Hypertensive

Disorders in
Pregnancy
NAVEED MOHAMMED
ROLL NO.130
HYPERTENSION IN PREGNANCY

 Most common medical problem encountered in pregnancy.

Seen in 5-10% of all pregnancies.
 Preeclampsia is the most dangerous among these.
 2nd most common cause of maternal mortality in India
HTN is defined as systolic BP>140 mmHg OR diastolic BP>90
mmHg on atleast 2 occasions taken 6 hours apart.
In terms of Mean Arterial Pressure, a rise of 20mmHg or an MAP
more than 105 is significant.
Mean arterial pressure: diastolic pressure+1/3 pulse pressure
CHANGES IN NORMAL
PREGNANCY
 Thediastolic BP begins to fall in early pregnancy and
continues to fall in 2nd trimester to reach minimum at 22-
24 weeks. Then increases steadily to reach prepregnant
levels by term
 REASON : Reduced vascular tone leading to peripheral
vasodilatation.
Classification
 According to National High Blood Pressure Education
Programme(NHBPEP),there are 4 types of hypertensive
disorders in pregnancy.
 Gestational HYPERTENSION
 Preeclampsia and eclampsia
 Chronic HYPERTENSION
 Chronic HYPERTENSION with superimposed
preeclampsia
Gestational Hypertension

 Hypertension that occurs after 20 weeks gestation in the

absence of proteinuria and biochemical or haematological
abnormalities.
BP returns to normal within 12 weeks postpartum.
 Proteinuriais the excretion of 300mg or more of protein in
24 hours urine. Hypertension and proteinuria define
preeclampsia.
Preeclampsia
 Multisystem disorder involving the placenta,liver ,
kidneys , blood , neurological and cardiovascular
systems.
 Both maternal and fetal morbidity / mortality are more
likely to occur with early – onset disease
 Placental abruption ,acute renal failure ,cerebral
HEMORRHAGE , DIC and Intrauterine growth
restriction ,prematurity are the outcomes. Delivery is the
only cure.
 Therefore, Antenatal care is directed towards identifying
women with hypertension and proteinuria
 Theprevious defn. was new onset hypertension+ new
onset proteinuria after 20 weeks of gestation or gestational
HTN with proteinuria
 Some may present with hypertension and multisystem
signs and symptoms even in the absence of proteinuria.
Chronic Hypertension

Presence of persistent hypertension of whatever cause before 20

weeks gestation
or
 Persistent hypertension beyond 6 weeks postpartum.
 Sustained BP of 140/90 mmHg or on > two occasions 6 hours apart
is considered hypertensive.
Superimposed preeclampsia

 Chronic hypertension with appearance of new onset

proteinuria or maternal organ dysfunction consistent with
preeclampsia
Diagnostic Criteria For Preeclampsia
 BP new onset HTN after 20 weeks of gestation
 Proteinuria >or= 300mg in 24 hrs
Or in the absence of proteinuria, hypertension with any of the following
 Thrombocytopenia Platelet count < 150,000/microL
 Renal insufficiency serum creatinine>1mg/dL
 Impaired liver function Elevated SGOT and SGPT
 Pulmonary oedema
 Cerebral or visual symptoms Severe headache, blurring of vision, blindness,
visual scotomata, eclampsia
 Uteroplacental dysfunction Fetal growth restriction, abnormal umbilical artery
Doppler or stillbirth
PROTEINURIA

 An indicator of severe disease and irreversible.

 Significant proteinuria is 300mg in 24 hours or more or
protein creatinine ratio of atleast 0.3
 Severe proteinuria is 5g in 24 hours or more.
 DIPSTICK PROTEINURIA can be used as a
semiquantitative method. 1+ is approx. equivalent to
300mg/L,2+ to 1g/L and 3+ to 3g/L
 Risk factors
l. GeneticFactors
Family history of preeclampsia
2. Obstetric Factors

• Primiparity
• Extremes of maternal age
• Previous history of preeclampsia
• New paternity
• Limited sperm
• Multiple pregnancy
• Hydrops fetalis with a large placenta •
Hydatidiform mole
triploidy where there is early onset preeclampsia
Medical Factors

 Diabetes
 Obesity
 Renal disease
 Antiphospholipid antibody syndrome and inherited
thrombophilias
 Connective tissue diseases like systemic lupus erythematosus
 Insulin resistance as in obesity and polycystic ovary syndrome
 Hyperhomocystinaemia
 Chronic infections
Aetiopathogenesis

Preeclampsia as a 2 stage disorder

 Stage 1- preclinical, characterised by poor placentation or
faulty endovascular trophoblastic remodelling of uterine
arteries, causing placental hypoxia
 Stage 2- caused by oxidative stress, causing release of
placental factors into maternal circulation.
 Sets up a systemic inflammatory response and endothelial
activation resulting in clinical syndromes.
Abnormal Trophoblastic Invasion

 In normal pregnancy ,the cytotrophoblast cells migrate through decidua

and myometrium to invade both the endothelium and tunica media of
spiral arteries.
 Occurs in 2 waves, and transforms the spiral arteries into wide mouthed
vessels unresponsive to vasomotor stimuli.
 Thus the blood supply is transformed from high resistance, low flow
system→low resistance, high flow system.
 Begins in late first trimester and completes by 18-20 weeks of gestation.
 In preeclampsia,trophoblast cells cannot invade the
myometrium.
 Vessels remain narrow,resulting in placental hypoperfusion.
 Results in reduced uteroplacental flow, which worsens as
gestation advances. This can also occur in growth restriction
without preeclampsia
 Ischemic placenta elaborate factors into maternal
bloodstream.
 Causes maternal endothelial dysfunction.
Abnormal Angiogenesis

 Angiogenic imbalance occurs in preeclampsia.

 Increased production of antiangiogenic factors.In normal
pregnancy,proangiogenic(Vascular Endothelial Growth
Factors,Placental growth factor)and antiangiogenic factors are
elaborated by placenta.
 Balance b/w these factors is imp for normal placental dev.
 Excessive amounts of antiangiogenic factors produced in response
to hypoxia disturbs the balance and cause systemic endothelial
dysfunction.
Endothelial cell dysfunction and
vasospasm
 Antiangiogenic factors, metabolic factors and other inflammatory
mediators provoke endothelial cell injury resulting in clinical syndrome
of preeclampsia.
 Caused by lipid peroxidation stimulated by free oxygen radicals because
of oxidative stress
 Cytokines like TNF and interleukins also contribute
 Toxic radicals are formed causing endothelial injury
Alteration in Nitric Oxide and
Prostaglandins
Prostacyclins- vasodilator and inhibitor of platelet aggregation and NO-
vasodilator
Thromboxane,endothelin-vasoconstrictors and helps in platelete
aggregation
In normal pregnancy,increase in prostacyclin causing vasodilatation
In preeclampsia, due to endothelial cell dysfunction,↓in prostacyclin,NO
and increase in endothelin and thromboxane leading to vasospasm,
platelet activation and activation of coagulation system.
 In normal pregnancy, peripheral resistance and thereby the
blood pressure falls due to acquired insensitivity to the
pressor effect of angiotensin II.
 In contrast, in preeclampsia, there is loss of this vascular
insensitivity.
 This results in vasospasm and thereby, an increase in
vascular resistance and increase in blood pressure.
Coagulation System and Platelets

 Endothelial dysfunction activation of platelets by tissue factor

 Widespread DIC and platelets and coagulation factors used up
 Thrombocytopenia
 Widespread multiple small haemorrhages and fibrin deposition
in many organs
Immunological Factors

 In normal pregnancy there is maternal immune tolerance

to paternally derived placental and fetal antigens.
 Loss of this tolerance is said to occur in preeclampsia
 Histologicalchanges at maternal placental interface
resemble acute graft rejection
 Explainshigh prevalence of preeclampsia in first
pregnancy and molar pregnancies
Metabolic Factors
 Central obesity and insulin resistance are risk factors
 Hyperlipidemia lead to endothelial dysfunction
 Calcium deficiency has also been linked
 Preeclampsia may be considered as the pregnancy associated
expression of metabolic syndrome.

Genotype and Phenotype

 There is an inherited maternal component in preeclampsia
 In normal pregnancy,Increased plasma volume -Increased
GFR-Increased renal blood flow-Expansion of ECF space-
Retention of sodium in ECF
 In preeclampsia,↓ in plasma vol, ↓ in GFR, ↓ in renal
blood flow.
 Sodium retention in blood-Shift of sodium into arerial
wall
Causing increased sensitivity to pressor agents
Pathophysiology
 PLACENTA

Vasospasm→decrease in uteroplacental blood flow→anoxia

→thromboplastic substances released from
placenta→intravascular coagulation
→IUGR,oligohydramnios,placental abruption and ultimately fetal
demise.
 KIDNEY

Swelling of endothelial cells, glomerular and tubular dysfunction

Leading to Proteinuria,decreased GFR,reduced renal blood
flow,hyperuricaemia.
 LIVER

Periportal thrombosis and fibrin deposition, haemorrhage and

necrosis
increase in liver enzymes(SGOT,SGPT)
subcapsular haematoma whichcause stretching of Glisson’s
capsule and epigastric pain

 EYES

Haemorrhages and papilloedema may be seen rarely in severe

hypertension. Visual disturbances are common,usually due to
oedema of occipital lobe
 CARDIOVASCULAR SYSTEM
- Increased afterload caused by hypertension
- diminished preload due to dimnished hyper-volaemia of pregnancy in preeclampsia
- endothelial cell activation with increased capillary permeability results in
pulmonary oedema
- Women with preeclampsia or eclampsia are unduly sensitive to vigorous fluid
therapy and can easily develop pulmonary oedema They are also sensitive to even
normal blood loss in delivery

 BLOOD AND COAGULATION

- -widespread subclinical to frank DIC ,may manifest as thrombocytopenia
- severe preeclampsia accompanied by micro angiopathic haemolysis caused by
endothelial cell damage with platelet adherence and fibrin deposition
 BRAIN
 -cerebral autoregulation lost and cerebral blood flow becomes dependant on
MAP
 -Increase in cerebral blood flow cause hypertensive encephalopathy
 -cerebral vasospasm
 -gross hemorrhage due to ruptured arteries caused by severe HTN
 -cerebral edema
 -localised hyperintense lesions at gray-white matter junction(primarily in
occipital lobe),termed as PRES ( Posterior Reversible Encephalopathy
Syndrome)
Severity of Preeclampsia
 Mild and severe
Based on the degree of hypertension,proteinuria and involvement of other
organ systems
<110mmHg diastolic bp –mild.
 Severe preeclampsia
Diastolic bp – 110mmHg or more
Systolic bp – 160mmHg or more
Proteinuria-5g in 24 hrs
Headache,visual disturbances,epigastric painOliguria and
thrombocytopaenia
Increased liver enzymes, serum creatinine,IUGR,Pulmonary edema
Imminent Eclampsia

 Headache
 Nausea or vomiting
 Flashing lights
 Epigastric or right upper quadrant pain
 Brisk deep tendon reflexes and ankle clonus
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