hypertensive disorders in pregnancy -i
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DEFINITION,CLASSIFICATION
ETIOPATHOGENESIS AND CLINICAL FEATURES OF
HYPERTENSIVE DISORDERS IN PREGNANCY
INTRODUCTION Commonest medical disorders during
pregnancy. Being the major cause of maternal and
perinatal morbidity and mortality. INCIDENCE Hypertensive disorders complicate 5-10
% of all pregnancies. Incidence of eclampsia is reduced due to
adequate and better antenatal care. GHTN : 6-17% in nullipara Pre eclampsia – 3-10% in nullipara
MATERNAL ADAPTATIONS IN PREG CARDIOVASCULAR SYSTEM :
-Cardiac output -Blood pressure
BP = CO * SVR CO increases ; SVR decreases
BP overall Diastolic BP &
M.A.P
MEASUREMENT BP can be recorded either in sitting or lateral recumbent posture. Brachial artery and mercury manometer should be at the level of
heart. Appropriate sized cuff should be used. DISAPPEARANCE OF KOROTKOFF
PHASE V
Diastolic BP
CLASSIFICATION By NHBPEP (2000)
GESTATIONAL HYPERTENSIONPRE ECLAMPSIA & ECLAMPSIAPRE ECLAMPSIA SUPER IMPOSED ON
CHRONIC HYPERTENSIONCHRONIC HYPERTENSION
GESTATIONAL HYPERTENSION BP ≥ 140/ 90 mmHg for first time
during pregnancy after 20 weeks of gestation
No proteinuria Returns to normal before 12
weeks postpartum With / without other symptoms of
pre eclampsia
PRE ECLAMPSIAAbnormality Mild SevereDiastolic BP <110 mmHg ≥110 mmHgSystolic BP <160 mmHg ≥160 mm HgProteinuria ≤2+ ≥3+Headache - +Visual disturbances - +Epigastric pain - +Oliguria _ +Convulsion - +Serum creatinine normal Thrombocytopenia _ +Serum transaminase minimal markedGrowth restriction - obviousPulmonary edema - +
ECLAMPSIA :Seizures that cannot be attributed to other
causes in a women with pre eclampsia.
CHRONIC HYPERTENSION : BP ≥140/ 90 mmHg before pregnancy or
diagnosed first before 20 wks of gestation
or Hypertension diagnosed after 20 wks and
persists after 12 wks postpartum
SUPER IMPOSED PRE ECLAMPSIA ON CHRONIC HTN :
New onset proteinuria ≥ 300mg/24 hrs in a hypertensive women but no proteinuria before 20 wks of gestation
orSudden in proteinuria / BP / in platelet
count in hypertensive women with proteinuria before 20 wks.
TRANSIENT HYPERTENSION :GHTN reclassified if pre eclampsia doesnot develop and BP returns to normal by 12 wks postpartum.
ATYPICAL PRE ECLAMPSIA :Without hypertension/ proteinuria/ both
Clinical findings Chronic HTN GHTN Pre eclampsia
Time of onset of hypertension
<20 wks 3rd trimester ≥20 wks
Degree of hypertension
Mild / severe Mild Mild/ severe
Proteinuria --- --- +
S.Uric acid >5.5 --rare -- +
hemoconcentration
- - Severe
Thrombocytopenia
- - „
Hepatic dysfunction
- - „
GESTATIONAL HYPERTENSION
Incidence : 6-17% in nullipara
CRITERIA FOR MILD GHTN : BP <160/110mmHg Proteinuria <300mg/24 hrs Platelet count > 100000 Normal liver enzymes Absent maternal symptoms Absent IUGR & OLIGO by
USG
PRE ECLAMPSIA INCIDENCE – 3-10% IN NULLIPARAOccurs before 20 wks in trophoblastic diseases.Clinical findings of pre eclampsia can manifest
either as maternal or fetal syndrome.RISK FACTORS1.AGE AND PARITY : Young primigravida Elderly > 40yrs Long interval between pregnancies Nulliparity2.MATERNAL OBESITY BMI > 35kg/m2 – 13.3%
3.Genetic : Family h/o pre eclampsia Genetic predisposition Race and ethnicity By ovum donation4. OBSTERIC : Prev h/o pre eclampsia Multifetal gestation Hydrops Hydatiform mole Congenital & chromosomal fetal anomalies5.PARTNER RELATED FACTORS Change of partner Partner who fathered a pre eclamptic preg Limited sperm exposure By donor Insemination
6. UNDERLYING MEDICAL DISORDERSChronic hypertensionRenal diseasesType I diabetes mellitusThrombophiliaFactor V leiden deficiencySickle cell disease or traitCollagen vascular diseasesPCOSUncontrolled hyperthyroidismMigraineAutoimmune diseases
CHRONIC HYPERTENSION CAUSES :
ESSENTIAL ( IDIOPATHIC / PRIMARY ) SECONDARY :
RENAL DISEASE Renal artery stenosis Glomerulonephritis Pyelonephritis Interstitial nephritis Polycystic disease TB Neoplasm
ADRENAL DISEASE Phaeochromocytoma Cushing syndrome Conn’s syndrome
CONNECTIVE TISSUE DISORDER Polyarteritis nodosa SLE Scleroderma
COARCTATION OF AORTA
ETIOPATHOGENESISPOOR PLACENTATION
PLACENTAL OXIDATIVE STRESS
FETALGROWTH
RESTRICTION
RELEASE OF PLACENTAL FACTORS
SYSTEMIC INFLAMMATORY
RESPONSE
ENDOTHELIAL ACTIVATION
STAGE I
STAGE II
ETIOLOGY Placental implantation with
abnormal trophoblastic invasion
Immunological maladaptive tolerance between maternal,paternal and fetal tissues.
Maternal maladaptation to CVS / inflammatory changes of normal pregnancy
Genetic factors – inherited predisposing genes & epigenetic influences
Coagulation abnormalities Dietary deficiency
ABNORMAL TROPHOBLAST INVASION
Incomplete trophoblast invasion
Shallow invasion upto decidual segments
Abnormally narrow spiral arteriolar lumen
Impairs blood flow
Diminished placental perfusion
Hypoxia Release of placental debris
Systemic inflammatory response
IMMUNOLOGICAL FACTORS uNK cells with HLA class I in extravillous
cytotrophoblasts control invasion.
Reduced expression of HLA-G by extravillous trophoblasts messenger RNA
Defective placental vascularisation
ENDOTHELIAL CELL ACTIVATIONDefective
placentation
Placental ischemia / hypoxia
Inflammatory mediators-
Il.TNF
Xanthine oxidase
activation
Oxidative stress
Free radical
PlacentaMaternal
endotheliumleucocytes
CEC
Platelet aggregation
fibrin ,thrombin
Lipid peroxides &Foam cells
NUTRITIONAL FACTORS : ascorbic acid < 85mg - incidenceGENETIC FATORS : - Multifactorial & Polygenic Disorder WARD AND LINDHEIMER (2009) 20-40 % for daughters of pre eclampsia
mothers 11-37 % for sisters of pre eclampsia women 22-47 % in twinsCANDIDATE GENES : Genome wide linkage studiesOUDEJANS Susceptibility loci on 10q22.1
2p122p259p13
GENETICS AND GENETIC IMPRINTINGGENETIC CONFLICT THEORY :
nutrients transfer limit the transfer
INCREASE BP REDUCE BP INADEQUATE UTEROPLACENTAL
BLOODFLOWFETAL RESCUE STRATEGY TO
INCREASE NON PLACENTAL RESISTANCE
ENDOTHELIAL DYSFUNCTION
FETAL GENES MATERNAL GENES
PATHOGENESISVASOSPASM : Vascular constriction increase in resistanceENDOTHELIAL CELL ACTIVATION : Placental factors activation & dysfunctionCEC of endothelial cells NO synthesisINCREASED PRESSOR RESPONSES - Sensitivity to AG
IINITRIC OXIDE – vasodilator
from L-arginine & fetal endothelium synthesisENDOTHELINS – vasoconstrictor human endothelium
PROSTAGLANDINS prostacyclin thrombaxene A2Vasodilatation & vasoconstrictionInhib plt aggregation plt aggregationIn pre eclampsia:PGI2 production TXA2 VasoconstrictionPGI2 : TXA2
endotheliumRenal cortex
PlateletTrophoblas
t
ANGIOGENIC AND ANTIANGIOGENIC PROTEINS
sFlt-1 reduced free VEGF & PLGF
endothelial dysfunction
sEng inhibits TGF- b
binding to endothelial receptors - NO dep vasodilatation
PATHOPHYSIOLOGYCVS : Preload affected Extravasation of fluid BLOOD VOLUME : HemoconcentrationBLOOD & COAGULATION :Endothelial activation plt activation &
aggreg plt exhaustion thrombocytopeniaHEMOLYSIS : LDH Schizocytosis,reticulocytosis,
spherocytosis
COAGULATION : INCREASED Factor VIII consumption fibrinopeptides & FDP DECREASED regulatory protein levelVOLUME HOMEOSTASIS :ENDOCRINE CHANGES
PLASMA NORMAL PRE ECLAMPSIA
ReninAngiotensin IIAldosterone
INCREASES DECREASES
Deoxycorticosterone
INCREASES NO CHANGE
Vasopressin Same SameANP -/ Increases Increases
FLUID AND ELECTROLYTE CHANGES :
Oncotic pressure Pathological fluid retention
LIVER :Periportal hemorrhage Subcapsular hemorrhage
stretching of glisson’s cap
Proteinuria Edema
SUBCAPSULAR LIVER HEMATOMA Can be unruptured or
ruptured. DD for unruptured :
Acute FLP, Ruptured uterus, abruption with DIC, TTP.
Presents with shoulder pain, shock, massive ascites, pleural effusion or respiratory difficulty.
BRAIN :
VISUAL CHANGES AND BLINDNESS : SCOTOMA, BLURRED VISION, DIPLOPIA BLINDNESS – Visual cortex of occipital lobe --AMAUROSIS Lateral geniculate nuclei Retina ---PURTSCHER RETINOPATHY RETINAL DETACHMENT
Acute and severe hypertension cerebrovascular over regulationVasospasm
Diminished cerebral flow – ischemia-cytotoxic edema-tissue infarction
Sudden in systemic BP exceed the normal cerebrovascular auto regulatory capacity
Posterior reversible encephalopathy syndrome
KIDNEY :- Renal Perfusion & GFR- Due to renal afferent arteriolar resistance- Glomerular capillery endotheliosis
blocking the filtration barrier.Pre renal
Urine osmolalityUrine :plasma
creatinineExcretion of
sodium
sr.creatinine- filtration
Uric acid - tubular
reabsorption
CLINICAL FEATURES–PRE ECLAMPSIA Onset : Insidious Symptoms :
MILD : Swelling over ankles, face, abdominal wall, vulva ALARMING : -Headache - Disturbed sleep
- Diminished urine output - Epigastric pain - Visual disturbances
Signs : -Abnormal weight gain -Rise of blood pressure -Oedema -Pulmonary edema -Abdominal examination
THANK YOU
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