hypetensive disorders in pregnancy 332.ppt

Hypertention

1. Hypertensive Hypertensive
disorders in disorders in
pregnancypregnancy
Presented by:Presented by:
Dr. A. KhalidDr. A. Khalid

2. Contents Contents
1.1.Factors affecting blood pressure in normal Factors affecting blood pressure in normal
pregnancy.pregnancy.
2.2.Pre eclmpsia.Pre eclmpsia.
3.3.Other causes of hypertension in pregnancy: Other causes of hypertension in pregnancy:
-Essential hypertension -Essential hypertension
(chronic) -(chronic) -
Phaeochromocytoma Phaeochromocytoma
-Coarctaition of the aorta -Coarctaition of the aorta
-Cushing syndrome -Cushing syndrome
-primary aldosteronism (conn’s syndrome). -primary aldosteronism (conn’s syndrome).
4.4.Cardiovascular changes in pregnancy.Cardiovascular changes in pregnancy.

3. Cardiovascular changes in Cardiovascular changes in
pregnancy (adaptation) pregnancy (adaptation)
Cardiac out put increases 40% and decreases Cardiac out put increases 40% and decreases
in the 3in the 3
rdrd
trimester. trimester.
Fall in the vascular tone (decrease resistance).Fall in the vascular tone (decrease resistance).
Increase in the heart rate.Increase in the heart rate.
Blood pressure decrease in the 1Blood pressure decrease in the 1
stst
and 2 and 2
ndnd

trimesters, become normal in the 3trimesters, become normal in the 3
rdrd
trimester. trimester.
Supine hypotension.Supine hypotension.

4. Factors affecting blood pressure Factors affecting blood pressure
in normal pregnancyin normal pregnancy
Error in measurement: small cuff in Error in measurement: small cuff in
obese lady.obese lady.
Patient’s position.Patient’s position.
Korotkoff sounds:Korotkoff sounds:
1.1.ІІ - systolic - systolic
2.2.ІІV-diastolicV-diastolic
Time of measurement. Time of measurement.

5. ACCURATE ACCURATE
MEASUREMENTS OF BPMEASUREMENTS OF BP
Sitting position.Sitting position.
Large cuff.Large cuff.
Korotkoff Korotkoff ІІ, , ІІV.V.
Not single reading.Not single reading.
Cut off line is 140/90 mmHg.Cut off line is 140/90 mmHg.

6. Pre eclampsia Pre eclampsia
NomenclatureNomenclature
Pre eclamptic toxaemia (P.E.T):Pre eclamptic toxaemia (P.E.T):
1.1.Pre eclampsia Pre eclampsia
2.2.GestosisGestosis
3.3.P.I.H P.I.H
syndrome of 2syndrome of 2
ndnd
half of pregnancy. half of pregnancy.

7. Aetiology and pathogenesisAetiology and pathogenesis
(PE) (PE)
Placenta :Placenta :
1.1.Decreased blood flow Decreased blood flow »» placental hypoxia »» infarction.»» placental hypoxia »» infarction.
2.2.Fibrin deposition.Fibrin deposition.
Maternal endothelial dysfunction:Maternal endothelial dysfunction:
1.1.Sequence hypertension.Sequence hypertension.
2.2.Renal impairment.Renal impairment.
3.3.Proteinuria. Proteinuria.
4.4.Convulsion.Convulsion.
5.5.Hepatic dysfunction, necrosis.Hepatic dysfunction, necrosis.
6.6.Jaundice.Jaundice.
7.7.Abdominal pain.Abdominal pain.
8.8.DIC. DIC.

8. Aetiology and pathogenesisAetiology and pathogenesis
(PE)(PE)
Cerebral haemorrhage. Cerebral haemorrhage.
Renal involvement, progressive Renal involvement, progressive
proteinurea (0.3 grams/L): poor proteinurea (0.3 grams/L): poor
prognosis, and that indicate prognosis, and that indicate
glomeruler involvement. glomeruler involvement.
Impaired renal function, decrease Impaired renal function, decrease
uric acid clearance. uric acid clearance.

9. Plasma volume changes Plasma volume changes
Decreased plasma volume.Decreased plasma volume.
Oedema is normally found in 85% of Oedema is normally found in 85% of
patients.patients.
Changes in the clotting system:Changes in the clotting system:
1.1.Hyperfibrinogenaemia.Hyperfibrinogenaemia.
2.2.Activation of platelets.Activation of platelets.
3.3.Deceased platelets count (late Deceased platelets count (late
complication). complication).

10. Liver changes Liver changes
Increased hepatic enzymes. Increased hepatic enzymes.
Jaundice.Jaundice.
Hepatic failure.Hepatic failure.
HELLP syndrome:HELLP syndrome:
-H: haemolysis.-H: haemolysis.
-EL: elevated liver enzymes.-EL: elevated liver enzymes.
-LP: low platelets count.-LP: low platelets count.

11. Possible causes of Possible causes of
ConvulsionsConvulsions

Hypertensive encephalopathy.Hypertensive encephalopathy.
Brain ischemia.Brain ischemia.
Brain oedema.Brain oedema.
Fibrin deposition.Fibrin deposition.
Vasoconstriction. Vasoconstriction.

12. Foetal syndrome in PEFoetal syndrome in PE
Placental dysfunction (infarction), this Placental dysfunction (infarction), this
leads to:leads to:
 Impaired transfer function, that leads to:Impaired transfer function, that leads to:
Intra uterine growth restriction (IUGR), that Intra uterine growth restriction (IUGR), that
leads to retro placental clots ( abruptio). leads to retro placental clots ( abruptio).
And that leads to foetal death.And that leads to foetal death.

13. Risk factors Risk factors
Maternal:Maternal:
1.1.PG.PG.
2.2.Increased maternal Increased maternal
age.age.
3.3.Previous PE.Previous PE.
4.4.ObesityObesity
5.5.Medical disorders:Medical disorders:
D.MD.M
Renal disease.Renal disease.
Ess. HTEss. HT
Foetal:Foetal:
1.1.Multiple pregnancy.Multiple pregnancy.
2.2.Hydatiform mole.Hydatiform mole.
3.3.Hydrops fetalis.Hydrops fetalis.
4.4.HyperplacentosisHyperplacentosis
5.5.Large babyLarge baby

14. Diagnosis of PEDiagnosis of PE
usually the condition is a symptomatic, usually the condition is a symptomatic,
so diagnosis depends on signs and so diagnosis depends on signs and
investigations.investigations.
Signs:Signs:
1.1.Increased blood pressure in the 2Increased blood pressure in the 2
ndnd
half half
of pregnancy.of pregnancy.
2.2.Excessive weight gain.Excessive weight gain.

15. Management of PEManagement of PE
Admission:Admission:
1.1.Rest .Rest .
2.2.Observation: general condition, foetal kick count, BP, Observation: general condition, foetal kick count, BP,
fundal measurements, oedema.fundal measurements, oedema.
3.3.Investigations: general (Hb , UG, BG), 24 hour urine Investigations: general (Hb , UG, BG), 24 hour urine
proteins collection, Renal function, liver function.CBC.proteins collection, Renal function, liver function.CBC.
Antihypertensive drugs: ( it prevents CVA)Antihypertensive drugs: ( it prevents CVA)
Criteria should not:Criteria should not:
1.1. cross the placenta.cross the placenta.
2.2. drop the BP sharply.drop the BP sharply.
3.3. reduce uteroplacental flow.reduce uteroplacental flow.

16. Continue Continue
Examples:Examples:
1.1.Methyl Dopa.Methyl Dopa.
2.2.Calcium channel blockers.Calcium channel blockers.
3.3.Hydralazine.Hydralazine.
4.4.Alfa & Beta Blockers (Labetalol)Alfa & Beta Blockers (Labetalol)

17. Management of labour & Management of labour &
delivery delivery
When? When?
Depends on gestational age and severity Depends on gestational age and severity
of the condition.of the condition.
How ?How ?
Depends on cervical condition, severity Depends on cervical condition, severity
of the condition & other indication of C/S .of the condition & other indication of C/S .
Sedation in case of induction.Sedation in case of induction.
Epidural anaesthesia.Epidural anaesthesia.

18. Other causes of HT in Other causes of HT in
Pregnancy Pregnancy
Chronic essential hypertensionChronic essential hypertension: :
Increase BP before 20 weeks.Increase BP before 20 weeks.
In old patients.In old patients.
Presence of family history of HT.Presence of family history of HT.
Superimposed by PE when Superimposed by PE when
proteinuria develops.proteinuria develops.

19. Continue Continue
Phaechromocytoma:Phaechromocytoma:
1.1.Rare and dangerous.Rare and dangerous.
2.2.Unstable HT.Unstable HT.
3.3.Urinary excretion of Vanillyl Mandelic Urinary excretion of Vanillyl Mandelic
Acid (VMA).Acid (VMA).
4.4.CT scan & MRI are helpful in diagnosis.CT scan & MRI are helpful in diagnosis.

20. Cushing’s syndrome Cushing’s syndrome
Associated with menstrual disturbances & Associated with menstrual disturbances &
Amenorrhea, so pregnancy is rare.Amenorrhea, so pregnancy is rare.
Presentation mimics pregnancy presentation Presentation mimics pregnancy presentation
e.g. wt. gain, striae, increased blood e.g. wt. gain, striae, increased blood
glucose, increased BP and pigmentation. glucose, increased BP and pigmentation.
Increase bound and unbound cortisol level.Increase bound and unbound cortisol level.
Dexamethazone suppression of cortisol is Dexamethazone suppression of cortisol is
diagnostic. diagnostic.