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ALEJANDRA VÉLEZ PEREA

Res. Ginecología y Obstetricia


TRASTORNO HIPERTENSIVOS DEL
EMBARAZO

Task Force. HYPERTENSION IN PREGNANCY. The American College of Obstetrician and Gynecologists. 2013
TA ≥ 140/90
PREECLAMPSIA Embarazo > 20ss

Proteinuria: > 300mg/24hr


Rx Proteinuria/Creatinuria > 0.3mg/dL
Proteinuria espontánea cualitativa > +

Trombocitopenia, PLT < 100.000

Disfunción hepática, elevación de las transaminasas dos


veces por encima de su valor normal
Falla renal, creatinina >1.1 o doblar su valor en menos
de 24hr en ausencia de enfermedad renal

Edema pulmonar

Cefalea, fosfenos, tinitus

Task Force. HYPERTENSION IN PREGNANCY. The American College of Obstetrician and Gynecologists. 2013
PREECLAMPSIA SEVERA

Task Force. HYPERTENSION IN PREGNANCY. The American College of Obstetrician and Gynecologists. 2013
MORTALIDAD POR PREECLAMPSIA

Complicación Frecuencia Mortalidad

Eclampsia 3 al 5% 14%

Síndrome Hellp 10% 3 al 10%

ACV 5% 40%

Edema 20% 1%
pulmonar
Ruptura 1% 75-90%
hepática
Sibai. Obstet Gynecol 2005; 105 (2): 402-410
E
T
G
I
Í
O
A
L
O
Factores Angiogenicos

• Diferenciación e
invasión del trofoblasto

• Desarrollo vascular
fetoplacentario

• Remodelación
vascular materna
FATORES ANTIANGIOGENICOS

 sFlt-1
 Trombospondina-1

 Endoglina

 Fragmentos truncados
de prolactina

 sEng
PREDICCIÓN Biochemical markers

Factores de riesgo maternos


Detection rate (FP 10%)

Doppler de arteria uterinas


early PE late PE
Fibronectina
PlGF 60% -
PAPP - A
PAPP-A 60% 45%
Proteína placentaria 13
sEng 47% -
Tensión arterial media
Inhibin A 40% 17%
Factor de crecimiento placentario
PP13
Factores Angiogénicos 38%
- Antiangiogénicos -

Poon 2009, Akolekar 2009, Poon 2010, Audibert 2010, Foidart 2010, Wortelboer 2010,
FACTORES DE RIESGO

Factor de Riesgo RR
Edad Materna > 40 años 1.96
Nulípara 3
IMC > 35 4
Gemelar 2,93
Sx Ac Anti-fosfolípidos 9.7
Antecedente personal 7.2
Antecedente familiar 2-4
Etnia 3.1
HTA Crónica 4–5
Diabetes 4
U T I L I D A D DE C O M B I N A C I O N D E P R U E B A S

Tasa de deteccion (IC 95%)

Falsos (+) 10%


HTA
PE TEMPRANA PE TARDIA
GESTACIONAL
Fx maternos 47 (22 – 65) 41 (32 – 50) 30 (23 – 39)
Fx maternos + I.P. 81 (65 – 92) 45 (36 – 54) 35 (27 – 43)
Fx maternos +
TAM 75 (58 – 88) 52 (43 – 61) 47 (39 – 56)

Todos 89 (74 – 96) 57 (48 – 65) 50 (41 – 58)

Poon LC., Karagiannis G., Leal A., Romero XC. And Nicolaides KH, Hypertensive disorders in pregnancy: screening by
uterine artery Doppler imaging and blood pressure at 11-13 weeks. Ultrasound Obstetric and Gynecoly. 2009 Nov;
34(5):497-502.
PREVENCIÓN

CALCIO
 1gr/día
 Antioxidantes:
 Ptes con déficit Vitamina C y E
en dieta
 Reposo en
ASPIRINA cama
 80-150mg <16ss
  riesgo 60%  Dite restrictiva
 PES NNT 50 / PENS NNT en sal
500

Ronilk et al, Combined Multimarker Screening and Randomized Patient Treatment with Aspirin for Evidence-Based Preeclampsia
Prevention , The new england journal of medicine; 2017, vol. 377 no. 7
C
O
M
P O
L N
I E
C S
A
C
I
CRISIS
HIPERTENSIVAS

El objetivo es disminuir
la presión arterial a un
nivel que se controle el
daño de órgano blanco y
evitar Hipotensión
Terminología Definición Metas de tratamiento

TA >180/120 + Lesión de Disminución inmediata de TA sin


Emergencia
órgano blanco llegar a niveles normales

TA >180/120 + No lesión de Reducción de TA en un periodo de


Urgencia
órgano blanco 24 horas

“Crisis hipertensivas”
Tensión arterial sistólica (TAS) ≥ 160 mmHg o
tensión arterial diastólica (TAD) ≥ 110 mmHg

 TAS > 160 mm Hg: ppal factor asociado con ACV siendo el limite indiscutible de
inicio de antihipertensivos en preeclampsia/eclampsia
 80% de gestantes con TAS mayor de 180 mmHg pueden hacer ACV

Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)
Marik, Varon. Chest 2007; 131:1949–1962
Mc Coy. Am J Health-Syst Pharm 2009; 66 (15): 337-349
Ghanem. Cardiovascular Therapeutics 2008; 26: 38–49
TRATAMIENTO

META TAS < 150 y TAD <100


 Meta-análisis: 21 estudios: 893 ptes
 8 compararon Hidralazina Vs Nifedipino
 5 estudios compararon Hidralazina Vs Labetalol

 Concluyó: Hidralazina NO podía ser droga de primera línea


 Fue menos efectiva que Nifedipina y similar a Labetalol pero con
peor resultado materno y perinatal
 Fue la peor tolerada de los antihipertensivos
 El principal problema del uso agudo de estos medicamentos es la
Hipotensión
 ECC: 200 ptes comparó: Hidralazina máx 25 mg Vs Labetalol máx
300 mg
 Evaluaron control de Presión Arterial e Hipotensión
 No hubo diferenias significativas para hipotensión materna
 Mayor incidencia de palpitaciones y taquicardia con Hidralazina ( p
=0.05)

 RN: resultados similares, con hipotensión y bradicardia


significativamente más frecuentes en Labetalol
 Concluyó que hidralazina y Labetalol son igual de efectivos en el
manejo de Emergencia HTA
 ECC: 50 mujeres

 Nifedipino 10 mg x 5 dosis

 Labetalol: 20 – 40- 80 – 80 – 80 (300mg)

 Meta disminuir TA < 150/100


MANEJO DE CRISIS HIPERTENSIVA
Inicie manejo anti-hipertensivo de inmediato hasta lograr TAS entre 140 -
150mmHg y TAD entre 90-100mmHg:

• Nifedipino cápsulas o tabletas de 10mg cada 20 minutos por 3 dosis.

• En caso de NO alcanzar objetivo terapéutico de presión arterial en la primera hora


administre
• Labetalol ampollas de 100 mg/20mL con el siguiente esquema: bolo
endovenoso inicial de 20 mg (4mL); si a los 20 minutos no se alcanza el
objetivo terapéutico aplique nuevo bolo endovenoso de 40mg (8mL); si pasados
otros 20 minutos no se alcanza el objetivo terapéutico aplique nuevo bolo
endovenoso de 80mg (16mL); este último bolo se repetirá cada 20 minutos (si el
objetivo terapéutico no se ha alcanzado) por 2 dosis adicionales mas, hasta
completar una dosis acumulada de 300mg.
O
• Hidralazina ampollas x 20 mg/ 4mL: aplicar 5 mg (1mL) endovenosos cada 20
minutos hasta alcanzar objetivo terapéutico, con una dosis máxima
acumulada de 20mg.

• Terapia de mantenimiento con: Nifedipino cápsulas o tabletas x 30mg 1 cápsula o


tableta vía oral cada 8 horas.
MANEJO DE CRISIS HIPERTENSIVA
Embarazada o en el puerperio TAS ≥ 160mmHg y/o TAD ≥
110mmHg en una toma con o sin síntomas premonitorios

• Iniciar sulfato de magnesio ampollas al 20%-10ml (2g)


de la siguiente forma:
– Impregnación → 2 ampollas + 100mL SSN 0.9% para
pasar en 10 a 15 minutos (4 g) y continuar con
– Mantenimiento → 4 ampollas + 500mL SSN 0.9%
para pasar a 1 g/h: 67mL /hr por bomba de infusión;
ó a 10 gotas/minuto por macrogotero 10 gotas = 1mL

• Tomar exámenes según la disponibilidad de su


laboratorio: hemograma con recuento de plaquetas;
pruebas hepáticas: lactato deshidrogenasa (LDH),
transaminasas (AST y ALT); creatinina.
CLINÍCA
 Anemia hemolítica microangiopatica
 Esquistocitos en el extendido de sangre periférica
  Abrupta niveles de Hgb
  Reticulocitos
  Bilirrubina, ppal/ BI >1,2md/dl
  Haptoglobina < 1gr/L

 Daño hepático
  AST y ALT
  Glutatión S Transferasa α-1

 Trombocitopenia
Haram K., Svendsen E. And Abildgaard U., The HELLP syndrome: Clinical issues and management. A Review, BMC
Pregnancy and Childbirth: February 2009
DIAGNÓTICO

Haram K., Svendsen E. And Abildgaard U., The HELLP syndrome: Clinical issues and management. A Review, BMC
Pregnancy and Childbirth: February 2009
TRATAMIENTO

 Finalizar el embarazo

 Medidas de soporte
• Prevención de las convulsiones.
• Control de la tensión arterial.
• Control de los trastornos de la coagulación.
• Control y reposición de volúmenes.
• Evaluación del estado materno-fetal.
TRANSFUSIÓN DE HEMODERIVADOS

 Transfusión de plaquetas en toda pte con PLT < 20000

 Transfusión de plaquetas en ptes con recuento entre


20000 – 50000 que van a ser llevadas a cirugía

 No se debe transfundir PLT en ningún caso en ptes


con recuento de PLT >50000

 En caso de transfusión de PLT se recomienda


administrar mínimo 6 unidades de PLT
ESTEROIDES

 Disminuye el edema

 Inhibe la activación endotelial

 Prevención de la anemia microhemolítica


angiopática

 Inhibición de la producción de citoquinas


bstetrics and Gynecology (2005) 193, 1591–8
www.ajog.org
www.ajog.org

EDI TORS’ CHOI CE


EDITORS’ CHOICE www.ajog.org

Dexamet hasone t reat ment does not improve t he out come


Dexamethasone treatment does not improve the outcome
E ofofwomen wit hHELLP
women with HELLP syndrome:
syndrome: A double-bl ind,
A double-blind,
placebo-cont
hasone rolled,
placebo-controlled,
t reat ment randomized
randomized
does clinicalclinical
not i trial
mprove t rialt he out come
n wi tJavier
Javiher EHE
E.
LLPMD,
. Fonseca,
Fonseca, MD,
syndrome:
MS
MSc,
a,b,c
c,Fabián
a,b,c Fabi APhD,
double-bl
án Méndez,
Méndez, MD,
a
aMD, PhD, Claudi
Claudia Cataño,
ib,cnd,
MD, a Cat año, MD,b,c
d
Fernando
Fernando Ari as,MD,
MD, PhD
d
ont rolled, Arias, randomi
PhD zed cli ni cal t ri al
a a and School of M edicine, b
School of ofPublic
School H ealth
Public Health
a,b,c and School of M edicine,b Universidad
Universidad del Valle;
del Valle; Department Department
of Gynecology
a of Gynecology and Obstetrics,
and Obstetrics, b,c
seca,H ospital
MD, MS c,
Universitario del F cabi
Valle, c án
Cali, Méndez,
Colombia; MD,
Department of P hD,
Obstetrics C
and laudi a C
Gynecology,
Hospital Universitario del Valle, Cali, Colombia; Department of Obstetrics and Gynecology, The Toledo Hospital, at Toledo
The año,H MD,
ospital,
d of OH dOH d
as, MD,
M edical PCollege
hD
M edical College of Ohio,
Ohio, Toledo,
Toledo,

 ECC
Received
Received forforpublication
publication MM
arch 15, 2005;
arch revisedrevised
15, 2005; April 4, 2005;
A prilaccepted Julyaccepted
4, 2005; 5, 2005 July 5, 2005

ealth and School of M edicine, b Universidad del Valle; Department of Gynecology and Obst etrics,
a

 Objetivo: Determinar le eficacia de la dexametaxona


r io del Valle, c Cali, Colombia; Department of Obstetr ics and Gynecology, The Toledo H ospital,
Ohio, KE YKEY
WO
Toledo,
WORDS
RDSOH d
Dexamethasone
Objective:
ObjectThe
ive:purpose of this study
The purpose of was
thistostudy
determine
wasthetoefficacy of dexamethasone
determine for of dexamethasone for
the efficacy

en el tratamiento del síndrome HELLP


D examethasone treatment of HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome.
treatment of H EL L P (hemolysis, elevated liver enzymes and low platelet count) syndrome.
HELLP (hemolysis, Study design: A prospective, double-blind clinical trial was conducted among 132 women with
H EL L P (hemolysis, St udy4,
design: A accepted
prospective, double-blind clinical trial was conducted among 132 women with
ion M arch 15, 2005; revised A pril
elevated liver 2005; July 5, 2005
HELLP syndrome who were assigned randomly to treatment or placebo groups. Pregnant women

 Octubre 2001 –experimental


Septiembre 2003, doses ofCali, Colombia. HUV
elevated liver
enzymes and lowH EL L P syndrome who were assigned randomly to treatment or placebo groups. Pregnant women
in the experimental group received 10-mg doses of dexamethasone intravenously every 12 hours
enzymes and low
platelet count)in the group received 10-mg dexamethasone intravenously every 12 hours
until delivery and 3 additional doses after delivery. Puerperal women received 3 10-mg doses of
platelet count)
syndrome until delivery and 3 additional doses after delivery. Puerperal women received 3 10-mg doses of
dexamethasone after delivery. The same schedule was used in the placebo group. The main
syndrome
Obj
Clinical trial dexamethasone
ect i ve: The outcome
purpose variableof after
this
was the delivery.
study
duration wasThe to
of hospitalization.same schedule
Indetermine
addition, was the
we evaluated used in the
efficacy
treatment placebo
effects group. The main for
of dexamethasone
Clinical treatment
trial of H EL outcome
L time
on the variable
P (hemolysis, was the
elevated
to recovery of laboratory duration liver
and clinical of hospitalization.
enzymes
parameters I n
and low
and on frequency addition, we evaluated
platelet count)
of complications. treatment effects
syndrome.
s, St udy desi gn: AResults:on the time to recovery
The mean duration
prospective, of laboratory
of hospitalization clinical
double-blind and clinical
of patients who
trial parameters
received
was dexamethasoneand
conducted on frequency
therapy of complications.
among 132 women with
H EL L P syndrome was R esult s:
shorter
who thanThe
were mean
in the duration
placebo
assigned group ofvshospitalization
(6.5
randomly 8.2 days),
tobut thisof
treatment patients
difference waswho
or received
not statistically
placebo dexamethasone
groups. Pregnant therapy
women
w significant
was (P =
shorter .37). No
than significant
in the differences
placebo were
group found
(6.5 in
vs
in the experimental group received 10-mg doses of dexamethasone intravenously every 12 hours the
8.2 time to
days), recovery
but thisof platelet
difference was not statistically
counts (hazard ratio,(P1.2;
= 95% CI,N 0.8-1.8), lactate dehydrogenase (hazard
wereratio, 0.9; in
95%theCI,time
0.5- to recovery of platelet
until delivery and significant
3 additional .37).
doses oafter
significant
delivery.differences
Puerperal found
women received 3 10-mg doses of
1.5),counts
aspartate(hazard
aminotransferase (hazard ratio, 0.6; 95% CI, 0.4-1.1) and
ratio, 1.2; 95% CI , 0.8-1.8), lactate dehydrogenase (hazardto the development of ratio, 0.9; 95% CI , 0.5-
dexamethasone complications.
after delivery. The results The same schedule
were found in both(hazard
pregnant and was
puerperal used
women. in the placebo group. The main
1.5), aspartate aminotransferase ratio, 0.6; 95% CI , 0.4-1.1) and to the development of
outcome variable was
Conclusion: the duration
The resultsThe
of this of hospitalization.
investigation do notinsupport I n addition,
the use of dexamethasone we evaluated treatment effects
complications. results were found both pregnant and puerperalforwomen.
k
Reference category.

Table IV Complications associated with HELLP syndrome


according to steroids use
Placebo Dexamethasone R.R. crude
Complication n (%) n (%) (95% CI)
Acute renal 8 (12.9) 6 (10.0) 0.8 (0.29-2.10)
failure*
Oliguria 4 (6.06) 5 (7.58) 1.3 (0.35-4.45)
Pulmonary 1 (1.54) 3 (4.62) 3.1 (0.32-28.09)
edema*
Eclampsia 10 (15.15) 8 (13.79) 0.8 (0.34-1.90)
Infections 10 (15.15) 5 (7.58) 0.5 (0.18-1.38)
Dead 1 (1.52) 3 (4.62) 3.0 (0.32-28.1)
Platelets 10 (15.15) 12 (18.18) 1.2 (0.56-2.58) Figure 3 I n
transfusión platelet cou
Plasma 6 (9.09) 5 (7.58) 0.8 (0.27-2.60) patients with
transfusión
* Only included patients without the event before randomization. tions, reco
need, or du
before randomization. Platelet transfusion was found to women, the
be associated with the development of renal failure be lower in
(odds ratio, 4.0; 95% CI , 1.1-14.3) and A ST levels at those wome
enrollment. vs 8.2 day
H
E
L
L
PLASMAFERESIS
 Pacientes que no a la finalización del embarazo, los esteroides
o la terapia de apoyo

 Recuperación mas rápida de los niveles de plaquetas, y


descenso de LDH, AST y ALT

 Disminución de la mortalidad

 Beneficio e Ptes con Sx HELLP clase I


Bulent Eser et al, The Role of Plasma Exchange in HELLP Syndrome, Clin Appl Thrombosis/Hemostasis: 2005; 11(2):211–217
 Universidad de Inonu, Turquía 2014
 Ptes con Sx HELLP clase I, sin respuesta al manejo inicial en las primeras 24hr
 3 Sesiones de plasmaferesis
Presencia de una o más convulsiones
generalizadas, estado de coma o ambos, en el E
embarazo o postparto en pacientes con
P
C
preeclampsia y en ausencia de otros trastornos
neurológicos
S
L
I
A
A
M
Sibai B., Diagnosis, Prevention, and Management of Eclampsia. The American College of Obstetricians
and Gynecologists; 2005: VOL. 105, Nº 2
Tiempo de presentación

• 0.95 – 2.2 % de todos los embarazos


 Anteparto 38 – 53%
• 38% de las convulsiones ocurren con
TA 140/90 o menos
 Intraparto 18 – 36%

 Posparto 11 – 44%
 >50% en las primeras 48 horas
 Reportes hasta 23 días postparto
Sibai B., Diagnosis, Prevention, and Management of Eclampsia. The American College of Obstetricians and Gynecologists; 2005: VOL. 105, Nº 2
Mortalidad 1-15%
Países desarrollados 0 – 1.8%
Países subdesarrollados 15 %

Causas de Mortalidad
Hemorragia cerebral 43%
Falla renal 26%
CID 11%
Edema cerebral 4%

MORTALIDAD
CON TTO <1%

1.
Ghulmiyyah Labib and Sibai Baha, Maternal Mortality From Preeclampsia/Eclampsia. Semin Perinatol; 2012: 36:56-59

2.
Vigil-De Gracia Paulino, Maternal deaths due to eclampsia and HELLP syndrome . International Journal of Gynecology and
Obstetrics. 2008
M agnesium Sulfate for the Treatment of Eclampsia : A Brief Review
Anna G. Euser and Marilyn J. Cipolla

M S A Vasodilatación
Stroke. 2009;40:1169-1175; originally published online February 10, 2009;
doi: 10.1161/STROKEAHA.108.527788
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2009 American Heart Association, Inc. All rights reserved.

E MC Print ISSN: 0039-2499. Online ISSN: 1524-4628

C O C Barrera Hemato-
I Encefalica
The online version of this article, along with updated information and services, is located on the
A World Wide Web at:
http://stroke.ahajournals.org/content/40/4/1169

N D Ò
I E N Anticonvulsivante
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Anna G. Euser and Marilyn J. Cipolla. Magnesium Sulfate for the Treatment of Eclampsia : A
Brief Review. Storke Journal American Heart association
A
AC
BN C
EE
AT
RR
RI
EE
RE
BB
ED
RR
RE
AA
AM
LL
A
Anna G. Euser and Marilyn J. Cipolla. Magnesium Sulfate for the Treatment of Eclampsia : A
Brief Review. Storke Journal American Heart association
A
A S
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TI V
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IV A
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CA N
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Anna G. Euser and Marilyn J. Cipolla. Magnesium Sulfate for the Treatment of Eclampsia : A
Brief Review. Storke Journal American Heart association
S
• 100% Renal
• Depuración total en 8 horas
• Alteración de la función renal
• Suspenderlo
• Disminuir su dosis a la
mitad si Cr >1.3
• En pte con falla renal las
manifestaciones tóxicas
aparecen a concentraciones
más bajas

DEPURACIÓN
Sulfato de Mg
EFECTOS ADVERSOS

• Flushing
• Nauseas
• Vomito
• Mareo
• Confusión
• Debilidad muscular
• Cefalea

• Dolor o quemazón en el sitio de la


infusión
• Sed
CONCENTRACION NORMAL DE MAGNESIO EN
SANGRE: 1.5 – 2.5mEq/l (1.8 to 3.0 mg/dL)

CONCENTRACION SERICA DE MAGNESIO


USADO EN PREECLAMPSIA 3.5 to 7 mEq/L (4.2
to 8.4 mg/dL)

TOXICIDAD
Arreflexia
8-10 mEq/L

La monitorización de los niveles


plasmáticos
Arresto
Cardiaco no es necesaria
Somnolencia
10-12 mEq/L
30 -35 mEq/L

Paro
Respiratorio
>13mEq/L
INTOXICACIÓN - MANEJO

 Interrumpir inmediata/ la administración de


sulfato de Mg

 GLUCONATO DE CALCIO
 Aumenta la concentración de Ach
 Presentación: Ampollas 10%  10cc  1gr
 Dosis: 1 g IV en10 min

 Realizar un EKG
 Diuréticos
EFECTIVIDAD
RR
SULFTATO Mg PLACEBO
IC 95%
Eclampsia 40 (0.8%) 96 (1.6%) 0.42 (0.29 – 0.60)

# Convulsiones
1 27 63
2 10 24
3 2 7
>4 1 1
Desconocido 0 1

ECLAMPSIA Reduce la aparición de convulsiones en


un 58%
SULFATO Mg Vs NNT 36 inminencia de eclampsia
PLACEBO 63 PE Severa y 129 para PE no severa
SULFTATO Mg PLACEBO

19Problemsatinjectionsite
DMorbilidad
A T A A NMaterna
D A N A L Y SES
1 9992 196Ri(3.9%)
skRatio (M-H,Fixed,95%CI) 183 (3.6%)1.78[1.52,2.08]
Depresión respiratoria 46 27
19.1 Intramuscul
Comparison 1.
Arresto arinjection 1 4553 Ris5kRatio (M-H,Fixed,95%CI) 2 1.49[1.25,1.79]
Magnesium sulphate versusnone/placebo (subgroupsby severity of pre-eclampsia)
respiratorio
Neumonía 14 6
19.2 Intravenousinjection 1
Outcome or subgroup title
Edema pulmonar
No. of
studies 5439 Ri32skRatio (M-H,Fixed,95%CI) 33 3.05[2.15,4.32]
No. of
participants Statistical method Effect size

1 Maternal death 2 10795 Risk Ratio (M -H , Fixed, 95% CI) 0.54 [0.26, 1.10]

20Placentalabrupti
Arresto cardiaco on
1.1 Severepre-eclampsia
1.2 Not severe pre-eclampsia
2 Eclampsia
2 2
1
6
8838 Ris4kRatio (M-H,Fixed,95%CI) 5 0.64[0.50,0.83]
3327
7468
11444
Risk
Risk
Risk
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
Difference (M -H , Fixed, 95% CI)
0.54 [0.19, 1.51]
0.54 [0.20, 1.45]
-0.01 [-0.02, -0.01]
Falla renal
2.1 Severepre-eclampsia 3 3555 49Risk 61
Difference (M -H , Fixed, 95% CI) -0.02 [-0.03, -0.01]

21Caesareansecti
Falla hepática on
2.2 Not severe pre-eclampsia
3 Serious maternal morbidity
3.1 Severepre-eclampsia
6 4
2
1
10096 Ri52skRatio (M-H,Fixed,95%CI) 67 1.05[1.01,1.10]
7889
10332
2642
Risk
Risk
Risk
Difference (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
-0.01 [-0.01, -0.00]
1.08 [0.89, 1.32]
1.23 [0.91, 1.66]
Coagulopatía
3.2 Not severe pre-eclampsia 2 7690
73Risk
86
Ratio (M -H , Fixed, 95% CI) 0.98 [0.75, 1.27]

22Inductionoflabour
4 Stroke
5 Pulmonary oedema
Accidente cerebrovascular
6 Pneumonia
1 1
3
1
8774 Ris3kRatio (M-H,Fixed,95%CI) 6 0.99[0.94,1.04]
10110
10560
10110
Risk
Risk
Risk
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
0.5 [0.13, 2.00]
0.97 [0.60, 1.57]
2.33 [0.90, 6.07]

23Postpartumhaemorrhage
7 Renal failure
8 Renal dialysis
9 Liver failure
2 1
2
1
8909 RiskRatio (M-H,Fixed,95%CI)
10110
10338
10110
Risk
Risk
Risk
0.96[0.88,1.05]
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
0.80 [0.55, 1.17]
0.70 [0.21, 2.32]
0.78 [0.54, 1.11]
10 Coagulopathy 1 10110 Risk Ratio (M -H , Fixed, 95% CI) 0.85 [0.62, 1.16]

24Manual removal of retai ned 1 - 8774 Ri skRati o (M-H,Fi xed,95%CI)


EN MORBILIDAD0.9MATERNA
0[0.72,1.12]
11 Cardiac arrest 1 10110 Risk Ratio (M -H , Fixed, 95% CI) 0.8 [0.21, 2.98]
12 Respiratory arrest 1 NO HAY
10110 DIFERENCIAS
Risk Ratio (M -H , Fixed, 95% CI) 2.5 [0.49, 12.88]

MORBILIDAD
13 Any antihypertensive therapy
14 Rapid acting antihypertensives
2
2
- SOLO HUBO UNA PEQUEÑA DIFERENCIA EN
10795 Risk
Risk
Ratio (M -H , Fixed, 95% CI)
Ratio (M -H , Fixed, 95% CI)
0.97 [0.95, 0.99]
Subtotals only
NECESIDAD DE CESAREA (RR 1.05, 95% CI 1.01-
placenta
14.1 Intravenous or
SULFATO Mg Vs
intramuscular hydralazine
14.2 Oral nifedipine
2

2
10338

10276
Risk Ratio (M -H , Fixed, 95% CI)

1.10) Risk Ratio (M -H , Fixed, 95% CI)


0.93 [0.86, 1.00]

0.93 [0.88, 0.99]


PLACEBO
15 Progression from mild to severe 2 - 357FACTOR PROTECTOR
Risk Ra ABRUPTIO
tio (M -H , Fixed, 95% CI) DE PLACENTA
0.91 [0.53, 1.55]

25Inspecial carebabyunit >7 1


pre-eclampsia
16 Toxicity
16.1 Absent or reduced
3
2
8260 RiskRatio (M-H,Fixed,95%CI)
10677
DISMINUYE RIESGO
Risk Ratio (M -H , Fixe26%
d, 95% CI)
Risk Ratio (M -H , Fixed, 95% CI)
1.02[0.93,1.11]
Subtotals only
1.00 [0.70, 1.42]
•  Recurrencia de convulsiones 59% (RR 0.41; 95% CI,
0.32-0.51)
• Mortalidad Materna 38% (RR 0.62; 95% CI, 0.39-0.99)

SIBAI Siba Baha Mi, Magnesium sulfate prophylaxis in preeclampsia: Lessons


learned from recent trials. American Journal of Obstetrics and
Gynecology; 2004: Vol190 Nº 1520e6
SULFATO DE
MAGNESIO
Which anticonvulsant for women with eclampsia? Evidence from
the Collaborative Eclampsia Trial
The Eclampsia Trial Collaborative Group*

Summary Introduction
Eclampsia, the occurrence of a seizure in association with Eclampsia is defined as the occurrence of one or more
pre-eclampsia, convulsions in association with the syndrome of pre-
Magnesium sulphateremains an important
versus diazepam of maternal
cause(Review)
for eclampsia
mortality. Although it is standard practice to use an eclampsia. Pre-eclampsia is a multisystem disorder that is
anticonvulsant for management of eclampsia, the choice of
Duley L, Henderson-Smart DJ, Walker GJA, Chou D
usually associated with raised blood pressure and
agent is controversial and there has been little properly proteinuria. In Europe and other developed countries
controlled evidence to support any of the options. 1687 eclampsia complicates about 1 in 2000 deliveries,’ while
women with eclampsia were recruited into an international
in developing countries estimates vary widely, from 1 in
100 to 1 in 1700.=-4
multicentre randomised trial comparing standard
Over half a million women die each year of pregnancy-
anticonvulsant regimens. Primary measures of outcome
related causes, and 99% of these deaths occur in the
were recurrence of convulsions and maternal death. Data
are available for 1680 (99&middot;6%) women: 453 allocated
developing world. 5,6 Although rare, eclampsia probably
accounts for 50 000 maternal deaths a year worldwide.7 In
magnesium sulphate versus 452 allocated diazepam, and areas where maternal mortality is very high, infection and
388 allocated magnesium sulphate versus 387 allocated
haemorrhage are the main causes of death;8 but as deaths
phenytoin. Most women (99%) received the anticonvulsant from these causes become less common, those associated
that they had been allocated. with hypertension and eclampsia assume greater
Women allocated magnesium sulphate had a 52% lower
importance. In the UK, eclampsia is a factor in 10% of
risk of recurrent convulsions (95% Cl 64% to 37% direct maternal deaths.9 Successful prevention of all cases
reduction) than those allocated diazepam (60 [13&middot;2%] vs of eclampsia is likely to be difficult,’ therefore it is
126 [27&middot;9%]; ie, 14&middot;7 [SD 2&middot;6] fewer women with recurrent important to assess the relative merits of alternative
convulsions per 100 women; 2p<0&middot;00001). Maternal treatments for eclampsia.
mortality was non-significantly lower among women Standard practice is to use anticonvulsants to control
Sulfato Mg Vs Diazepam
Sulfato Mg 70
Vs
60
Diazepam
50

Número de mujeres
40

SULFATO MG
30
DIAZEPAM

20

A 10

0
1 2 3 4 5 >5

M
Número de recurrencia de convulsiones
Sulfato Mg
Vs
Diazepam
 Mortalidad materna RR 0,59; IC del 95%: 0,38 a 0,92

 Recurrencia de convulsiones NNT 7; IC del 95% 5 a


9 mujeres

 No hubo diferencia en morbilidad materna


extrema

 No hubo diferencias en muerte perinatal

 Diferencias significativas en el puntaje de APGAR y


los días de estancia en uci neonatal
Sulfato Mg Sulfato Mg Vs Fenitoina
Vs
40

35
Fenitoina 30

Número de mujeres
25

20
SULFATO MG
15
FENITOINA

I
10

0
1 2 3 4 5 >5

N
Número de recurrencia de convulsiones

O
*Not known whether prior anticonvulsant was given to 11 women allocated MgS04 and to 7 allocated diazepam
tNot known whether prior anticonvulsant was given to 3 women allocated MgS04 and to 6 allocated phenytoin
Sulfato Mg
Vs
Fenitoina
 No hay diferencias en mortalidad materna

MORBILIDAD MATERNA
 Menor necesidad de ventilación mecánica
 Menor Neumonía
 Menor necesidad de ingreso a UCI

MORTALIDAD PERINATAL
 No hay diferencias

MORBILIDAD PERINATAL
 Mejor puntaje de APGAR
 Menor necesidad de ventilación mecánica
 Menor ingreso a UCI (RR 0.73, 95% CI 0.58–0.91)
CUANTO TIEMPO

ECC compara la administración sulfato de magnesio


durante 12 horas Vs 24 horas en el postparto inmediato de
mujeres con preeclampsia severa estable.
120 Ptes postparto con preeclampsia severa,
estables : 24 horas vs 12 horas
Manejo alternativo del sulfato de Magnesio
en mujeres con preeclampsia severa e
inminencia de eclampsia
Embarazo Normal
Velocidad sistólica

Presión
perfusión Resistencia

Flujo sanguíneo cerebral aumenta 10%


Rango de TAM: 65 y 120 mmHg

Autorregulación cerebral
BAROTRAUMA
 Presión persistentemente elevada debilita y destruye tejido
especialmente el endotelio

 Daño del vaso sanguíneo:


 Extravasación de fluido

 Daño endotelial

 Daño de muscular
Medicamento ideal  CPP Pero q mantenga el CFI
NIMODIPINO

 Calcio antagonista

 Vasodilatador periférico arteriolar   RVS y


la postcarga

 El efecto en circulación venosa es mínimo

  Diuresis (natriuretico)  Vasodilatador renal

  FC  y el Índice cardiaco

 La perfusión cerebral


RR 3.2 ( IC 95 1.1 - 9.1).
LABETALOL
 Bloqueador selectivo α1 y bloquedor No selectivo β
1 -2

  RVS

  FC y el consumo de oxigeno

 No compromete el flujo periférico: cerebro, riñón y


coronarias

 No compromete el flujo uteroplacentario


Labetalol como profilaxis de eclampsia
 2002-2005 estudio piloto Labetalol Vs Sulfato Mg

 Eclampsia labetalol 1.1% vs MgSO4 1.4%, P 0.7

 No hubo diferencias significativas en:


 Abruptio de placenta (2,6% labetalol vs 0% MgSO4)
 Cesárea por sufrimiento fetal (35% Labetalol vs 46% MgSO4)
 HHP (2,0% labetalol vs 0,5% MgSO4)
 Edema pulmonar (0,5% labetalol vs 0% MgSO4)
 El grupo de MgSO4 requiro mas antihipertensivos

 Iguales resultados neonatales

PRELIMINARY DATA FROM THE


LABETALOL VERSUS MAGNESIUM SULFATE
STUDY
Labetalol versus Magnesium Sulfate for the
Prevention of Eclampsia Trial

• ECC
• 4000 ptes reciben Labetalol Vs 4000 ptes reciben sulfato
Magnesio
• Resultado primario: Incidencia de convulsiones

LAMPET
CONCLUSIONES

La preeclampsia es una enfermedad de alto


impacto mundial con una significativa morbi-
mortalidad

Identificar las Ptes a riesgo

Prevención primaria

Diagnostico temprano y oportuno

Manejo de la crisis hipertensivas. Prevención


de las convulsiones y el edema pulmonar
GRACIAS

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