Hypertensive Disorders in Pregnancy 1
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Transcript of Hypertensive Disorders in Pregnancy 1
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Hypertensive Disorders in
Pregnancy
Preeclampsia and Eclampsia
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Definition
Preeclampsia
It is defined as the development of
hypertension and proteinuria after the 20th wk
of gestation.
Eclampsia
This is defined once the CNS is also involved.
HELLP
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Epidemiology
Preeclampsia is a disorder of unknown
etiology affecting 6-8% of all
pregnancies.Between 1979 and 1986incidence of severe preeclampsia
increased from 2.4 per 1000 deliveries to
5.2.
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Pathogenesis
Immunologic factors 50% of the genes is paternal which interacts with maternal tissue as the fetal trophoblast migrates into the maternal decidua. There is a second wave of trophoblastic invasion around 14-16 wks which results in disruption of muscular integrity of the spiral
arteries, leading to their adrenergic denervation and converts them from high resistance to low resistance vessels.
Biochemical adaptations occur in the maternal vasculature with dominance of prostacyclin and nitric oxide in comparison tothromboxane.
Genetic factors A familial tendency exists in some population and it may result from a recessive genetic inheritance.
Angiotensinogen gene T235 has been noted in association with preeclampsia.
Increased resistance to activated protein C, caused by a mutation of Factor V (Factor V Leiden mutation) predisposes topreeclampsia.
Glutamine substitution for arginine in position 506 in Factor V molecule. This renders the protein resistant to proteolytic inactivationby activated protein C and predisposes to thrombosis.
Endothelial Factors Vascular endothelial damage and dysfunction is the common pathological factor. Metabolic end-products of normal vascular
endothelium are PGI2 and EDRF(nitric oxide) Failure of trophoblastic invasion increases production of free radicals and lipidperoxides. The latter activate cyclooxygenase and impair PGI2.synthetase.
In the absence of PGI 2 and nitric oxide surface mediated platelet activation occurs causing adhesion a nd damage to spiralarteriesnreleasing contents of dense granules, like TXA2 and serotonin
Lack of the normal stimulation of RAAS and hence increased response to angiotensin II
Coagulation Factors
Women with preeclampsia have thromboembolic tendencies which maybe in part due to alteration between vWF and Factor VIIIcoagulant activity.Endothelial cell damagereleases vWF factor and thrombin inactivates factor VIII C activity hence increasing ratioof vWF: VIII C.
Calcium Intracellular free Ca is important for the vascular tone and contractility. In normal pregnancy it increases slowly but in preeclampsia
this increase is significantly higher in the 3rd trimester.
Fatty Acid Metabolism Altered handling of fatty acids by the liver is key in the pathogenesis of preeclampsia.
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Criteria and Classification for
Diagnosis Hypertension
Sustained BP of 140 systolic or 90 mm Hg diastolic
Proteinuria
>300 mg protein in 24 hr urine collection
Preeclampsia
Mild
Severe Eclampsia
HELLP
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Features of Severe Preeclampsia
BP >160 systolic or 110 diastolic on two occasions atleast 6 hrsapart.
Proteinuria > 5gms in 24 hr urine
Oliguria: UO < 400 ml in 24 hrs
Cerebral or visual disturbances like HA, blurred vision or alteredconsciousness.
Pulmonary edema or Cyanosis
Epigastric or RUQ pain- Glissons cpasule being stretched
Hepatic rupture
Impaired liver function
Thrombocytopenia HELLP Syndrome
Fetal compromise-IUGR, Oligohydramnios
LV dysfunction
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Cardiovascular changes
ANP is higher
LV dysfunction
CVP can be misleading No correlation between CVP and PCWP
Blood volume can be lower from 9% to 30-
40% below the expected. Higher SVR
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Hematologic Changes
Colloid oncotic pressures are lower than in
normal pregnancy
Hypercoagulability(accentuation of thenormal hypercoagulablr state of
pregnancy.
Activation of the fibrinolytic system
Platelet activation (severe cases it causes
thrombocytopenia)
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Changes that imply
Hypercoagulability Increased common pathway activity Decreased Fibrinogen
Increased FDP
D-dimer positive
Decreased Antithrombin III ( AT III )
Increased AT III antithrombin complex
Decreased platelets
Increased platelet aggregability
Decreased sensitivity to prostacyclin Increased Beta-thromboglobulin
AT III levels are low. It is a protease inhibitor that inhibitsactive forms of Factors IX, X, XI, XII.
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Renal Function
Decreased GFR 25% below normal
122ml/hr in non-pregnant pts and 170ml/hr in pregnantpts
Glomerulopathy causes proteinuria
Serum creatinine rarely increase but if it does, it signifiessubstantial involvement
Urate clearance decreases and uric acid increases.
Mild preeclampsia often is associated with uric acidlevels between 5.4-6.1mg/dl and severe is associated
between 6.7-8.2 mg/dl. Sodium excretion also diminishes.
Oliguria parallels the severity of preeclampsia
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Endocrine
RAAS Renin, angiotensin I, II, aldosteroneincrease markedly in normal pregnancy as alsoprostaglandin (PGI2) synthesis and Nitric oxide.
Breakdown of this normal balance betweenvasodilators or normalization of vascularresponse to angiotensin II.
Deficient production of PGI2
Lower ionized calcium levels RAAS suppression and lower levels of plasma
renin conc. and activity.
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Respiratory, Hepatic, Neurologic
Function Pharyngolaryngeal edema Pulmonary edema in 3%
Increased LFTs
Distention of liver capsule
Hepatic hemorrhage or rarely rupture
Headache, visual disturbances, CNS hyperexcitabilityand hyperreflexia.
Hypertensive encephalopathy and loss of cerebralautoregulation when MAP exceeds a critival value.
Other proposed etiologies for seizures are vasospasm,microinfarctions, punctate hemorrhages, thrombosis andcerebral edema.
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Uteroplacental Perfusion
Decreased uteroplacental perfusion with
increased downstream resistance,
diastolic velocity decreases and
systolic/diastolic ratio increases.
IUGR and Oligohydramnios
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Treatment
Lab tests CBC, Coagulation assay, Electrolytes, BUN andcreatinine, uric acid, LFTs, Urine 24 hr protein
Magnesium Sulfate. 4-6 gms bolus over 20 mins followed by 1 to 2gms /hr. Pts should be monitored by reflexes respiratory rate, urineoutput and serum levels.
Therapeutic levels for Magnesium is 5-7 mg/dl Loss of patellar reflexes at 10-12mg/dl, respiratory arrest at 15mg/dl
and asystole at >20mg/dl.
Cardiac arrest is treated with Calcium gluconate 1gm or calciumchloride 300mg
Magnesium acts on cerebral NMDA receptors and peripheral
neuromuscular junctions. Decreased uterine activity, prolonged labor, excessive bleeding and
neonatal depression.
Other drugs that can be used are Hydralazine, Labetalol,Nitroglycerine, Sodium nitroprusside and Nifedipine.