2. Hypertensive disorders in pregnancy
Dr. Wael Al,Halaki
Professor in Qasyoun Private university
Hama University 2017

3. Hypertensive disorders in pregnancy

4. Hypertensive disorders are the most common and yet serious conditions seen in obstetrics

5. INTRODUCTION Incidence is 5-10%.
The most frequent cause of iatrogenic prematurity.
Preterm delivery
Intrauterine growth restriction (IUGR)
Perinatal death
Maternal cerebrovascular accidents ( CVA).
Placental abruption.

6. Normal Blood Pressure changes in Pregnancy
Decreases during the first trimester,
Reaching its lowest point at 20 weeks,
Returns to pre-pregnancy levels during the third trimester.

7. Classification Pre-eclampsia Eclampsia Gestational hypertension
Preeclampsia superimposed on chronic hypertension
Chronic hypertension with pregnancy
Gestational hypertension

8. GESTATIONAL HYPERTENSION
Blood Pressure ≥ 140/90mmHg on two or more occasions
- In a previously normotensive patient
- After 20 weeks gestation
- Without proteinuria
- Returning to normal 12 weeks after delivery
Almost half of these develop preeclampsia syndrome

9. GESTATIONAL HYPERTENSION SUSTAINED HYPERTENSION ( ≥ 140/90)
GESTATION ≥ 20 WEEKS
SUSTAINED HYPERTENSION ( ≥ 140/90)
No proteinuria

10. GESTATIONAL HYPERTENSION
Sustained B.P
No proteinuria
DEFINITION
SYMPTOMS
NONE
EXAMINATION
Unremarkable

11. Preeclampsia
It is defined as hypertension of at least 140/90mm Hg recorded on two separate occasions at least 4 hours apart and in the presence of at least 300mg protein in a 24 hour collection of urine, arising after the 20th week of gestation in a previously normotensive woman and resolving completely by the 6th postpartum week.

12. Gestational Hypertension
Preeclampsia
Preeclamsia
Gestational Hypertension
Proteinuria

13. RISK FACTORS for PREECLAMPSIA
NULLIPARA
(Age extremes <20yrs ,
>35yrs )
DEMOGRAPHIC
Multiple gestation
Molar pregnancy
Non-immune hydrops
OBSTETRICS
Diabetes mellitus
Chronic HTN
Renal disease
SLE
MEDICAL

14. Genetic Age &Parity Partner Factors
Genetic Predisposition
Family History
Race & Ethnicity
More Common in black & Asians
Pregnancy by ovum donation
Age &Parity
Teenage pregnancy <18 yrs
Age>35 yrs
Long interval between pregnancy >10 years
Nulliparity
Partner Factors
Change of partner
Limited sperm exposure
Pregnancy by donor insemination
Partner fathered an eclamptic pregnancy

15. Pregnancy Factors Underlying Medical Diseae Others
Multiple pregnancy
Hydatiform mole
Hydrops fetalis
Fetal chromosomal anomaly
(trisomy 13)
Underlying Medical Diseae
Chronic hypertension
Diabetes mellitus
Renal Disease
Cardiovascular disease
Hyperthyroidism
Metabolic Syndrome
Others
Obesity BMI> 35 kg/m2
Psychological stress & strain
Smoking
Previous history of preeclamsia
insulin resistance, obesity, atherogenic dyslipidemia and hypertension. 
Hyperhomocysteinemia ,
Autoimmune disease
Antiphospholipid antibodies,
Thrombophilia

16. SUSTAINED HYPERTENSION (≥ 140/90)
MILD PREECLAMPSIA
GESTATION ≥ 20 WEEKS
SUSTAINED HYPERTENSION (≥ 140/90)
Proteinuria (≥300mg /24 hr)

17. MILD PREECLAMPSIA LABORATORY FINDINGS Proteinuria (1-2+)
Hemoconcentration
< 36 wks Conservative
>36 wks MgSO4 and Delivery
MANAGEMENT

18. GESTATIONAL HYPERTENSION
GESTATION ≥ 20 WEEKS
SUSTAINED HYPERTENSION (≥ 140/90)
NO PROTEINURIA
MILD PREECLAMPSIA
GESTATION ≥ 20 WEEKS
SUSTAINED HYPERTENSION ( ≥ 140/90)
Proteinuria ( ≥ 300mg /24 hr)

19. CRITERIA: SEVERE PREECLEMPSIA
≥ 170/110
GREEN TOP GUIDELINE 2010
BLOOD PRESSURE
≥ 5grams
GREEN TOP GUIDELINE 2010
PROTEINURIA
Headache
Epigastric pain
Visual changes
SYMPTOMS

20. ECLAMPSIA
New onset of seizures or unexplained coma during pregnancy in patients with pre-existing preeclampsia and without pre-existing neurological disorder.

21. Eclampsia addition of convulsions in a woman with preeclampsia
occurs in 0.5-4% of deliveries
25% have eclamptic seizures before labour, 50% during labour, and 25% after delivery.
Eclampsia
Preeclampsia
Seizure/
Convulsion/
Coma

22. ECLAMPSIA Same as Preeclampsia RISK FACTORS PATHO -PYSIOLOGY
Cerebral vasospasm , ischemia and edema
Generalized tonic-clonic
SEIZURES
SYMPTOMS

23. ECLAMPSIA Proteinuria Hemoconcentration LABORATORY FINDINGS MANAGEMENT
DIC
Elevated Liver enzymes
Stop convulsions with MgSO4
Prompt delivery at any gestational age
Lower diastolic BP mm/Hg
MANAGEMENT

24. MANAGEMENT IV MgSO4 – To prevent convulsions
( continue 24 hrs post-partum )
LOWER B.P ( hydralazine or labetalol)
INDUCE LABOR (IV oxytocin and amniotomy )

25. CHRONIC HYPERTENSION OR
Blood pressure ≥ 140/90 before 20 weeks of gestation. OR
persistence of hypertension beyond 12 weeks after delivery.

26. CHRONIC HYPERTENSION GESTATION < 20 WEEKS OR Prepragnancy
SUSTAINED HYPERTENSION (≥140/90)
+/- PROTEINURIA

27. CHRONIC HTN PREGNANCY PROGNOSIS
B.P 140/90 to 179/109
No end organ damage
GOOD PROGNOSIS
KIDNEYS: Renal disease
EYES : Retinopathy
HEART : Left Ventricular Hypertrophy (B.P >180/110)
POOR PROGNOSIS
Uncontrolled HTN
Chronic HTN +Superimposed Pre-eclampsia
WORST PROGNOSIS

28. MANAGEMENT OF CHRONIC HYPERTENSION
antihypertensive meds
(if B.P >100 mm Hg diastolic)
If antihypertensive meds needed
- Methyl dopa is drug of choice (or labetalol)
Serial ultrasounds (increase risk of IUGR >30 weeks )
Serial B.P and urine protein
(watch for superimposed preeclampsia)
Induce labor at term

29. SUPERIMPOSED PREECLAMPSIA (on Chronic Hypertension)
New-onset proteinuria > 300 mg/24 hrs in hypertensive women but no proteinuria before 20 wks gestation.
A sudden increase in proteinuria or blood pressure or platelet count < 100,000/ cu mm in women with hypertension and proteinuria before 20 wks gestation.

30. CHRONIC HTN SUPERIMPOSED PRE-ECLAMPSIAS
CHRONIC HYPERTENSION
Worsening BLOOD PRESSURE
Worsening proteinuria

31. MANAGEMENT of Chronic HTN and superimposed PRE-ECLAMPSIA
MgSO4 – To prevent convulsions
( continue 24 hrs post-partum )
LOWER B.P - Diastolic mm Hg
( hydralazine or labetalol)
INDUCE LABOR (IV oxytocin and amniotomy )

32. HELLP Syndrome
HTN patients with hemolysis (H), elevated liver enzymes (EL), low platelet count (LP)
4-12% of pt. with severe preeclampsia and eclampsia develop HELLP syndrome

33. HELLP Syndrome
Cardiovascular stabilization, correction of coagulation abnormalities, and delivery
PLT transfusion before or after delivery if PLT count is <20,000/mm3 (advised at <50,000/mm3 before cesarean)
<32 weeks gestation; steroid therapy may help stabilize maternal PLT count

34. PATHOPHYSIOLOGY Complex disease
Appears to be triggered by the placenta
Can occur in molar pregnancies where fetus absent
Can also occur in abdominal pregnancy (pregnancy not in uterus)

35. Poor Immunoregulation Clinical manifestation
Mechanisms
Stage 0
3-8 weeks
Stage 1
8-18 weeks
Stage 2
20 weeks to birth
Poor Immunoregulation
Inadequate tolerance to feto-paternal antigens during conception and implantation
Poor Placentation
Deficient trophoblast invasion and spiral artery remodelling
Clinical manifestation
Over activation of maternal endothelium and systemic inflammatory network
Oxidative Stress
Endoplasmic reticulum Stress
Inflammatory Stress
Abnormal placentation (stage 1), particularly lack of dilatation of the uterine spiral arterioles, is the common starting point in the genesis of pre-eclampsia, which compromises blood flow to the maternal–fetal interface. Reduced placental perfusion activates placental factors and induces systemic hemodynamic changes. The maternal syndrome (stage 2) is a function of the circulatory disturbance caused by systemic maternal endothelial cell dysfunction resulting in vascular reactivity, activation of coagulation cascade and loss of vascular integrity. Pre-eclampsia has effects on most maternal organ systems, but predominantly on the vasculature of the kidneys, liver and brain.

36. Mechanisms Normal Pregnancy
invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries
transforms them from small-caliber resistance vessels to high-caliber capacitance vessels
capable of providing placental perfusion adequate to sustain the growing fetus
Normal Pregnancy
process of vascular invasion, the cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as "pseudovasculogenesis" 

37. cytotrophoblasts fail to adopt an invasive endothelial phenotype
Mechanisms
Preeclampsia
cytotrophoblasts fail to adopt an invasive endothelial phenotype
invasion of the spiral arteries is shallow and they remain small caliber, resistance vessels
placental ischemia

39. Pre-eclampsia is two stage disease
Maternal Syndrome
Fetal Syndrome

40. Organ Specific Changes associated with Pre-eclampsia
Cardiovascular
Renal
Generalized vasospasm
Increased peripheral resistance
Reduced central venous/ pulmonary pressure
Proteinuria
Decreased glomerular filtration rate
Decreased urate excretion
Hepatic
Organ Specific Changes associated with Pre-eclampsia
Periportal necrosis
Subscapular hematoma
Hematological
Central Nervous System
Platelet activation and depletion
Coagulopathy
Decreased plasma volume
Increased blood viscosity
Cerebral oedema
Cerebral haemorrhages

41. Treatment of Hypertension:
Antihypertensive drugs used in pregnancy are
Methyldopa
Hydralazine
labetalol

42. Seizure Prophylaxis Routinely used in severe PE.
Magnesium sulphate: most commonly used.
Initiated with onset of labor till 24h postpartum.
For caesarean, started 2hrs before the section till 12hrs postpartum.

43. Recommended regime for MgSO4
it can be given either IV or IM IV has good prognosis.
Loading dose for IV is 4g. i.e. 8 ml diluted in 12ml normal saline. This 20 ml is given in 20 minutes.
Maintenance dose is 20 g i.e. 40ml diluted in 60ml normal saline and given at rate of 1g/hr.

44. Recommended regime for MgSO4
IM is also used.
Loading dose is as IV.
Maintenance dose is 5g every 4 hrs in alternate buttocks for 24hrs.
Mgso4 acts on NM junction and inhibit entry of Ca++ ions thus inhibiting excitability of neurons.

45. Management of MgSO4 Toxicity
Calcium gluconate is antagonist for MgSO4. it is usually given as 10 ml of 10% Calcium gluconate in 10 minutes

46. Delivery The only definitive treatment
Preeclamptic patients divided into 3 categories
A- Preeclampsia features fully subside
B- partial control, but BP maintains a steady high level
C- persistently increasing BP to severe level or addition of other features

47. Management: A: can wait till spontaneous onset of labor
don’t exceed Expected Date of Delivery
B: >37wk terminate without delay
<37wk, expectant management at least
till 34wks
C: terminate irrespective of POG
start seizure prophylaxis and steroids if<34wks

48. Delivery in Eclampsia
Unless contraindicated: Eclamptic women should undergo normal vaginal delivery
Indications for caesarean section -
Fetal distress
Placental abruption
Unfavourable cervix
Failed induction of labour
Recurrent seizures

49. Investigations Urine: 24 hour urine, Proteinuria.
Kidney functions: serum creatinine, urea, creatinine clearance and uric acid.
Liver functions: bilirubin, Enzymes
Blood: CBC, HCt , Hemolysis and Platelet count (Thrombocytopenia).
Coagulation Profile: Bleeding and clotting time

50. PREVENTION Regular Antenatal checkup: Rapid gain in weight
Rising blood pressure
Edema
Proteinuria/Deranged liver or renal profile
Low dose Aspirin in High risk group: ↑PGs and↓TXA2
(nice guideline)
Calcium supplementation: no effects unless women are calcium deficient
Antioxidants- Vitamin C and E
Nutritional supplementation: zinc, magnesium, fish oil, low salt diet

51. Uterine Artery Doppler Velocimetry (abnormal flow resistance/ diastolic notch in 2nd/ 3rd trimester)
is most promising, but currently, none of them is completely suitable for clinical use. (Conde-Agudelo, 2014; Kleinrouweler, 2012; Myatt, 2012a).
These have value for fetal-growth restriction but not preeclampsia (ACOG, 2013a).
As a result of these trials, some methods to prevent Preeclampsia have been theorized…

52. uterine artery DOPPLER
at 24 weeks of pregnancy: Flow velocity waveform from the uterine artery at 24 weeks of gestation in a pregnancy with impaired placentation; in early diastole there is a notch (yellow arrow) and in late diastole there is decreased flow (orange arrow).
In preeclamptic mother:
Showing early diastolic NOTCH
Decreased EDF
(due to high resistance)
In normal mother