa de 135/85 mmHg o menor

MONITOREO
Presión arterial Por lo menos cada 48 horas
Una o dos veces Cada 15-30 minutos Cada 15-30 minutos
por semana Más frecuentemente si se
encuentra hospitalizada

Proteinuria Una o dos veces

Diario Solo repetir si existe indicación clínica
por semana

Exámenes
de Laboratorio
Al momento del diagnóstico
Biometría hemática
completa Posteriormente una vez por semana
2 veces por semana 3 veces por semana
Pruebas de funcion- Ofrecer prueba de PlGF (Factor de Crecimiento Placentario)
amiento hepático si existe sospecha de preeclampsia
Pruebas de
funcionamiento renal

EVALUACIÓN FETAL
Auscultación En cada visita prenatal En cada visita prenatal
cardiaca

Ultrasonografía Al momento del diagnóstico Al momento del diagnóstico Al momento del diagnóstico
Posteriormente, cada
Posteriormente cada
2 a 4 semanas, si existe Posteriormente cada 2 semanas
2 semanas
indicación clínica

Cardiotocografía Al momento del diagnóstico Al momento del diagnóstico

Si existe indicación clínica
Posteriormente, si existe Posteriormente si existe indicación clínica
indicación clínica

Brindar una Considerar el uso de modelos

Repetir prueba con nueva muestra Incertidumbre sobre evaluación de predicción de riesgo
Si la tira reactiva es
el diagnóstico clínica completa
positiva para proteinuria
fullPIERS PREP-S
en cada visita
Interpretar hallazgos dentro del contexto de prenatal En cualquier Hasta las 34
Relación momento semanas de
una revisión clínica completa, incluyendo: del embarazo gestación
proteína/creatinina
Usar 30 mg/mmol Síntomas y signos de preeclampsia, como:
como punto de Cefalea severa Alteraciones visuales Vómito
corte Dolor severo en epigastrio o debajo de las costillas Ingresar al hospital si existen datos de
o alarma maternos o fetales, como:
Sudoración súbita en cara, manos o pies
Relación Presión arterial sistólica >160 mmHg persistente
albumina/creatinina Investigación de otros resultados, como:
Usar 8 mg/mmol Preocupación con respecto a los resultados
Evidencia de hemólisis Deterioro de la función renal hematológicos o bioquímicos maternos
como punto de
corte Función hepática anormal
Signos de edema pulmonar inminente
Descenso en la cuenta plaquetaria
Signos de eclampsia inminente Signos de
preeclampsia
Sospecha de compromiso fetal severa
Cualquier otro signo que genere preocupación
Sin evidencia de proteinuria, sin hallazgos clínicos de preeclampsia Diagnóstico de preeclampsia

Continuar monitoreo < 37 semanas > 37 semanas Considerar las Incluir a un obstetra experimentado en cualquier
indicaciones decisión relativa al momento del nacimiento en la
maternas y fetales para el mujer con preeclampsia
No ofrecer un nacimiento prematuro planeado a nacimiento; así como el
aquellas mujeres cuya presión arterial se momento, generando un 37 semanas de gestación Después de las 37
encuentre por debajo de 160/110 mmHg, a no o antes semanas
acuerdo entre la paciente
ser que existan otras indicaciones médicas y el obstetra Considerar un nacimiento Inducir el nacimiento
prematuro planeado en caso dentro de las primeras
de preeclampsia severa 24 a 48 horas

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completo en línea http://bit.ly/BMJhypreg © 2019 BMJ Publishing Group Ltd.
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asumen ninguna responsabilidad por ningún aspecto del tratamiento administrado con la ayuda de esta información. Cualquier confianza depositada en esta información es estrictamente bajo el riesgo del usuario. Para consultar el documento completo de
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 ACOG PRACTICE BULLETIN
Clinical Management Guidelines for Obstetrician–Gynecologists
NUMBER 202
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Committee on Practice Bulletins—Obstetrics. This Practice Bulletin was developed by the American College of Obstetricians and
Gynecologists’ Committee on Practice Bulletins—Obstetrics in collaboration with Jimmy Espinoza, MD, MSc; Alex Vidaeff, MD,
MPH; Christian M. Pettker, MD; and Hyagriv Simhan, MD.

Gestational Hypertension and

Preeclampsia
Hypertensive disorders of pregnancy constitute one of the leading causes of maternal and perinatal mortality worldwide. It
has been estimated that preeclampsia complicates 2–8% of pregnancies globally (1). In Latin America and the Caribbean,
hypertensive disorders are responsible for almost 26% of maternal deaths, whereas in Africa and Asia they contribute to 9%
of deaths. Although maternal mortality is much lower in high-income countries than in developing countries, 16% of
maternal deaths can be attributed to hypertensive disorders (1, 2). In the United States, the rate of preeclampsia increased
by 25% between 1987 and 2004 (3). Moreover, in comparison with women giving birth in 1980, those giving birth in 2003
were at 6.7-fold increased risk of severe preeclampsia (4). This complication is costly: one study reported that in 2012 in the
United States, the estimated cost of preeclampsia within the first 12 months of delivery was $2.18 billion ($1.03 billion for
women and $1.15 billion for infants), which was disproportionately borne by premature births (5). This Practice Bulletin
will provide guidelines for the diagnosis and management of gestational hypertension and preeclampsia.

20 weeks of gestation and frequently near term. Although

Background
Risk Factors
A variety of risk factors have been associated with
increased probability of preeclampsia (Box 1) (6–12).
Nonetheless, it is important to remember that most cases
of preeclampsia occur in healthy nulliparous women with
no obvious risk factors. Although the precise role of
genetic–environmental interactions on the risk and inci-
dence of preeclampsia is unclear, emerging data suggest
the tendency to develop preeclampsia may have some
genetic component (13–16).
Definitions and Diagnostic Criteria for
Hypertensive Disorders of Pregnancy
Preeclampsia (With and Without
Severe Features)
Preeclampsia is a disorder of pregnancy associated with
new-onset hypertension, which occurs most often after
often accompanied by new-onset proteinuria, hyperten-
sion and other signs or symptoms of preeclampsia may
present in some women in the absence of proteinuria
(17). Reliance on maternal symptoms may be occasion-
ally problematic in clinical practice. Right upper quad-
rant or epigastric pain is thought to be due to periportal
and focal parenchymal necrosis, hepatic cell edema, or
Glisson’s capsule distension, or a combination. However,
there is not always a good correlation between the
hepatic histopathology and laboratory abnormalities
(18). Similarly, studies have found that using headache
as a diagnostic criterion for preeclampsia with severe
features is unreliable and nonspecific. Thus, an astute
and circumspect diagnostic approach is required when
other corroborating signs and symptoms indicative of
severe preeclampsia are missing (19, 20). Of note, in
the setting of a clinical presentation similar to preeclamp-
sia, but at gestational ages earlier than 20 weeks, alter-
native diagnoses should to be considered, including but

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 Box 1. Risk Factors for Preeclampsia
Nulliparity
Multifetal gestations
Preeclampsia in a previous pregnancy
Chronic hypertension
Pregestational diabetes
Gestational diabetes
Thrombophilia
Systemic lupus erythematosus
Prepregnancy body mass index greater than 30
Antiphospholipid antibody syndrome
Maternal age 35 years or older
Kidney disease
Assisted reproductive technology
Obstructive sleep apnea
not limited to thrombotic thrombocytopenic purpura,
hemolytic–uremic syndrome, molar pregnancy, renal
disease or autoimmune disease.
Although hypertension and proteinuria are consid-
ered to be the classical criteria to diagnose preeclampsia,
other criteria are also important. In this context, it is
recommended that women with gestational hypertension
in the absence of proteinuria are diagnosed with pre-
eclampsia if they present with any of the following
severe features: thrombocytopenia (platelet count less
than 100,000 3 109/L); impaired liver function as indi-
cated by abnormally elevated blood concentrations of
liver enzymes (to twice the upper limit of normal con-
centration); severe persistent right upper quadrant or epi-
gastric pain and not accounted for by alternative
diagnoses; renal insufficiency (serum creatinine concen-
tration greater than 1.1 mg/dL or a doubling of the serum
creatinine concentration in the absence of other renal
disease); pulmonary edema; or new-onset headache unre-
sponsive to acetaminophen and not accounted for by
alternative diagnoses or visual disturbances (Box 2). Ges-
tational hypertension is defined as a systolic blood pres-
sure of 140 mm Hg or more or a diastolic blood pressure
of 90 mm Hg or more, or both, on two occasions at least
4 hours apart after 20 weeks of gestation in a woman
with a previously normal blood pressure (21). Women
with gestational hypertension with severe range blood
pressures (a systolic blood pressure of 160 mm Hg or
higher, or diastolic blood pressure of 110 mm Hg or
higher) should be diagnosed with preeclampsia with
severe features. These severe ranges of blood pressure
or any of the severe features listed in Box 3 increase
the risk of morbidity and mortality (22).
e2 Practice Bulletin Gestational Hypertension and Preeclampsia
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Box 2. Diagnostic Criteria for
Preeclampsia
Blood pressure
c Systolic blood pressure of 140 mm Hg or more or
diastolic blood pressure of 90 mm Hg or more on
two occasions at least 4 hours apart after 20
weeks of gestation in a woman with a previously
normal blood pressure
c Systolic blood pressure of 160 mm Hg or more or
diastolic blood pressure of 110 mm Hg or more.
(Severe hypertension can be confirmed within
a short interval (minutes) to facilitate timely
antihypertensive therapy).
and
Proteinuria
c 300 mg or more per 24 hour urine collection (or
this amount extrapolated from a timed collection)
or
c Protein/creatinine ratio of 0.3 mg/dL or more or
c Dipstick reading of 2+ (used only if other quan-
titative methods not available)
Or in the absence of proteinuria, new-onset hyper-
tension with the new onset of any of the
following:
c Thrombocytopenia: Platelet count less than
100,000 3 109/L
c Renal insufficiency: Serum creatinine concen-
trations greater than 1.1 mg/dL or a doubling of
the serum creatinine concentration in the
absence of other renal disease
c Impaired liver function: Elevated blood concen-
trations of liver transaminases to twice normal
concentration
c Pulmonary edema
B New-onset headache unresponsive to medi-
cation and not accounted for by alternative
diagnoses or visual symptoms
Proteinuria during pregnancy is defined as 300 mg/dL
of protein or more in a 24-hour urine collection (21, 23)
or a protein-to-creatinine ratio of 0.30 or more (24).
When quantitative methods are not available or rapid
decisions are required, a urine protein dipstick reading
can be substituted. However, dipstick urinalysis has high
false-positive and false-negative test results. A test result
of 1+ proteinuria is false-positive in 71% of cases com-
pared with the 300 mg cutoff on 24-hour urine collection,
and even 3+ proteinuria test results may be false-positive
in 7% of cases. Using the same 24-hour urine collection
standard, the false-negative rate for dipstick urinalysis is
9% (25). If urinalysis is the only available means of
OBSTETRICS & GYNECOLOGY

Box 3. Severe Features
c Systolic blood pressure of 160 mm Hg or more, or
diastolic blood pressure of 110 mm Hg or more
on two occasions at least 4 hours apart (unless
antihypertensive therapy is initiated before this
time)
c Thrombocytopenia (platelet count less than
100,000 3 109/L)
c Impaired liver function as indicated by abnormally
elevated blood concentrations of liver enzymes
(to twice the upper limit normal concentration),
and severe persistent right upper quadrant or
epigastric pain unresponsive to medication and
not accounted for by alternative diagnoses
c Renal insufficiency (serum creatinine concentra-
tion more than 1.1 mg/dL or a doubling of the
serum creatinine concentration in the absence of
other renal disease)
c Pulmonary edema
c New-onset headache unresponsive to medication
and not accounted for by alternative diagnoses
c Visual disturbances
assessing proteinuria then overall accuracy is better using
2+ as the discriminant value (25, 26).
Gestational Hypertension
Gestational hypertension is defined as a systolic blood
pressure 140 mm Hg or more or a diastolic blood pres-
sure of 90 mm Hg or more, or both, on two occasions at
least 4 hours apart after 20 weeks of gestation, in
a woman with a previously normal blood pressure (21).
Gestational hypertension is considered severe when the
systolic level reaches 160 mm Hg or the diastolic level
reaches 110 mm Hg, or both. On occasion, especially
when faced with severe hypertension, the diagnosis
may need to be confirmed within a shorter interval (mi-
nutes) than 4 hours to facilitate timely antihypertensive
therapy (27). Gestational hypertension occurs when
hypertension without proteinuria or severe features de-
velops after 20 weeks of gestation and blood pressure
levels return to normal in the postpartum period (21). It
appears that this diagnosis is more of an exercise of
nomenclature than a pragmatic one because the manage-
ment of gestational hypertension and that of preeclamp-
sia without severe features is similar in many aspects, and
both require enhanced surveillance. Outcomes in women
with gestational hypertension usually are good, but the
notion that gestational hypertension is intrinsically less
concerning than preeclampsia is incorrect. Gestational
hypertension is associated with adverse pregnancy out-
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comes (17) and may not represent a separate entity from
preeclampsia (28). Up to 50% of women with gestational
hypertension will eventually develop proteinuria or other
end-organ dysfunction consistent with the diagnosis of
preeclampsia, and this progression is more likely when
the hypertension is diagnosed before 32 weeks of gesta-
tion (29, 30). Although investigators have reported
a higher perinatal mortality rate in women with nonpro-
teinuric hypertension compared with proteinuric pre-
eclampsia (31), in a cohort of 1,348 hypertensive
pregnant patients, the women with proteinuria progressed
more frequently to severe hypertension and had higher
rates of preterm birth and perinatal mortality; however,
women without proteinuria had a higher frequency of
thrombocytopenia or liver dysfunction (17). Women with
gestational hypertension who present with severe-range
blood pressures should be managed with the same
approach as for women with severe preeclampsia. Ges-
tational hypertension and preeclampsia may also be un-
distinguishable in terms of long-term cardiovascular
risks, including chronic hypertension (32).
Hemolysis, Elevated Liver Enzymes and
Low Platelet Count Syndrome
The clinical presentation of hemolysis, elevated liver
enzymes, and low platelet count (HELLP) syndrome is
one of the more severe forms of preeclampsia because it has
been associated with increased rates of maternal morbidity
and mortality (33). Although different diagnostic bench-
marks have been proposed (34), many clinicians use the
following criteria (35) to make the diagnosis: lactate dehy-
drogenase (LDH) elevated to 600 IU/L or more, aspartate
aminotransferase (AST) and alanine aminotransferase
(ALT) elevated more than twice the upper limit of normal,
and the platelets count less than 100,000 x 109/L. Although
HELLP syndrome is mostly a third-trimester condition, in
30% of cases it is first expressed or progresses postpartum.
Furthermore, HELLP syndrome may have an insidious and
atypical onset, with up to 15% of the patients lacking either
hypertension or proteinuria (36). In HELLP syndrome, the
main presenting symptoms are right upper quadrant pain
and generalized malaise in up to 90% of cases and nausea
and vomiting in 50% of cases (35, 37).
Eclampsia
Eclampsia is the convulsive manifestation of the hyper-
tensive disorders of pregnancy and is among the more
severe manifestations of the disease. Eclampsia is
defined by new-onset tonic-clonic, focal, or multifocal
seizures in the absence of other causative conditions such
as epilepsy, cerebral arterial ischemia and infarction,
intracranial hemorrhage, or drug use. Some of these
e3
alternative diagnoses may be more likely in cases in
which new-onset seizures occur after 48–72 hours post-
partum (38) or when seizures occur during administration
of magnesium sulfate.
Eclampsia is a significant cause of maternal death,
particularly in low-resource settings. Seizures may lead
to severe maternal hypoxia, trauma, and aspiration
pneumonia. Although residual neurologic damage is rare,
some women may have short-term and long-term con-
sequences such as impaired memory and cognitive
function, especially after recurrent seizures or uncor-
rected severe hypertension leading to cytotoxic edema or
infarction (39). Permanent white matter loss has been
documented on magnetic resonance imaging after
eclampsia in up to one fourth of women, however, this
does not translate into significant neurologic deficits
(39).
Eclampsia often (78–83% of cases) is preceded by
premonitory signs of cerebral irritation such as severe
and persistent occipital or frontal headaches, blurred
vision, photophobia, and altered mental status. However,
eclampsia can occur in the absence of warning signs or
symptoms (40, 41). Eclampsia can occur before, during,
or after labor. Of note, a significant proportion of women
(20–38%) do not demonstrate the classic signs of pre-
eclampsia (hypertension or proteinuria) before the sei-
zure episode (42). Headaches are believed to reflect the
development of elevated cerebral perfusion pressure,
cerebral edema, and hypertensive encephalopathy (43).
The term preeclampsia implies that the natural
history of patients with persistent hypertension and
significant proteinuria during pregnancy is to have
tonic–clonic seizures if no prophylaxis if instituted.
However, the results of two randomized placebo-
controlled trials indicate that seizure occurred in only
a small proportion of patients with preeclampsia (1.9%)
(44) or severe preeclampsia (3.2%) (45) allocated to the
placebo arm of both studies. It is also noteworthy that
there is a significant proportion of patients who had
abrupt-onset eclampsia without warning signs or symp-
toms (40). In a nationwide analysis of cases of eclampsia
in the United Kingdom, it was noted that in 38% of
eclamptic cases the seizure occurred without any prior
documentation of either hypertension or proteinuria in
the hospital setting (46). Thus, the notion that preeclamp-
sia has a natural linear progression from preeclampsia
without severe features to preeclampsia with severe fea-
tures and eventually to eclamptic convulsions is
inaccurate.
Nervous system manifestations frequently encoun-
tered in preeclampsia are headache, blurred vision,
scotomata, and hyperreflexia. Although uncommon,
temporary blindness (lasting a few hours to as long as
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a week) also may accompany preeclampsia with severe
features and eclampsia (47). Posterior reversible enceph-
alopathy syndrome (PRES) is a constellation of a range
of clinical neurologic signs and symptoms such as vision
loss or deficit, seizure, headache, and altered sensorium
or confusion (48). Although suspicion for PRES is
increased in the setting of these clinical features, the
diagnosis of PRES is made by the presence of vasogenic
edema and hyperintensities in the posterior aspects of the
brain on magnetic resonance imaging. Women are par-
ticularly at risk of PRES in the settings of eclampsia and
preeclampsia with headache, altered consciousness, or
visual abnormalities (49). Another condition that may
be confused with eclampsia or preeclampsia is reversible
cerebral vasoconstriction syndrome (50). Reversible
cerebral vasoconstriction syndrome is characterized by
reversible multifocal narrowing of the arteries of the
brain with signs and symptoms that typically include
thunderclap headache and, less commonly, focal neuro-
logic deficits related to brain edema, stroke, or seizure.
Treatment of women with PRES and reversible cerebral
vasoconstriction syndrome may include medical control
of hypertension, antiepileptic medication, and long-term
neurologic follow-up.
Pathophysiology
Several mechanisms of disease have been proposed in
preeclampsia (1, 51, 52), including the following:
chronic uteroplacental ischemia (53), immune maladap-
tation (53), very low-density lipoprotein toxicity (53),
genetic imprinting (53), increased trophoblast apoptosis
or necrosis (54, 55), and an exaggerated maternal inflam-
matory response to deported trophoblasts (56, 57). More
recent observations suggest a possible role for imbalan-
ces of angiogenic factors in the pathogenesis of pre-
eclampsia (58). It is possible that a combination of
some of these purported mechanisms may be responsible
for triggering the clinical spectrum of preeclampsia. For
example, there is clinical (59, 60) and experimental evi-
dence (61, 62) suggesting that uteroplacental ischemia
leads to increased circulating concentrations of antiangio-
genic factors and angiogenic imbalances (63).
Vascular Changes
In addition to hypertension, women with preeclampsia or
eclampsia typically lack the hypervolemia associated
with normal pregnancy; thus, hemoconcentration is
a frequent finding (64). In addition, the interaction of
various vasoactive agents, such as prostacyclin (vasodi-
lator), thromboxane A2 (potent vasoconstrictor), nitric
oxide (potent vasodilator), and endothelins (potent vaso-
constrictors) results in another significant change
OBSTETRICS & GYNECOLOGY
described in preeclampsia: intense vasospasm. Attempts
to correct the contraction of the intravascular space in
preeclampsia with vigorous fluid therapy are likely to
be ineffective and could be dangerous because of the
frequent capillary leak and decreased colloid oncotic
pressure often associated with preeclampsia. Aggressive
fluid therapy may result in elevation of the pulmonary
capillary wedge pressure and increased risk of pulmonary
edema. A study using invasive hemodynamic monitoring
in women with preeclampsia found that before intrave-
nous fluid therapy, women with preeclampsia had hyper-
dynamic ventricular function with low pulmonary
capillary wedge pressure (65). However, after aggressive
fluid therapy, the pulmonary capillary wedge pressure
increased significantly above normal levels (65) with
increased risk of pulmonary edema.
Hematologic Changes
Various hematologic changes also may occur in women
with preeclampsia, especially in preeclampsia with
severe features. Thrombocytopenia and hemolysis may
occur and may reach severe levels as part of HELLP
syndrome. Thrombocytopenia results from increased
platelet activation, aggregation, and consumption (66)
and is a marker of disease severity. A platelet count less
than 150,000 x 109/L is found in approximately 20% of
patients with preeclampsia, varying from 7% in cases
without severe manifestations to 50% in cases with
severe manifestations (67). However, reduced platelet
counts are not found in all cases of preeclampsia or
eclampsia (68). Interpretation of hematocrit levels in pre-
eclampsia should take into consideration that hemolysis
and hemoconcentration may occur (69). In some cases,
the hematocrit may not appear decreased despite hemo-
lysis because of baseline hemoconcentration. Lactate
dehydrogenase is present in erythrocytes in high concen-
tration. High serum concentrations of LDH (more than
600 IU/L) may be a sign of hemolysis (34, 35).
Hepatic Changes
Hepatic function may be significantly altered in women
with preeclampsia with severe features. Alanine amino-
transferase and AST may be elevated. Aspartate amino-
transferase is the dominant transaminase released into the
peripheral circulation in liver dysfunction due to pre-
eclampsia and is related to periportal necrosis. The fact
that AST is increased to a greater extent than ALT, at
least initially, may help in distinguishing preeclampsia
from other potential causes of parenchymal liver disease
in which ALT usually is higher than AST. Increased
serum levels of LDH in preeclampsia are caused by
hepatic dysfunction (LDH derived from ischemic, or
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necrotic tissues, or both) and hemolysis (LDH from red
blood cell destruction). Increase in bilirubin secondary to
significant hemolysis may develop only in the late stages
of the disease. Similarly, alterations in hepatic synthetic
function, as reflected by abnormalities of prothrombin
time, partial prothrombin time, and fibrinogen, usually
develop in advanced preeclampsia. Evaluation of these
coagulation parameters is probably only useful when the
platelet count is below 150,000 x 109/L, there is signif-
icant liver dysfunction, or there is suspected placental
abruption (70).
Renal Changes
The histopathologic renal changes classically described
in preeclampsia as glomerular endotheliosis consist of
swollen, vacuolated endothelial cells with fibrils, swollen
mesangial cells, subendothelial deposits of protein re-
absorbed from the glomerular filtrate, and tubular casts
(71, 72). Proteinuria in preeclampsia is nonselective, as
a result of increased tubular permeability to most large-
molecular-weight proteins (albumin, globulin, transfer-
rin, and hemoglobin). Urinary calcium decreases because
of an increased tubular reabsorption of calcium.
In women with preeclampsia, contraction of the
intravascular space secondary to vasospasm leads to
worsening renal sodium and water retention (73). The
normal increase in renal blood flow and glomerular fil-
tration rate and the expected decrease in serum creatinine
may not occur in women with preeclampsia, especially if
the disease is severe. Preeclampsia with severe features
may include acute renal deterioration as part of the clin-
ical spectrum. Oliguria in severe preeclampsia is a conse-
quence of intrarenal vasospasm with an approximate
25% reduction in glomerular filtration rate. In these pa-
tients, transient oliguria (less than 100 mL over 4 hours)
is a common observation in labor or the first 24 hours of
the postpartum period. Plasma concentrations of uric acid
normally increase in late pregnancy, and this is thought
to be due to increased rates of fetal or placental produc-
tion, or both, decreased binding to albumin, and
a decrease in uric acid clearance. The serum uric acid
concentration increases to a greater extent in preeclamp-
sia (74). The most commonly accepted explanation for
hyperuricemia in preeclampsia, besides increased pro-
duction, is the increased reabsorption and decreased
excretion of uric acid in the proximal renal tubules.
Fetal Consequences
As a result of impaired uteroplacental blood flow
secondary to failure of physiologic transformation of
the spiral arteries or placental vascular insults, or both,
manifestations of preeclampsia also may be seen in the
e5
fetal–placental unit (63). Abnormalities in the placental
bed and subsequent failure of physiologic transformation
of the spiral arteries in the first or early second trimester
(75, 76) limit the blood flow to the uteroplacental unit.
Additional mechanisms for chronic uteroplacental
ischemia include placental vascular insults (77, 78).
Among women with preeclampsia, clinical manifes-
tations that follow from this uteroplacental ischemia
include fetal growth restriction, oligohydramnios, pla-
cental abruption, and nonreassuring fetal status demon-
strated on antepartum surveillance. Consequently, fetuses
of women with preeclampsia are at increased risk of
spontaneous or indicated preterm delivery.
Clinical Considerations
and Recommendations
< Are there screening methods that are useful to iden-
tify women at risk of developing hypertensive disor-
ders of pregnancy?
Several studies have evaluated the role of biochemical
markers or a combination of biochemical and biophysical
markers in the prediction of preeclampsia in the first and
second trimesters of pregnancy (79). Regardless of the
parameters used, screening for preeclampsia in low-risk
women is associated with very low positive predictive
values ranging from 8% to 33% (79). Thus, most
screen-positive patients will not develop the disease
and any prophylactic intervention in the screen-positive
group would unnecessarily expose a large number of
patients who would not benefit from these interventions.
In general, the sensitivity and specificity for the
prediction of early-onset preeclampsia using first-
trimester (80–82) and second-trimester biochemical (81,
83) or biophysical parameters (84–87) are better than for
late-onset preeclampsia. The reason for this is still
unclear but it is possible that the timing of the insults
to the fetal supply line or the fetal response to these
insults may be different between early-onset and late-
onset preeclampsia. Even so, there is limited evidence
that an accurate prediction of early-onset preeclampsia
can be followed by interventions that improve maternal
or fetal outcome.
Regardless of the index or combinations of indices
used, uterine artery Doppler studies alone have a low
predictive value for the development of early-onset
preeclampsia and an even lower value for late-onset
preeclampsia (88). Extensive work has identified some
angiogenic factors (soluble fms-like tyrosine kinase-
[sFlt-1], placental growth factor [PlGF], and soluble
endoglin) in the second trimester as likely tools for
the prediction of early-onset preeclampsia. However,
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no single test reliably predicts preeclampsia and further
prospective investigation is required to demonstrate
clinical utility. In the first trimester of pregnancy, it
has been reported that a combination of low maternal
serum concentrations of PlGF, high uterine artery pul-
satility index, and other maternal parameters, identified
93.1% of patients who would develop preeclampsia
requiring delivery before 34 weeks of gestation (82).
However, the results of this study are based on mathe-
matical modeling derived from a nested case2control
study applied to a large cohort of almost 7,800 patients
in which PlGF was measured only in the case2control
group. The calculated positive predictive value was only
21.2%, indicating that approximately 79% of the
women in the screen-positive group would not develop
hypertensive disorders during pregnancy (82). Of note,
a similar algorithm underperformed in a subsequent ran-
domized trial performed by the same research group
(89). Thus, biomarkers and ultrasonography cannot
accurately predict preeclampsia and should remain
investigational.
< Are there prevention strategies for reducing the risk
of hypertensive disorders of pregnancy?
Strategies to prevent preeclampsia have been studied
extensively over the past 30 years. To date, no interven-
tion has been proved unequivocally effective at elimi-
nating the risk of preeclampsia. With regard to nutritional
interventions, evidence is insufficient to demonstrate
effectiveness for vitamins C and E (90), fish oil (91),
garlic supplementation (92), vitamin D (93), folic acid,
(94) or sodium restriction (95) for reducing the risk of
preeclampsia. A meta-analysis of 13 trials (15,730
women) reported a significant reduction in preeclampsia
with calcium supplementation, with the greatest effect
among women with low-baseline calcium intake (96).
Yet, this is not the case in the United States or other
developed countries. Likewise, data do not support effec-
tiveness of bed rest and, thus, it should not routinely be
recommended (97).
Investigators hypothesized that an imbalance in
prostacyclin and thromboxane A2 metabolism was
involved in the pathogenesis of preeclampsia, leading
to the initial studies of aspirin for preeclampsia preven-
tion because of its preferential inhibition of thromboxane
A2 at lower doses (98, 99). In a recent meta-analysis of
aggregate data from 45 randomized trials, only a modest
reduction in preeclampsia was noted when low-dose
aspirin was started after 16 weeks of gestation (relative
risk [RR], 0.81; 95% CI, 0.66–0.99) but a more signifi-
cant reduction in severe preeclampsia (RR, 0.47; 95% CI,
0.26–0.83) and fetal growth restriction (RR, 0.56; 95%
CI, 0.44–0.70) was demonstrated when low-dose aspirin
OBSTETRICS & GYNECOLOGY
was started before 16 weeks of gestation (100). In con-
trast, in pooled individual data from 31 high-quality ran-
domized trials, the beneficial effects of low-dose aspirin
were consistent, whether treatment was started before or
after 16 weeks of gestation (101). Women with any of the
high-risk factors for preeclampsia (previous pregnancy
with preeclampsia, multifetal gestation, renal disease,
autoimmune disease, type 1 or type 2 diabetes mellitus,
and chronic hypertension) and those with more than one
of the moderate-risk factors (first pregnancy, maternal
age of 35 years or older, a body mass index [BMI; cal-
culated as weight in kilograms divided by height in me-
ters squared] of more than 30, family history of
preeclampsia, sociodemographic characteristics, and per-
sonal history factors) should receive low-dose (81 mg/
day) aspirin for preeclampsia prophylaxis initiated
between 12 weeks and 28 weeks of gestation (optimally
before 16 weeks of gestation) and continuing until deliv-
ery (Table 1).
In a recent multicenter, double blind, placebo-
controlled trial, pregnant women at increased risk of
preterm preeclampsia (less than 37 weeks of gestation)
were randomly assigned to receive aspirin, at a higher
dose (150 mg/day), or placebo from 11 weeks to 14
weeks of gestation until 36 weeks of gestation (89).
Preterm preeclampsia occurred in 1.6% of the partic-
ipants in the aspirin group, as compared with 4.3% in
the placebo group (odds ratio, 0.38; 95% CI,
0.2020.74; P5.004). The authors also reported that
there were no significant differences in the incidence
of neonatal adverse outcomes between groups. The
authors concluded that low-dose aspirin in women at
high risk of preeclampsia was associated with a lower
incidence for preterm preeclampsia. However, there
were no differences in the rates of term preeclampsia
between study groups. Of note, as a possible study
limitation, the prevalence of preterm preeclampsia in
the placebo group was one half of that expected for

Table 1. Clinical Risk Factors and Aspirin Use*

Level of
Risk Risk Factors Recommendation

High†
History of preeclampsia, especially when Recommend low-dose aspirin if the patient
accompanied by an adverse outcome has one or more of these high-risk factors

Multifetal gestation

Chronic hypertension

Type 1 or 2 diabetes

Renal disease

Autoimmune disease (ie, systemic lupus
erythematosus, the antiphospholipid syndrome)
Moderatez
Nulliparity Consider low-dose aspirin if the patient has

Obesity (body mass index greater than 30) more than
§
one of these moderate-risk
factors

Family history of preeclampsia (mother or sister)

Sociodemographic characteristics (African American
race, low socioeconomic status)

Age 35 years or older

Personal history factors (eg, low birth weight or small
for gestational age, previous adverse pregnancy
outcome, more than 10-year pregnancy interval)
Low
Previous uncomplicated full-term delivery Do not recommend low-dose aspirin
*Includes only risk factors that can be obtained from the patient’s medical history. Clinical measures, such as uterine artery
Doppler ultrasonography, are not included.
†
Single risk factors that are consistently associated with the greatest risk of preeclampsia. The preeclampsia incidence rate
would be approximately 8% or more in a pregnant woman with one or more of these risk factors.
z
A combination of multiple moderate-risk factors may be used by clinicians to identify women at high risk of preeclampsia. These
risk factors are independently associated with moderate risk of preeclampsia, some more consistently than others.
§
Moderate-risk factors vary in their association with increased risk of preeclampsia.
Modified from LeFevre, ML. U.S. Preventive Services Task Force. Low-dose aspirin use for the prevention of morbidity and mortality
from preeclampsia: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med 2014;161(11):819–26.

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Copyright ª by the American College of Obstetricians

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Unauthorized reproduction of this article is prohibited.
a high-risk population based on first-trimester param-
eters (89).
The use of metformin for the prevention of pre-
eclampsia has been suggested. In a meta-analysis of five
randomized controlled trials comparing metformin treat-
ment (n5611) with placebo and control (n5609), no
difference in the risk of preeclampsia was found
(combined/pooled risk ratio, 0.86; 95% CI, 0.33–2.26;
P5.76; I2566%) (102). Because preeclampsia was a sec-
ondary outcome in most studies in this meta-analysis, the
effect of metformin needs to be assessed by a study de-
signed to evaluate the reduction in the prevalence of pre-
eclampsia as a primary endpoint. In the meantime, the
use of metformin for the prevention of preeclampsia re-
mains investigational, as is the use of sildenafil and sta-
tins (103–105). These drugs are not recommended for
this indication outside of the context of clinical trials.
< What is the optimal treatment for women with ges-
tational hypertension or preeclampsia?
Delivery Versus Expectant Management
At the initial evaluation, a complete blood count with
platelet estimate, serum creatinine, LDH, AST, ALT, and
testing for proteinuria should be obtained in parallel with
a comprehensive clinical maternal and fetal evaluation.
In the settings of diagnostic dilemmas, such as in the
evaluation of possible preeclampsia superimposed upon
chronic hypertension, a uric acid test may be considered.
Fetal evaluation should include ultrasonographic evalu-
ation for estimated fetal weight and amount of amniotic
fluid, as well as fetal antepartum testing. Subsequent
management will depend on the results of the evaluation
and gestational age. The decision to deliver must balance
the maternal and fetal risks.
Continued observation is appropriate for a woman
with a preterm fetus if she has gestational hypertension or
preeclampsia without severe features (21). There are no
randomized controlled trials in this population, but retro-
spective data suggest that without severe features, the
balance should be in favor of continued monitoring until
delivery at 37 0/7 weeks of gestation in the absence of
abnormal antepartum testing, preterm labor, preterm prel-
abor rupture of membranes (also referred to as premature
rupture of membranes) or vaginal bleeding, for neonatal
benefit (106). The risks associated with expectant man-
agement in the late preterm period include the develop-
ment of severe hypertension, eclampsia, HELLP
syndrome, placental abruption, fetal growth restriction
and fetal death; however, these risks are small and coun-
terbalanced by the increased rates of admission to the
neonatal intensive care unit, neonatal respiratory compli-
cations and neonatal death that would be associated with
e8 Practice Bulletin Gestational Hypertension and Preeclampsia
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delivery before 37 0/7 weeks of gestation (39). In the
HYPITAT trial, women with gestational hypertension
and preeclampsia without severe features after 36 weeks
of gestation were allocated to expectant management or
induction of labor. The latter option was associated with
a significant reduction in a composite of adverse maternal
outcome including new-onset severe preeclampsia,
HELLP syndrome, eclampsia, pulmonary edema, or pla-
cental abruption (RR, 0.71; 95% CI, 0.59–0.86) (107). In
addition, no differences in rates of neonatal complica-
tions or cesarean delivery were reported by the authors
(107).
Continued monitoring of women with gestational
hypertension or preeclampsia without severe features
consists of serial ultrasonography to determine fetal
growth, weekly antepartum testing, close monitoring of
blood pressure, and weekly laboratory tests for pre-
eclampsia. The frequency of these tests may be modified
based on clinical findings and patient symptoms. Fol-
lowing the initial documentation of proteinuria and the
establishment of the diagnosis of preeclampsia, addi-
tional quantifications of proteinuria are no longer neces-
sary. Although the amount of proteinuria is expected to
increase over time with expectant management, this
change is not predictive of perinatal outcome and should
not influence the management of preeclampsia (108,
109). Women should be advised to immediately report
any persistent, concerning, or unusual symptoms. In
women with gestational hypertension without severe fea-
tures, when there is progression to preeclampsia with
severe features, this progression usually takes 1–3 weeks
after diagnosis, whereas in women with preeclampsia
without severe features, the progression to severe pre-
eclampsia could happen within days (72). Gestational
hypertension and preeclampsia are known risk factors
for fetal death and antenatal testing is indicated. How-
ever, limited-to-no data exist regarding when to start
testing, the frequency of testing, and which test to use.
In women with gestational hypertension or preeclampsia
without severe features at or beyond 37 0/7 weeks of
gestation, delivery rather than expectant management
upon diagnosis is recommended.
Preeclampsia with severe features can result in acute
and long-term complications for the woman and her
newborn. Maternal complications include pulmonary
edema, myocardial infarction, stroke, acute respiratory
distress syndrome, coagulopathy, renal failure, and
retinal injury. These complications are more likely to
occur in the presence of preexistent medical disorders.
The clinical course of preeclampsia with severe features
is characterized by progressive deterioration of maternal
and fetal condition. Therefore, delivery is recommended
when gestational hypertension or preeclampsia with
OBSTETRICS & GYNECOLOGY

Box 4. Conditions Precluding Expectant
Management∗
Maternal
c Uncontrolled severe-range blood pressures (per-
sistent systolic blood pressure 160 mm Hg or
more or diastolic blood pressure 110 mm Hg or
more not responsive to antihypertensive
medication
c Persistent headaches, refractory to treatment
c Epigastric pain or right upper pain unresponsive
to repeat analgesics
c Visual disturbances, motor deficit or altered
sensorium
c Stroke
c Myocardial infarction
c HELLP syndrome
c New or worsening renal dysfunction (serum cre-
atinine greater than 1.1 mg/dL or twice baseline)
c Pulmonary edema
c Eclampsia
c Suspected acute placental abruption or vaginal
bleeding in the absence of placenta previa
Fetal
c Abnormal fetal testing
c Fetal death
c Fetus without expectation for survival at the time
of maternal diagnosis (eg, lethal anomaly,
extreme prematurity)
c Persistent reversed end-diastolic flow in the
umbilical artery
Abbreviation: HELLP, hemolysis, elevated liver enzymes,
and low platelet count.
∗In some cases, a course of antenatal steroids can be
considered depending on gestational age and maternal
severity of illness.
Data from Balogun OA, Sibai BM. Counseling, manage-
ment, and outcome in women with severe preeclampsia
at 23 to 28 weeks’ gestation. Clin Obstet Gynecol
2017;60:183–9.
severe features (Box 3) is diagnosed at or beyond 34 0/7
weeks of gestation, after maternal stabilization or with
labor or prelabor rupture of membranes. Delivery should
not be delayed for the administration of steroids in the
late preterm period.
In women with preeclampsia with severe features
at less than 34 0/7 weeks of gestation, with stable
maternal and fetal condition, expectant management
may be considered. Two randomized controlled trials
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of delivery versus expectant management of preterm
preeclampsia with severe features demonstrated that
expectant management is associated with higher ges-
tational age at delivery and improved neonatal out-
comes (110, 111). These observations were reiterated
by a Cochrane systematic review (112). The limited
available randomized data are consistent with observa-
tional evidence suggesting that expectant management
of early preeclampsia with severe features prolongs
pregnancy by 1–2 weeks, has low maternal risk, and
improves neonatal outcomes (113). In contrast, in
a multicenter randomized controlled trial in Latin
America, the authors found no neonatal benefit with
expectant management of preeclampsia with severe
features from 28 weeks to 34 weeks of gestation
(114). These different results may reflect the limita-
tions in neonatal intensive care in low-resource
settings.
Embarking on a course of expectant management
necessitates adherence to principles of shared decision
making with discussions of maternal and fetal risks and
benefits, appropriate resources (levels of care), and
ongoing vigilant surveillance. Close maternal and fetal
clinical monitoring is necessary, and laboratory testing
(complete blood count including platelets, liver enzymes,
and serum creatinine) should be performed serially (115).
The expectant management of preeclampsia with
severe features before 34 0/7 weeks of gestation is based
on strict selection criteria of those appropriate candidates
and is best accomplished in a setting with resources
appropriate for maternal and neonatal care (116).
Because expectant management is intended to provide
neonatal benefit at the expense of maternal risk, expec-
tant management is not advised when neonatal survival is
not anticipated. During expectant management, delivery
is recommended at any time in the case of deterioration
of maternal or fetal condition, which may include some
of the criteria in Box 4. Indications for expedited delivery
irrespective of gestational age after maternal stabilization
are described in Box 4 (115).
If delivery is indicated at less than 34 0/7 weeks of
gestation, administration of corticosteroids for fetal lung
maturation is recommended (115); however, delaying
delivery for optimal corticosteroid exposure may not
always be advisable. Maternal or fetal deterioration
may preclude completion of the course of steroid treat-
ment. Previously, fetal growth restriction was considered
an indication for delivery. In the setting of normal fetal
parameters (eg, amniotic fluid volume, Doppler findings,
antenatal fetal testing), continuation of expectant man-
agement may be reasonable in the absence of other,
aforementioned maternal and fetal criteria.
Practice Bulletin Gestational Hypertension and Preeclampsia e9
Inpatient Versus
Outpatient Management
Ambulatory management at home is an option only for
women with gestational hypertension or preeclampsia
without severe features and requires frequent fetal and
maternal evaluation. Hospitalization is appropriate for
women with severe features and for women in whom
adherence to frequent monitoring is a concern. Because
assessment of blood pressure is essential for this clinical
condition, health care providers are encouraged to follow
the recommendations from regulatory bodies regarding
the proper technique for blood pressure measurement.
Having a blood pressure cuff that is too small or too large
may result in erroneous evaluations. To reduce inaccurate
readings, an appropriate size cuff should be used (length
1.5 times upper arm circumference or a cuff with
a bladder that encircles 80% or more of the arm). The
blood pressure level should be taken with an
appropriately-sized cuff with the patient in an upright
position after a 10-minute or longer rest period. For
patients in the hospital, the blood pressure can be taken
with either the patient sitting up or in the left lateral
recumbent position with the patient’s arm at the level of
the heart (117). The patient should not use tobacco or
caffeine for 30 minutes preceding the measurement
because these agents can temporarily lead to increased
blood pressure (118).
If home management is selected, frequent fetal and
maternal evaluation are required. No randomized trials
have determined the best tests for fetal or maternal
evaluation. Among women with gestational hypertension
or preeclampsia without severe features, expectant man-
agement up to 37 0/7 weeks of gestation is recommen-
ded, during which frequent fetal and maternal evaluation
is recommended. Fetal monitoring consists of ultraso-
nography to determine fetal growth every 3–4 weeks of
gestation and amniotic fluid volume assessment at least
once weekly. In addition, an antenatal test one-to-two
times per week for patients with gestational hypertension
or preeclampsia without severe features is recommended.
Maternal evaluation consists primarily of frequent
evaluation for either the development of or worsening of
preeclampsia. In women with gestational hypertension or
preeclampsia without severe features, weekly evaluation
of platelet count, serum creatinine, and liver enzyme
levels is recommended. In addition, for women with
gestational hypertension, once weekly assessment of
proteinuria is recommended. However, these tests should
be repeated sooner if disease progression is a concern. In
addition, women should be asked about symptoms of
preeclampsia with severe features (eg, severe headaches,
visual changes, epigastric pain, and shortness of breath).
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Blood pressure measurements and symptom assessment
are recommended serially, using a combination of in-
clinic and ambulatory approaches, with at least one visit
per week in-clinic.
Intrapartum Management
In addition to appropriate management of labor and
delivery, the two main goals of management of women
with preeclampsia during labor and delivery are 1)
prevention of seizures and 2) control of hypertension.
Seizure Prophylaxis
The prevention of eclampsia is empirically based on the
concept of timely delivery, as previously discussed, once
preeclampsia has been diagnosed. A significant body of
evidence attests to the efficacy of magnesium sulfate to
prevent seizures in women with preeclampsia with severe
features and eclampsia. In the Magpie study, a random-
ized placebo-controlled trial with 10,110 participants
(two thirds originating from developing countries), the
seizure rate was reduced overall by more than one half
with this treatment. It is interesting to note that the
reduction in the rate of eclampsia was not statistically
significant in the subset of women enrolled in high-
resource countries in the Western world (RR, 0.67; 95%
CI, 0.19–2.37) (44). In a subsequent systematic review
that included the Magpie study and five other studies,
magnesium sulfate compared with placebo more than
halved the risk of eclampsia (RR, 0.41; 95% CI, 0.29–
0.58), reduced the risk of placental abruption (RR, 0.64;
95% CI, 0.50–0.83), and reduced the risk of maternal
mortality albeit nonsignificantly (RR, 0.54; 95% CI,
0.26–1.10). There were no differences in maternal mor-
bidity or perinatal mortality. A quarter of women re-
ported adverse effects with magnesium sulfate,
primarily hot flushes, and the rate of cesarean delivery
was increased by 5% when magnesium sulfate was used
(119).
There is no consensus regarding the prophylactic use
of magnesium sulfate for the prevention of seizures in
women with gestational hypertension or preeclampsia
without severe features. Two small randomized trials
(total n5357) allocated women with preeclampsia with-
out severe features to either placebo or magnesium sul-
fate and reported no cases of eclampsia among women
allocated to placebo and no significant differences in the
proportion of women that progressed to severe pre-
eclampsia (120, 121). However, given the small sample
size, the results of these studies cannot be used for clin-
ical guidance (122, 123).
The rate of seizures in preeclampsia with severe
features without magnesium sulfate prophylaxis is four
OBSTETRICS & GYNECOLOGY
times higher than in those without severe features (4 in
200 versus 1 in 200). It has been calculated that 129
women need to be treated to prevent one case of
eclampsia in asymptomatic cases, whereas in symptom-
atic cases (severe headache, blurred vision, photophobia,
hyperreflexia, epigastric pain), the number needed to
treat is 36 (124). The evidence regarding the benefit-to-
risk ratio of magnesium sulfate prophylaxis is less sup-
portive of routine use in preeclampsia without severe
features (122). The clinical decision of whether to use
magnesium sulfate for seizure prophylaxis in patients
with preeclampsia without severe features should be
determined by the physician or institution, considering
patient values or preferences, and the unique risk-
benefit trade-off of each strategy. Although the benefit-
to-risk ratio for routine prophylaxis is less compelling for
patients in high resource settings, it is recommended that
magnesium sulfate should be used for the prevention and
treatment of seizures in women with gestational hyper-
tension and preeclampsia with severe features or eclamp-
sia (124, 125).
Magnesium sulfate is more effective than phenytoin,
diazepam, or nimodipine (a calcium-channel blocker
used in clinical neurology to reduce cerebral vasospasm)
in reducing eclampsia and should be considered the drug
of choice in the prevention of eclampsia in the intra-
partum and postpartum periods (119, 126, 127). Benzo-
diazepines and phenytoin are justified only in the context
of antiepileptic treatment or when magnesium sulfate is
contraindicated or unavailable (myasthenia gravis, hypo-
calcemia, moderate-to-severe renal failure, cardiac ische-
mia, heart block, or myocarditis).
There are still sparse data regarding the ideal dosage
of magnesium sulfate. Even the therapeutic range of 4.8–
9.6 mg/dL (4–8 mEq/L) quoted in the literature is ques-
tionable (128, 129). Although there is a relationship
between toxicity and plasma concentration of magne-
sium, with higher infusion rates increasing the potential
for toxicity, the accurate magnesium concentration clin-
ically effective in prevention of eclampsia has not been
established. Seizures occur even with magnesium at
a therapeutic level, whereas several trials using infusion
rates of 1 g/hour, frequently associated with subtherapeu-
tic magnesium levels, were able to significantly reduce
the rate of eclampsia or recurrent convulsions (44, 130).
Further complicating aspects are that steady magnesium
levels are reached more slowly during the antepartum
period than postpartum period. Larger volume of distri-
bution and higher BMI also affect the dosage and dura-
tion needed to reach adequate circulating levels. It has
been reported in patients with a high BMI (especially
greater than 35) that the antepartum level of magnesium
may remain subtherapeutic for as long as 18 hours after
VOL. 133, NO. 1, JANUARY 2019 Practice Bulletin Gestational Hypertension and Preeclampsia
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Unauthorized reproduction of this article is prohibited.
infusion initiation when an intravenous loading dose of
4.5 g followed by 1.8 g/hour is used (131). However,
infusion rates in excess of 2 g/hour have been associated
with increased perinatal mortality in a systematic review
of randomized studies of magnesium sulfate used for
tocolysis (132). These data may be considered supportive
for the regimen generally preferred in the United States
(intravenous [IV] administration of a 4–6 g loading dose
over 20–30 minutes, followed by a maintenance dose of
1–2 g/hour). For women requiring cesarean delivery
(before onset of labor), the infusion should ideally begin
before surgery and continue during surgery, as well as for
24 hours afterwards. For women who deliver vaginally,
the infusion should continue for 24 hours after delivery.
In case of difficulties with establishing venous access,
magnesium sulfate can be administered by intramuscular
(IM) injection, 10 g initially as a loading dose (5 g IM in
each buttock), followed by 5 g every 4 hours. The
medication can be mixed with 1 mL of xylocaine 2%
solution because the intramuscular administration is
painful. The rate of adverse effects is also higher with the
intramuscular administration (44). The adverse effects of
magnesium sulfate (respiratory depression and cardiac
arrest) come largely from its action as a smooth muscle
relaxant. Deep tendon reflexes are lost at a serum mag-
nesium level of 9 mg/dL (7 mEq/L), respiratory depres-
sion occurs at 12 mg/dL (10 mEq/L), and cardiac arrest at
30 mg/dL (25 mEq/L). Accordingly, provided deep ten-
don reflexes are present, more serious toxicity is avoided.
(Table 2) Because magnesium sulfate is excreted almost
exclusively in the urine, measuring urine output should
be part of the clinical monitoring, in addition to moni-
toring of respiration status and tendon reflexes. If renal
function is impaired, serum magnesium levels will
increase quickly, which places the patient at risk of sig-
nificant adverse effects. In patients with mild renal failure
(serum creatinine 1.0–1.5 mg/dL) or oliguria (less than
30 mL urine output per hour for more than 4 hours), the
loading dose of 4–6 g should be followed by a mainte-
nance dose of only 1 gm/hour. Using a lower loading
dose, such as 4 g, may be associated with subtherapeutic
levels for at least 4 hours after loading (133). In cases
with renal dysfunction, laboratory determination of
serum magnesium levels every 4 hours becomes neces-
sary. If the serum level exceeds 9.6 mg/dL (8 mEq/L),
the infusion should be stopped and serum magnesium
levels should be determined at 2-hour intervals. The infu-
sion can be restarted at a lower rate when the serum level
decreases to less than 8.4 mg/dL (7 mEq/L) (133). The
serum concentration of magnesium is related to the
occurrence of adverse effects and toxicities (see Table 2)
(128, 134). Patients at risk of impending respiratory
depression may require tracheal intubation and
e11
Table 2. Serum Magnesium Concentration and Toxicities

Serum Magnesium Concentration

mmol/L mEq/L mg/dL Effect

2–3.5 4–7 5–9 Therapeutic range

.3.5 .7 .9 Loss of patellar reflexes
.5 .10 .12 Respiratory paralysis
.12.5 .25 .30 Cardiac arrest
Data from Duley L. Magnesium sulphate regimens for women with eclampsia: messages from the Collaborative Eclampsia Trial. Br
J Obstet Gynaecol 1996;103:103–5 and Lu JF, Nightingale CH. Magnesium sulfate in eclampsia and preeclampsia: pharmacokinetic
principles. Clin Pharmacokinet 2000;38:305–14.

emergency correction with calcium gluconate 10% solu-
tion, 10 mL IV over 3 minutes, along with furosemide
intravenously to accelerate the rate of urinary excretion.
Antihypertensive Approach: Drugs and
Thresholds for Treatment
The objectives of treating severe hypertension are to
prevent congestive heart failure, myocardial ischemia,
renal injury or failure, and ischemic or hemorrhagic
stroke. Antihypertensive treatment should be initiated
expeditiously for acute-onset severe hypertension
(systolic blood pressure of 160 mm Hg or more or
diastolic blood pressure of 110 mm Hg or more, or
both) that is confirmed as persistent (15 minutes or
more). The available literature suggests that antihy-
pertensive agents should be administered within 30–
60 minutes. However, it is recommended to administer
antihypertensive therapy as soon as reasonably possi-
ble after the criteria for acute-onset severe hyperten-
sion are met. Intravenous hydralazine or labetalol and
oral nifedipine are the three agents most commonly
used for this purpose (see Table 3). A recent Cochrane
systematic review that involved 3,573 women found
no significant differences regarding either efficacy or
safety between hydralazine and labetalol or between
hydralazine and calcium channel blockers (135). Thus,
any of these agents can be used to treat acute severe
hypertension in pregnancy (135, 136). Although par-
enteral antihypertensive therapy may be needed ini-
tially for acute control of blood pressure, oral
medications can be used as expectant management is
continued. Oral labetalol and calcium channel blockers
have been commonly used. One approach is to begin
an initial regimen of labetalol at 200 mg orally every
12 hours and increase the dose up to 800 mg orally
every 8–12 hours as needed (maximum total 2,400 mg/
d). If the maximum dose is inadequate to achieve the
desired blood pressure goal, or the dosage is limited by
adverse effect, then short-acting oral nifedipine can be
added gradually.

Table 3. Antihypertensive Agents Used for Urgent Blood Pressure Control in Pregnancy

Onset of
Drug Dose Comments Action

Labetalol 10–20 mg IV, then 20–80 mg every Tachycardia is less common and fewer 1–2 minutes
10–30 minutes to a maximum cumulativeadverse effects.
dosage of 300 mg; or constant infusion
Avoid in women with asthma,
1–2 mg/min IV preexisting myocardial disease,
decompensated cardiac function, and
heart block and bradycardia.
Hydralazine 5 mg IV or IM, then 5–10 mg IV every Higher or frequent dosage associated 10–20 minutes
20–40 minutes to a maximum with maternal hypotension, headaches,
cumulative dosage of 20 mg; or constant and abnormal fetal heart rate tracings;
infusion of 0.5–10 mg/hr may be more common than other agents.
Nifedipine 10–20 mg orally, repeat in 20 minutes if May observe reflex tachycardia and 5–10 minutes
(immediate needed; then 10–20 mg every 2–6 hours; headaches
release) maximum daily dose is 180 mg
Abbreviations: IM, intramuscularly; IV, intravenously.

e12 Practice Bulletin Gestational Hypertension and Preeclampsia OBSTETRICS & GYNECOLOGY

Copyright ª by the American College of Obstetricians

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Unauthorized reproduction of this article is prohibited.
Monitoring for Disease Progression
Because the clinical course of gestational hypertension or
preeclampsia without severe features can evolve during
labor, all women with gestational hypertension or pre-
eclampsia without severe features who are in labor must
be monitored for early detection of progression to severe
disease. This should include monitoring of blood pres-
sure and symptoms during labor and delivery as well as
immediately after delivery. Magnesium sulfate therapy
should be initiated if there is progression to preeclampsia
with severe features. The evidence regarding the benefit-
to-risk ratio of magnesium sulfate prophylaxis is less
supportive of routine use in preeclampsia without severe
features (122). The clinical decision of whether to use
magnesium sulfate for seizure prophylaxis in patients
with preeclampsia without severe features should be
determined by the physician or institution, considering
patient values or preferences and the unique risk-
benefit trade-off of each strategy.
Mode of Delivery
The mode of delivery in women with gestational
hypertension or preeclampsia (with or without severe
features) should be determined by routine obstetric
considerations. Vaginal delivery often can be accom-
plished, but with labor induction in preeclampsia with
severe features this is less likely with decreasing
gestational age at diagnosis. The likelihood of cesarean
delivery at less than 28 weeks of gestation could be as
high as 97%, and at 28–32 weeks of gestation as high as
65% (137–139). For gestational hypertension or pre-
eclampsia without severe features, vaginal delivery is
preferred (137–139). Retrospective studies comparing
induction of labor with cesarean delivery in women with
preeclampsia with severe features remote from term con-
cluded that induction of labor was reasonable and was
not harmful to low-birth-weight infants (140, 141). The
decision to perform cesarean delivery should be individ-
ualized, based on anticipated probability of vaginal deliv-
ery and on the nature and progression of preeclampsia
disease state.
Anesthesia Considerations
With improved techniques over the past decades,
regional anesthesia has become the preferred technique
for women with preeclampsia with severe features and
eclampsia for labor and delivery. A secondary analysis of
women with preeclampsia with severe features in
a randomized trial of low-dose aspirin reported that
epidural anesthesia was not associated with an increased
rate of cesarean delivery, pulmonary edema, or renal
failure (142). Also, in a prospective study, the incidence
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Copyright ª by the American College of Obstetricians
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Unauthorized reproduction of this article is prohibited.
and severity of hypotension did not appear to be
increased with spinal anesthesia for cesarean delivery
in women with preeclampsia with severe features (n 5
65) compared with women without preeclampsia (143).
When the use of spinal or epidural anesthesia in
women with preeclampsia with severe features was
compared in a randomized trial (144), the incidence of
hypotension was higher in the spinal group (51% versus
23%) but was easily treated and of short duration (less
than 1 minute). General anesthesia carries more risk to
pregnant women than regional anesthesia does because
of the risk of aspiration, failed intubation because of
pharyngolaryngeal edema, and stroke secondary to
increased systemic and intracranial pressures during intu-
bation and extubation (145, 146). However, neuraxial
anesthesia and analgesia are contraindicated in the pres-
ence of a coagulopathy because of the potential for hem-
orrhagic complications (147). Thrombocytopenia also
increases the risk of epidural hematoma. There is no
consensus in regard to the safe lower-limit for platelet
count and neuraxial anesthesia. The literature offers only
limited and retrospective data to address this issue, but
a recent retrospective cohort study of 84,471 obstetric
patients from 19 institutions combined with a systematic
review of the medical literature support the assertion that
the risk of epidural hematoma from neuraxial anesthetics
in a parturient patient with a platelet count of more than
70 3 109/L is exceptionally low (less than 0.2%) (148).
Extrapolating this expanded data to previous recommen-
dations (149) would suggest that epidural or spinal anes-
thesia is considered acceptable, and the risk of epidural
hematoma is exceptionally low, in patients with platelet
counts of 70 3 109/L or more provided that the platelet
level is stable, there is no other acquired or congenital
coagulopathy, the platelet function is normal, and the
patient is not on any antiplatelet or anticoagulant therapy
(148, 149).
Magnesium sulfate has significant anesthetic impli-
cations because it prolongs the duration of nondepolariz-
ing muscle relaxants. However, women with
preeclampsia who require cesarean delivery should
continue magnesium sulfate infusion during the delivery.
This recommendation is based on the observation that
magnesium sulfate half-life is 5 hours and that discon-
tinuation of the infusion of magnesium sulfate before
cesarean delivery would only minimally reduce magne-
sium concentration at the time of delivery while possibly
increasing the risk of seizure (150). Women with pre-
eclampsia with severe features undergoing cesarean
delivery remain at risk of developing eclampsia. The
induction of general anesthesia and the stress of delivery
may even reduce the seizure threshold and increase the
likelihood of eclampsia in the immediate postpartum
e13
period if the infusion of magnesium sulfate is stopped sulfate is not necessary to arrest the seizure but to
during delivery. prevent recurrent convulsions.
During eclamptic seizures, there are usually pro-
Postpartum Hypertension and longed fetal heart rate decelerations, even fetal brady-
Postpartum Headache cardia, and sometimes an increase in uterine contractility
and baseline tone. After a seizure, because of maternal
Postpartum hypertension and preeclampsia are either
hypoxia and hypercarbia, the fetal heart rate tracing may
persistent or exacerbated hypertension in women with
show recurrent decelerations, tachycardia, and reduced
previous hypertensive disorders of pregnancy or a new-
variability. However, only after maternal hemodynamic
onset condition. It is important to increase the awareness
stabilization should one proceed with delivery. Further-
among health care providers and to empower patients to
more, maternal resuscitation is usually followed by
seek medical advice if symptoms that precede eclampsia,
normalization of the fetal tracing.
hypertensive encephalopathy, pulmonary edema, or
Cochrane reviews, including data originating from
stroke are noted in the postpartum period. Most women
developing countries, indicate a significant reduction in
who present with eclampsia and stroke in the postpartum
recurrent seizures and eclampsia-related maternal mor-
period have these symptoms for hours or days before
tality with the use of magnesium sulfate. Magnesium
presentation (151–154). Some common medications and
sulfate administered intramuscularly or intravenously is
substances used in the postpartum period may potentially
superior to phenytoin, diazepam, or lytic cocktail (usu-
aggravate hypertension through three major mechanisms:
ally chlorpromazine, promethazine, and pethidine) and
volume retention, sympathomimetic activation, and
also is associated with less maternal and neonatal
direct vasoconstriction. Of particular interest are
morbidity (126, 158, 159). Thus, these data support the
nonsteroidal antiinflammatory drugs (NSAIDs), which
use of magnesium sulfate as the drug of choice to prevent
are frequently prescribed as postpartum analgesics.
recurrent seizures in women with eclampsia. In the rare
These medications decrease prostaglandins leading to
cases of an extremely agitated patient, IV clonazepam 1
a lack of vasodilation and increased sodium retention.
mg, diazepam 10 mg, or midazolam may be used for
Nonsteroidal anti-inflammatory medications should con-
sedation to facilitate the placement of the IV lines and
tinue to be used preferentially over opioid analgesics;
Foley catheter, and the collection of blood specimens.
however, women with chronic hypertension may theoret-
These drugs should be used cautiously and only if abso-
ically require intensification of blood pressure monitor-
lutely necessary because they inhibit laryngeal reflexes,
ing and regimen adjustments when on these medications.
increasing the risk of aspiration and also may depress the
Overall, data support the safe use of NSAIDs in post-
central respiratory centers leading to apnea.
partum patients with blood pressure issues. In a random-
Women with eclampsia should be delivered in
ized trial comparing use of ibuprofen to acetaminophen
a timely fashion. However, eclampsia by itself is not an
in postpartum patients with preeclampsia with severe
indication for cesarean delivery. Once the patient is
features, ibuprofen did not lengthen the duration of
stabilized, the method of delivery should depend, in part,
severe-range blood pressures (155). In a cohort of 399
on factors such as gestational age, fetal presentation, and
patients with preeclampsia with severe features, there
the findings of the cervical examination. A high rate of
was no association of NSAID use with postpartum blood
failure may be anticipated with induction or augmenta-
pressure elevations (156). Further, another cohort study
tion in pregnancies less than 30 weeks of gestation if the
of postpartum patients on magnesium for seizure prophy-
patient is not in active labor and the Bishop score is
laxis for preeclampsia did not show differences in blood
unfavorable. In these cases, it may be preferable to opt
pressure, antihypertensive requirements, or other adverse
for cesarean delivery without further delay. However,
events for patients managed with NSAIDs in the post-
patients that adequately progress in labor could be
partum period (157).
allowed to continue labor even after an eclamptic seizure.
< What is the optimal treatment for eclampsia? It has been proposed that when convulsions recur,
The initial steps in the management of a woman with a further 2–4 grams of magnesium sulfate could be
eclampsia are basic supportive measures such as calling administered IV over 5 minutes (130). In cases refractory
for help, prevention of maternal injury, placement in to magnesium sulfate (still seizing at 20 minutes after the
lateral decubitus position, prevention of aspiration, bolus or more than two recurrences), a health care pro-
administration of oxygen, and monitoring vital signs vider can use sodium amobarbital (250 mg IV in 3 mi-
including oxygen saturation. Only subsequently is atten- nutes), thiopental, or phenytoin (1,250 mg IV at a rate of
tion directed to the administration of magnesium sulfate. 50 mg/minute). Endotracheal intubation and assisted ven-
Most eclamptic seizures are self-limited. Magnesium tilation in the intensive care unit are appropriate in these

e14 Practice Bulletin Gestational Hypertension and Preeclampsia OBSTETRICS & GYNECOLOGY

Copyright ª by the American College of Obstetricians

and Gynecologists. Published by Wolters Kluwer Health, Inc.
Unauthorized reproduction of this article is prohibited.
circumstances. Head imaging should also be considered
because most of cases refractory to magnesium sulfate
therapy may prove to have abnormal findings on brain
imaging (160).
< What is the management of acute complications for
preeclampsia with HELLP?
The clinical course of HELLP syndrome often is
characterized by progressive and sometimes sudden
deterioration in maternal and fetal condition. Considering
the serious nature of this entity, with increased rates of
maternal morbidity and mortality, many authors have
concluded that women with HELLP syndrome should be
delivered regardless of their gestational age. Because the
management of patients with HELLP syndrome requires
the availability of neonatal and obstetric intensive care
units and personnel with special expertise, patients with
HELLP syndrome who are remote from term should
receive care at a tertiary care center (116, 161).
It has been hypothesized that the antiinflammatory
and immunosuppressive effects of corticosteroids may
modify some of the proinflammatory features of pre-
eclampsia with severe features and favorably affect the
clinical course. Several randomized controlled trials of
high-dose corticosteroid treatment for antepartum or
postpartum stabilization of HELLP syndrome have been
conducted. The use of corticoids in the management of
HELLP syndrome compared with placebo or no treat-
ment was reviewed in a Cochrane Database Systematic
Review, which included 11 randomized trials (550
women) (162). There was no difference in the risk of
maternal death, severe maternal morbidity, or perinatal
or infant death. The only effect of treatment on individual
outcomes was improved platelet count (standardized
mean difference [SMD] 0.67; 95% CI, 0.2421.10).
The authors concluded that the evidence is insufficient
to support the use of corticosteroids for attenuation of the
disease process in HELLP syndrome (162).
Very close monitoring is required in HELLP syn-
drome until delivery and in the postpartum period, with
laboratory testing at least at 12-hour intervals. Aspartate
aminotransferase levels more than 2,000 IU/L or LDH
more than 3,000 IU/L suggest an increased mortality risk.
In the natural history of HELLP syndrome there is an
inverse relationship between the trends in platelet values
and liver enzymes level. During the aggravation slope in
the disease evolution, platelet count usually decreases at
an average rate of approximately 40% per day, whereas
the liver enzymes values tend to increase. The lowest
observed platelet count occurs at a mean of 23 hours after
delivery. The disease may achieve peak intensity during
the first 2 days after delivery, including a downward
trend in hematocrit. If the platelet count continues to drop
VOL. 133, NO. 1, JANUARY 2019 Practice Bulletin Gestational Hypertension and Preeclampsia
Copyright ª by the American College of Obstetricians
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Unauthorized reproduction of this article is prohibited.
and liver enzymes to increase after 4 days postpartum,
the validity of the initial diagnosis of HELLP syndrome
should be reassessed. With supportive care alone, 90% of
patients with HELLP syndrome will have platelet count
more than 100,000 3 109/L and reversed trend
(decrease) in liver enzymes values within 7 days after
delivery. Not infrequently, a rebound phenomenon in
platelet count follows reaching values of 400,000–
871,000 3 109/L (163). Women with HELLP syndrome
are also at increased risk of pulmonary edema, acute
respiratory distress syndrome and renal failure (164).
< What are the risks of subsequent cardiovascular
disease among women with hypertensive disorders
of pregnancy and are there prevention strategies
that modify this risk?
Women with a history of preeclampsia continue to
have an elevated risk of cardiovascular disease in sub-
sequent years. Several systematic reviews and meta-
analyses have linked preeclampsia with an increased risk
of cardiovascular disease (hypertension, myocardial
infarction, congestive heart failure), cerebrovascular
events (stroke), peripheral arterial disease, and cardio-
vascular mortality later in life, with an estimated
doubling of odds compared with women unaffected by
preeclampsia (165–167). Meta-regression analysis re-
veals a graded relationship between the severity of pre-
eclampsia or eclampsia and the risk of cardiac disease
(mild RR, 2.00; 95% CI, 1.83–2.19; moderate RR, 2.99;
95% CI, 2.51–3.58; severe RR, 5.36; 95% CI, 3.96–7.27,
P,.0001) (168). The risk is even higher (428 times the
risk for women with normal pregnancies) in women with
recurrent preeclampsia (169) and women with early-
onset preeclampsia or preeclampsia requiring preterm
delivery (170). More recent evidence suggests that all
hypertensive conditions in pregnancy are associated with
later cardiovascular disease with an approximately dou-
bling of the rate of incident cardiovascular disease and
a five times higher rate of hypertension (171).
The mechanisms that account for an increased risk of
cardiovascular disease in women with a history of
preeclampsia are not yet well understood, but endothelial
dysfunction, which has been linked to atherosclerosis,
persists in women with a history of preeclampsia many
years after an affected pregnancy (172). A study of car-
diovascular risk factors present before and after preg-
nancy suggested that nearly one half of the elevated
risk of future hypertension after preeclampsia can be ex-
plained by prepregnancy risk factors (173). Yet, it may
be possible that the stress incurred to the cardiovascular
system during gestation triggers a biological response
that would otherwise not have occurred despite any
genetic predisposition or risk factors (171). It remains
e15
unclear if cardiovascular changes associated with pre-
eclampsia during pregnancy causally lead to cardiovas-
cular remodeling increasing the risk of cardiovascular
disease later in life or if preeclampsia is a manifestation
of an underlying increased risk of cardiovascular disease
(for example, a common genetic–environmental risk
factor(s) interaction [such as hyperlipidemia, obesity,
diabetes mellitus, or renal disease] that predisposes
women to develop preeclampsia during pregnancy and
cardiovascular diseases later in life) (174). Preventive
strategies to be considered by patients and health care
providers may warrant closer long-term follow-up and
lifestyle modifications to better manage risk factors for
cardiovascular disease (eg, achieving healthful weight,
exercise, diet, smoking cessation), for which women
and their primary care providers may maintain ongoing
care and vigilance.
Clinical Considerations
and Recommendations
The following recommendations are based on good and
consistent scientific evidence (Level A):
< Women with any of the high-risk factors for pre-
eclampsia (previous pregnancy with preeclampsia,
multifetal gestation, renal disease, autoimmune
disease, type 1 or type 2 diabetes mellitus, and
chronic hypertension) and those with more than one
of the moderate-risk factors (first pregnancy,
maternal age of 35 years or older, a body mass
index of more than 30, family history of pre-
eclampsia, sociodemographic characteristics, and
personal history factors) should receive low-dose
(81 mg/day) aspirin for preeclampsia prophylaxis,
initiated between 12 weeks and 28 weeks of ges-
tation (optimally before 16 weeks of gestation) and
continuing until delivery.
< In women with gestational hypertension or pre-
eclampsia without severe features at or beyond 37 0/7
weeks of gestation, delivery rather than expectant
management upon diagnosis is recommended.
< Magnesium sulfate should be used for the prevention
and treatment of seizures in women with gestational
hypertension and preeclampsia with severe features
or eclampsia.
< Nonsteroidal anti-inflammatory medications should
continue to be used preferentially over opioid an-
algesics. Postpartum patients on magnesium for sei-
zure prophylaxis for preeclampsia did not show
differences in blood pressure, antihypertensive re-
e16 Practice Bulletin Gestational Hypertension and Preeclampsia
Copyright ª by the American College of Obstetricians
and Gynecologists. Published by Wolters Kluwer Health, Inc.
Unauthorized reproduction of this article is prohibited.
quirements, or other adverse events for patients
managed with NSAIDs in the postpartum period.
The following recommendations are based on limited or
inconsistent scientific evidence (Level B):
< Delivery is recommended when gestational hyper-
tension or preeclampsia with severe features is
diagnosed at or beyond 34 0/7 weeks of gestation,
after maternal stabilization or with labor or prelabor
rupture of membranes. Delivery should not be de-
layed for the administration of steroids in the late
preterm period.
< The expectant management of preeclampsia with
severe features before 34 0/7 weeks of gestation is
based on strict selection criteria of those appropriate
candidates and is best accomplished in a setting with
resources appropriate for maternal and neonatal care.
Because expectant management is intended to pro-
vide neonatal benefit at the expense of maternal risk,
expectant management is not advised when neonatal
survival is not anticipated. During expectant man-
agement, delivery is recommended at any time in the
case of deterioration of maternal or fetal condition.
< Antihypertensive treatment should be initiated expe-
ditiously for acute-onset severe hypertension (systolic
blood pressure of 160 mm Hg or more or diastolic
blood pressure of 110 mm Hg or more, or both) that
is confirmed as persistent (15 minutes or more). The
available literature suggests that antihypertensive
agents should be administered within 30–60 minutes.
However, it is recommended to administer antihy-
pertensive therapy as soon as reasonably possible
after the criteria for acute-onset severe hypertension
are met.
The following recommendations are based primarily on
consensus and expert opinion (Level C):
< It is recommended that women with gestational
hypertension in the absence of proteinuria are diag-
nosed with preeclampsia if they present with any of
the following severe features: thrombocytopenia
(platelet count less than 100,000 x 109/L); impaired
liver function as indicated by abnormally elevated
blood concentrations of liver enzymes (to twice the
upper limit of normal concentration); severe persis-
tent right upper quadrant or epigastric pain and not
accounted for by alternative diagnoses; renal insuf-
ficiency (serum creatinine concentration more than
1.1 mg/dL or a doubling of the serum creatinine
concentration in the absence of other renal disease);
pulmonary edema, or new-onset headache
OBSTETRICS & GYNECOLOGY
 unresponsive to acetaminophen and not accounted
for by alternative diagnoses, or visual disturbances.
< Women with gestational hypertension who present
with severe-range blood pressures should be managed
with the same approach as for women with severe
preeclampsia.
< Among women with gestational hypertension or pre-
eclampsia without severe features, expectant man-
agement up to 37 0/7 weeks of gestation is
recommended, during which frequent fetal and
maternal evaluation is recommended. Fetal monitor-
ing consists of ultrasonography to determine fetal
growth every 3–4 weeks of gestation, and amniotic
fluid volume assessment at least once weekly. In
addition, an antenatal test one-to-two times per week
for patients with gestational hypertension or pre-
eclampsia without severe features is recommended.
< Epidural or spinal anesthesia is considered acceptable,
and the risk of epidural hematoma is exceptionally
low, in patients with platelet counts 70 x 109/L or
more provided that the platelet level is stable, there is
no other acquired or congenital coagulopathy, the
platelet function is normal, and the patient is not on
any antiplatelet or anticoagulant therapy.
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169. Funai EF, Paltiel OB, Malaspina D, Friedlander Y, Deutsch
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171. Grandi SM, Vallee-Pouliot K, Reynier P, Eberg M, Platt
RW, Arel R, et al. Hypertensive disorders in pregnancy
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172. Powe CE, Levine RJ, Karumanchi SA. Preeclampsia,
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173. Romundstad PR, Magnussen EB, Smith GD, Vatten LJ.
Hypertension in pregnancy and later cardiovascular risk:
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Pre-eclampsia and future cardiovascular risk among
women: a review. J Am Coll Cardiol 2014;63:1815–22.
(Level III)

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were reviewed, and additional studies were located by Gestational hypertension and preeclampsia. ACOG Practice
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reliable research was not available, expert opinions from necologists. Obstet Gynecol 2019;133:e1–25.
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Unauthorized reproduction of this article is prohibited.
 new england
The
journal of medicine
established in 1812 August 17, 2017 vol. 377  no. 7

Aspirin versus Placebo in Pregnancies at High Risk

for Preterm Preeclampsia
Daniel L. Rolnik, M.D., David Wright, Ph.D., Liona C. Poon, M.D., Neil O’Gorman, M.D., Argyro Syngelaki, Ph.D.,
Catalina de Paco Matallana, M.D., Ranjit Akolekar, M.D., Simona Cicero, M.D., Deepa Janga, M.D.,
Mandeep Singh, M.D., Francisca S. Molina, M.D., Nicola Persico, M.D., Jacques C. Jani, M.D.,
Walter Plasencia, M.D., George Papaioannou, M.D., Kinneret Tenenbaum‑Gavish, M.D., Hamutal Meiri, Ph.D.,
Sveinbjorn Gizurarson, Ph.D., Kate Maclagan, Ph.D., and Kypros H. Nicolaides, M.D.​​

a bs t r ac t

BACKGROUND
Preterm preeclampsia is an important cause of maternal and perinatal death and From King’s College Hospital (D.L.R.,
complications. It is uncertain whether the intake of low-dose aspirin during preg- N.O., A.S., R.A., K.H.N.), King’s College
London (L.C.P.), Homerton University
nancy reduces the risk of preterm preeclampsia. Hospital (S.C.), North Middlesex Univer-
sity Hospital (D.J.), and University College
METHODS London Comprehensive Clinical Trials
In this multicenter, double-blind, placebo-controlled trial, we randomly assigned Unit (K.M.), London, University of Exeter,
Exeter (D.W.), Medway Maritime Hospi-
1776 women with singleton pregnancies who were at high risk for preterm pre- tal, Gillingham (R.A.), and Southend Uni-
eclampsia to receive aspirin, at a dose of 150 mg per day, or placebo from 11 to versity Hospital, Westcliff-on-Sea (M.S.)
14 weeks of gestation until 36 weeks of gestation. The primary outcome was de- — all in the United Kingdom; Chinese Uni-
versity of Hong Kong, Hong Kong (L.C.P.);
livery with preeclampsia before 37 weeks of gestation. The analysis was performed Hospital Clínico Universitario Virgen de la
according to the intention-to-treat principle. Arrixaca, Murcia (C.P.M.), Hospital Uni-
versitario San Cecilio, Granada (F.S.M.),
RESULTS and Hospiten Group, Tenerife (W.P.) — all
A total of 152 women withdrew consent during the trial, and 4 were lost to follow in Spain; Ospedale Maggiore Policlinico,
Milan (N.P.); University Hospital Brug-
up, which left 798 participants in the aspirin group and 822 in the placebo group. mann, Université Libre de Bruxelles, Brus-
Preterm preeclampsia occurred in 13 participants (1.6%) in the aspirin group, as sels (J.C.J.); Attikon University Hospital,
compared with 35 (4.3%) in the placebo group (odds ratio in the aspirin group, Athens (G.P.); Rabin Medical Center, Pet-
ach Tikva (K.T.-G.), and HyLabs Diagnos-
0.38; 95% confidence interval, 0.20 to 0.74; P = 0.004). Results were materially tics, Rehovot (H.M.) — both in Israel; and
unchanged in a sensitivity analysis that took into account participants who had University of Iceland, Reykjavik (S.G.). Ad-
withdrawn or were lost to follow-up. Adherence was good, with a reported intake dress reprint requests to Dr. Nicolaides at
the Harris Birthright Research Centre for
of 85% or more of the required number of tablets in 79.9% of the participants. Fetal Medicine, Fetal Medicine Research
There were no significant between-group differences in the incidence of neonatal Institute, King’s College Hospital, Den-
adverse outcomes or other adverse events. mark Hill, London SE5 8BB, United King-
dom, or at ­k ypros@​­fetalmedicine​.­com.
CONCLUSIONS Drs. Poon and Nicolaides contributed
Treatment with low-dose aspirin in women at high risk for preterm preeclampsia equally to this article.

resulted in a lower incidence of this diagnosis than placebo. (Funded by the This article was published on June 28, 2017,
and updated on July 11, 2017, at NEJM.org.
European Union Seventh Framework Program and the Fetal Medicine Foun­
N Engl J Med 2017;377:613-22.
dation; EudraCT number, 2013-003778-29; Current Controlled Trials number, DOI: 10.1056/NEJMoa1704559
ISRCTN13633058.) Copyrightº © 2017 Massachusetts Medical Society.

n engl j med 377;7 nejm.org  August 17, 2017 613

The New England Journal of Medicine
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Copyright © 2017 Massachusetts Medical Society. All rights reserved.
 The n e w e ng l a n d j o u r na l
P
reeclampsia is an important cause
of death and complications for the mother
and baby. The risk of such complications
is considerably higher when the disease is severe
and of early onset, leading to preterm birth at less
than 37 weeks of gestation.1-4 Major challenges
A Quick Take is
available at in modern obstetrics are the identification of
NEJM.org women at high risk for preterm preeclampsia
early in pregnancy and interventions to reduce
the prevalence of the disease.
In 1979, a study showed that women who had
taken aspirin regularly during pregnancy were
less likely to have preeclampsia than women
who had not.5 In the subsequent decades, more
than 30 trials have investigated the benefit of low-
dose aspirin (at a dose of 50 to 150 mg per day)
for the prevention of preeclampsia; a meta-analy-
sis of these studies showed that such therapy
resulted in a 10% lower incidence of preeclamp-
sia.6 In a meta-analysis of individual-participant
data from the trials, the effect of aspirin was not
affected by the gestational age at the onset of
therapy.7 In contrast, other meta-analyses showed
that aspirin started at or before 16 weeks of
gestation resulted in halving the rates of pre-
eclampsia, fetal-growth restriction, and perina-
tal death, whereas aspirin started after 16 weeks
of gestation did not have a significant benefit.8,9
In addition, the beneficial effect of aspirin that
was started at or before 16 weeks of gestation
was dose dependent, with a greater reduction in
the incidence of preeclampsia being associated
with a daily dose of aspirin of 100 mg or more.10
Professional associations now recommend the
prophylactic use of low-dose aspirin (60 to 80 mg
per day) in women who are considered to be at
high risk for preeclampsia. In the United King-
dom, the National Institute for Health and Clini-
cal Excellence recommends the identification of
the high-risk group on the basis of 10 factors,
including maternal characteristics and features
of the medical and obstetrical histories.11 How-
ever, the performance of such screening is poor,
with detection of approximately 40% of cases of
preterm preeclampsia and 33% of cases of term
preeclampsia, at a screen-positive rate of 11%.12
In the United States, the American College of
Obstetricians and Gynecologists recommends
the use of aspirin in women with a history of
preeclampsia in more than one pregnancy or a
history of preeclampsia that resulted in delivery
614 n engl j med 377;7 nejm.org  August 17, 2017
The New England Journal of Medicine
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Copyright © 2017 Massachusetts Medical Society. All rights reserved.
of m e dic i n e
before 34 weeks of gestation.13 However, this
subgroup constitutes only approximately 0.3% of
all pregnancies and includes only 5% of women
in whom preterm preeclampsia develops and 2%
of those in whom term preeclampsia develops.14
An alternative approach to screening is the use
of Bayes’ theorem to combine the a priori risk
from maternal factors with biophysical and bio-
chemical measurements obtained at 11 to 13 weeks
of gestation. A study involving approximately
60,000 women with singleton pregnancies showed
that such screening detected 76% of cases of
preterm preeclampsia and 38% of cases of term
preeclampsia, at a screen-positive rate of 10%.15
The Combined Multimarker Screening and Ran-
domized Patient Treatment with Aspirin for Evi-
dence-Based Preeclampsia Prevention (ASPRE) trial
was designed to test the hypothesis that, among
women who are identified as being at high risk
for preterm preeclampsia on the basis of the
above-mentioned factors, aspirin at a dose of
150 mg per day, taken from 11 to 14 weeks of
gestation until 36 weeks of gestation, would re-
sult in an incidence of preterm preeclampsia that
was half the incidence observed with placebo.
Me thods
Trial Design and Participants
In this double-blind, placebo-controlled trial, we
compared aspirin at a dose of 150 mg per day
with placebo that was administered from 11 to
14 weeks of gestation until 36 weeks of gesta-
tion in women with singleton pregnancies who
were at high risk for preterm preeclampsia. We
conducted the trial at 13 maternity hospitals in
the United Kingdom, Spain, Italy, Belgium,
Greece, and Israel.
All the women who had a routine prenatal visit
at 11 weeks 0 days of gestation through 13 weeks
6 days of gestation in the participating hospitals
were offered screening for preeclampsia by means
of an algorithm that combines maternal factors,
mean arterial pressure, uterine-artery pulsatility
index, and maternal serum pregnancy-associated
plasma protein A and placental growth factor.
(The algorithm is provided in the Supplementary
Appendix, available with the full text of this ar-
ticle at NEJM.org.)15
Gestational age was determined from the
measurement of the fetal crown–rump length.16
 Aspirin vs. Placebo for Preterm Preeclampsia
Maternal characteristics and medical and obstet-
rical histories were recorded, and the maternal
weight and height were measured. The mean
arterial pressure was measured by validated auto-
mated devices with the use of a standardized
protocol.17 Transabdominal color Doppler ultra-
sonography was used to measure the left and
right uterine-artery pulsatility index, and the
average value was recorded.18 Serum concentra-
tions of pregnancy-associated plasma protein A
and placental growth factor were measured by an
automated device (PAPP-A and PlGF 1-2-3 kits and
DELFIA Xpress random access platform, Perkin­
Elmer). Quality control was applied to achieve
consistency of the measurement of biomarkers
across trial centers. Quality control of screening
and verification of adherence to the protocol
were performed by the University College London
Comprehensive Clinical Trials Unit.
Inclusion criteria for the trial were the follow-
ing: an age of 18 years or more, singleton preg-
nancy, live fetus at the time that scanning was
performed at 11 to 13 weeks of gestation, and a
high risk (>1 in 100) for preterm preeclampsia
according to the screening algorithm. Exclusion
criteria were the following: unconscious or severe­
ly ill status, learning difficulties or serious men-
tal illness, major fetal abnormality identified at
the time that scanning was performed at 11 to
13 weeks of gestation, regular treatment with
aspirin within 28 days before screening, bleeding
disorder such as von Willebrand’s disease, peptic
ulceration, hypersensitivity to aspirin, long-term
use of nonsteroidal antiinflammatory medication,
and participation in another drug trial within
28 days before screening. Potential trial partici-
pants were given written information about the
trial, and those who agreed to participate pro-
vided written informed consent.
Approval for the trial was obtained from the
relevant research ethics committee and compe-
tent authority in each country in which the trial
was conducted. The trial was conducted with
fidelity to the protocol, which is available, with
the statistical analysis plan, at NEJM.org. The
funding organizations and the companies that
supplied and distributed the aspirin and placebo
had no role in the trial design, the collection,
analysis, or interpretation of the data, the writ-
ing of the manuscript, or the decision to submit
the manuscript for publication. The authors vouch
n engl j med 377;7 nejm.org  August 17, 2017
The New England Journal of Medicine
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Copyright © 2017 Massachusetts Medical Society. All rights reserved.
for the accuracy and completeness of the data
and analyses.
Randomization and Trial-Group Assignment
Eligible women were randomly assigned, in a 1:1
ratio, with the use of a Web-based system (Sealed
Envelope), to receive either aspirin or placebo,
and in the random-sequence generation there
was stratification according to participating cen-
ter. The aspirin and placebo tablets were manu-
factured by Actavis UK and were packaged, labeled,
stored, and distributed by Mawdsley-Brooks. The
placebo tablets were identical to the aspirin tab-
lets with respect to variables such as size, thick-
ness, physical properties, and appearance. After
randomization, the participants were prescribed
the assigned trial product and received instruc-
tions to take one tablet every night throughout
the trial and to stop taking tablets at 36 weeks
of gestation or, in the event of early delivery, at
the onset of labor.
Outcome Measures
The primary outcome measure was delivery with
preeclampsia before 37 weeks of gestation. Pre-
eclampsia was defined according to the Interna-
tional Society for the Study of Hypertension in
Pregnancy (see the Supplementary Appendix).19
Secondary outcomes were adverse outcomes of
pregnancy before 34 weeks of gestation, before
37 weeks of gestation, and at or after 37 weeks
of gestation; stillbirth or neonatal death; death
and neonatal complications; neonatal therapy;
and poor fetal growth (birth weight below the 3rd,
5th, or 10th percentile) (Table S1 in the Supple-
mentary Appendix).20
Adverse Events and Adherence
Adverse events and adherence were assessed
and recorded at follow-up clinical visits at 19 to
24 weeks of gestation, 32 to 34 weeks of gesta-
tion, and 36 weeks of gestation and during three
telephone interviews, which occurred at 16 weeks
and 28 weeks of gestation and 30 days after the
last tablet was taken. Participants were encour-
aged to record any side effects or adverse events
in a diary that was reviewed at each trial visit,
and they were specifically asked about such
events during each telephone interview.
We assessed adherence by counting the tab-
lets that were returned by participants at each
615
 The n e w e ng l a n d j o u r na l
visit and by the participants’ reporting of tablet
counts during each telephone interview. The
total number of tablets taken was calculated by
subtracting the number of tablets returned
from the number of tablets prescribed. Adher-
ence was considered to be good if the reported
intake of tablets was 85% or more of the total
number that participants were expected to have
taken between the date of randomization and
the date of the visit at 36 weeks of gestation or
the date of delivery if delivery occurred before
36 weeks of gestation. Adherence was consid-
ered to be moderate if the intake was between
50% and 84.9% and considered to be poor if it
was less than 50%.
Statistical Analysis
The sample-size estimation was based on the
assumption that first-trimester screening would
detect 76% of the cases of preterm preeclampsia
at a screen-positive rate of 10%.15 It was hypoth-
esized that low-dose aspirin would result in a rate
of preterm preeclampsia that was 50% lower
than the rate with placebo,8,9 for an estimated
rate of 7.6% in the placebo group and 3.8% in
the aspirin group. We calculated that the enroll-
ment of 1600 participants would give the trial
90% power to show a treatment effect at a two-
sided alpha level of 5%. The target recruitment
number was inflated to 1776 to account for
attrition.
Statistical analyses were performed on an
intention-to-treat basis, and no interim analyses
were performed. Logistic-regression analysis was
used to determine the significance of the between-
group difference in the incidence of preterm
preeclampsia, with adjustment for the effect of
the estimated risk of preeclampsia at screening
and the participating center. The treatment ef-
fect was quantified as the odds ratio with a 95%
confidence interval in the aspirin group. Pre-
specified analyses were also performed in sub-
groups that were categorized according to the
estimated risk of preterm preeclampsia and his-
tory of preeclampsia; a post hoc subgroup analy-
sis was performed according to country of the
participating centers. A sensitivity analysis was
performed to take into account the effect of
withdrawal of consent and loss to follow-up. We
also produced Kaplan–Meier estimates of the
cumulative incidence of preeclampsia according
616 n engl j med 377;7 nejm.org  August 17, 2017
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of m e dic i n e
to trial group, in which deliveries that were not
with preeclampsia were excluded. The treatment
effect for the secondary outcomes was quanti-
fied as the odds ratio with a 99% confidence
interval in the aspirin group, with adjustment
for the effect of the estimated risk for pre-
eclampsia at screening and the participating
center, and no corrections were made for mul-
tiple comparisons. The statistical software pack-
age R was used for data analyses.21
R e sult s
Trial Participants
The trial started at King’s College Hospital, in the
United Kingdom, in April 2014 but was stopped
in June 2014 after the recruitment of 56 partici-
pants because of administrative problems with
the supply of the trial products. The manufac-
ture and composition of the products were the
same throughout the trial, and the women who
were enrolled during this period were included
in the trial population. The trial was restarted
in July 2015, and recruitment was completed in
April 2016.
A total of 26,941 women with singleton preg-
nancies underwent screening,15 and 2971 (11.0%)
were found to be at high risk for preterm pre-
eclampsia. However, 332 of these women (11.2%)
were excluded from recruitment to the trial be-
cause they did not fulfill the eligibility criteria
(Fig. 1). Of the 2641 eligible women, 1776 (67.2%)
agreed to participate in the trial. After random-
ization, 152 women (8.6%) withdrew consent. Of
the women who participated in the trial, 4 were
lost to follow-up.
There were no significant differences between
the aspirin group and the placebo group with
regard to the characteristics of the participants
at baseline (Table 1). In the aspirin group, there
were 11 miscarriages before 24 weeks of ges­
tation, 2 pregnancy terminations for fetal ab-
normalities at or before 24 weeks of gestation,
1 pregnancy termination for severe fetal growth
restriction and preeclampsia at 24 weeks of ges-
tation, 7 stillbirths at or after 24 weeks of gesta-
tion, 1 neonatal death within 28 days after birth,
and 776 live births of infants who survived until
discharge from the hospital. In the placebo
group, there were 12 miscarriages before 24 weeks
of gestation, 4 pregnancy terminations for fetal
 Aspirin vs. Placebo for Preterm Preeclampsia

26,941 Women were screened for preterm

preeclampsia

2971 (11.0%) Were at high risk for preterm

preeclampsia

332 Were excluded

253 Were receiving aspirin
47 Had hypersensitivity to aspirin
17 Had peptic ulcer or bleeding disorder
10 Participated in another drug trial
2 Had miscarriage before randomization
3 Had termination of pregnancy
before randomization

2641 Were eligible for inclusion

865 Declined to participate

1776 Underwent randomization

878 Were assigned to receive aspirin 898 Were assigned to receive placebo

78 Withdrew consent 74 Withdrew consent

2 Were lost to follow-up 2 Were lost to follow-up

798 Were included in the primary analysis 822 Were included in the primary analysis

Figure 1. Screening, Randomization, and Follow-up.

abnormalities at or before 24 weeks of gestation,
no pregnancy terminations for severe fetal growth
restriction and preeclampsia at 24 weeks of ges-
tation, 12 stillbirths at or after 24 weeks of
gestation, 2 neonatal deaths within 28 days after
birth, and 792 live births of infants who survived
to discharge from the hospital.
Primary Outcome
Preterm preeclampsia occurred in 13 of 798 par-
ticipants (1.6%) in the aspirin group, as compared
with 35 of 822 (4.3%) in the placebo group (ad-
justed odds ratio in the aspirin group, 0.38; 95%
confidence interval, 0.20 to 0.74; P = 0.004) (Ta-
ble 2). The size of the treatment effect was con-
sistent across estimated risk groups at the time
of screening, across groups defined according to
obstetrical history, and across countries of the
participating centers (Figs. S1 and S2 in the Sup-
plementary Appendix). The cumulative percent-
ages of participants who had delivery with pre-
eclampsia are shown in Figure 2.
Of the 152 women who withdrew consent, 74
did not want any of their data to be reported and
78 allowed reporting of their screening data; the
baseline characteristics of the women who with-
drew consent were similar between those as-
signed to receive aspirin and those assigned to

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 The n e w e ng l a n d j o u r na l of m e dic i n e

Table 1. Characteristics of the Trial Participants.*

Aspirin Group Placebo Group

Characteristic (N = 798) (N = 822)
Gestational age at randomization — wk
Median 12.7 12.6
Interquartile range 12.3–13.1 12.3–13.0
Age — yr
Median 31.5 31.4
Interquartile range 27.3–35.8 26.9–35.8
Body-mass index†
Median 26.7 26.5
Interquartile range 23.3–31.1 23.0–31.5
Race or ethnic group — no. (%)‡
White 528 (66.2) 559 (68.0)
Black 208 (26.1) 201 (24.5)
South Asian 37 (4.6) 37 (4.5)
East Asian 13 (1.6) 16 (1.9)
Mixed race 12 (1.5) 9 (1.1)
Method of conception — no. (%)
Natural 747 (93.6) 779 (94.8)
Assisted by use of ovulation drugs 6 (0.8) 7 (0.9)
In vitro fertilization 45 (5.6) 36 (4.4)
Cigarette smoking — no. (%) 57 (7.1) 59 (7.2)
Mother had preeclampsia — no. (%) 66 (8.3) 74 (9.0)
Medical history — no. (%)
Chronic hypertension 49 (6.1) 61 (7.4)
Systemic lupus erythematosus 3 (0.4) 1 (0.1)
Antiphospholipid syndrome 2 (0.3) 2 (0.2)
Diabetes mellitus type 1 7 (0.9) 2 (0.2)
Diabetes mellitus type 2 8 (1.0) 8 (1.0)
Obstetrical history — no. (%)
Nulliparous 547 (68.5) 543 (66.1)
Multiparous without preeclampsia 164 (20.6) 195 (23.7)
Multiparous with preeclampsia 87 (10.9) 84 (10.2)
Interval from last pregnancy — yr
Median 4.2 4.6
Interquartile range 2.5–7.0 2.9–7.5
Gestational age at delivery of last pregnancy — wk 39 (37–40) 39 (36–40)
Risk of preterm preeclampsia as assessed at screening 2.3 (1.4–4.8) 2.6 (1.5–4.8)
at 11–13 wk (95% CI) — %§

* There were no significant between-group differences with regard to the characteristics at baseline. CI denotes confidence
interval.
† The body-mass index is the weight in kilograms divided by the square of the height in meters.
‡ Race or ethnic group was reported by the participants.
§ The risk of preterm preeclampsia was assessed by means of an algorithm that combined maternal factors, mean arterial
pressure, uterine-artery pulsatility index, and maternal serum pregnancy-associated plasma protein A and placental
growth factor (see the Supplementary Appendix).

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 Aspirin vs. Placebo for Preterm Preeclampsia

Table 2. Outcomes According to Trial Group.

Aspirin Group Placebo Group Odds Ratio

Outcome (N = 798) (N = 822) (95% or 99% CI)*
Primary outcome: preterm preeclampsia at <37 wk of 13 (1.6) 35 (4.3) 0.38 (0.20–0.74)
gestation — no. (%)
Secondary outcomes according to gestational age
Adverse outcomes at <34 wk of gestation
Any — no. (%) 32 (4.0) 53 (6.4) 0.62 (0.34–1.14)
Preeclampsia — no. (%) 3 (0.4) 15 (1.8) 0.18 (0.03–1.03)
Gestational hypertension — no. (%) 2 (0.3) 2 (0.2) 1.02 (0.08–13.49)
Small-for-gestational-age status without 7/785 (0.9) 14/807 (1.7) 0.53 (0.16–1.77)
preeclampsia — no./total no. (%)†
Miscarriage or stillbirth without preeclampsia 14 (1.8) 19 (2.3) 0.78 (0.31–1.95)
— no. (%)
Abruption without preeclampsia — no. (%) 1 (0.1) 3 (0.4) 0.36 (0.02–7.14)
Spontaneous delivery without preeclampsia 12 (1.5) 12 (1.5) 1.07 (0.37–3.10)
— no. (%)
Adverse outcomes at <37 wk of gestation
Any — no. (%) 79 (9.9) 116 (14.1) 0.69 (0.46–1.03)
Gestational hypertension — no. (%) 8 (1.0) 7 (0.9) 1.19 (0.31–4.56)
Small-for-gestational-age status without 17/785 (2.2) 18/807 (2.2) 1.01 (0.42–2.46)
preeclampsia — no./total no. (%)†
Miscarriage or stillbirth without preeclampsia 14 (1.8) 19 (2.3) 0.78 (0.31–1.95)
— no. (%)
Abruption without preeclampsia — no. (%) 2 (0.3) 4 (0.5) 0.52 (0.06–4.91)
Spontaneous delivery without preeclampsia 40 (5.0) 49 (6.0) 0.83 (0.47–1.47)
— no. (%)
Adverse outcomes at ≥37 wk of gestation
Any — no. (%) 178 (22.3) 171 (20.8) 1.12 (0.82–1.54)
Preeclampsia — no. (%) 53 (6.6) 59 (7.2) 0.95 (0.57–1.57)
Gestational hypertension — no. (%) 72 (9.0) 62 (7.5) 1.24 (0.78–1.98)
Small-for-gestational-age status without 54/785 (6.9) 56/807 (6.9) 1.00 (0.60–1.66)
preeclampsia — no./total no. (%)†
Stillbirth without preeclampsia — no. (%) 2 (0.3) 2 (0.2) 1.01 (0.08–13.40)
Abruption without preeclampsia — no. (%) 2 (0.3) 2 (0.2) 1.05 (0.08–13.92)

* The confidence interval was 95% for the primary outcome and 99% for the secondary outcomes.
† The status of being small for gestational age was defined as a birth weight below the 5th percentile. The birth weight
for neonates delivered before 24 weeks of gestation was not recorded.

receive placebo (Table S2 in the Supplementary
Appendix). A sensitivity analysis to evaluate the
effect of the withdrawals22 showed no substan-
tive difference from the primary analysis (Fig. S3
in the Supplementary Appendix).
Tables 2 and 3, and in Figures S4 and S5 in the
Supplementary Appendix. There was no signifi-
cant between-group difference in the incidence
of any secondary outcomes, but the trial was not
powered for these outcomes.

Secondary Outcomes Adverse Events

The treatment effect for secondary outcomes, In the aspirin group, at least one serious adverse
quantified as the odds ratio in the aspirin group event occurred in 13 participants (1.6%) and at
with a 99% confidence interval, is shown in least one adverse event occurred in 207 partici-

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 The n e w e ng l a n d j o u r na l of m e dic i n e

aspirin at a dose of 150 mg per day from 11 to

100 25 14 weeks of gestation until 36 weeks of gesta-
tion was associated with a significantly lower
Incidence of Delivery with Preeclampsia (%)

Placebo
20 incidence of preterm preeclampsia than was
75 placebo. There was no significant between-
15 group difference in the incidence of other preg-
nancy complications or of adverse fetal or
10 Aspirin neonatal outcomes. However, the trial was not
50
adequately powered for the secondary outcomes.
5 Unlike previous trials of strategies to reduce
the risk of preeclampsia among high-risk women,
25 0
we identified women at high risk for preterm pre-
0 24 26 28 30 32 34 36 38 40 42 eclampsia by means of combined screening with
maternal demographic characteristics and his-
torical factors and biomarkers — a strategy that
0
0 24 26 28 30 32 34 36 38 40 42 has been shown to be superior to other cur-
Week of Gestation at Delivery rently used methods.11,13,14,23 Decisions regarding
No. at Risk
the gestational-age range at the onset of treat-
Placebo 807 802 793 783 775 764 734 619 285 10 ment (11 to 14 weeks of gestation) and the pri-
Aspirin 785 781 778 776 772 760 740 627 295 12 mary outcome measure (preterm preeclampsia
rather than total preeclampsia) were informed
Figure 2. Kaplan–Meier Plot of Incidence of Delivery with Preeclampsia. by the results of meta-analyses suggesting that
The gray box highlights the rate of preeclampsia before 37 weeks of gestation. aspirin confers greater benefit if it is started at
Data were censored after deliveries not associated with preeclampsia. The
or before 16 weeks of gestation and that preven-
inset shows the same data on an enlarged y axis.
tion is confined to preterm preeclampsia.8,9,24
The dose of 150 mg of aspirin per day was se-
lected on the basis of previous evidence of a
pants (25.9%); in the placebo group, at least one dose-dependent benefit to therapy10; in addition,
serious adverse event occurred in 26 participants the commonly used dose of 81 mg of aspirin per
(3.2%) and at least one adverse event occurred in day has no appreciable effect on platelet func-
210 participants (25.5%). There was no significant tion in up to one third of pregnant women.25 The
between-group difference in the incidence of recommendation that participants take aspirin
these events (Tables S3 and S4 in the Supple- at night, rather than during the day, was based
mentary Appendix). on the observation from a randomized trial that
treatment at this time may be superior in reduc-
Adherence ing the rate of preeclampsia.26 The incidence of
Adherence was good in 1294 of 1620 partici- preterm preeclampsia in the placebo group was
pants (79.9%), moderate in 241 (14.9%), and poor lower than what was anticipated (4.3%, vs. the
in 85 (5.2%). There were no significant between- expected value of 7.6%), and this finding is likely
group differences in the degree of adherence to be the consequence of differences between
(Table S5 in the Supplementary Appendix). A the demographic characteristics of the screened
sensitivity analysis that took into account adher- population and those of the population that was
ence to the assigned regimen is shown in Figure used for the development of the algorithm.
S6 in the Supplementary Appendix. Screening at 11 to 13 weeks of gestation has
been shown to identify less than 40% of cases of
term preeclampsia.15 In our trial, aspirin did not
Discussion
reduce the incidence of term preeclampsia.
In this multicenter, randomized, placebo-con- In conclusion, this randomized trial showed
trolled trial involving women with singleton preg- that among women with singleton pregnancies
nancies who were identified by means of first- who were identified by means of first-trimester
trimester screening as being at high risk for screening as being at high risk for preterm pre-
preterm preeclampsia, the administration of eclampsia, the administration of aspirin at a dose

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 Aspirin vs. Placebo for Preterm Preeclampsia

Table 3. Neonatal Outcomes According to Trial Group.

Aspirin Group Placebo Group

Outcome (N = 798) (N = 822) Odds Ratio (99% CI)
Stillbirth or death — no. (%)
All stillbirths or deaths 8 (1.0) 14 (1.7) 0.59 (0.19–1.85)
With preeclampsia or status of being small for 5 (0.6) 8 (1.0) 0.65 (0.15–2.90)
gestational age
Without preeclampsia or status of being small for 3 (0.4) 6 (0.7) 0.51 (0.08–3.19)
gestational age
With placental abruption or bleeding 0 2 (0.2) 0.00 (0.00–∞)
Without placental abruption or bleeding 8 (1.0) 12 (1.5) 0.69 (0.21–2.28)
Death or complications — no. (%)
Any 32 (4.0) 48 (5.8) 0.69 (0.37–1.27)
Miscarriage, stillbirth, or death 19 (2.4) 26 (3.2) 0.76 (0.35–1.68)
Intraventricular hemorrhage of grade ≥II 2 (0.3) 1 (0.1) 2.23 (0.09–52.70)
Sepsis with confirmed bacteremia in cultures 3 (0.4) 6 (0.7) 0.52 (0.08–3.32)
Anemia resulting in blood transfusion 5 (0.6) 11 (1.3) 0.47 (0.11–1.92)
Respiratory distress syndrome treated with surfactant 11 (1.4) 22 (2.7) 0.53 (0.20–1.40)
and ventilation
Necrotizing enterocolitis resulting in surgery 2 (0.3) 1 (0.1) 2.10 (0.09–49.54)
Therapy — no. (%)
Any 55 (6.9) 60 (7.3) 0.97 (0.58–1.60)
Admission to intensive care unit 48 (6.0) 54 (6.6) 0.93 (0.55–1.59)
Ventilation with positive airway pressure or intubation 37 (4.6) 46 (5.6) 0.85 (0.47–1.52)
Poor fetal growth — no./total no. (%)*
Birth weight <3rd percentile 57/785 (7.3) 63/807 (7.8) 0.92 (0.57–1.51)
Birth weight <5th percentile 82/785 (10.4) 96/807 (11.9) 0.86 (0.57–1.30)
Birth weight <10th percentile 148/785 (18.9) 187/807 (23.2) 0.77 (0.56–1.06)

* The birth weight for neonates who were delivered before 24 weeks was not recorded.

of 150 mg per day from 11 to 14 weeks of gesta-
tion until 36 weeks of gestation resulted in a
significantly lower incidence of preterm pre-
eclampsia than that with placebo.
Supported by grants from the European Union Seventh Frame-
work Program (FP7-HEALTH-2013-INNOVATION-2; ASPRE Proj-
ect number, 601852) and from the Fetal Medicine Foundation.
No potential conflict of interest relevant to this article was
reported.
Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
We thank all the participants and their attending obstetri-
cians and midwives; Zarko Alfirevic, University of Liverpool;
Bryony Jones, Imperial College Healthcare NHS Trust; George
Attilakos, University College London Hospital; Mark Turner,
University of Liverpool; Christina Yu, Imperial College Health-
care NHS Trust; and Ian Bradbury, Statistics at Frontier Science
Scotland, for serving as members of the trial steering commit-
tee or independent data and safety monitoring committee;
Emilia Caverly, Hannah Lever, and Susan Tebbs, team mem-
bers of the University College London Comprehensive Clinical
Trials Unit, for project management and oversight of the trial;
Alan Wright for quality control of measurement of biomarkers;
and the following medical professionals who helped in the re-
cruitment and follow-up of participants: Silvia Andrietti, Jean
Edgard Aupont, Mercedes de Alvarado, Mercedes Campanero,
Stefania Carlucci, Irene Ceccacci, Siobhan Chaplin, Tunay Efe-
turk, Ilaria Fantasia, Madgalena Fiolna, Alex Frick, Paula Gar-
cia, Gavin Guy, Evgenia Kapeti, Natalia Karagiotis, Sofia Ka-
trantzi, Lemonia Koutoulas, Mirian Machuca, Sofia
Mastrodima, Olivia Mendez, Natalia Prodan, Anoop Rehal,
Min Yi Tan, Mayumi Tokunaka, Athanasios Tzelepis, Maria
Tziomaki, Gulen Yerlikaya, and Ling Zen, from London; Juan
Luis Delgado, Marisol Quezada, Rocio Revello, and Macarena
Quesada Rojas, from Murcia, Spain; Andrea Pazos, from
Granada, Spain; Vivien Dutemeyer, from Brussels; Ilma Car-
bone and Francesco D’Ambrosi, from Milan; Nikolaos Papan-
toniou and Nikos Evangelinakis, from Athens; and Eran Ha-
dar, Anna Idelson, and Lihi Rothman from Petah Tikva, Israel.
University College London, represented by the Comprehensive
Clinical Trials Unit, acted as the regulatory sponsor of this
trial for all sites within the European Union.

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 Aspirin vs. Placebo for Preterm Preeclampsia

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.
21st Annual Meeting Society for Maternal-
Fetal Medicine. Reno, Nevada, USA, 09-02-
2001 (Comunicación personal, 21-05-2001).
 Recordemos que……..


L. D. Macchi
Patología de Urgencia, Año 9, Nro. 2, Junio de 2001
 Morbilidad perinatal

✓
❑púrpura trombocitopénica trombótica,

❑síndrome urémico-hemolítico,

❑ púrpura trombocitopénica idiopática

❑atrofia amarilla aguda del embarazo.

 Tratamiento

 a. Reducir morbilidad y mortalidad

maternoperinatal.
 b. Prevenir progresión de la afección a clase
1.
 c. Precaver complicaciones de PE-E o
eclampsia, o ambos.
 d. Limitar los procedimientos invasivos y
operatorios a aquellos de absoluta necesidad.
1-
.
 El parto puede intentarse por vía VAGINAL
siempre que no exista una indicación medica u
obstétrica que indique la interrupción por
cesárea.
Antibioticoterapia de amplio espectro
postoperatorio
 PRONÓSTICO PARA LA MADRE Y EL PERINATO

 es muy reservado, cuando no "sombrío".

la morbilidad perinatal reúne las siguientes
condiciones esenciales:
- Nacimiento pretérmino
- Bajo peso al nacer
- Crecimiento intrauterino retardado
- Asfixia en el periparto y sus secuelas
- Membrana hialina (enfermedad y síndrome)
- Hemorragia intraventricular
- Enterocolitis necrotizante
· Síndrome del distrés respiratorio del adulto
· Insuficiencia renal
· Sepsis
· Encefalopatía hipoxicoisquémica
I. Cardiopulmonares

dolor torácico
II. Hematológicas y de la coagulación
❑Sangramiento que requiere transfusión de sangre
o sus derivados
❑Equimosis
❑Hematoma
❑Coagulopatía intravascular diseminada (con
tiempo de PTT > 40 segundos)
IV. Renales
❑Insuficiencia renal aguda
❑Necrosis tubular aguda
VI. Infecciosas
❑ Endometritis
❑ Pielonefritis
❑ Infección de la herida
.
 Bibliografía
 . Lipton R. Mutación de proteína como responsable de la hipertensión en
el embarazo. Rev Science / Bol 10-07-2000. URL disponible en:
www.sciencemag.org
. Johns C, Knowlton J, Nelson L, Ward K. The angiotensin II receptor I 1166A
to C allelic variant is not associated with preeclampsia Am J Obstet
Gynecol 2001;184:S72-3.
 Cotter A, Molloy A, Scott J, Daly S. Elevated plasma homocysteine in
early pregnancy: a risk factor for the development of severe preeclampsia
Am J Obstet Gynecol 2001;184:S11.
. Kim Y. Genetic susceptibility to preeclampsia: roles of Asp9Asn mutation, -
93G promoter mutation, Asn291Ser mutation in the lipoprotein lipase
gen. Am J Obstet Gynecol 2001;184:S72.
. Whitecar P, Boggess K, McMahon M, Thorp J, Taylor D. T-cell zeta chain
expression in women with preeclampsia compared to normotensive
pregnant controls. Am J Obstet Gynecol 2001;184:S76.
. Sorensen T. A prospective study of maternal dietary and plasma folate,
vitamin B12 and homocysteine status in relation to preeclampsia risk. Am
A Acosta y Cols. Ginecologia y Obstetricia- 200
Parto prematuro o pre termino
Parto- pre termino
Demografía
• RN de bajo peso : < 2500 gr
• RN de muy bajo peso: < 1500 gr
• Embarazo de Pre-Termino: < 37 sem.

• Ambos están relacionados ( Parto PT da

productos de BP)
 Definición
parto que se produce

Pre termino moderado: 36-32 semanas

Pre termino severo: < 32 sem
Pretermino extremo: <28 semanas

Parto inmaduro: e/ 22 y 27 semanas

Frecuencia
• En Paraguay : 10% (MSP).

Entre 5- 9 %
 Etiología
Multi factorial
Recept miometrio
Factores potencialmente removibles
durante el embarazo
Marcadores biológicos predictores
Fibronectina
Pasa al líquido amniótico y vagina hasta las
20 semanas, luego de la cual el sellado de las
membranas fetales impide su secreción a la
vagina
Después de la 22ª semana, la
fibronectina fetal no se evidencia hasta
la ruptura de membranas al término del
embarazo
Prevención del PP
Dx precoz
Edad del embarazo
Contracciones uterinas
Modificaciones del cuello uterino
Tratamiento
Reposo
Tocólisis

o
:
Inducción de la madurez fetal
Uso de tocoliticos
CUANDO FINALIZAR UNA TOCOLISIS?
Cuando reanudar?
• Si aparecen contracciones
• Se intentara otra infusión pero no mas de 6-8 hs

• Si no logra uteroinhibicion

• Se suspende definitivamente
Tratamiento de sostén
• Al finalizar el tratamiento inicial:
Reposo relativo en cama por 48 hs
Restricción de exámenes vaginales
Indometacina VO: 25 mg c/ 6 hs o VR: 100
mg/día
Betametasona
Cuando dar el alta?
Tratamiento ambulatorio
Contraindicaciones de uteroinhibicion
Cuidados en un parto prematuro
Cuidados en un parto prematuro
LA APP ES CONSIDERADA UNA DE LAS
PRINCIPALES CAUSAS DE RN DE BAJO
PESO.

EL TRATAMIENTO DEBE SER

ADMINISTRADO A TIEMPO Y LA
INTERRUPCION DE LA GESTACION TIENE
LIMITES ESTRECHOS RELACIONADOS A
LA MADUREZ FETAL.

COMUNICACIÓN CON NEONATOLOGIA

Factores Pre disponentes
Factores pre-existentes
Factores que aparecen durante el embarazo.
Factores socio/ económicos.
I) Factores Pre existentes
• Antecedentes de partos prematuros
• Antecedentes de abortos
• Antecedentes de muerte fetal y neonatal
• Antecedentes de Hemorragias e ISO inmunidad.
• Edad temprana o tardía: <18 y > 35 años.
• Multiparidad
• Malformaciones uterinas: bicorne, tabiques.
• Malformaciones adquiridas del útero: sinequias,
miomas submucosos.
• Tumores intra y extrauterinos: miomas.
• Incompetencia Istmico-cervical.
• Factores socioeconómicos.
II) Factores que se instalan durante el
embarazo
Embarazo múltiple
Polihidramnios
Placenta previa y DNP
RPM
HIE
Enfermedades infecciosas
Mala nutrición
Exceso de nicotina, alcohol
GPM < percentil normal
Anemia
Agotamiento físico
Traumatismos
Excesos sexuales
Fisiopatología
Control actividad miometrial
Mecanismos:
I. Miogenico
II. Neurogenico
III.Hormonales
I. Control Miogenico Llave para la regulación

ATP + Bomba calcio

actina y miosina

Excitación/ Contracción
II. Control Neurogenico
Liberación de neurotransmisores
(fibras adrenérgicas post
ganglionares)
Drogas beta miméticas
Contracción y relajación
III. Control hormonal
La contractilidad uterina se encuentra bajo
control de Hormonas esteroideas y
derivados:
I. estrógenos,
II. progesterona,
III. oxitocina,
IV. prostaglandinas,
V. relaxina.
 learn the facts: Predicting Prematurity
• Some tests are fairly accurate in identifying women who are at increased risk of premature delivery, while others have proven
ineffective.
Cervical length. The length of a woman’s cervix is measured using vaginal ultrasound. Women with a shorter-than-
average cervix and those whose cervix shortens on subsequent exams are at increased risk of premature delivery. This
test is fairly accurate in determining which women are at lower risk of premature delivery.
Fetal fibronectin. Fibronectin is a biological glue that helps attach the fetal sac to the uterine lining. It is normally seen
in vaginal secretions up to 22 weeks of pregnancy, then not until one to three weeks before delivery. A swab is used to
take a sample of vaginal secretions between 22 and 34 weeks of pregnancy. If fibronectin is seen, a woman appears to
be at increased risk of premature labor. This test shows moderate success in predicting who will not deliver
prematurely. In some cases, this test may be combined with a measurement of cervical length to increase accuracy.
Salivary estriol. Because levels of this hormone in the saliva appear to increase just before labor, attempts have been
made to measure it. Studies show that this test is not accurate.
Home uterine monitoring. Women at high risk have been monitored for painless contractions in an attempt to
diagnose premature labor early, when it was most treatable. A number of studies have shown that home uterine
monitoring is not effective in preventing premature delivery.
May 2007
Martin, J.A., et al. Births: Final Data for 2003. National Vital Statistics Reports, volume 54, number 2, September 8,
2005.
Risk Factors for Premature Birth compiled by the March of Dimes.
American College of Obstetricians and Gynaecologists (ACOG). Intrauterine Growth Restriction. ACOG Practice Bulletin,
number 12, January 2000.
Resnik, R. Intrauterine Growth Restriction. Obstetrics and Gynaecology, volume 99, number 3, March 2002, pages 490-
496.
U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon
General—2004. Centres for Disease Control and Prevention, Office on Smoking and Health, Atlanta, GA, May 2004.
• 6. Siega-Riz, A., et al. Second Trimester Folate Status and Preterm Birth. American Journal of Obstetrics and Gynaecology, volume 191, 2004, pages 1851-
1857.
• 7. Meis, P.J., et al. Prevention of Recurrent Preterm Delivery by 17 Alpha-Hydroxyprogesterone Caproate. New England Journal of Medicine, volume 348,
number 24, June 12, 2003, pages 2379-2385.
• 8. Petrini, J.R., et al. Estimated Effect of 17 Alpha-Hydroxyprogesterone Caproate on Preterm Birth in the United States. Obstetrics and Gynecology, volume
5, number 2, February 2005, pages 267-272.
•
November 2005
• MEDLINE LIBRARY
Pruebas predictoras de APP
1. Longitud cervical: < 25 mm
2. Fibronectina fetal: presente en un 50,4% de
los embarazos con contracciones
prematuras
3. Estriol salival: antes del parto.
4. Monitoreo electrónico de contracciones
subliminales

May 2007
Martin, J.A., et al. Births: Final Data for 2003.
National Vital Statistics Reports, volume 54,
number 2, September 8, 2005.
Fibronectina fetal
sensibilidad de 81,7%
especificidad de 82,5%.
VPP: 83,1%
VPN: 81%.
Por lo tanto, el riesgo relativo (RR) de parto
prematuro para aquellos embarazos con un test
positivo para fFN es de 4,88 (IC 94% 2,54-,.55).
La fibronectina fetal
es una proteína multifuncional de
la matriz extracelular involucrada en la adhesión
celular, opsonización y trombosis.

• La fibronectina fetal es la proteína más

grande de la matriz extracelular de las
membranas amnióticas.
• sintetizada por el trofoblasto
extravelloso durante el embarazo.
Pasa a:
 líquido amniótico y vagina hasta las
20 semanas, luego de la cual el sellado de las
membranas fetales impide su secreción a la
vagina
Después de la 22ª semana, la
fibronectina fetal no se evidencia hasta
la ruptura de membranas al término del
embarazo
 Cuando la interfase es agredida por infección
ascendente, isquemia, contracción
mecánica o cualquier otro proceso que
conduce a compromiso de la membrana, la
fibronectina fetal aparece en las secreciones
cérvicovaginales.
Este proceso bioquímico puede ocurrir hasta
las tres semanas previas a la aparición de
signos visibles del parto prematuro
Petrini, J.R., et al. Estimated Effect of 17 Alpha-Hydroxyprogesterone & fibrinectin
Caproate on Preterm Birth in the United States. Obstetrics and Gynecology, volume 5,
number 2, February 2005, pages 267-272.
Infección corioamniotica
 Diagnostico
• API: 22 a 27 semanas
• APP: >27 a < 37 semanas.

3 parámetros de DX:
I. EG
II. CONTRACTILIDAD UTERINA ANORMAL
III. MODIFICACIONES DEL C. UTERINO.

Resnik, R. Intrauterine Growth Restriction. Obstetrics and Gynecology,

volume 99, number 3, March 2002, pages 490-496
 PARAMETROS DE DX

I. EDAD GESTACIONAL (Resnik,2002)

Confirmada por Ecografía ( 1er trimestre)

DBP
CC
CA
LF
LH
 II. CONTRACTILIDAD
UTERINA
FISIOLOGICAS: Braxton - Hicks
ANORMALES: no ceden con reposo, a la noche
ni con antiespasmódicos.

Características(Carreras &cols):
1 o mas contracciones c/ 10’
Síntomas acompañantes
1. Dolor tipo menstruación
2. Dolor irradiado a la región lumbar.
3. Dolores abdominales.
4. Sensación de pujo
5. Perdida de limos.
III. Modificaciones del cuello
Borramiento
Dilatación: paridad?: 2 o mas cm. No existe dilatación
fisiológica en nulíparas

Posición : mas anterior.

Altura de la presentación: apoya sobre el
cuello.
Otros parámetros
Irritabilidad uterina
Estado de M. ovulares

Cuello maduro antes de las 37 sem + útero

irritable + presentación baja
Tratamiento
• Tratamiento preventivo
• Tratamiento medicamentoso.

Dependiendo de la gravedad del cuadro al

inicio del Dxco
I) Preventivo
1. Identificar mujeres con riesgo.
2. Abstinencia sexual.
3. Reposo. Limitación de actividad física.
4. Tratamiento de infecciones cervico vaginales.
II) Medicamentoso: ataque
sostén
Ataque : reposo en cama
inhibición de contracciones
maduración pulmonar

Sostén : Reposo absoluto en cama ( 48 hs)

restricción de exámenes vaginales
Beta miméticos

Maduración pulmonar.
Drogas uteroinhibidoras
Isoxuprine ( uterine®)

• VO: comprimidos 10 mg: 1 c/ 6 a 8 hs

IV: 1 ampolla (10 mg) : diluir 10 ampollas (100
mg) en 500 cc de suero glucosado.( 20
gotas/min).
IM: 1 ampolla c/ 4-6 hs.
• Ampollas de 0,5 mg: 4 ampollas en 250 cc :
goteo 20 x’ o D/R

• VO: tabletas de 20 mg.

Tocoferol ( partusisten®)
IV: 2 ampollas en 500 cc: 20 gotas/min
LM no deben pasar de 120
Hexoprenalina ( argocian®)
•
Controlar cada 30 min.
Si no cede duplicar la dosis del goteo

Luego de 7 horas sin DU iniciar V.O.

Luego de 2 hs evaluar DU:

Pte sin DU: se suspende V.Parenteral
Salbutamol (Ventolin®)
Ritodrina
• IV: 3 ampollas de 150 mg en 500 cc de Ringer
Lactato. ( 300 ug /ml)
• Se inicia con 100 ug/min
Hexoprenalina
Formada por 2 moléculas de adrenalina unidas
e/si:
0,1 a 0,2 ug/min
(D. Máxima: 0,35 ug/min)
Otras medicaciones
• Sulfato de Mg: igual esquema que en la pre-
eclampsia severa
• Nifedipina: VO: 10 mg c/ 6 hs
• Indometacina: 100 mg c/ 12 hs (48-72 hs)
Consideraciones
Toco líticos deben ser administrados hasta
lograr la madurez minina fetal.

En DBT gestacional se deben aumentar las

dosis de insulina
Finalización del cuadro de ataque IV
a. Cuando la contracción descendió a menos de
2-3 por minuto por lo menos 4 horas

tratamiento
de sostén.

b. Si no mejora: fracaso( no disminuyen las

contracciones a < 2-3 en 10 min y la dilatacion
es > a 4 cm durante el Tto.
Tratamiento de sostén ambulatorio
Hasta las 37/38 semanas
 Usar la vía oral de preferencia.
Dosis modificable de acuerdo a la respuesta
uterina y cardiovascular materna y fetal.
Continuar con medidas generales de reposo
físico, sin estrés.
 Contraindicaciones para el Tto
inhibidor
• RPM
• Malformaciones congénitas severas.
• Feto muerto
• Madurez comprobada.
• Nefropatías.
• Alteración del bienestar fetal
• Hipertiroidismo .
• Cardiopatías no compensadas.
• Alteraciones del ritmo cardiaco.
Maduración pulmonar
• Betametasona: 12 mg IM. Se repite a las 24 hs
• Ambroxol: 1 gr diluido en 100 ml de sol.
Fisiologica ( goteo en no menos de 2hs). Por 5
dias seguidos.
• Dexametasona: 6 mg cada 6 hs ( 4 dosis) IM.
24 mg en 24 hs
A tener en cuenta durante el T. P.
• MF intraparto
• Reducir los exámenes vaginales al mínimo.
• Mantener las membranas integras hasta
dilatación completa.
• Control estricto de D.U. (fetos lábiles)
• Episiotomía amplia
• Buena aspiración bucal/nasal.
• Pinzar el cordón luego de 45 a 60 ’’
Muchas gracias
Mortalidad perinatal en la
DBT hoy
DESCENSO DEL 40% AL
4%. (2000)

DECADA DEL 50: >40%

 FRECUENCIA

 DBT MELLITUS Y EMBARAZO : 0,1

a 5%

 DBT GESTACIONAL: 1 – 5 %
DEFINICION
 ESTADO DE HIPERGLICEMIA
CRONICA COMO CONSECUENCIA DE
FACTORES GENETICOS Y
AMBIENTALES (OMS)
 intolerancia o anormal tolerancia a
la glucosa,
 resultante en hiperglucemia de grado
variable, que se inicia o se reconoce por
vez primera durante un embarazo y que
la condición termina con el mismo o
persiste después del mismo.
diabetes conocida antes del
embarazo.
“diabetes pre gestacional”
DIABETES PRE -
GESTACIONAL
❖no se considera una afectación
pancreática exclusivamente sino
una perturbación del
metabolismo de
 ETIOPATOGENIA
EMBARAZO OBESIDAD TRAUMATISMOS

BASE GENETICA

STRESS INFECCIONES INTERVENCIONES

 SISTEMA DE REGULACION HORMONAL
EN EL EMBARAZO

 GLANDULAS MODIFICAN SU SECRESION:

: HIPERINSULINISMO HIPOGLICEMIA(1ER TRIM)

: CORTISOL LIBRE GLUCONEOGENESIS

ACTIVIDAD PANCREATICA
 ACTH HIDROXICORTICOIDES

HIPERGLICEMIA INSULINA

PLACENTA: ESTROGENOS,
PROGESTERONA,
GONADOTROFINAS HIPERGLUCEMIA
 Comportamiento de la
insulina en el embarazo
de 10 – 24 semanas: hiper insulinismo
✓ mejor tolerancia
✓ tendencia hipoglicemica
✓ tendencia a compensación de
hiperglicemia
de las 24 – 36 semanas:
disminución en la tolerancia
hiperglicemia
cetoacidosis
 36 – 37 sem
necesidad de insulina
leve mejoría en la DBT

lactancia:
mas la necesidad de insulina
 HISTOPATOLOGIA
vascularitis generalizada
causa:
CHOQUE INMUNOLOGICO DEPOSITOS DE
MUCOPOLISACARIDOS EN VASOS

FACTOR GENETICO: GEN ANORMAL UNICO ( AUTOSOMAL)

A NIVEL TISULAR
 Diagnostico
clínico
➢
Diagnostico
ecográfico

.
 TTGO ( Test O’Sullivan)

 CURVA DE TOLERANCIA A GLUCOSA

ORAL
CRITERIOS DIAGNOSTICOS
 según la OMS:
TTGO: 75 grs de glucosa oral
diluida en 200/300 ml de agua
❖glicemia basal: ayuno de 10-14 hs
❖glicemia a las 2hs de la glucosa
oral
 Interpretación de TTGO para Dx de
DBT gestacional
Ayunas (O): igual o mayor 92 mg/dl

A la hora Post-Carga (1hr): 180 mg/dl

A las 2 hrs Post-Carga (2hr): 153 mg/dl

DBT GESTACIONAL
 CLASIFICACION:

❑NORMOTOLERANTE A LA
GLUCOSA.
❑ITG
❑DIABETICA

6 SEM POST PARTO

 TODA MUJER
EMBARAZADA
1RA CONSULTA
DBT
PREGESTACIONAL
PREPARACION PARA SU EMBARAZO

EDUCACION SEXUAL.
CONTROLES CLINICO ENDOCRINOLOGICOS
MEDIDAS HIGIENICO DIETETICAS
 DBT GESTACIONAL
EN POBLACIONES DE RIESGO:
➢población hispana
➢alta prevalencia de anormal
tolerancia a glucosa
➢alta paridad
➢estilo de vida
 DIABETES MATERNA FETO HIPERGLICEMICO

 INSULINA
BARRERA
 GLUCAGON PLACENTARIA

 GLUCOSA
FETO
 CLASIFICACION DE LA DBT SEGÚN OMS
I)DBT MELLITUS: TIPO I Y II
II)DBT SECUNDARIA:
A. enf. pancreática
B. hormonal
C. inducida( fármacos, agentes
químicos
D. sx genéticos
III) TOLERANCIA ALTERADA DE LA
GLUCOSA
A. OBESIDAD
B. NO OBESIDAD
C. RELACIONADA A SINDROMES.

IV) DBT GESTACIONAL.

DETECCION EN MUJERES SIN
RIESGO
GLICEMIA EN AYUNAS (1ra consulta)
 NORMAL NUEVA PESQUIZA A 24
Y 28 SEM

 ANORMAL TTGO
 MUJERES CON RIESGO
 se inicia con test O’Sullivan (50 gr
glucosa)

 normal nuevo control 24 y 28 sem.

 anormal CONFIRMAR CON CURVA T. G. O

ANORMAL= DBT
 FACTORES DE RIESGO (CLAP)
 ANTECEDENTES GENETICOS : FLIARES EN 1ER
GRADO

 ANTECEDENTES OBSTETRICOS:
❖ MUERTES PERINATALES SIN CAUSA CONOCIDA.
❖ ABORTOS A REPETICION
❖ HIE
❖ POLIHIDRAMNIOS A REPETICION
 FACTORES FETALES:
✓MACROSOMIA ( >4000 GR)
✓MALFORMACIONES.
FACTORES METABOLICOS:
✓ OBESIDAD AL INICIO DEL EMBARAZO
✓ GP ENCIMA DEL PERCENTIL NOMAL.
✓ DBT EN GESTACIONES ANTERIORES.
✓ GLICEMIAS > 90 EN AYUNAS
EDAD MATERNA : > 35 AÑOS
 hgb glicosilada:
❑ informa del metabolismo glúcido de las ultimas
8 semanas
❑ pronostico de posibilidad de malformaciones

buen pronostico: < 8%

mal pronostico: > 10
 CRITERIOS DX: SON GEST.
DIABETICAS
 embarazadas con 2 o mas
determinaciones de glicemia
en ayunas > 92 mg/dl. en
cualquier momento del embarazo.

 embarazadas con

PTG ( test de O’ Sullivan)

SI LOS RESULTADOS SON NORMALES
INICIO
24 Y 28 SEMANAS
PERO…..
PACIENTE CON FACTORES DE RIESGO

 REPETIR entre LAS 31 Y 33 SEM

EFECTOS DE LA DBT SOBRE
LA MADRE
EFECTOS DE LA DBT SOBRE
LA MADRE
DURANTE EMBARAZO: INFECCIONES URINARIAS
MONILIASIS
VASCULITIS

DURANTE EL PARTO:
HEMORRAGIAS HIPERDISTENSION

FETO MACROSOMICO
POLIHIDRAMNIOS
EFECTOS DE LA DBT SOBRE
EL FETO
 mortalidad intrauterina
 prematuridad
 parto distócico
 sx membrana hialina
 hipoglucemia neonatal.
 abortos
 malformaciones
 viceromegalia ( todos menos el cerebro)
TRATAMIENTO
OBJETIVOS GENERALES
 USO DE DROGAS
 CONTROL DE SALUD FETAL
 CONDUCTA OBSTETRICA
 ANTICONCEPCION
 CONTROL CLINICO Y METABOLICO
OBJETIVOS
GENERALES
1. asegurar la sobrevida materna
2. control de la glicemia
3. proteger contra enfermedad
vascular
4. profilaxis de toxemia
5. obtener feto vivo sin
malformaciones
6. establecer dieta adecuada
 USO DE DROGAS
insulina: no tiene riesgo excepto ….
la hipoglicemia materno - fetal
 hipoglucemiantes orales:
derivados de la sulfonil urea: aumenta
el hiperinsulinismo en el feto.
no se usan ( GLIBENCLAMIDA ?????)

maduración pulmonar:
USAR SOLO EN CASOS BIEN INDICADOS
CONTROL DE LA
SALUD FETAL
 ECOGRAFIAS SERIADAS
SCREENING 1ER TRIM
MORFOLOGICA
CURVA DE CRECIMIENTO.
 MONITOREO FETAL
 PERFIL BIOFISICO + DOPPLER
 CONDUCTA
OBSTETRICA
EN CONCORDANCIA CON
PEDIATRA, ANESTESISTA,
ENDOCRINOLOGO,
PERINATOLOGO

MOMENTO DE LA INTERRUPCION

ELECCION DE VIA DEL PARTO

 DURANTE EL PARTO
Mantener la glicemia entre 80 – 120
utilizar dextrosa al 5%

en las insulino dependientes se

realiza el mismo tto que en las
DBT pre- gestacionales
 PUERPERIO EN DBT NO
INSULINO DEPENDIENTES
24 – 48 HS POST- PARTO:
✓ CONTROLES DE GLICEMIA
SERIADAS
✓ Dieta
PUERPERIO TARDIO:
✓ CONTROLES CLINICO/ENDOCRINOLOGICOS
✓ Dieta
PUERPERIO EN LAS INSULINO DEPENDIENTES
Alumbramiento
Períodos del Parto

◼ 1er período: Dilatación

◼ 2do período: Expulsivo.

◼ 3er período: Alumbramiento

◼ 4to período: Involución uterina

Alumbramiento
Expulsión de la placenta y
membranas tras la expulsión
del feto.
 Tipos de Alumbramiento

◼ Natural: Expulsión espontánea de la placenta y

membranas.

◼ Dirigido: mediante el uso de oxitócicos. Ayuda

a prevenir hemorragias.

◼ Manual: Bajo anestesia general. Extracción por

desprendimiento manual.
En casos especiales ( Retención, hemorragias)
 Alumbramiento Natural
Se verifica espontáneamente por las
contracciones del útero.
Comprende dos tiempos:
* desprendimiento *expulsión.

Contracciones destruyen las adherencias.

 Signos clínicos de
desprendimiento:
Sangramiento,
momento en que se
produce, y
cuantificarlo.
Reaparición de las
dinámica uterina.

, útero
palpable a 3 cm.
supraumbilical y
lateralización a
derecha.
 , es la
inmovilidad de la
pinza que está
unida al cordón, al
traccionar el fondo
del útero hacia
arriba.
 , es el descenso espontaneo de la
pinza unida al cordón.
Se considera que el desprendimiento es completo al
descender más de 10 cms.
 ,
se tracciona el cordón y se palpa el
fondo del útero. No es aconsejable.
Descenso de la placenta
Se produce por
el hematoma retroplacentario
las contracciones
uterinas,
el peso de la placenta y los
anexos
la gravedad.
 Expulsión:
Es la expulsión de la placenta y los anexos al exterior
ayudados por los pujos y prensa abdominal.
◼ Irritación del cuello del útero por la presencia de la masa que
acaba de caer sobre él, reacciona sobre el cuerpo uterino que
se contrae, se entreabre el cuello y deja pasar la placenta a la
vagina, y la presión que se ejerce entonces sobre el intestino
excita a la mujer a hacer pujos cuyo resultado es ayudar a la
expulsión.

PARA AYUDAR AL DESPRENDIMIENTO TOTAL DE

LAS MEMBRANAS GIRAR LA PLACENTA DEJANDO
QUE DESCIENDA POR SU PROPIO PESO
 UNA VEZ EXPULSADA LA
PLACENTA DEBE SER
EXAMINADA
1- LOS COTILEDONES
2- LAS MEMBRANAS
3- LA INSERCION DEL CORDON
4 - CARACTERISTICAS DEL PARENQUIMA
DURANTE UNA CESAREA

EXTRACCION DE LA PLACENTA DURANTE UNA CESAREA

Tiempo de expectación
20 a 30 minutos
post expulsión
fetal
 Maniobras que ayudan al
desprendimiento de la
placenta
*Tracción suave del
cordón

* Masaje en fondo
uterino
 Tipos de alumbramiento natural

desprendimiento por los

bordes.
Dx: sangrado continuo
transvaginal
hasta la expulsión de la
placenta.
Por el centro
Sale con hematoma
Retro-placentario
COMPLICACIONES DURANTE EL
PREOCESO DE ALUMBRAMIENTO

1- Hemorragias

2- Retención.

3- Encastillamiento.

4- Engatillamiento
Distocias del
alumbramiento
PARTE DE LA PLACENTA
QUEDA RETENIDA POR
EL CIERRE
INTEMPESTIVO DEL
CUELLO.
Hemorragias Post Parto
Manejo activo del 3er
periodo
 MANEJO ACTIVO.
ALUMBRAMIENTO DIRIGIDO

MALEATO DE ERGONOVINA IM
CUANDO AFLORA EL HOMBRO
ANTERIOR FETAL.
 III-Alumbramiento
Manual
Extracción manual de la placenta al
cumplirse un tiempo prudente de
expectación o ante una hemorragia o
retención anormal.
Indicaciones: Retención simple,
sospecha de acretismo, hemorragias,
atonía uterina, parto prolongado con
“cansancio uterino”, feto muerto y
retenido, eclampsia.
 HEMORRAGIA POST
ALUMBRAMIENTO
UNO DE LOS CUADROS CON MAS
MORBIMORTALIDAD .
LA PERDIDA NORMAL: 300- 500 ML, Y
DEBE CESAR EN SU MAYOR PARTE
LUEGO DE LA EXPULSION DE LA
PLACENTA.
EN CASO CONTRARIO TOMAR LAS
MEDIDAS CLINICO QUIRURGICAS
DEL CASO.
FORMACION DEL
GLOBO DE
SEGURIDAD DE
PINARD QUE
SIGNIFICA QUE EL
UTERO ESTA
PRODUCIENDO EN
FORMA EFECTIVA
SU “LIGADURA
VIVIENTE.”
 LA MORBIMORTALIDAD DURANTE EL
◼
ALUMBRAMIENTO SE EQUIPARAN A LAS
DEL PERIODO EXPULSIVO .
◼ LA VENTAJA ES QUE UNA VIDA, LA DEL
FETO, YA ES DIFERIDA AL NEONATOLOGO

◼ NOS QUEDA EL CONTROL Y DIRECCION

DE LA EXPULSION SIN
COMPLICACIONES DE LA PLACENTA.

◼ CUALQUIER MANIOBRA INTEMPESTIVA

COMPLICA EL PERIODO DEL
ALUMBRAMIENTO.
MUCHAS GRACIAS
La hemorragia es la
complicación más
importante del
alumbramiento
 Federación
Internacional de
Gineco-Obstetricia

Programas de
prevención de la
mayor causa de
mortalidad post
parto
 MORTALIDAD MATERNA

¿Cuál es la mayor
amenaza para la vida y
la salud de la mujer en
los países en
desarrollo?
Las complicaciones
del embarazo y del
parto.
 MORTALIDAD MATERNA
PANORAMA MUNDIAL Y CAUSAS

Causas Indirectas 20%

Hemorragia Grave
25%

Otras causas directas 8%

Parto Obstruído 15% Infección 15%

Eclampsia 12% CADA AÑO:

Aborto en Condiciones de Riesgo
13 %
➢180-200 millones de embarazos
➢75 millones de embarazos no deseados
➢50 millones de abortos inducidos
➢20 millones de abortos realizados en condiciones de
riesgo
➢Casi 600.000 muertes maternas
1 muerte materna= 30 morbilidades maternas
 MORTALIDAD MATERNA
CADA MINUTO:
✓380 mujeres quedan embarazadas
✓190 mujeres se enfrentan a un embarazo no
planificado o no deseado
✓110 mujeres sufren de complicaciones
relacionadas con el embarazo
✓200 adquieren alguna enfermedad de
transmisión sexual
✓40 mujeres tienen un aborto realizado en
condiciones de riesgo
✓1 mujer muere por complicaciones relacionadas
con el embarazo
MORTALIDAD MATERNA
❖ La Hemorragia es la mayor causa directa de muerte materna –
25-50% de todas ellas.
❖ No existe manera de prevenirla en un 100 %.
❖ La mayoría de las hemorragias post parto son causadas por
atonía uterina.
❖ Existen intervenciones basadas en evidencia, aplicables y de
bajo costo que ofrecen resultados efectivos para prevenirlas.
❖ El manejo activo de la tercera etapa del parto puede prevenir
cerca del 60 % de ellas.
❖ La prevención de la HPP reduce significativamente la
morbilidad y mortalidad materna.
Mortalidad Materna en América Latina y el Caribe

❖ 80% de las muertes maternas se deben a

causas obstétricas directas
❖ 80% de las muertes que ocurren en el post
parto ocurren en los primeros 7 días
❖ 15% de las mujeres de parto presentan una
complicación seria
❖ 1-2% de las mujeres que dan a luz necesitan
una intervención obstétrica mayor para
sobrevivir

Fuente:
 MORTALIDAD MATERNA i nternational

Confederation of
Midwives
Declaración Conjunta

MANEJO ACTIVO DE LA TERCERA ETAPA DEL PARTO

PARA EVITAR LA HEMORRAGIA POST-PARTO

El manejo activo de la tercera etapa del parto

se debe ofrecer a las mujeres porque reduce el
índice de hemorragia post-parto debido a
atonía uterina.
Paciente anémica, hipovolemica o toxemica
Pte con útero muy distendido (gemelar,
polihidramnios, DBT)
Asociación de mioma y embarazo
Óbito fetal intrauterino
Comprende anomalías
✓ Desprendimiento

✓ Descenso

✓ Expulsión
 Retención Total:
✓ Distocias dinámicas
inercia
anillos de contracción: A. Bandl

✓ Distocias Anatómicas: plac. adherente

placenta acreta
increta
percreta
Retención parcial:
Prevención . Tratamiento
Manejo activo del 3er periodo
 III. Atonía o inercia uterina post
alumbramiento

Este fenómeno ocurre en el 2 al 5 % de los

partos por vía baja.

Principal causa de muerte materna debidas a

complicaciones del alumbramiento
Mecanismo de hemostasia normal
Post Alumbramiento
 Factores predisponentes
Antecedentes
Multiparidad
Edad avanzada
P. vaginal Post cesárea
Anestesia general( fluotane, alotane, éter)
Útero hiperdistendido( polihidramnios, gemelar,
macrosomia)
Parto con actividad uterina vigorosa que en
el P. expulsivo.
Parto con actividad uterina débil (oligo o hipo
sistolia)
Parto precipitado (Hiperdinamias, incomp.
Cervical)
RPM, Amnionitis
Parto Prolongado.
Parto con Óbito fetal intrautero.
Embolia del liquido amniótico
Pre eclampsia eclampsia
Mala conducción del T.P.
Globo vesical intraparto.
Diagnostico
 Tratamiento
Preventivo
Etiológico
Medidas generales Pre y post parto/
cesárea

Control de la perdida sanguínea

Control en sala de partos hasta
recuperación
Control clínico preoperatorio
 Tratamiento de la hemorragia
❑Revisión manual de cavidad
❑Oxitócicos endovenosos en bolo o goteo
❑Taponamiento uterino/vaginal
❑Factores de coagulación
❑Inyección ergonovinicos en miometrio
❑Uso de Misoprostol ( 1000 mg) V. Rectal
 Ante persistencia de hemorragia o
agravamiento
❑
• Tipo de histerectomía preferente: total
Tratamiento de la Hipotensión-Shock
Abrir una segunda vía ( vía venosa central)
Movilizar equipo medico ( internista,
anestesista, transfusionista)
Preparar UTI
Control estricto de S. Vitales
Transfusión (sangre, plasma y albuminas)
Control de diuresis y función renal.
 Ante persistencia del cuadro
Descartar:
✓ Rotura uterina/hematoma retroperitoneal

✓ CiD
III. Lesiones por desgarro y
traumatismos del parto
Lesiones
 Tratamiento
Reparación adecuada

Controles cercanos posteriores PP p/ evolución

 IV. Coagulopatias
Poco frecuente

Modificaciones de la función COAGULO LITICA

Las modificaciones de los factores de la

coagulación observadas durante el embarazo
( aumento de fibrinógeno y plaminógeno)
disminuyen al momento del parto y
alumbramiento
Coagulopatias por alteración de la fase
formativa de la fibrina
CID: o coagulopatia de consumo
1 de C/ 2000 partos
Deposito de fibrina en la micro circulación

Consumo de factores de coagulación

 Causas
Feto muerto y retenido
Aborto séptico
Placenta previa
“Abruptio placentae”
Eclampsia
Embolia del LA
Hematoma retro placentario
Hemolisis intravascular
Embolia pulmonar masiva
Embarazo molar
Placenta acreta
DNP
 Tratamiento
Tratar el SHOCK
Supresión de causa: asegurar la vacuidad
uterina ( , )
Corrección de Trast. hemostasia: a
bajas dosis.
total fresca, plasma fresco
Concentrado de
puro.
Purpura Trombocitopenica
Inmunologica
Tratamiento