Hypertension complications pregnancy

1. HYPERTENSIVE
DISORDERS IN
PREGNANCY

2. • Complicates 5-10% of all pregnancies
• Leading cause of maternal mortality
• One among the deadly triad that contribute
greatly to maternal mortality- others being
h’ge and infection

3. Normal changes in bp in pregnancy
• Brachial SBP an DBP
lowers 6 to 7 weeks of
gestation
• Arterial pressure
decreaes to a lowest
by 24-26 weeks and
rises thereafter

5. DBP SBP
Mild
hypertension
90-99 mmHg 140-149 mmHg
Moderate
hypertension
100-109 mmHg 150-159 mmHg
Severe
hypertension
110 mmHg or
greater
160 mmHg or
greater
NICE guidelines

6. • GESTATIONAL HYPERTENSION
New hypertension presenting after 20 weeks without significant proteinuria (NICE)
• PREECLAMPSIA
New hypertension presenting after 20 weeks with significant proteinuria (NICE)
• ECLAMPSIA
In a woman with preeclampsia, a convulsion that cannot be attributed to another
cause is termed eclampsia
• CHRONIC HYPERTENSION
Women with documented e/o bp > 140/90 before pregnancy, or before 20 weeks
gestation

7. ■ Diagnosis of Hypertensive Disorders

8. DELTA HYPERTESION

9. RISK FACTORS
1.genetic factors-
2.obstretic factors
• Age and parity:
Young, nulliparous-preclampsia
(Older-c/c HTN)
• Multifetal gestation
• Hydatidiform mole
• Limited sperm exposure
• Previous h/o preeclampsia
3.medical factors
• chronic hypertension
• Obesity
• Diabetes
• Renal diseases
• Insulin resistance in obesity &
PCOD
• Hyperhomocysteinemia
• Connective tissue disorders
SLE
Smoking-Reduced risk for HTN during pregnancy!!!

10. Etiopathogenesis
HTNve disorders are more likely to develop in women who
• Are exposed to chorionic villi for the first time
• Are exposed to a superabundance of chorionic villi, as with twins or hydatidiform
mole
• Have preexisting conditions of endothelial cell activation or inflammation such as
diabetes or renal or cardiovascular disease
• Are genetically predisposed to hypertension developing during pregnancy

11. “2 stage disorder hypothesis”
Stage 2:
Maternal
Syndrome
Stage 1:
Reduced
Placental
perfusion
Abnrml
placentation
?
“maternal and placental preeclampsia”
•Cardiovascular d/s
•Renal d/s
•DM
•Obesity
•Immunologic d/o
•Hereditary
ETIOLOGY PATHOGENESIS PATHOPHYSIOLOGY

12. Etiology
1. Placental implantation with abnormal
trophoblastic invasion of uterine vessels
2. Immunological maladaptive tolerance between
maternal,paternal (placental), and fetal tissues
3. Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancy
4. Genetic factors

13. 1.Abnormal trophoblastic invasion
• NORMAL implantation:
extensive remodelling of
spiral arterioles within the
decidua

15. • In preeclampsia:
Incomplete
Trophoblastic
Invasion

16. SPIRAL ARTERIOLES
•BEFORE TROPH.
INVASION
•AFTER INVASION –
NORMAL
•INCOMPLETE INVASION –
PREECLAMPSIA
•Narrow lumen
•Muscular
•High resistance
•Low flow
•Sensitive to vasomotpr
stimuli
•Low resistance
•High flow
•Arteries refractory to
vasomotor stimuli
•High resistance
•Low flow
•Arteries highly sensitive to
vasomotor stimuli

17. 2.Immunologic factors
• Normal maternal tolerence to paternally derived
placental and fetal antigens is lost /
dysregulated
• Factors asso. with this dysregulation
– Molar pregnancy(paternal antigenic load incr,/
double dose)
– 1st pregnancy(prev pregnancy immunise against
preeclampsia!)
– Inherited HLA abnormality

18. 3. Endothelial cell activation
In response to placental factors released by
ischemic changes/ any other Inciting Cause
Endothelial cell injury

19. 4. Nutritional factors
-vit.C
-Ca.
5. Genetic factors
-family history

20. Pathogenesis

21. 1.Endothelial cell injury
Release of
placental
factors into
maternal
circulation
Activation &
Dysfunction of
endothelium
•Reduced NO prodn &
Promote coagulation
•Increased sensitivity to
vasopressor

22. 1.Endothelial cell injury
•Reduced NO prodn &
Promote coagulation
•Increased sensitivity to
vasopressor
Intact endothelium:
-anticoagualant properties
-NO:Potent Vasodilator
When ‘NO’ reduced:
•Incr. MAP
•Reduc HR
•Incresd sensitivty to vasopressor
Normal preg.: refractoriness
to infused vasopressors –
PG
Here reduced PG
ie., reducd PGI2:TXA2
Reduced NO

23. 2.Endothelins
➢Increased release d/t endothelial activation
(happens even in normal pregnacncy, here it is
much more)
➢Potent vasoconstrictor
➢Increased release of endothelins Impt-ET1
➢MgSO4 → reduces ET1

24. 3.Angiogenic and antiangiogenic
proteins• Hypoxia in uteroplacental interface→ excessive
antiangiogenic factors
• Inactivate and reduce VEGF & Pl.GF
→Endothelial dysfunction
• Reduced NO dependent VD

25. Pathophysiology

26. CVS changes
d/t 3 main causes
1. Increased cardiac afterload caused by HTN
2. Reduced cardiac preload d/t reduced
hypervolemia of pregnancy
3. Endothelial activation with extravasation of
fluid; into lungs causing pulmonary oedema

27. -Blood volume changes
• Hemoconcentration is a hallmark of Eclampsia
• Hemoconc. is d/t
– Generalised VC
– Leakage of plasma
• Preeclampsia: Hemoconcentration is not that
marked
• GHTN: Blood volume is usually normal

28. A women with preeclampsia is:
• Unduly sensitive to vigorous fluid therapy
• Sensitive to amounts of blood loss at
delivery that are considered nl for a
normotensive

29. -Hematological changes
• Thrombocytopenia
• Hemolysis
– Incr. S.LDH
– Decr. Haptoglobin
– Periph.blood: schizocytosis, reticulocytosis,
spherocytosis

30. Renal
• Nl preg: renal perf. & GFR increas
• Preeclampsia: renal perf. & GFR decreas
• d/t reducd GFR → S.Creatinine incr.
• Oliguria
• Elevated plasma uric acid
• PROTEINURIA- d/t increased capillary
permeability

31. • Swollen endothelial cells called glomerular
capillary ENDOTHELIOSIS– d/t
antiangiogenic factors
• ARF- develops when there is associated
severe hemorragic hypotension or HELLP s’
or abruption

32. Hepatic
• Periportal h’ge, hepatic infarction
• Elevated transaminases
• Symptomatic involvement of liver or asymptomatic
elevation of transaminases is a sign of severe
preeclampsia
• symptoms? – moderate to severe R upper quadrant
or mid epigastric pain
• LIVER FAILURE: if combined with h’gc hypotension

33. HELLP SYNDROME
• Hemolysis
• ELevated liver enzymes
• Low Platelet
• In 10% cases of preeclampsia
• Increased maternal and fetal risk
• m/c symptom: R upper quadrant pain, nausea and
vomiting
• Asso. elevated liver enzymes(SGOT OR SGPT>
70U/L)
• May hav asso.thrombocytopenia, bleeding
tendencies;

34. Brain
• Cortical and subcortical petechial h’ge; Widespread
intracerebral h’ge; cerebral oedema
• Headaches , visual symptoms- scotomata, diplopia (severe
preeclampsia)
o d/t cerebrovascular hypererfusion
• Convulsion : eclampsia
o d/t excessive release of excitatory neurotransmitters esp. glutamate
• Blindness
• Mental changes ranging from confusion to coma
o may be d/t generalised cerebral oedema

35. Uteroplacental perfusion
• Compromised→ perinatal morbidity and
mortality
• By normal placentation – impedence to
blood flow is reduced
• Abnl placentation – high resistance persists

36. Severity of Preeclampsia

37. Impending or imminent eclampsia
• Headache or flashing lights
• Nausea or vomiting after midpregnacy
• Epigastric or right upper quadrant pain
• Brisk deep tendon reflexes and ankle clonus

38. Complications
❑ Maternal
❑ CNS:
– Eclampsia
– Cerebral hemorrhage
– Cortical blindness, Retinl
detachment
❑ Renal
– Cortical necrosis
– Renal tubular necrosis
❑ Hematological
– DIC
❑ Respiratory system
– Pulmonary oedema
– ARDS
• Liver
– HELLP syndrome
– Hepatic rupture
• Placental
– Abruptio placenta
• Fetal
• Immediate
– Prematurity
– IUGR
• Late
– Long term cardiovascular
morbidity

39. Management of pre
eclampsia

40. Investigations
1.Renal function test
• 24 hr urine protein
• Urine for pus cells,cast
• ↑blood urea,serum creatinine
• ↑serum uric acid:helps to differentiate with chronic
hypertension
2.LFT
• ↑SGPT,SGOT
• ↑Bilirubin

41. 3.Haematologic test
• ↑haematocrit
• Haemolysis
• ↑LDH
• Thrombocytopenia
• Coagulation profile

42. 4.fundoscopy
o Arteriolar spasm and vascular damage
o Retinal oedema
o Cotton wool exudates
o Retinal haemorrhages
o Retinal detachment

43. PREDICTIVE TESTS FOR
PREECLAMPSIA
TESTS RELATED TO….
• Vascular resistance/placental perfusion
• Fetoplacental unit endocrine dysfunction
• Endothelial dysfunction/oxidative stress
• Others

44. RELATED TO VASCULAR RESISTANCE
• 1.MAP in second trimester >/=90mmHg
women who don’t develop normal midtrimester fall
in diastolic BP more likely.

45. • 2.Gant’s roll over test→Women turned from
LL to Supine position
increase in diastolic pressure of 20 mm or more
• 3.Angiotensin sensitivity test
if pressor response occurs with <8ng/kg/min of
infused angiotensin

46. • 4.UTERINE ARTERY DOPPLER
• Persistance of diastolic notch in the
uterine artery or increased resistance
at 20-22 weeks

48. Tests to assess fetoplacental unit
endocrine dysfunction
• Elevated 2 nd trimester maternal serum
alpha fetoprotein,beta hcg,inhibin A.
• PAPP –A ,PP-13

49. OXIDATIVE STRESS RELATED TEST
✓Fibronectin,thrombocytopenia,hyperhomoc
ystinaemia –seen before clinical syndrome
develop
✓Decrease in angiogenic factors –
VEGF,increase in soluble Fms like
tyrosine kinase &soluble endoglin .

50. OTHER TESTS
• Antithrombin 3
• Atrial natriuretic peptide
• low Ca creatinine ratio in urine<0.04
• Increase in urinary Ca excretion
• Raised serum uric acid
• microalbuminuria

51. Prophylaxis
• Low dose aspirin 75 mg daily
• Selectively inhibits COX ,thromboxane syn
• Thus restore normal balance of thromboxane &
Prostacyclin.
• Started at 10 – 12 week & continued untill birth of
baby
• Indicn→high risk women
• DM, hypertension,renal disease, APLA
syndrome, previous history of pre eclampsia

52. • CALCIUM SUPPLEMENTATION
• Women with low Ca intake are at
increased risk of preeclampsia.
• Hence given for women at high risk of
preeclampsia in communities with low
dietary Ca intake.

53. • Folic acid
• hyperhomocystinaemia has association with
early onset preeclampsia
• reduce homocysteine levels

54. Management
MILD PRE ECLAMPSIA(140/90 to 149/99mmHg)
• Admit / Op or day care basis
• Bed rest in left lateral position
• High protein diet
• No salt restriction ,sedatives or diuretics needed

55. • Anti hypertensives
indicn→early onset disease
SBP>160,DBP>100
Drugs→ labetalol
a methyl dopa
nifedipine
hydralazine

56. Adv→help to prolong pregnancy
Disadv→they mask the severity of disease
ACE inhibitors,ARB’s & diuretics are
contraindicated in pregnancy.

58. • Monitoring
Maternal:daily weighing
BP at least 4 times daily& daily dipstick proteinuria
Haematocrit,platelet count,RFT,LFT→twice weekly
Fetal→DFMC
USG→fetal growth & well being
NST & amniotic fluid volume
doppler velocimetry in IUGR

59. • DELIVERY--.definitive treatment
• If pre eclampsic features subsided→induce labour at37- 38 wks
• Early termination-if there is progression to severe preeclampsia or
eclampsia
• Antenatal corticosteroids ,if preterm
• If cervix unfavourable,PG’s given.
• Continuous cardiotocography during labour.
• Epidural analgesia for pain relief.
• Ergometrine avoided as it can lead to sudden rise in BP.

60. • Induction
IF cervix favourable →ARM +oxytoxin infusion
Ifcervix unfavourable→PGE2 gel
• CTG monitoring during labour
• Cut short 2nd stage
• No prophyllactic ergometrine
• Post partum→ observe 48 hrs

61. • SEVERE PRE ECLAMPSIA
hospitalise,rest diet
delivery is definitive treatment
after 34 wk→terminate
before34 wk→
if initial condn stabilises→exp mngmt
if not termination.
before 24 wk→terminate after proper counselling
Expectant management
at tertiary care centre with close maternal and fetal monitoring

62. Anti hypertensives
To prevent cerebral haemorrhage.
Labetalol,nifedipine,hydralazine, alpha methyl
dopa
Close monitoring
Biochemical &physiological parameters repeated
twice daily
Close monitoring of maternal and fetal
conditions.

63. Maternal monitoring
-Bp monitoring >4 times depending on clinical circumstances
-Biochemical & hematological parameters repeated twice daily.
-Haematocrit,platelet count,blood urea,serum -creatinine,SGOT,SGPT -3 times
a week
-Total urinary protien or urinary total protein/creatinine ratio-to quantify
proteinuria
-Coagulation studies and evaluation of haemolysis if platelet count below
100,000/cumm,liver enzymes evelated,evidence of abruption.

64. Fetal monitoring
- USG,doppler,liquor volume assessed.
- Fetal wellbeing by nonstress test,biophysical profile,
doppler if there is IUGR.
Antenatal corticosteroids
- For lung maturity

65. • Indications for immediate termination
• Uncontrolled hypertension
• Imminent eclampsia or eclampsia
• Abnormal RFT,LFT, coagulopathy
• abruption
• HELLP syndrome
• Fetal distress
• Severe IUGR
• Attainment of 34 wks

66. Intrapartum medical management
• Control BP
• DBP<110 mm Hg
• Labetalol IV infusion 2mg/kg or 20 mg IV bolus over 2 min
• Oral nifedipine
• Hydralazine 5 mg IV bolus
• sublingual nifedipine-Rapid fall in BP avoided

67. Anti convulsants
• Prophylactic MgSO4
loading dose-
4gm(8ml)+12ml NS in 20ml syringe over 5 min IV
4gm(8ml)+1ml local IM along with 50% lignocaine on one
buttock
Maintainance dose-
4gm(8ml) in 92ml NS as IV slowly over 4hrs(1gm/hr)
Continue till 24 hr post partum

68. • Fluid management
• Fluid restriction,excessive fluid causes fluid overload & pulmonary
oedema.
• Total fluid limited to 80 ml/hr or 1 ml/kg/hr.
• In coagulopathy/HELLP syndrome-blood ,blood products like
FFP,platelet concentrate
• Post partum haemorrhage-CVP line mandatory
• Obstetric management
-Induce labour
-Continuous CTG monitoring
-Epidural analgesia

69. • Indications for CS
• associated obstetric indications
• failed induction
• rapid worsening of maternal condition and
delivery not imminent
• Fetal distress or severe IUGR

70. POSTPARTUM MANAGMENT
Postpartum haemorrhage
• Prophylatic ergometrine & methergin are
contraindiacted.
• Oxytocin &15-methyl analogue of PGF2 alpha
used.
• PGE1 analogue tablets used rectally
• Fluid and blood may have to be replaced
under CVP monitoring.

71. Monitoring
• Biochemical and haematological parameters.
• Pulmonary oedema is more common in this
period.
• Oliguria common but recovers spontaneously
• MgSo4 continued for another 24 hrs.
• Close monitoring of vitals at least 48 hrs.

72. Thromboprophylaxis
✓ Severe preeclampsia –risk factor for DVT
ANTIHYPERTENSIVES
✓ Continued after delivery ,reduction in dose done step wise.
✓ Methyldopa avoided-causes depression
✓ Can stop medication in 6-8 wks.
✓ If it persists beyond 8 wks ,diagnosis of chronic hypertension
considered.

73. HELLP syndrome-
management• Obstetric emergency
• Immediate termination in maternal interest.
• Supportive trt for coagulation abnormality-FFP,fresh blood,platelet
transfusion.
• Steriod therapy –dexamethasone-used previously
• Doesn’t mandate cs and pt with favourable cervix –induction of
labour.
• If unfavourable cervix-cs
• Mgso4 and antihypertensives given
• If platelet count low,GA necessary.
• Intraperitoneal & subfascial drain used.
• Intensive monitoring for 24 hrs postpartum.

74. ECLAMPSIA

75. ECLAMPSIA
• Occurrence of seizures in a woman with
preeclampsia, that cannot be attributed to any
other cause.
• ECLAMPSIA : “ FLASHES OF LIGHT”
• Seizures are generalized and may appear before,
during, of after labour
• PP eclampsia unlikely after 4days

76. • One third of women may experience eclampsia before
the development of hypertension & proteinuria
• It may be asymptomatic or preceded by the classical
symptoms of impending eclampsia: headache, visual
disturbances, epigastric pain

77. • Other associated problems
• Neurological defecit(cerebral vasospasm
& oedema)
• Cortical blindness (reversible)
• Pulmonary oedema
• Aspiration
• Cerebral haemorrhage
• Tongue bite

78. PHASES OF ECLAMPTIC SEIZURE
Prodromal phase(30s) :
aura followed by convulsive movements
beginning around the mouth
Tonic phase (15-20s) :
whole body rigid,
face contorted,
respiration ceases
CLINICAL FEATURES

79. Clonic phase (1min) :
grand mal convulsions starting from facial
muscles
involves entire body
frothing at mouth
Recovery phase : (variable duration)
convulsions subside
respiration resumes
Stage of coma

80. D/D
• Epilepsy
• CVA like hghe, cerebral thrombosis (should be
considered when more than 48 hrs has elapsed
since delivery or when there are FND or
prolonged coma.)
• Infection like encephalitis, meningitis & cerebral
malaria
• Brain tumours
• Metabolic disturbances
FND / prolonged coma –CT ,MRI , to exclude
haemorrhage and thrombosis.

81. • PROGNOSIS
• Maternal mortality
• Adequate trtmnt mortality < 2%
• Bad prognostic factors
a) long interval btw fits & delivery
b) late referrals
c) coma
d) very high BP
e) oliguria & severe proteinuria
f) abnormal liver function test & HELLP
syndrome

82. • Perinatal mortality
• Upto 30%
• Due to prematurity, hypoxia & effects of
drugs used

83. MANAGEMENT
• INVESTIGATIONS
• RFT
• LFT
• HAEMATOCRIT
• PLATELET COUNT
• COAGULATION STUDIES
• HAEMOLYSIS
• URINE-PROTEINURIA

84. General measures:
• Left lateral position
• Airway should be kept patent
• IV line should be established (RL)
• MEASUREMENT OF OXYGEN SATURATION USING Pulse oximetry
• Catheterize, input Output monitoring
• Mouth gag is placed during convulsions, to prevent tongue bite
• After the attack air passages should be cleared by suction

85. MEDICAL MANAGEMENT
• Anticonvulsant therapy
Magnesium sulphate
Can be given IV/IM
MOA: compete with Ca ion at neuromuscular junction

86. • CONTINUOUS IV INFUSION
1. Give 4-6 gm of loading dose of MgSO4 diluted in
100ml of iv fluid administrated over 15-20 min.
2. Begin 2gm/hr in 100ml of iv maintenance
infusion.
3. Monitor for magnesium toxicity
4. MgS04 is discontinued 24 hr after delivery.

87. • INTERMITTANT INTRAMUSCULAR INJECTIONS
1.Give 4gm of mgso4 as a 20% solution iv at a rate not to
exceed 1 gm/ min
2. Follow promtly with 10 gm of 50%MgSO4 solution – half
injected deeply in the upper outer quadrant of both buttocks.
If convulsions persist after 15 min , give upto 2 gm more iv
as 20% solution.
3. Every hr thereafter give 5 gm of 50% solution of MgSO4 INJ
deeply into upper outr qudrant of alternate buttocks.
4. It is discontinued 24 hr after delivery.

88. Anti convulsants
loading dose-
4gm(8ml)+12ml NS in 20ml syringe over 5 min IV
4gm(8ml)+1ml local IM along with 50% lignocaine on
one buttock
Maintainance dose-
4gm(8ml) in 92ml NS as IV slowly over 4hrs(1gm/hr)
Continue till 24 hr post partum

89. MONITOR FOR:
• Patellar reflex
• Urine output (at least 100ml in preceding 4hrs)
• Respiratory rate (normal>16/min)

90. • Therapeutic range is about 4-8mEq/L
• Once patellar reflux is absent blood level
of mgso4 is about 10mEq/L
• Respiratory arrest occurs when level is
12mEq/L

91. ANTIDOTE
Oxygen & 10ml 10% Ca Gluconate or calcium chloride IV if
respiratory depression
If resp arrest occurs,CPR started & pt intubated.
Recurrent seizures
• a further bolus of 2g mgso4
• Sometimes midazolam 0r lorazepam may have to be given
ABSOLUTE CONTRAINDICATION
• myasthenia gravis
• recent myocardial infarction

92. • ANTI HYPERTENSIVES
• Similar to pre eclampsia:
• Labetalol
• Alpha methyl-dopa
• Nifedipine
• Hydralazine

93. Obstetric management
• Immediate termination is advisable after controlling
seizures
• Stabilize maternal condition.
• No contraindication for vaginal delivery & labour can
be induced.
• Cs section-if convulsions not controlled,maternal
condition worsens.
• Mgso4 continued throughout labour and for at least 24
hr postpartum.

94. Status eclampticus
• Midazolam,lorazepam or Thiopentone sodium given slow iv.
• If it fails, transfer to icu & intubation & assisted ventilation

95. GESTATIONAL HTN
HTN arising for 1st time after 20weeks of
gestation in the absence of proteinuria &
BP returns to normal 12weeks postpartum
• Reclassified as transient htn ,if evidence for
preclampsia doesnot develop and bp returns
to normal by 12 weeks postpartum.

96. MANAGEMENT
• Mild cases managed on an outpatient basis with close
monitoring of BP,proteinuria,blood tests.
• Follow up –twice weekly,when lab tests should be
done.
• Ask to report if any symptoms appear or tests show
abnormalities.
• Antihypertensives if BP more than 150/100 mm Hg
• Mild cases delivered at 37-38 wks

97. • Severe cases-admitted
• Managed like severe
preeclampsia,terminated at 34 wks.
• Persistently high BP is to be viewed
seriously even in absence of
proteinuria and managed as case of
severe preeclampsia.

98. • Postnatally,if BP is normal ,continue on
antihypertensives.
• Usually medication stopped in 6-8 wks.
• If HTN persists beyond 8 wks,diagnosis of
chronic HTN should be considered.
• If it persists at 12 wks ,should be referred to a
specialist.

99. CHRONIC HTN
• HTN occuring prior to pregnancy or prior to 20
weeks of gestation.
• HTN first diagnosed before 20 weeks and
perssting 12 weeks pp is also considered chronic
htn.
• 1 – 5% of pregnancies
• Increasing maternal age & race(blacks)
• 2 types :
a) primary htn / essential htn – 90%
b) secondary htn – 10%

100. • Aetiology
• Essential htn 90%
• Renal disease
• Collagen d/s
• Pheochromocytoma
• Cushings syndrome
• Conn syndrome
• Coarctation of aorta
• Renal artery stenosis

101. • COMPLICATIONS
• Superimposed preeclampsia with all its
complications
• Abruption
• Cerebral hghe
• Congestive cardiac failure
• Renal damage

102. MANAGEMENT
Preconceptional evaluation
• Bp should be controlled prior to pregnancy.
• Changing of drugs like ACE’s inhibitors,ARB’s
and diuretics –to avoid risk of teratogenicity.
• Fundoscopy,RFT,LFT,ECG and
echocardiography performed in all pts to
evaluate end organ damage.

103. Find out the cause
• If first detected in pregnancy,investigations aimed
to find out cause.
• Vanyl mandelic acid- pheochromocytoma
• Antinuclear antibody & ds DNA for SLE
• Electrolyte level for Conn syndrome.
• Serum uric acid help to differentiate chronic HTN
from preeclampsia

104. ANTIHYPERTENSIVES
• ACE inhibitors & ARBs avoided during 2 nd & 3 rd
trimester-causes IUGR,renal
agenesis,oligohydramnios,pulmonary hypoplasia.
• Diuretics continued if pt was previously on the
same.
• Reduce salt intake
• Aim –bp below 140/90 mm Hg

105. Obstetric management
• Closely monitored for dev of superimposed
preeclampsia and IUGR
• Pt considered low risk if they have mild HTN without
end organ damage
• Can continue upto 40 wks
• High risk include severe HTN or mild HTN with end
organ damage.
• Managed as any other case of severe preeclampsia.

106. THANK YOU