HYPERTENSION IN PREGNANCY ADDIS GETAHUN

1. HYPERTENSIVE
DISORDERS IN
PREGNANCY
ADDIS GETAHUN,
2014,@ chiro Hospital

2. Introduction
1. Hypertensive disorders of
pregnancy are leading causes of
maternal mortality.
2. Worldwide: 50,000 women die
each year.
3. Egypt: 18% of maternal mortality.

3. Introduction
Homeostasis during normal pregnancy:
is an example of the principle of
priorities, where the pregnant women
must alter her entire physiological and
biochemical environment to provide
conditions best suited for the fetus to whom
she is hostess, that is the price of
viviparity.

4. Introduction
In hypertension:
many complex homeostatic
modifications occur, some are
harmful to the mother and fetus,
while others are beneficial.

5. Definitions
Hypertension in pregnancy:
– Bl/P of 140/90 or more is abnormal.
– If there is a rise of 30 mmHg or more in the systolic
blood pressure or 15 mmHg or more in the diastolic
blood pressure In 2 occasions 6 hours apart.
– Mean arterial BP> 105 mmHg .
Mean arterial BP = Systolic + 2 Diastolic
-----------------------------
3

6. Classifications

7. National High Blood Pressure Education
Program Classification ( NHEP) 2000
Gestational hypertension.
Preeclampsia (mild, severe).
Eclampsia.
Superimposed preeclampsia
upon chronic hypertension.
Chronic hypertension with
pregnancy.

8. Definitions
Gestational hypertension:
– Hypertension for first time after 20 w,
without Proteinuria. BP returns to normal
before 12 weeks postpartum.
Chronic hypertension with pregnancy:
– Hypertension antedates pregnancy and
detected before 20 w, & lasts more than 12
weeks postpartum.

9. Definitions
– Preeclampsia:
The development of hypertension and
Proteinuria after 20 w
May occur earlier in vesicular mole or twins.
– Eclampsia (in Greek= Flash of light):
The occurrence of tonic-clonic convulsions
(without any neurological disease) in a woman
with pre-eclampsia.

10. Definitions
Superimposed pre-eclampsia:
¤ It is the new development of
Proteinuria after 20 weeks gestation
in a patient with chronic
hypertension

11. Definitions
Proteinuria:
– ≥ 300mg/24 hours urine.
– ≥ +1 dipstick.
Heavy Proteinuria :
–= ≥ 2gm/24 hours
– or ≥ +2 in dipstick.

12. Preeclampsia

13. Epidemiology of preeclampsia
Incidence:
Is a disease of humans only.
Is the most common medical disorder
complicating pregnancy 5-15%
Is the most common hypertensive disorder in
pregnancy.
More common in primigravidas and elderly
multipara.
More common in winter.
More in black races.

14. Epidemiology
Risk factors:
Chronic hypertension.
Chronic nephritis.
Past history .
Family history.
Obesity.
Multiple pregnancy.

15. Epidemiology ( risks)
Polyhydramnios.
Vesicular mole.
Diabetes mellitus.
Nulliparity.
Teenage Pregnancy.
Smoking.
Stress

16. Etiology= theories
Genetic Predisposition.
Free Radicals Theory
In pre-eclampsia the levels of free
radicals are higher than normotensive
women leading to endothelial damage.

17. Oxidative stress
Antioxidant capacity
ROS synthesis
O2
._
H2O2
ONOO
_
Vitamin C
SOD

18. Etiology= theories
Endothelial injury:
Endothelin 1(potent vasoconstrictors).
Nitric Oxide ( vasodilator action).
Vascular Endothelial Growth
Factor (VEGF).

19. Etiology= theories
Prostaglandins:
There is decrease in
prostacyclin /TX A2 ratio
leading to :
vasoconstriction and
tendency to thrombosis.

20. Etiology= theories
Inflammatory Factors:
Pre-eclampsia is considered an inflammatory
disease due to increased number of activated
leukocytes in the maternal circulation.
Immunological Factor:
primigravidas
Multipara with 1st pregnancy from a
new husband.
Abundant trophoblast ( vesicular
mole and multiple pregnancy.

21. The Central Players
(Hemostats) in PET
1. The Endothelium
2. Neutrophils
3. Platelets
4. Coagulation system.
Once one is triggered
Co- Workers are released (NO, PGs, ROS,
Homosystein, etc)

22. Triggers for PET
Genetic Modulators
Pre-existing Vascular
Pathology
Central players
Cytokines
Ros

23. The Constant
Pathophysiological Changes
Is
Vascular endothelial:
Damage +Dysfunction
+ Spasm

24. Pathology
PET is the clinical ice-
berg tip manifestation
of the disturbances in
the maternal
homeostasis, involving
many systems and
organs.

25. Multisystem Features Of
Preeclampsia
Hypertension Proteinuria
Eclampsia HELLP syndrome
IUGR
Multi-organ disease
Cerebral vessels
Fetus
Liver
Systemic blood vessels Kidneys

26. Diagnosis
1) Prediction.
2)CL/P & Severity
3)Eclampsia

27. Diagnosis
I. Prediction:
High risk factors.
Rapid weight gain during the
2nd half of pregnancy (due to
occult edema).
Any increase above 3/4 kg/week in late
pregnancy is abnormal.

28. Tests for Prediction
Roll over test is positive (rise of diastolic blood
pressure 20 mmHg or more after turning from left
lateral to dorsal position).
Increased pressor response.
Uric acid: is elevated.
Hypercalciuria.
Doppler velocimetry to detect Uteroplacental hypo
perfusion.

29. Diagnosis Of PET
Hypertension + Proteinuria
=
Two facets of a complex pathophysiological
process

30. A): Signs: :
it is a disease of signs :
2 cardinal signs + or - Edema:
Hypertension:
– usually precedes Proteinuria,
Proteinuria: detected by
– Boiling test.
– Quantitative assay.
– Dipstick test.

31. + or - Edema
occult or manifest:
The lower extremities.
Abdominal wall, vulva or may be
generalized anasarca.
usually after hypertension.

32. Peripheral edema is not a
useful diagnostic criterion
1) it is common in normal pregnancy.
2) PET can occur without edema (dry type).
so its presence does not ensure a poor
prognosis and its absence not ensure a
favorable outcome.

33. B) Symptoms (non specific):
Headache.
Blurring of vision.
Nausea and vomiting.
Epigastric pain (distension of the liver
capsule)
Oliguria or anuria

34. Severity Of Pre-eclampsia
The severity of pre-eclampsia is
assessed by:
–The frequency and intensity
of the signs and symptoms.
–The more the severity of PET,
the more likely is the need to
terminate pregnancy.

35. DD ,mild & severe PET
Severe
Mild
Abnormality
110 mm Hg or higher
< 100 mg Hg
Diastolic blood pressure
Persistent 2+ or more
Trace to 1+
Proteinuria
Present
Absent
Headache
Present
Absent
Visual disturbances
Present
Absent
Upper abdominal pain
Present
Absent
Oliguria
Present (eclampsia)
Absent
Convulsion
Elevated
Normal
Serum creatinine
Present
Absent
Thrombocytopenia
Marked
Minimal
Liver enzyme elevation
Obvious
Absent
Fetal growth restriction
Present
Absent
Pulmonary edema

36. 4) Diagnosis Of Eclampsia:
Eclamptic fit stages ( 4 stages):
–Premonitory stage (1/2 minute):
Eye rolled up.
Twitches of the face and hands.
–Tonic stage (1/2 minute):
Generalized tonic spasm with
episthotonus.
Cyanosis.
Tongue may be bitten between the
clenched teeth.

37. 4) Diagnosis Of Eclampsia:
Clonic stage (1-2 minutes):
Convulsions .
Tongue may be bitten.
face is congested and cyanosed.
conjunctival congestion.
blood stained froth from the mouth,
Stertorous breathing,
temperature may rise.
involuntary passage of urine or stool.
Gradually convulsions stop.

38. 4) Diagnosis Of Eclampsia:
Coma:
– Variable duration due to respiratory and
metabolic acidosis.
– Deep coma may occurs (cerebral
hemorrhage).
– Labor usually starts shortly after the fit.
– Sometimes labor does not start and
convulsions recur again the so called
‘intercurrent eclampsia’ and carries a bad
prognosis.

39. Classifications of Eclampsia
–Intercurrent Eclampsia:
eclampsia in which the
eclamptic fits recur in the same
pregnancy.
–Recurrent Eclampsia:
eclampsia that recurs in
subsequent pregnancy.
Classifications of Eclampsia

40. Classifications of Eclampsia
– Ante partum (65%) with the best
prognosis.
–Intrapartum (20%).
–Postpartum (15%) with the worst
prognosis as it indicates extensive
pathology and multisystem
damage..

41. Classifications of Eclampsia
1)Mild
2) Severe (Eden's criteria):
Coma > 6 hours.
Temperature > 39 (pneumonia or
pontine hge)
Systolic Bp > 200 (risk of cerebral hge)
Pulse > 120/min ( acute heart failure).
Anuria or Oliguria( renal failure).
Respiratory rate > 40/min( pneumonia)
More than 10 fits (status eclampticus).

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

43. Investigations
B. Instrumental
Fundus Examination .
C. Imaging techniques :
CT scan for the brain.
Ultrasonograghy .
E. Doppler Velocimetry .

44. VI. Differential Diagnosis:
A. Hypertension With Pregnancy.
B. Proteinuria With Pregnancy.
C. Edema With Pregnancy:

45. VI. Differential Diagnosis:
D. Convulsions With Pregnancy:
Eclampsia.
Epilepsy.
Hysteria.
Meningitis and Encephalitis.
Tetanus.
Tetany.
Strychnine poisoning.
Brain tumors.
Uremic convulsions

46. VI. Differential Diagnosis:
E. Coma With Pregnancy:
Hypoglycemic .
Hyperglycemic coma
Uremic coma.
Hepatic coma.
Alcoholic coma.
Cerebral coma.

47. VI. Differential Diagnosis:
F. HELLP Syndrome:
Acute fatty liver in pregnancy
Hepatitis
TTP
HUS

48. Treatment
PREVENTION.
Antepartum ttt.
Proper antenatal care
Expectant treatment.
Control hypertension.
Treatment of eclampsia .
Prevention and control of convulsions.
Termination of pregnancy .
Intrapartum care.
Postpartum care.

49. Prevention
Low dose aspirin: 75 mg/day.
Decrease TxA2 (from Platelets).
Not affect endothelial prostacyclin
(PGI2 )
Calcium supplementation:
Ca++ supplementation may
increase the production of
prostacyclin (PGI2 ) from
endothelial cells.

50. The most effective preventive
measures for OCCURANCE
of pre-eclampsia IS
PREVENTION OF
PREGNANCY
“contraception”
Prevention

51. TTT of preeclampsia
Expectant Treatment .
Control of Hypertension.
Prevention of convulsions .
Termination of pregnancy .

52. 1) Expectant Treatment
Rest: Complete Physical and mental rest.
Diet: Increase protein and carbohydrate
with low Na diet !!!!!.
Sedation AND TRANQULIZER:
Phenobarbitone & DIAZEPAM.
Observation ( MATERNAL & FETAL).

53. 1) Expectant Treatment
(Observation)
Maternal:
– Blood pressure.
– Pulse and Respiratory rate.
– Urine output.
– Proteinuria.
– Any new symptoms.
– Investigations (creatinine, creatinine clearance,
blood picture, coagulation profile,….)
Fetal:
fetal well-being

54. 2) Control of
Hypertension:
A)Parentral drugs:
– 1) Hydralazine:
It is a peripheral VD.
The best Antihypertensive drug worn during
Pre-eclampsia and Eclampsia.
Dose: 5-10mg IV or IM as initial dose.
Repeated every 20-30 minutes until blood
pressure is controlled.

55. 2)Control of Hypertension:
– 2) Labetalol (Trandate):
α and non selective β- adrenergic blocker
resulting in VD.
Dose: 10-20mg IV .
The dose can be doubled every 10 minutes if
proper response is not achieved.
– 3) Diaz oxide (Hyperstat):
Used in severe dangerous resistant hypertension
as a last resort.
Dose: 50-150mg IV bolus dose.
Repeated every 1-2 minutes until BP decreases.

56. 2)Control of Hypertension:
A )Oral drugs:
1) α-methyl DOPA (aldomet):
It is the most commonly used.
It is α-adrenergic agonist causing depletion
of catecholamine stores.
Dose: 500mg 3-4 times/day orally.
2) Monohydralazine (Aprisoline):
It is a weak Antihypertensive when given
alone.
It used in combination with β- blockers to
increase its efficacy and decrease its side
effects.

57. 2)Control of Hypertension:
– 3) β- adrenergic blockers:
– Atenolol (tenormin) 50-100mg 4 times daily.
– Labetalol (Trandate) 10-20mg 3 times daily.
– 4) Prazocin (minipres):
It is postsynaptic α-adrenergic receptor blocker
resulting in VD and reflex tachycardia.
It is a weak Antihypertensive drug so used in
combination with other drugs.
– 5) Calcium Channel Blocker:
Nifedipine (adalat or Epilat) .

58. TTT of Preeclampsia
3)Prevention of convulsions ( vide infra ).
4)Termination of pregnancy( vide infra)

59. Treatment of Eclampsia
1)General and first aid measures:
– Isolation in a single, quite, semi dark room
(eclampsia room).
– An efficient nurse should be present.
– The following equipments must be present
Oxygen source.
Airway.
Suction apparatus.
Bed with movable head and legs with limb
ties.

60. Treatment of Eclampsia
1) General and first aid measures( A &B &C
&D …………cont )
–Ensure patent airway with tracheal and
bronchial suction.
–Put the patients in Trendlenburg position
(to avoid aspiration of secretions) .
–Insert a catheter.
– Nasogastric tube may be inserted .
–Nothing by mouth and fluid chart.
– Full laboratory investigation.

61. Treatment of Eclampsia
2) Observation:
–Pulse, temperature, BP
and RR.
– Level of consciousness.
–Duration of coma.
–Fetal heart sounds.
– Urine output and albuminuria .
–Number of convulsions

62. Treatment of Eclampsia
– 3) Sedation :
Morphine
– 10-20mg IM then maintain by diazepam 10mg IV or
IM/8 hours.
Lytic cocktail
– 25mg chlorpromazine + 50mg phenergan + 100mg
pethidine.
– Given in 500CC fluid over 4 hours .
– Can be repeated after 6 hours.
– Never give 3rd dose.

63. 4) Control of Convulsions:
A) Magnesium Sulfate (MgSO4):
It is the drug of choice.
Mechanism:
–CNS depression.
–Mild VD.
–Mild diuresis.
–Inhibits platelet aggregation.
–Increase PGI2 synthesis.

64. Magnesium Sulfate (MgSO4):
It can be given IV (20%) or IM (50%) or SC
(15%):
– The therapeutic level is 4-7mEq/L.
– The total dose of MgSO4 should not exceed 24 gms in
24 hours .
– The dose of MgSO4 is monitored by:
Preserved patellar reflex.
Respiratory rate >16/min.
Urine output >100ml/4hours.
Serum Mg++ level.
– Is stopped 24 hours after delivery.
N.B Antidote is ca gluconate

65. Magnesium Sulfate (MgSO4):
IV regimen:
– initially 4-6 gm (20%) in 100ml solution .
Given over 15-20 minutes.
– Then, 2 gm/hour by IV drip.
IM regimen:
– 10 gms of 50% solution are given deeply
IM (5 gms in each buttock).
– Maintain with 5 gm/6 hours of 50%
solution.

66. Side effects of MgSO4 (small safety margin)
– At a level of 8-10mEq/L patellar reflex is lost and
starts myometrial inhibition.
– 10-15mEq/L respiratory depression.
– >15mEq/L cardiac depression.
– Curare like action.
– Synergistic effect with Ca++ channel blockers.
– Uterine inertia.
– Neonatal hypermagnesemia.
– Decreased beat to beat variability in FHS.
Antidote : 10ml of 10 percent calcium gluconate

67. 4) Control of Convulsions:
B ) Pheyntoin (Epanutin):
In severe pre-eclampsia
In imminent eclampsia .
The dose is 15mg/kg.

68. 4) Control of Convulsions:
– C) Diazepam (Valium):
– This regimen is mainly for eclamptic
patients.
– Initially 20-40mg IV slowly over 5 minutes.
– then 10-20mg/6hours.
– then the dose is adjusted at 10mg/hour to
maintain drowsiness.
– Side effects:
Neonatal low APGAR score.
Neonatal hyperbilirubinemia.

69. Modified Stroganoff method:
The original Stroganoff method is
MgSO4 6gm initially then 4 gm/4hours
+ 20mg morphine IM.
4) Control of Convulsions:

70. Treatment of Eclampsia
5) Control of hypertension (VIDE SUPRA)
6)Other drugs:
– Prophylactic digitalis to guard against HF
– Antibiotic for infection.
– IV glucose 25% as a liver support, increases
the urine output and improves
Hemoconcentration.

71. Treatment of Eclampsia
7)Termination of Pregnancy
– Indications:
Eclampsia.
Retinal hemorrhage: by CS to avoid bearing
down.
Deteriorated cardiac, renal or liver functions.
Severe PET not controlled after 24 hours.
Mild PET reaching 38 weeks and not controlled.
Expectant treatment reaching maturity.
Deterioration of the fetal conditions.
Other obstetric indications as CPD,
malpresentations, APH,…(by CS).

72. 7)Termination of Pregnancy
Methods:
– As a rule vaginal delivery is safer and better
than CS.
Artificial rupture of membranes and pitocin drip.
– CS.

73. Treatment of Eclampsia
8) Management during labor:
With the onset of labor give IV
hypotensives and sedation.
The patient must be at rest with oxygen
source and other equipments for treating
fits.
Maternal observation.
Continuous electronic fetal monitoring.

74. 8) Intrapartum management:
Epidural anesthesia is the best for both CS
and vaginal delivery (provided that DIC is
excluded).
Avoid straining in the second stage.
Shorten the 2nd stage by forceps or
ventouse.
No ergometrine Intrapartum.
Management during CS:
Best done 4-6 hours after the last fit (allow time
for recovery from acidosis).

75. Treatment of Eclampsia
9) Postpartum management
Improvement is monitored by:
– Increased urine output.
– Decreased edema.
– Disappearance of Proteinuria within 1 week
– Decreased hemotocrite value to normal level.
– BP normalize within 2 weeks
No ergometrine postpartum.
MgSO4 stopped 24 hours postpartum.

76. Prognosis:
BP usually normalize after placental
delivery .
Hypertension may persist.
Postpartum eclampsia carries the worst
prognosis.
Maternal mortality is about 2% in severe
preeclampsia and 10% in eclampsia.
Perinatal mortality rate is about 5% in
mild cases, 25% in severe cases and 30%
in eclampsia.