Professional Documents
Culture Documents
Scope
Terminology Risk
and classification
Incidence
3.7
I. Gestational hypertension
BP
>= 140/90 mmHg for first time during 140/ pregnancy No proteinuria BP returns to normal < 12 wk postpartum Final diagnosis made only postpartum May have other signs & symptoms of preeclampsia , eg. epigastric discomfort or thrombocytopenia
>= 140/90 mmHg before pregnancy or 140/ diagnosed before 20 wk , not attributable to GTD or Hypertension first diagnosed after 20 wk and persistent after 12 wk postpartum
Essential familial hypertension Obesity Arterial abnormalities Endocrine disorders Glomerulonephritis Renoprival hypertension Connective tissue disease PCKD ARF
III. Preeclampsia
Preeclampsia
Mild preeclampsia BP >= 140/90 mmHg after 20 wk gestation 140/ Proteinuria >= 300 mg/24hr or >=1+ dipstick mg/24hr >=1
Severe preeclampsia
Anyone who meets at least two of the following signs:
BP >= 160/110 mmHg 160/ Proteinuria 5 g/24hr or >= 2+ dipstick (persistent) g/24hr Cr > 1.2 mg/dl Platelets < 100,000 /mm3 100, /mm3 Microangiopathic hemolysis Elevated ALT or AST Persistent headache , visual disturbance , epigastric pain
IV. Eclampsia
Seizures Seizures
are generalized May appear before , during or after labor 10% develop after 48 hr postpartum 10%
V. Superimposed preeclampsia
New
onset proteinuria >= 300mg/24 hr in 300mg/24 hypertensive women but no proteinuria before 20 wk A sudden increase in proteinuria or BP or platelet count < 100,000 in women with 100, hypertension and proteinuria before 20 wk
Diagnosis
Gestational HT
Also
called transient HT Final Dx : after delivery , by exclusion BP : resting BP , Korotkoff phase V is used to defined diastolic pressure GHT may later develop preeclampsia 10% of eclamptic seizures develop before 10% overt proteinuria is identified BP rise , increase both mother and fetus risks
Preeclampsia
Described
as pregnancy-specific pregnancysyndrome of reduced organ perfusion secondary to vasospasm and endothelial activation Proteinuria & glomerular pathology develop late in the course , pathophysiologic process begin as early as implantation
Preeclampsia
Diastolic hypertension >= 95 , increase fetal death rate 3 fold Worsening proteinuria resulted in increasing preterm delivery Epigastric pain from hepatocellular necrosis , ischemia and edema that stretches Glisson capsule Thrombocytopenia from platelet activation & aggregation , microangiopathic hemolysis induced by severe vasospasm
Preeclampsia
Hematuria
, Hyperbilirubinemia : indicative of severe disease Cardiac dysfunction , pulm edema , obvious IUGR : indicative of severe disease Severity of preeclampsia assess by freq & intensity of abnormalities
maternal age Race and ethnicity (genetic predisposition & envoronmental factor) Multifetal gestation Obesity BMI > 35 kg/m2
Superimposed preeclampsia
1. Hypertension (>=140/90) is documented (>=140/90) antecedent to pregnancy 2. Hypertension is detected before 20 wk , unless there is GTD 3. Hypertension persists long after delivery Additional previous Hx or family Hx of HT End organ damage : LVH , retinal change Risk abruption , IUGR , preterm & death
Etiology?
Etiology
Theory account for the observation hypertensive disorder more likely to develop in : 1. exposed to chorionic villi for first time 2. exposed superabundance of chorionic villi (Twin ,mole) 3. Preexisting vascular disease 4. Genetic predisposition
Etiology
1. Abnormal trophoblastic invasion of uterine vessels 2. Immunological intolerance between maternal and fetoplacental tissues 3. Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy (vasculopathy) 4. Dietary deficiencies 5. Genetic influences
implantation , uterine spiral arteries undergo extensive remodeling as they are invaded by endovascular trophoblasts Incomplete invasion (decidual vessels , not myometrial vessels) : preeclampsia
Atherosis : pathology
Endothelial damage Insudation of plasma constituents into vessel walls Proliferation of myointimal cells Medial necrosis Lipid accumulation in myointimal cells & macrophages Aneurysmal dilatation Obstruction of spiral arteriole
2. Immunological factors
Acute
graft rejection Impaired formation of blocking antibodies to placental antigenic sites Lack of effective immunization in first pregnancies Lower proportion of Th1 , Th2 dominance Th1 Th2
2. Immunologic factors
Increased
risk for first conception , new partner , conception very shortly after beginning sexual relation (5% if > 12mo) (5 12mo) Any kind of previous pregnancy (completed , spontaneous miscarriage or elective abortion) protective against preeclampsia Tolerate semi-allogenic graft through semifathers alloantigen
2. Immunological factors
IL10 IL10
regulate s arterial pressure in early primate pregnancy IL-10 & TNF : vasodilation of early ILpregnancy Anti-human IL-10 MAb caused significant AntiILincrease in MAP TNF- alone or combine with IL-10 not TNFILalter MAP
2. Immunological factors
Serum
from preeclamptic pt contains IgG autoantibody Reacts with AT1 receptor AT1 AT1-AA induce signaling in vascular cells AT1 and trophoblasts Including AP-1 and NF-kB activation APNF Results in tissue factor production , reactive oxygen species (ROS)generation
changes Decidua activated , release noxious agents provoke endothelial cell injury Endothelial cell dysfunction Cytokines : TNF , IL
stress (ROS , free radical) selfselfpropagating lipid peroxides formation Generate highly toxic radicals injure endothelial cells Modify NO2 production NO2 Interfere PG balance
stress : produce lipid-laden lipidmacrophage foam cells Activation of microvascular coagulation : Thrombocytopenia Increased capillary permeability : proteinuria and edema
4. Nutritional factors
Dietary
taboos : meat , protein , purines , fat , dairy products , salt Supplement of Zn , Ca , Mg prevent preeclampsia ? Fruits & vegetables : antioxidant Ascorbic acid intake < 85 mg/d , predispose preeclmapsia 2 fold Obesity increase risk preeclampsia
5. Genetic factors
Hereditary
hypertension, preeclampsia ,
eclampsia Polygenic inheritance Asso with HLA-DR4 HLA-DR4 Maternal Ab against fetal anti HLA-DR Ig HLA Heterozygous for angiotensinogen gene variant T235 T235 Polymorphisms of genes for TNF , IL 1 , Lymphotoxin
Genetics of preeclampsia
Familial
predisposition AGT(encode angiotensinogen) & NOS 3 (encode nitric oxide synthestase) genes mutation
IgG Ab against HSV-2 , CMV , HSVEBV , Toxoplasma gondii at first ANC Seronegative for HSV-2, CMV , EBV HSVincreased risk preeclampsia (OR 1.7 ,1.6, 3 .5) Seronegative for Toxo not associated with increase risk preeclampsia (OR 1.0)
Pathogenesis
Vasospasm Endothelial
cell activation
Increased pressor resonses Prostaglandins Nitric oxide Endothelins Angiogenic factors (VEGF , PIGF)
Pathogenesis
Increased
vascular reactivity to vasopressor Decrease PG I2 production by endothelium Increase TxA2 secretion by platelet Increased NO2 synth by endothelium Decrease NO2 synthease
Pathophysiology
Endothelial
damage Interstitial leakage Platelet & fibrinogen deposit Increase subendothelial a. resistance Decreased blood flow Ischemia necrosis , hemorrhage Multiorgan involvement
Complications
Cardiovascular system
Increase
after load Preload diminish Endothelial activation with extravasation Decreased cardiac output Hemoconcentration from generalized vasoconstriction and endothelial dysfynction Decreased blood volume
from platelet activation, aggregation & consumption Increased platelets activating factor & thrombopoietin Clotting factors decrease Erythrocytes rapid hemolysis (increase LDH , schizocyte , MAHA)
Volume homeostasis
Decrease
plasma levels of renin , AT II , aldosterone DOC increase Vasopressin normal despite decreased plasma osmolality ANP increased Extracellular fluid : edema : endothelial injury , reduced oncotic pressure
Kidney
RPF
& GFR reduced Uric acid elevated Creatinine clearance reduced , oliguria Diminished urinary Ca due to increased tubular reabsorption Urine sodium elevated Urine osmolality , U:P Cr , FE Na : prerenal mechanism
Kidney
Proteinuria
: glomerulopathy : increased permeability : albumin , Hb , globulin , transferins changes : glomeruli enlarge , capillary loops dilated & contracted , endothelial cells swollen fibrils deposit (glomerular capillary endotheliosis)
Anatomical
Kidney
Renal
tubular lesions : degenerative change , accumulation with casts ARF from ATN Oliguria , azotemia induced by hypovolemia Preeclampsia with ARF occur in HELLP syndrome , placental abruption 1/3 Rarely , irreversible renal cortical necrosis
Liver
Periportal Elevated
transaminase HELLP syndrome Bleeding cause hepatic rupture(mortality 30%) 30%) , subcapsular hematoma Conservative treatment Recombinant factor VIIa
HELLP syndrome
No
strict definition Incidence 20% of severe preeclampsia or 20% eclampsia Factors contributing to death : include stroke , coagulopathy , ARDS , ARF , sepsis Insufficient evidence : adjunctive steroid
Brain
Headache
& visual symptoms associated with eclampsia Two cerebral pathology related 1. gross hemorrhage due to ruptured a. caused by severe HT 2. more widespread , edema hyperemia , ischemia , thrombosis & hemorrhage caused by preeclampsia
Neuroimaging
CT
: hypodense area in cortex , correspond to petechial hemorrhage and infarctions Remarkable changes in area of distribution of posterior cerebral a.
MRI
: hyperperfusion due to vasogenic edema Eclampsia : 25% were area of infarction 25%
doppler ultrasonography Preeclampsia : increase perfusion pressure , counter by increase cerebrovascular resistance(net no change) Eclampsia : loss of autoregulation , hyperperfusion similar to hypertensive encephalopathy Eclampsia caused by transient loss of cerebrovascular autoregulation
Blindness
Visual
disturbance common in SPE It follows eclampsia in >10% >10% Develop upto 1 wk or more after delivery Called Amaurosis Extensive ocipital lobe vasogenic edema Resolve completely in all case Rare cerebral infarct or retinal a. ischemia Retinal detach : resolve within 1 wk
Cerebral edema
Widespread
vasogenic edema S&S : Lethargy , confusion , blurred vision, coma Waxed & waned Rx : Manitol , Dexamethasone
Uteroplacental perfusion
Compromised
uteroplacental perfusion from vasospasm Mean diameter of myometrial spiral arterioles decrease Doppler flow velocity of uterine artery Ring-like : higher in peripheral than in Ringcentral vessels Preeclampsia was higher resistance
Prediction
Biological
faulty placentation reduced placental perfusion , endothelial cell activation & dysfunction , activation of coagulation
HOW?
1. Roll-over test Roll2828-32 wk Abnormally sensitive to infused angiotensin II Positive predictive value 33% 33%
Uric acid
Decreased
renal urate excretion in preeclampsia Serum uric acid exceeding 5.9 at 24 wk (PPV 33%) 33%) Not useful in differentiating GHT from preeclampsia
Fibronectin
Endothelial
cell activation Low sensitivity 69% 69% Positive predictive vaules 12% 12% Higher levels by 12 wks (PPV 29% NPV 29% 98%) 98%)
Coagulation activation
Thrombocytopenia
and platelet
dysfunction Increased destruction cause platelet volumes increase (younger platelet) Preeclampsia : PAI-1 increase increased PAIrelative to PAI-2 because of endothelial PAIcell dysfunction
Cytokines
Released
by vascular endothelium & leukocytes , and macrophages & lymphocytes at decidua Interleukin , TNF , CRP : inflammatory response Possibly predictive preeclampsia
Fetal DNA
Fetal
DNA in maternal serum At the time endothelial activation , fetal cells released into maternal circulation Elevations after 28 wk indicate impending disease
Placental peptides
Corticotropin-releasing Corticotropin-
hormone , hCG ,
Activin A , inhibin A Variably elevated depend on duration & severity of preeclampsia Overlap with normal pregnancy VEGF and PIGF : regulate placental development , both antagonized by sFlt1 sFlt1 Excessive sFlt1 , PIGF in 1st trimester : sFlt1 high risk
hCG
hCG
in second trimester , > 2.0 MoM Sensitivity 23.7% 23. Specificity 89.4% 89. Relative risk 2.54 Positive predictive value 9.5% Negative predictive value 96.6% 96.
A : control trophoblast differentiation in first trimester : high in preeclampsia Inhibin A 15-19 wk , > 2.0 MoM 15 Sensitivity 48.6% 48. Specificity 23.6% 23. Activin A more sensitive than inhibin A at 2121-25 wk
Vasoactive
Decrease
active renin , AT I & I , aldosterone , activity of ACE in 3rd trim AT II infused test : positive at less than 10 ng/kg Ratio inactive urinary kallikrein /urine creatinine at 16-20 wk : lower 5 fold in who 16developed preeclampsia
trophoblastic invasion of spiral arteries , leading to reduction in uteroplacental blood flow 8-22 wk , sensitivity 78% , PPV 28% , 78% 28% unreliable in low risk pregnancies Combined inhibin A & activin A , sensitivity 86% 86% Combined hCG & AFP , sensitivity 2-40% 40%
Prevention
Salt
restriction : ineffective Inappropriate diuretic therapy Low dietary calcium increased risk GHT Fish oil capsules : modify abnormal PG balance : ineffective Low dose aspirin (60mg) : ineffective (60mg) Antioxidants : vitamin C & E : reduced endothelial cell activation , reduction in preeclampsia
control study Mean milk intake per day in preeclampsia < control group Drinking more than 5 glasses per day has evident protective effect of developing preeclampsia (odd ratio 0.1)
Eur J of Obs & Gyn & Repro Bio 105 (2002) 11-14 2002) 11-
Calcium supplement
Reduction
in high BP (RR 0.58) 58) The effect greater among women at high risk of developing HT and those with low baseline dietary calcium (RR 0.47 & 0.38) 38) Reduction risk of preeclampsia (RR 0.35) 35) The effect greatest in women at high risk of developing HT and those with low baseline dietary calcium (RR 0.22 & 0.29) 29)
Aspirin
Significant
benefit in reducing preeclampsia (odds ratio 0.55) 55) Baseline risk of preeclampsia in women with abnormal uterine a doppler was 16% 16%
risk : Hx preclampsia ,CHT , DM , renal disease , FH of preeclampsia Significant benefit in reducing perinatal death (OR 0.79) & preeclampsia (OR 79) 0.86) 86) Reduction in rates of spontaneous preterm birth (OR 0.86) 86) Increase of mean birth weight No increase risk of placental abruption
reduction in risk of preeclampsia (RR 0.81) 81) Greater reduction in risk of preeclampsia in aspirin >75 mg/d (RR 0.49 VS RR 0.86) >75 86) 7% reduction in risk of preterm delivery (RR 0.84) 84) 16% reduction in baby deaths (RR 0.84) 16% 84) 8% reduction in SGA babies (RR 0.92) 92)
high risk (previous SPE , DM , CHT , renal dis , autoimmune disease) : 27% 27% reduction in risk of preeclampsia For mod risk (first preg , mild rise BP no proteinuria , abnormal uterine a doppler, positive roll over test , multiple preg , FH SPE , teenage) : 15% reduction 15% Started before implantation & trophoblast invasion ,crucial time before 16 or 12 wk
Vitamin E supplement
Either
at high risk of preeclampsia or with established preeclampsia No difference in risk of stillbirth , neonatal death , perinatal death , preterm birth , IUGR & birthweight Decrease risk of developing clinical preeclampsia (RR 0.44) using fixed-effect 44) fixedmodels (no diff using random-effects randommodels)
Vitamin E supplement
Dosage
: above recommended dietary intake of 7 mg of alpha-TE (daily 400 iu or alpha800 iu) GA : no difference in risk of stillbirth , preterm birth ,IUGR & preeclampsia between before to 20 wk and both before & after 20 wk No difference side-effect (acne , transient sideweakness, skin rash)
Vitamin C supplement
No
difference in risk of stillbirth , perinatal death, IUGR , birthweight Increase risk of preterm birth (RR 1.38) 38) Heterogeneity : Decreased preeclampsia (RR 0.47) 47) Dosage : above RDI of 60 mg (500 , (500 1000mg) 1000mg) GA : no difference before & after 20 wk
Antioxidant
39% 39%
reduction in risk of preeclampsia (RR 0.61) 61) Reduced risk of SGA infant (RR 0.64) 64) More preterm birth (RR 1.38) 38) No difference in develop preeclampsia among low & high risk (RR 0.66 & 0.44) 44) GA : no diff (<20wk VS before & after (<20wk 20wk) 20wk)
Dietary salt
Reduce
dietary salt intake vs continue a normal diet No effect in preeclampsia (RR 1.11) 11) Insuffient evidence for reliable conclusions about effect of advice to reduce diet salt
in risk of preeclampsia in supplemented groups ( 200 ug & 5 mg/d) In low serum folate pregnancy & women with Hx preeclampsia Odd ratios of preeclampsia no diff between receive folic 200 ug VS 5 mg/d (0.46 VS 0.59) 59)
Management
Management
Early
prenatal detection Antepartum hospital management Termination of pregnancy Antihypertensive drug therapy Delayed delivery with SPE
preeclampsia without overt HT : increased surveillance New-onset diastolic BP 81-89 mmHg or New81sudden abnormal wt gain (> 2 lb/wk during 3rd trimester) OPD surveillance unless overt HT , proteinuria , visual disturbances or epigastric discomfort
2. Antepartum management
Admit
if new onset HT , esp persistent or worsening HT or develop proteinuria Detail examine : headache , visual disturbances , epigastric pain , weight gain Proteinuria at least every 2 d BP q 4 hr , except midnight & morning Creatinine , hematocrit , platelets , liver enzymes.
Antepartum management
Evaluate
fetal size , AF Reduced physical activity Sedative not prescribed Ample, not excess, protein & calories diet Sodium & fluid intake not limit or forced Further Mg depend on : severity , Gestational Age , condition of cervix
PreeclampsiaPreeclampsia-Initial Evaluation
Serial
blood pressure measurements Urine protein excretion Fetal monitoring Tests to rule out HELLP and other complications: Hematocrit, platelets, uric acid, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH)
deliver at term, unless superimposed preeclampsia, HELLP syndrome Avoid ACE inhibitors (renal failure, oligohydramnios, pulmonary hypoplasia, IUGR) and atenolol (IUGR)
PreeclampsiaPreeclampsia-Management
Seizure
PreeclampsiaPreeclampsia-Term Pregnancy
Delivery
is a short-term goal short Induction of labor is appropriate after maternalmaternal-fetal observation/stabilization Cesarean reserved for standard obstetric indications Cesarean may be recommended in cases of severe preeclampsia where delivery is remote
PreeclampsiaPreeclampsia-Preterm Pregnancy
Mild
preeclampsia - expectant management is acceptable under certain conditions Close maternal-fetal surveillance maternal Ability to intervene either if conditions worsen or if acceptable gestational age reached In-hospital vs. home care? In-
PreeclampsiaPreeclampsia-Preterm Pregnancy
Severe
preeclampsia - controversial Delivery for poor maternal condition is likely to be necessary over the short term Sibai has advocated expectant management for selected patients to attempt to reduce perinatal morbidity and mortality due to prematurity
PreeclampsiaPreeclampsia-Preterm Pregnancy
Expectant
PreeclampsiaPreeclampsia-Preterm Pregnancy
24-34 24
Deliver
3. Termination of pregnancy
Delivery
is the cure for preeclampsia Headache , visual disturbances or epigastric pain : indicative convulsions (imminent eclampsia) Oliguria : ominous sign SPE : objectives to forestall convulsions , prevent intracranial hemorrhage , & serious vital organ damage
Termination of pregnancy
Preterm
: conservative justified in mild preeclampsia, closed observation and monitoring to complications severe preeclampsia : prompt delivery
Induction
4. Antihypertensive drug
To
lower mean BP, no difference : mean pregnancy prolongation , birthweight , c/s rate IUGR 2 fold
Antihypertensive drug
RCT
: blocker (Labetolol) , calcium channel blockers (Nifedipine , Isradipine) no benefit Meta-analysis : treatment induced Metadecrease maternal BP , may adversely affect fetal growth Prophylactic atenolol decrease incidence preeclampsia
Antihypertensive drug
Inhibitor should avoid in 2nd & 3rd trimester Complication : oligohydram , IUGR , bony malformations , limb contractures , persistent PDA , pulm hypoplasia , RDS , prolonged neonatal hypotension , neonatal death Early preg taken ACE Inhb : discontinued as soon as possible
ACE
Nicardipine
Nicardipine
mg/hr Target DBP < 100 or < 90 in HELLP syndrome pt Median time to obtained target 23 min Delivery postponed 4.7 days Potential use for second line drug when other antiHT drugs failed
remote from term Conservative or expectant management in selected group Sibai 1985 : SPE 18-27 wk : perinatal 18mortality 87% , no mothers died , placental 87% abruption eclampsia , consumptive coagulopathy , RF , encephalopathy , intracerebral hemorrhage , ruptured hepatic hematoma
1994 : SPE 28-32 wk (exclude 28HELLP) : prolonged mean of 15.4 d : 15. sustained 4% placental abruption Abramovici 1999 :
better neonatal outcomes in SPE , IUGR not relate to severity of disease , IUGR affected survival infants , median elapsed time 0 , 1 , 2 days in HELLP , partial , & SPE
2003 : bed rest , MgSO4 48 hr , bolus MgSO4 antihypertensive drug , volume expansion, & Dexa Indications for delivery : uncontrollable BP, fetal distress , placental abruption , renal failure, HELLP synd , persistent symptom Average pregnancy prolong 8d No maternal deaths, 6 stillbirth , 11 placental abruption , 28 IUGR
Intervention VS Expectant
Insufficient
data for reliable conclusions on maternal outcome For baby : insufficient reliable conclusions on stillbirth or death after delivery (RR 1.50) 50) More RDS (RR 2.3) , NEC (RR5.5) (RR5 Less likely to SGA (RR 0.36) 36)
Glucocorticoids
Not
worsen maternal HT Decrease RDS , improve fetal survival No evidence : benefit to ameliorate severity of HELLP syndrome Transient improve hematological lab : platelet counts 2 Maternal death , 18 stillbirth
EclampsiaEclampsia-Management
Preeclampsia
complicated by generalized tonictonic-clonic convulsions OR Fatal coma without convulsions also Major complications included placental abruption (10%) , neuro deficit (7%) , (10%) (7 aspiration pneumonia (7%) , pulm edema (7 (5%) , arrest (4%) , ARF (4%) , death (1%) (4 (4 (1
Eclampsia
Appear
before, during or after labor Most common in last trimester Shift in incidence toward postpartum Usually begin in facial twitch , entire body rigid , generalized muscle contraction , jaw open & close violently
Diaphragm
Eclampsia
Duration
of coma variable Hypercarbia , lactic acidemia , fetal brady cardia High fever Proteinuria Diminished urine output , hemoglobinuria Pronounced edema Proteinuria & edema disappear within 1 wk BP return within a few days to 2 wk PP
Eclampsia
Pulmonary
edema from aspiration pneumonitis or heart failure Death from massive cerebral hemorrhage Hemiplegia from sublethal hemorrhage Blindness from retinal detachment or occipital lobe ischemia & edema Persistent coma due to uncal herniation Rarely eclampsia followed by psychosis
Eclampsia
Differential
diagnosis : epilepsy , encephalitis , meningitis , cerebral tumor , cysticercosis , ruptured cerebral aneurysm Prognosis always serious 6% of Maternal death relate to eclampsia Among PIH patient , maternal death 16% 16%
Treatment
1. control of convulsions using IV MgSO4 MgSO4 2. Intermittent IV or oral of antihypertensive drug to lower Diastolic BP <100 <100 3. Avoidance of diuretics , limit IV fluid adminstration , avoid hyperosmotic agents 4. Delivery
Continuous IV regimen
4-6 gm MgSO4 dilute in 100 ml fluid , admin MgSO4 over 15-20 min 15Begin 2 g/hr in 100 ml IV maintenance Measure Mg level at 4-6 hr , adjust level between 4-7 mEq/L MgSO4 MgSO4 discontinued 24 hr after delivery
Intermittent intramuscular
Give
4 g MgSO4 IV , rate not exceed 1 MgSO4 g/min Follow with 10 g MgSO4 : 5 g injected MgSO4 each buttock through 3 inch long , 20 gauge needle , (add 1 ml of 2% lidocaine) If convulsions persist after 15 min , give 2 g more IV slowly Give 5 g MgSO4 IM q 4 hr MgSO4 MgSO4 discontinue 24 hr after delivery MgSO4
MgSO4 MgSO4
Effective
anticonvulsant without producing CNS depression in either mother or infant Not given to treat HT Exert specific on cerebral cortex 10-15% after MgSO4 : subsequent 10-15% MgSO4 convulsion Sodium amobarbital & thiopental , if excessive agitate in postconvulsion state In Eclampsia , admin for 24 hr after onset of convulsion
MgSO4 MgSO4
Almost
totally cleared by renal excretion Monitor urine output , DTR , RR Maintained level 4-7 mEq/L IM & IV regimen , no significant difference Mg level Mg 10 mEq/L : patellar reflex disappear > 10 mEq/L : respiratory depression > 12 mEq/L : respiratory paralysis & arrest Cr >1.3 : half dose MgSO4 >1 MgSO4
MgSO4 MgSO4
Acute
cardiovascular effect Decrease MAP Increase CO 13% 13% Decrease SVR Transient nausea & flushing Persist for only 15 min
MgSO4 MgSO4
Uterine
effects Depress myometrial contractility Inh calcium entry to myometrial cell Dose dependent : at least 8-10 mEq/L No uterine effect , when given for prophylaxis eclampsia (oxytocin stimulation of labor , admit to delivery intervals , route of delivery)
MgSO4 MgSO4
Fetal effects Promptly cross placenta Neonatal depression occurs only if severe hypermagnesemia at delivery Decrease in beat-to-beat variability beat-toPossible protective effect against cerebral palsy in VLBW infants Substantial gross motor dysfunction reduced No serious harmful effects
reduce recurrent sz 50% 50% compared to diazepam , reduce maternal & perinatal morbidity (not sig) Maternal mortality reduced compared to phenytoin (not sig) , less neonatal intubation & NICU admission Prevent eclamptic sz superior to phenytoin Lower risk placental abruption
with placebo Reduce risk eclampsia (RR 0.41) 41) Reduce risk of dying (RR 0.56) 56) More Side effect (flushing) (24% VS 5%) (24% Reduce risk placental abruption (RR 0.64) 64) 5% Increase risk c/s No difference in stillbirth or neonatal death (RR 1.04) 04)
to phenytoin Better Reduce risk of eclampsia (RR 0.05) 05) Increase risk c/s (RR 1.21) 21) Compared to diazepam Too small for any reliable conclusions
to Nimodipine Lower risk of eclampsia (RR 0.33) 33) Increase respiratory problem (RR 3.61) 61) Greater need for additional antihypertensive drugs (RR 1.19) 19) No difference in morbidity
MgSO4 MgSO4
Sz
rate in preeclampsia , no sz prophylaxis 3.9% reduced to 1.5% Mild preeclampsia , estimated risk without prophylaxis 1 in 100 , & not asso with severe maternal morbidity Do not given sz prophylaxis in Mild PE
Antihypertensive
Hydralazine
suggested if persistent systolic > 160 , or diastolic > 105 mmHg (NHBPEP2000) (NHBPEP2000) 5-10 mg doses at 15-20 min inervals 15 Satisfactory response ante or intrapartum : diastolic 90-100 90 Seldom another antihypertensive needed FHR deceleration when BP fell to 110/80 110/
Antihypertensives
Labetolol
: IV 1& nonselective -blocker Lower BP more rapidly , associated tachycardia NHBPEP(2000) : recommends 20 mg IV NHBPEP(2000) bolus , if not effective within 10 min , followed by 40 mg , then 80 mg q 10 min but not exceed 220 mg total dose per episode treated
Antihypertensives
Nifedipine
10 mg Oral , repeated in 30 min , if necessary (NHBPEP 2000) 2000) Fewer dose required to achieve BP control without increased adverse effects Sublingual : potent & rapid : cerebrovascular ischemia , MI , conduction disturbance , death Not superior to other hypertensives
Antihypertensives
Verapamil
IV 5-10 mg/hr Nimodipine IV & oral Ketanserin IV (selective 5-HT blocker) Nitroprusside not recommend unless no response , continuous IV , start 0.25 ug/kg/min , increase to 5 ug/kg/min , fetal cyanide toxicity may occur after 4 hr
Persistent postpartum HT
Hydralazine
10-25 mg IM q 4-6 hr 10 If HT persists or recur : oral labetolol or thiazide diuretic are given Two mechanisms :
Persistent postpartum HT
Atypical
syndrome in which SPESPEeclampsia persists despite delivery Single or multiple plasma exchange Plasma exchange performed in postpartum women with HELLP syndrome Very few women : persistent Hypertension , thrombocytopenia and renal dysfunction due to thrombotic microangiopathy
: deplete intravascular volume , compromise placental perfusion , limited used to pulmonary edema Hyperosmotic agents : leaks of agents through capillaries into lungs & brain promote accumulation of edema
Fluid therapy
Lactate
Ringers Solution , rate 60 ml to 125 ml/hr Unless unusual fluid loss : N/V , diarrhea , excessive blood loss Oliguria : maternal blood volume constricted, admin IV fluid more vigorously Women with eclampsia already has excessive extracelular fluid
volume expansion for treatment of preeclampsia Compared colloid with no plasma volume expansion Insufficient evidence for any reliable effect
Pulmonary edema
Most often do so postpartum Aspiration should be exclude Majority have cardiac failure Decrease plasma oncotic pressure , increase extravascular oncotic pressure , increase capillary permeability , hemoconcentration , reduced CVP , PCWP Excessive colloid & cyrstalloid cause pulm edema
Invasive monitoring
Use
of pulmonary artery catheterization Reserved for women with severe cardiac disease , renal disease , refractory hypertension , oliguria , pulmonary edema Pulmonary edema by more than one mechanism If questionable pulmonary edema : furosemide IV , hydralazine IV
Delivery
After
eclamptic sz , labor often ensues spontaneously or can be induced successfully even in remote from term Because lack of normal pregnancy hypervolemia , so less tolerant of blood loss at delivery
the past , SAB , EB were avoid GA caused by tracheal intubation, sudden HT ,pulm edema , intracranial hge Epidural preferred : no serious maternal or fetal complication , lower MAP , Cardiac output not fall
LongLong-term consequence
More
prone to hypertensive complications in future pregnancies Earlier diagnosed , greater recurrence Diagnose before 30 wk , recur 40% 40% Recurrence rate for women with 1 episode of HELLP 5% Subsequent preeclampsia , high incidence of preterm , IUGR , placental abruption , c/s delivery
LongLong-term consequence
Multiparous
develop preeclampsia , increased risk recur in subsequent pregnancy compared with nulliparas Early-onset SPE may have underlying Earlythrombophilias, complicate subsequent pregnancies Preeclampsia not cause chronic hypertension