PIH

 Normally during pregnancy blood

pressure decreases  main hormone during
pregnancy is progesterone  progesterone is
smooth muscle relaxant  so peripheral
vascular resistance decreases  so blood
pressure decreases.

 Systolic, diastolic and main arterial pressure

decreases.
 Diastolic blood pressure mainly decreases; this
is more during 2nd trimester. Blood pressure
decrease more during supine position, called
supine hypotension syndrome.

 Hypertension in pregnancy:
 BP > 140/90 of Hg on 2 occasion 4-6 hour
apart.
 PIH
 In pregnancy: diastolic BP indicated by
disappearance of sound (KORTOKOFF sound
5)

 2 situations:
 Hypertensive female has conceived, called
chronic HTN in pregnancy.
 Normotensive female has conceived, but
during pregnancy due to some placental
pathology (=20 weeks of pregnancy), her BP
increases, called PIH.

Chronic HTN in PIH

pregnancy
Past H/O of HTN present No past history
BP raise even before 20 BP raised after 20 weeks of
weeks of pregnancy pregnancy
BP does not come back BP comes back to normal
to normal after 12 weeks within 12 weeks of delivery.
of delivery.
 PIH

 PIH: two types.

 Gestational hypertension.
 Preeclampsia.

 Preeclampsia: proteinuria and end organ

damage present.
 Gestational HTN: absent

 Proteinuria.
 30 mg/dl in urine or
 300 mg in 24 hours or
 >0.3 ratio of urinary protein / creatinine
 It is always pathological in pregnancy.
 Glycosuria is physiological in pregnancy.

 Sign of end organ damage:

 PIH is a multi organ dysfunction.
 ↓Platelet count < 1 lac
 PIH

↑Serum creatinine
 ↑Liver serum enzyme to more than 2 times than

normal value.
 Pulmonary edema
 Cerebral edema / visual symptoms.

 Preeclampsia;
 Mild
 Severe (preeclamtic toxiemia)

Mild Severe
BP BP
140/90 > 160 / 110
< 160/110
End organ damage End organ damage
Absent Present

 Outdated criteria:
 Proteinuria.
 PIH
 Oliguria.
 IUGR.

 Chronic HTN with superimposed

preeclampsia:
 A hypertensive female conceives and all of a
sudden @ 20 weeks of pregnancy
 BP becomes uncontrollable
 Starts having proteinuria.
 Signs of end organ damage.

 Pathology of PIH:
PIH is due to placental pathology.
 Cytotrophoblast:
 They replace the lining of maternal spiral
arteries and surrounds them and coverts these
spiral arteries into low resistance vessels.
 Low resistance vessels:
 It means pressure↓ and volume of blood in inter
villous space↑.
 PIH
 This is called TROPHOBLASTIC invasion.

 This trophoblastic invasion happens in 2 steps:

 10 – 12 weeks of pregnancy.
 16 – 18 weeks of pregnancy.

 If second phase do not happens – called

incomplete trophoblastic invasion.
 So, resistance in maternal artery remains high.
The blood pressure will increase leads to PIH.

 Pathophysiology of PIH:

BP in mother is high
↓

Volume of blood which comes to inter villous

 PIH
Space decreases
↓
Placental ischemia
Placenta size is small.
↓
Inflammatory mediators are released.
↓
They act on capillary endothelium
↓
Makes capillary endothelium leaky
↓
Plasma leaks out and leads to edema.
↓
Inside the capillary there is hemoconcentration
happens + abnormal function of platelets leads to
end organ damage.
↓
 PIH
Due to hemoconcentration – we cannot use
diuretics
 Indication of diuretics in pregnancy;
 Left ventricular failure
 Raised intracranial tension
 Pulmonary edema

 Size of placenta is big in:

 Twin pregnancy
 Diabetes
 Rh negative pregnancy

 In severe preeclampsia;
Decrease blood flow to brain
↓
Cerebral blood flow decreases
↓
Cerebral hypoxia
 PIH
↓
Leads to convulsion, called eclampsia.

Decrease blood flow to fetus

↓
Growth of fetus decreases
↓
IUGR
↓
Renal blood flow decreases
↓
GFR decreases
↓
Urine output decrease
↓
Oligohydraminos
 PIH
↓
Fetus collect blood from all peripheral organ and
send it to brain called brain sparing effect.

Decrease renal blood flow in mother

↓
Decrease GFR
↓
Oliguria happens in mother
↓
Serum urea, uric acid, creatinine increase in
mother.

 Histopathological finding seen in kidney

 Glomeruloendotheliosis
 PIH
 Most common organ involvement in PIH:
kidney

 Normally in pregnancy: TH2 cell increases

during pregnancy.
 In females who have PIH: TH2 do not
increase.

 Risk factors for PIH:

1. Primi gravida female
2. New paternity
3. molar pregnancy
4. Rh negative pregnancy
5. Twin pregnancy
6. metabolic X syndrome
7. anti phospholipid antibody [APLA]
syndrome
 PIH
 Otherwise risk factor for PIH;
 Past history of PIH
 Family history of HTN
 Obese
 Diabetic

 Smoking is protective in PIH.

 Eclampsia:
 Generalized tonic clonic convulsion in a severe
preeclampsia patients.

 Sign and symptoms of impending eclampsia;

 Oliguria
 Headache
 Visual symptoms (most common is scotoma,
blurring of vision, diplopia, blindness – this is
due to hypertensive retinopathy)
 Epigastric pain
 PIH

 Incidence of eclampsia:
 India: 1-5 %
 Maternal mortality due to eclampsia: 2-6 %

 Eclampsia / convulsion:
 During pregnancy: ante partum eclampsia
 During delivery: intra partum eclampsia
 After delivery: within 48 hour of delivery
called post partum eclampsia.
 Most common variety: ante partum eclampsia.
 Worst prognosis: ante partum eclampsia. Bcoz
prognosis depends upon duration of eclampsia.
 MC cause of death – intra cranial bleeding.
 MC cause of convulsion – cerebral hypoxia.
 MC MIR finding in eclampsia: sub cortical
white matter edema.
 DOC for prevent and treat convulsion in
hypertensive female: mgSO4