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HYPERTENSIVE
DISORDERS IN
PREGNANACY
BY: DR.K.S.K JUSU
DEPARTMENT OF O&G
SCHOOL OF CLINICAL SCIENCES
CONTENTS
 OVERVIEW OF HTNSIVE DISORDERS IN PREG
 CLASSIFICATION OF HTNSIVE DISODERS IN PREGNANCY
 PRE-ECLAMPSIA:
Definition
Incidence
Aetiology and pathophysiology
Clinical features
Investigations
Managements
Complications
 ECLAMPSIA :
Definition
Types
Pathophysiology
Clinical features
Investigtions
Differentials
Management
Complications
HPERTENSIVE DISORDERS IN
PREGNANCY
It’s the most common medical
problem seen in pregnancy.it
constitute major threats to maternal
life during pregnancy,labour and
immediate postpartum Period.In
developing countries,due to
inadequate facilities for
investigation,its not easy to
differentiate btw PIH,ESS.HTN &CRDz
CLASSIFICATION OF HTNsive
DISORDERS IN PREG
(1)PIH:
(a)PIH without proteinuria
(b)PIH with proteinuria ie PRE-
ECLAMPSIA
(2)CHTN of any etiology
(a)Essential htn
(b)CRDz
(3)CHTN with superimposed PE
PIH
Defined as development of
hypertension in the second half
of pregnancy measured at least
in 2 occasions about 4hrs apart,in
a woman who has previously
been normotensive and in which
BP returns to normal within 6
weeks of delivery
DEFINATION CONT......
PIH with proteinuria Is
a benign condition and usually occur in
the 3rd trimester,during labour or
peuperium
 CHTN:Present b4 20th week of pregnancy
or that present b4 pregnancy
 CHTN WITH SUPERIMPOSED PE: Define as
proteinuria developing for the 1st time
during pregnancy in a woman with known
CHTN
PIH with proteinuria or pre-
eclampsia
PRE-ECLAMPSIA is a multi-systemic disorder
characterized by HYPERTENTION and
PROTEINURIA that develops after 20 weeks
gestation in a previously normotensive
woman and in whom BP goes to normal
immediately within 6 weeks of delivery
HYPERTENSION in pregnancy is define as a
BP > or=140/90mmHg or rise in blood
pressure (BP) of > +30/+15 during the course
of pregnancy.
PIH with proteinuria or pre-
eclampsia
PROTEINURIA is defined as the presence of
>or = 300mg of protein in a 24-hr urine
collection or a protein measurement of
2+(1g albumin/l in random urine specimen.
Note Oedema is present in > 80% of normal
pregnant women and should not be a
diagnostic criteria .Condition resolves by 6
weeks postpartum
CLASSIFICATION
 MILD PE:
 Proteinuria 1+
 BP<160/100
 Mild oedema
 Minimal liver enzymes
 SEVERE PE:
 Proteinuria 2+
 BP>160/110
 Headache,blurred vision,abdominal pain
 Marked oedema
INCIDENCE OF PRE-
ECLAMPSIA
 There is an increase risk in the following cases
 Primigravidae<20 or >35 years
 FHx of PE
 First pregnancy with a new partner
 Multiple pregnancy
 Maternal obesity
 Fetal/placental hydrops
 Pre-existing DM,HTN or Renal dz
ETIOLOGY AND
PATHOGENESIS
 Basic etiology is ABNORMAL
PLACENTATION:failure of
trophoblast invasion
 Failure of second wave of
endovascular trophoblast
migration resulting in reduction
of blood supply to the
fetoplacental unit
ETIOLOGY AND
PATHOGENESIS
 2 main things we should
remember:ENDOTHELIAL
DYSFUNCTION:due to oxidative
stress and inflammatory
mediators,VASOSPASM due to
imbalance btw
vasodilators(Prstcyl,NO) and
vasoconstriction(TXA2,ANG
II,ENDOTHELIN
POSSIBLE MECHANISM OF
ACTION OF PIH
Abnormal cystotrophoblast
invasion->decrease in uterine
placental blood flow->placental
ischaemia->placental release of
cytokine factors(TNF,IL6,placental
syncytiotrophoblast microvillous
membranes)->endothelial
dysfunction->decrease renal
pressure natriuresis->HTN
CLINICAL FEATURES
 Increase BP
 Proteinuria
 Headache
 Double vision
 Blurred vision
 Epigastic pain
 Flashing lights
 Nausea and vomiting
 Rapidly increasing oedema
INVESTIGATION
 Hb and Haematocrit values increases
due to haemoconc. Caued by
decreased plasma volume
 Pl count decreases due to incr
intravascular destruction
 Clotting profile:clotting
time,PT,partial thromboplastin time &
Fibrinogen level.
INVESTIGATION
 Serum uric acid tends to be raised but
falls in normal pregnancy.
 Serum urea and critenine increases
 Liver enzymes elevated ie Alanin &
Aspartate transaminases.
 Urinalysis-daily for proteinuria
Management
Aims of management:
 To prevent maternal complications
 To prevent fetal mobidity & mortality.
Patient with mild hypertension without
proteinuria are given out-patient treatment,
councelled & follow up.
Management
Aims of management:
Those with proteinuria & severe HTN require
hospital admission for further Investigation &
MX.
But in general the maturity of the fetus
determines the line of action. For
instance,pregnancy of 37-42 weeks with
proteinuria, severe htn requires immediate
BP control and delivery of the baby.
Management.........
 For cases in which the baby is
immature,conservative
management is adopted to
achieve reasonable maturity to
minimize prenatal death.
However, if BP bcomes
uncontrolled,conservative
management must be
abandoned regardless of the
gestational age of fetus.
Conservative management
 Bed rest
 Monitor urine output & Bp
 Review results of maternal and fetal invs
 Further management plan
Antihypertensive drugs
LIST OF DRUGS USED
 -methyldopa
 -hydralazine
 -Beta blockers
Conservative management
 -mix beta & alpha blockers eg.Labetelol
 -CCBs eg Nifedipine
 In severe HTN,pre treatment with IV
colloids such as haemacel or human
solution not>500mls.useful for improving
renal & uteroplacental blood flow.also help
to reduce BP
Fetal assessment
 Wellbeing of the fetus can be can
assessed by
-fetal heart rate monitoring
-daily fetal kick charts
-fetal growth
-liquor volume & umbilical artery
dopplers
COMPLICATIONS
 compromised utero-placenta perfusion
 IUGR
 uterine and neonatal death
 Eclampsia
 ARF
 Pulmonary oedema
 Abruptio placentae
 DIC
PREVENTION OF PE
 Low doses of aspirin(75mg)start
early in 2nd trimester
 Calcium supplement is
beneficial in women@high risk
of PE and in those with low
dietary calcium intake
ECLAMPSIA
 It is defined as PIH
experiencing convulsive attacks
or fits
INCIDENCE
 It varies frm one part of the
world to another.
 It is low in western countries as
compared to developing
TYPES
There are 3 types
 Antepartum
 Intrapartum
 postpartum
Pathology
 The pathological features seen in
Eclampsia are mainly due to vascular
spastic effect on some organs.
 On the kidneys,bcos of marked spasm of
the glomerular arterioles with narrow
lumina which subsequently enlarge & the
capillary end arterial cells are swollen
with wide spread tubular necrosis.
 On the liver,it shows subscapular
haemorrhage & haemorrhagic infarcts.
pathology
 On the brain,vascular changes
occur in which edema is often
marked.Tiny or large
haemorrhage are often
present.
 The lungs show evidence of
congestion,infection or
aspiration pneumonia.
CLINICAL FINDINGS
 Increased BP
 Gross proteinuria
 Edema of limbs & face
 Convulsion
INVESTIGATIONS
 Urine testing for proteinuria
 FBC
 Uric acid,creatinine
electrolytes
 Abdominal scan
DIFFERENTIAL DX
 Idiopathic epilepsy
 Meningitis
 Encephalitis
 HIV encephalopathy
 Cerebral malaria
 Diabetic or hypoglycaemic
coma
MX
 Control convulsion by giving
magnesium sulphate
 Control hypertension using
antihypertensive drugs eg
Hydralazine
 Fluid & electrolyte balance
 Delivery of the baby.
COMPLICATIONS
 Cardiac failure
 Renal failure.
 Hyperpyrexia with or without evidence of
infection.
 Cerebrovascular accident
 HELLP(Haemolysis, Elevation of Liver
enzyme, Low Platelets) syndrome
 Mendelson’s syndrome
Complications.......
NOTE THAT;
 Delivery is the only cure
 Antihypertensive only lower the BP but does not prevent
progress of the dz
 Don’t stop giving a bolus dose of magnesium sulphate
THANK YOU

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PIH.pptx8888888888888888888888888888888888

  • 1. HYPERTENSIVE DISORDERS IN PREGNANACY BY: DR.K.S.K JUSU DEPARTMENT OF O&G SCHOOL OF CLINICAL SCIENCES
  • 2. CONTENTS  OVERVIEW OF HTNSIVE DISORDERS IN PREG  CLASSIFICATION OF HTNSIVE DISODERS IN PREGNANCY  PRE-ECLAMPSIA: Definition Incidence Aetiology and pathophysiology Clinical features Investigations Managements Complications  ECLAMPSIA : Definition Types Pathophysiology Clinical features Investigtions Differentials Management Complications
  • 3. HPERTENSIVE DISORDERS IN PREGNANCY It’s the most common medical problem seen in pregnancy.it constitute major threats to maternal life during pregnancy,labour and immediate postpartum Period.In developing countries,due to inadequate facilities for investigation,its not easy to differentiate btw PIH,ESS.HTN &CRDz
  • 4. CLASSIFICATION OF HTNsive DISORDERS IN PREG (1)PIH: (a)PIH without proteinuria (b)PIH with proteinuria ie PRE- ECLAMPSIA (2)CHTN of any etiology (a)Essential htn (b)CRDz (3)CHTN with superimposed PE
  • 5. PIH Defined as development of hypertension in the second half of pregnancy measured at least in 2 occasions about 4hrs apart,in a woman who has previously been normotensive and in which BP returns to normal within 6 weeks of delivery
  • 6. DEFINATION CONT...... PIH with proteinuria Is a benign condition and usually occur in the 3rd trimester,during labour or peuperium  CHTN:Present b4 20th week of pregnancy or that present b4 pregnancy  CHTN WITH SUPERIMPOSED PE: Define as proteinuria developing for the 1st time during pregnancy in a woman with known CHTN
  • 7. PIH with proteinuria or pre- eclampsia PRE-ECLAMPSIA is a multi-systemic disorder characterized by HYPERTENTION and PROTEINURIA that develops after 20 weeks gestation in a previously normotensive woman and in whom BP goes to normal immediately within 6 weeks of delivery HYPERTENSION in pregnancy is define as a BP > or=140/90mmHg or rise in blood pressure (BP) of > +30/+15 during the course of pregnancy.
  • 8. PIH with proteinuria or pre- eclampsia PROTEINURIA is defined as the presence of >or = 300mg of protein in a 24-hr urine collection or a protein measurement of 2+(1g albumin/l in random urine specimen. Note Oedema is present in > 80% of normal pregnant women and should not be a diagnostic criteria .Condition resolves by 6 weeks postpartum
  • 9. CLASSIFICATION  MILD PE:  Proteinuria 1+  BP<160/100  Mild oedema  Minimal liver enzymes  SEVERE PE:  Proteinuria 2+  BP>160/110  Headache,blurred vision,abdominal pain  Marked oedema
  • 10. INCIDENCE OF PRE- ECLAMPSIA  There is an increase risk in the following cases  Primigravidae<20 or >35 years  FHx of PE  First pregnancy with a new partner  Multiple pregnancy  Maternal obesity  Fetal/placental hydrops  Pre-existing DM,HTN or Renal dz
  • 11. ETIOLOGY AND PATHOGENESIS  Basic etiology is ABNORMAL PLACENTATION:failure of trophoblast invasion  Failure of second wave of endovascular trophoblast migration resulting in reduction of blood supply to the fetoplacental unit
  • 12. ETIOLOGY AND PATHOGENESIS  2 main things we should remember:ENDOTHELIAL DYSFUNCTION:due to oxidative stress and inflammatory mediators,VASOSPASM due to imbalance btw vasodilators(Prstcyl,NO) and vasoconstriction(TXA2,ANG II,ENDOTHELIN
  • 13. POSSIBLE MECHANISM OF ACTION OF PIH Abnormal cystotrophoblast invasion->decrease in uterine placental blood flow->placental ischaemia->placental release of cytokine factors(TNF,IL6,placental syncytiotrophoblast microvillous membranes)->endothelial dysfunction->decrease renal pressure natriuresis->HTN
  • 14. CLINICAL FEATURES  Increase BP  Proteinuria  Headache  Double vision  Blurred vision  Epigastic pain  Flashing lights  Nausea and vomiting  Rapidly increasing oedema
  • 15. INVESTIGATION  Hb and Haematocrit values increases due to haemoconc. Caued by decreased plasma volume  Pl count decreases due to incr intravascular destruction  Clotting profile:clotting time,PT,partial thromboplastin time & Fibrinogen level.
  • 16. INVESTIGATION  Serum uric acid tends to be raised but falls in normal pregnancy.  Serum urea and critenine increases  Liver enzymes elevated ie Alanin & Aspartate transaminases.  Urinalysis-daily for proteinuria
  • 17. Management Aims of management:  To prevent maternal complications  To prevent fetal mobidity & mortality. Patient with mild hypertension without proteinuria are given out-patient treatment, councelled & follow up.
  • 18. Management Aims of management: Those with proteinuria & severe HTN require hospital admission for further Investigation & MX. But in general the maturity of the fetus determines the line of action. For instance,pregnancy of 37-42 weeks with proteinuria, severe htn requires immediate BP control and delivery of the baby.
  • 19. Management.........  For cases in which the baby is immature,conservative management is adopted to achieve reasonable maturity to minimize prenatal death. However, if BP bcomes uncontrolled,conservative management must be abandoned regardless of the gestational age of fetus.
  • 20. Conservative management  Bed rest  Monitor urine output & Bp  Review results of maternal and fetal invs  Further management plan Antihypertensive drugs LIST OF DRUGS USED  -methyldopa  -hydralazine  -Beta blockers
  • 21. Conservative management  -mix beta & alpha blockers eg.Labetelol  -CCBs eg Nifedipine  In severe HTN,pre treatment with IV colloids such as haemacel or human solution not>500mls.useful for improving renal & uteroplacental blood flow.also help to reduce BP
  • 22. Fetal assessment  Wellbeing of the fetus can be can assessed by -fetal heart rate monitoring -daily fetal kick charts -fetal growth -liquor volume & umbilical artery dopplers
  • 23. COMPLICATIONS  compromised utero-placenta perfusion  IUGR  uterine and neonatal death  Eclampsia  ARF  Pulmonary oedema  Abruptio placentae  DIC
  • 24. PREVENTION OF PE  Low doses of aspirin(75mg)start early in 2nd trimester  Calcium supplement is beneficial in women@high risk of PE and in those with low dietary calcium intake
  • 25. ECLAMPSIA  It is defined as PIH experiencing convulsive attacks or fits INCIDENCE  It varies frm one part of the world to another.  It is low in western countries as compared to developing
  • 26. TYPES There are 3 types  Antepartum  Intrapartum  postpartum
  • 27. Pathology  The pathological features seen in Eclampsia are mainly due to vascular spastic effect on some organs.  On the kidneys,bcos of marked spasm of the glomerular arterioles with narrow lumina which subsequently enlarge & the capillary end arterial cells are swollen with wide spread tubular necrosis.  On the liver,it shows subscapular haemorrhage & haemorrhagic infarcts.
  • 28. pathology  On the brain,vascular changes occur in which edema is often marked.Tiny or large haemorrhage are often present.  The lungs show evidence of congestion,infection or aspiration pneumonia.
  • 29. CLINICAL FINDINGS  Increased BP  Gross proteinuria  Edema of limbs & face  Convulsion
  • 30. INVESTIGATIONS  Urine testing for proteinuria  FBC  Uric acid,creatinine electrolytes  Abdominal scan
  • 31. DIFFERENTIAL DX  Idiopathic epilepsy  Meningitis  Encephalitis  HIV encephalopathy  Cerebral malaria  Diabetic or hypoglycaemic coma
  • 32. MX  Control convulsion by giving magnesium sulphate  Control hypertension using antihypertensive drugs eg Hydralazine  Fluid & electrolyte balance  Delivery of the baby.
  • 33. COMPLICATIONS  Cardiac failure  Renal failure.  Hyperpyrexia with or without evidence of infection.  Cerebrovascular accident  HELLP(Haemolysis, Elevation of Liver enzyme, Low Platelets) syndrome  Mendelson’s syndrome
  • 34. Complications....... NOTE THAT;  Delivery is the only cure  Antihypertensive only lower the BP but does not prevent progress of the dz  Don’t stop giving a bolus dose of magnesium sulphate