This document discusses hypertensive disorders in pregnancy, including preeclampsia. It defines the different types of hypertension during pregnancy and outlines risk factors and pathophysiology of preeclampsia. The key theories around the abnormal trophoblastic invasion and immunological and vasoconstrictor/vasodilator imbalances are summarized. Diagnosis, management including controlling blood pressure, preventing eclampsia and timely delivery, and potential complications are covered at a high level. Management involves careful monitoring, controlling hypertension and seizures, delivering the baby when indicated based on gestational age and severity of symptoms, and following up postpartum.

1. HYPERTENSIVE DISORDER IN
PREGNANCY.

2. CONTENTS.
• Introduction .
• Risk factors.
• Pathophysiology
• Diagnosis
• Management
• Complications
• Prevention.

3. INTRODUCTION.
• Hypertension:
BP ≥ 140/90 mm Hg measured 2 times with at least a 6-hour interval
• Gestational hypertension:
Elevation of BP ≥ 140/90 mm Hg in pregnancy after 20 weeks, without proteinuria.
• Preeclampsia:
is a multisystem disorder characterized by the new onset of hypertension
and proteinuria, or hypertension and end-organ dysfunction with or
without proteinuria after the 20th week in a previously normotensive and
non protein uric woman.

4. Cont..
• Eclampsia:
is the occurrence of grand mal seizure in a woman with preeclampsia
in the absence of other neurological conditions that account for
seizure.
• Chronic hypertension:
Known hypertension before pregnancy or hypertension diagnosed first time before 20
weeks of pregnancy.
Preeclampsia superimposed on chronic hypertension:
• Women with pre existing hypertension develops systemic features of preeclampsia
after 20 weeks of GA.

5. PREECLAMPSIA.
Risk factors.
• Primigravida
• Family history.
• Placental abnormalities , Hyperplacentosis and Placental ischemia.
• Obesity.
• Pre-existing vascular disease
• New paternity.
• Thrombophilia. (antiphospholipid syndrome, protein C, S deficiency, Factor V Leiden)

6. PATHOPHYSIOLOGY OF PRECLEMPSIA.
The causes are unknown but there are some theories support this condition.
These are;
• The abnormal trophoblastic invasion.
• The immunological factors.
• Imbalance between vasoconstrictor and vasodilator.

7. Abnormal trophoblastic invasion.
Normal implantation is characterized by :
Extensive remodeling of the spiral arterioles within the decidua basalis.
In the first trimester (10–12 weeks) endovascular trophoblasts invades up to decidual
segments and in the second trimester (16–18 weeks) another wave of trophoblasts
invades up to the myometrial segments.
The spiral arterioles thereby become distended, tortuous, and funnel shaped.
This physiological change transforms the spiral arterioles into a low
resistance, low pressure, high flow system.

8. Abnormal trophoblastic invasion.
In case of preeclampsia:
There may be incomplete trophoblastic invasion decidual vessels, but not myometrial
vessels, become lined with endovascular trophoblasts.
Also, there is changes like endothelial damage, insudation of plasma constituents into vessel
walls, proliferation of myointimal cells, and medial necrosis, lipid laden cell changes.
These all causes spiral arteriole narrowing, atherosis, and infarcts in placentas
This change lead the spiral arterioles into high resistance, high pressure and low blood flow
to the baby.

9. The immunological factors
Normally there is maternal immune tolerance to paternally derived placental and
fetal antigens.
Loss of this tolerance, or dysregulation, account for preeclampsia syndrome.
Dysregulation include “immunization” from a previous pregnancy, some inherited
human leukocyte antigen (HLA) and natural killer (NK)-cell receptor haplotypes,
and possibly shared susceptibility genes with diabetes and hypertension

10. Imbalance between vasoconstrictor and
vasodilator
Normally, placenta liberates angiotensinase which degrade angiotensin II.
Vascular synthesis of prostaglandin I2 and NO neutralizes the vasoconstrictive effect of
angiotensin II.
Increased level of Vascular Endothelial Growth Factor (VEGF) restores the uteroplacental
blood flow to normal.
All these maintain blood pressure in normal state during pregnancy

11. Imbalance between vasoconstrictor and
vasodilator
But in preeclampsia;
• There are imbalance between vasoconstrictor and vasodilator.
• There are increases synthesis of thromboxane A2, endothili-1, cytokines
(TNF-alpha, IL-6) elevated and oxidative stress that lead vasoconstriction.
• Depressed activity of angiotensinase thereby increasing vascular activity of
angiotensin 11, deficiency of NO, prostaglandin I2 and VEGF
• All of these contribute to vasospasm resulting in hypertension.

13. CLASSIFICATION OF PREECLAMPSIA.
Preeclampsia may be classified as
Severe (also called preeclampsia with severe
features) or
Mild (also called Preeclampsia without severe
features )

15. CLINICAL FEATURES OF
PRREECLAMPSIA.
Symptoms .
Mild symptoms:
Slight swelling over the ankles which persists on rising from the bed in the
morning or tightness of the ring on the finger is the early manifestation of pre-eclampsia
Gradually, the swelling may extend to the face, abdominal wall, vulva and even the whole
body
.

16. Cont..
Alarming symptoms:
• Headache — either located over the occipital or frontal region
• Disturbed sleep.
• Diminished urinary output; less than 400 ml in 24 hours.
• Epigastric pain.
• Eye symptoms—there may be blurring, scotomata, dimness of vision or at
times complete blindness.

17. Cont..
Signs:
• Abnormal weight gain:
A rapid gain in weight of more than 5 lb (2.3kgs) a month or more than
1 lb (0.45kg) a week in later months of pregnancy is significant.
• Rise of blood pressure
• Edema

19. Eclampsia
• Eclampsia : is the occurrence of grand mal seizure in a woman with
preeclampsia in the absence of other neurological conditions that account
for seizure.
• “Preeclampsia with generalized tonic-clonic seizure is called eclampsia”
• Labor and delivery is a more likely time for convulsions to develop

20. Stages of eclampsia.
Premonitory stage.
Tonic stage.
Clonic stage.
Coma stage.

21. INVESTIGATIONS.
• Complete urine examination.
• Take blood for; ( MPS, RBG, serum electrolytes, FBP).
• Renal function tests: serum uric acid > 6 mg % is abnormal during pregnancy.
Serum creatinine level over 1.1mg/dl.
• Liver function test ; (AST of >70 U/L and LDH of >600 U/L) & Indirect
bilirubin level over 1.2 mg/dL

22. Cont..
• Coagulation status: Platelet count, Elevated PT or a PTT
Decreased fibrinogen as DIC may develop.
• Eye fundus examination.
• Tests for foetal well being: as
– ultrasound,
– daily foetal movement count,
– non-stress test,
– oxytocin challenge test (if needed).

23. Cont..
• CT Scanning and MRI.
To detect cerebral edema, focal infarction, intracranial hemorrhage in patient
having sudden severe headaches, focal neurologic deficits, seizures with a
prolonged postictal state, or atypical presentation for eclampsia.

24. MANAGEMENT.
Principles of management.
• To control BP.
• To prevent eclampsia
• Control convulsion
• Deliver the baby
• Follow up post natal clinic
• To prevent the complications

25. 1. To control blood pressure.
For mild hypertension(140-149/90-99)mmHg or moderate
hypertension(150-159/100-109).
1. Methyldopa (250-500)mg tds. PO OR
2. Nifedipine 10mg bd PO. OR
3. Labetalol 100mg twice a day.

26. To control blood pressure
For severe hypertension, BP is 160/110mmHg or higher.
• Hydralazine 10mg iv start , then recheck BP after 20/ 30minutes ,
If DBP is 110mmHg or more give another dose of (5-10) mg of hydralazine
iv. AND
• Methyldopa 500mg (PO) 8hourly. OR
• Nifedipine 20mg orally 12 hourly. THEN
• Labetalol 100mg orally twice a day.

27. 2. To control convulsion.
Provide magnesium sulphate.
• Loading dose of 14gm IV then maintenance dose 5g 4hrly in alternate
buttocks for 24hrs or after delivery or last fits whatever come last.
• Give 2gm IV if seizure recur after 15mints or
if persist give Diazepam 10-20mg slowly

28. 2. To control convulsion
• Before repeating MgSO4 administration ensure that
-respiration rate at least 16b/mn
-patellar reflex are present
-urinary output at least 30mls/hr over the preceding 4hrs.
Withhold or delay MgSO4, if there is any sign of magnesium toxicity
Give calcium gluconate 1gm(10mls of 10% solution )

29. How to dilute MgSO4
Route Dose 50% of Mgso4 (10mls solution)
IV slowly for 10-20min 4gm 8mls of MgSO4 +12mls of normal
saline (make 20mls solution)
2gm 4mls of MgSO4 +6mls of normal
saline (make 10mls solution)
IM 5gm 10mls of MgSO4 +1mls of
2%lignocaine)

30. Advantages of MgSO4
Advantages of MgSO4
• Controls fits effectively without any depression to mother and fetus
• Reduce risk of recurrent convulsion
• Significant decrease in maternal and foetal death
• Reduces perinatal mortality.

31. 3. Delivery
Preeclampsia without severe features
 At term: delivery is recommended at 37weeks
 Preterm :conservative management is indicated when
1. mother and fetus are stable
2.without finding of serious end organ dysfunction.

32. Delivery
At 28-34weeks
- Treatment of hypertension
-Administration of corticosteroids(inj dexamethasone 12mg 12hrly for 1/7 or 6mg
12hrly for 48hrs)
-Assessment of fetal growth and well being.
At 34-36weeks: uncertainity on conservative management , recommended delivery
to reduce maternal risk.
- During conservative management laboratory evaluation should repeated weekly.
( RFT,LFT, FBP)

33. Delivery
• Pre eclampsia with severe features or if imminent eclampsia manage as
eclampsia.
• Preeclampsia with severe features
terminate pregnancy –below viable gestational age
_above 34weeks of GA
_unstable maternal or fetal condition

34. Delivery
• patient with eclampsia should be delivered within 6-8 hrs from the onset
of seizure regardless of gestational age.
• Vaginal delivery is the safest mode of delivery if there is no
contraindication.

35. Methods of delivery
• Induction of labor.
• Cesarean section.

36. Indications for induction of labor
• Aggravation of the preeclamptic features in spite of medical treatment
and/or appearance of newer symptoms.
• Hypertension persists in spite of medical treatment with pregnancy
reaching 37 weeks or more.
• Acute fulminating pre-eclampsia irrespective of the period of gestation.

37. Indications for cesarean section
• When an urgent termination is indicated and the cervix is unfavorable
(unripe and closed).
• Severe pre-eclampsia with a tendency to prolong the induction (delivery
interval).
• Associated complicating factors, such elderly primigravida, contracted
pelvis, malpresentation.

39. FETAL COMPLICATIONS.
(1) Prematurity — spontaneous or induced
(2) Intrauterine asphyxia due to placental insufficiency.
(3) Effects of the drugs used to control convulsions,
(4) Trauma during operative delivery.

40. DIFFERENTIAL DIAGNOSIS.
(1) Epilepsy
(2) Hysteria
(3) Encephalitis,
(4) Meningitis,
(5) Puerperal cerebral thrombosis,
(6) Poisoning,
(7) Cerebral malaria in tropics,
(8) Intracranial tumor

41. Preventions .
• Patient education on risk factors
• Low dose aspirin from 12-36weeks
• Calcium supplement 1,5-2g/day
• Weight loss
• Proper antenatal care BP, urine for protein

42. reference
• DC DUTTAS TEXT BOOK OF OBSTETRIC
• KAPLAN OF OBSTETRIC AND GYNAECOLOGICAL..