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Hypertensive Disorders
in Pregnancy
Dr. Jograjiya G.R.
Post Graduate Student
ESI-PGIMSR, Basaidarapur, New Delhi.
INTRODUCTION
 It is associated with severe maternal obstetric
complications.
 Incidence is 5-10%.
 The most frequent ca...
Hypertension in Pregnancy
 Systolic B.P. ≥ 140 mmHg
 and/or
 Diastolic B.P. ≥ 90 mmHg
 Documented on two occasions
 A...
SEVERITY HYPERTENSION
 Non-severe hypertension: SBP
140-159 mmHg or DBP 90-109
mmHg.
Mild: SBP 140-149 mmHg or
DBP 90-99...
How to Measure Blood
Pressure
 Sitting Position
 Patient Relaxed
 Arm well supported
 Measured in right arm
 Cuff at ...
Normal Blood Pressure
changes in Pregnancy
• Decreases during the first
trimester,
• Reaching its lowest point at 20
weeks...
What is Significant
Proteinuria in Pregnancy
Total protein in 24 hours urine
> 300mg
Protein : Creatinine ratio in
rando...
Calcification and
Definitions
Classification
2. Pre-
eclampsia
4. Eclampsia
3.
Preeclampsia
superimposed
on chronic
hypertension
5. Chronic
hypertension...
GESTATIONAL HYPERTENSION
New onset of hypertension after
20 weeks of gestation without
proteinuria or other features of
p...
Gestational HTN:
DIAGNOSIS
 Determine the severity of
hypertension
 Measure protein excretion
24-hour urine collection
...
Gestational HTN: DIAGNOSIS
CRITERIA FOR MILD GESTATIONAL HYPERTENSION
Blood Pressure > 140 to < 160 mm Hg, systolic
> 90 t...
Gestational HTN: MANAGEMENT
 Mild Gestational HTN
Managed as outpatients (weekly antepartum
visits)
Daily fetal movemen...
Gestational HTN: MANAGEMENT
Severe Gestational HTN
SBP ≥160 mmHg or DBP
≥110 mmHg is treated with
antihypertensive agent...
Gestational HTN:
Risk of Progression to Preeclampsia
15-25% risk
Women with early onset of
gestational hypertension
are ...
Gestational HTN:
RECURRENCE
Prevalence: 22 - 47 % (2nd
pregnancy)
tends to recur with
subsequent pregnancies
Gestational HTN:
LONG-TERM PROGNOSIS
associated with
development of HTN later
in life
associated with
development of dis...
PREECLAMSIA
 New onset of hypertension after 20
weeks of gestation along with properly
documented proteinuria or end-orga...
Note it……………………..
 Preeclampsia can also occur
without proteinuria, with end-
organ dysfunction manifestations.
 Edema i...
Risk Factors
Genetic
Age & parity
Partner factors
Pregnancy Factors
Underlying Medical
Conditions
Others
Risk Factors
Risk Factors: Cont.
Genetic
Genetic
Predisposition
Family History
Race & Ethnicity
More Common in
black & Asians
Pregnancy...
Risk Factors: Cont.
Pregnancy Factors
Multiple pregnancy
Hydatiform mole
Hydrops fetalis
Fetal chromosomal
anomaly
(trisom...
PATHOPHYSIOLOGY
2 stage model for
preeclampsia
Stage 2
Maternal syndrome
(HTN, proteinuria,
Endothelial
dysfunction)
Stage1
Reduced placen...
Reduced placental
implantation –Stage-1
PREDISPOSING FACTORS:
Abnormal implantation
Association with microvascular
dise...
Net effect
Replacement of endothelial lining & muscular
arterial wall by trophoblast cells
Distended tortuous spiral arter...
ETIOLOGICAL FACTORS
Placental hypoxia
Immunological factors
Placental enzymes
Genetic factors (MTHFR, F5,)
Oxidative ...
What causes maternal
syndrome
Stage 2
Maternal syndrome
(HTN, proteinuria,
Endothelial
dysfunction)
Stage1
Reduced placent...
Maternal Syndrome
stage-II
Not just hypertension and
proteinuria
But also involves different end
organs
Physiology of maintain
uteroplacental flow in
Normal pregnancy
 Placenta releases angiotensinase
 destruction of angiot...
Normal balance of agonist &
anta-gonistic factors:
1.vasodialator &
vasoconstrictor
2. angiogenic and
antiangiogenic fac...
1.vasodialator & vasoconstrictor
vasodialator
NO
PGI-2
vasoconstrictor
Angiotensin-
II
Endothelin-I
Thromboxane A2
placent...
2. angiogenic and
antiangiogenic factors
Angiogenic
factor
• VEGF
• TFG-beta
• PlGF
Antiangiogenic
factor
• sFlt-1
• sEng
Gestational Hypertension
Basic mechanism of different
organ damage
Increased vasoconstriction
Decreased organ perfusion
Increased endothelial dy...
Multisystem Features
Of Preeclampsia
Hypertension Proteinuria
Eclampsia HELLP syndrome
Intra-uterine growth restriction
Mu...
Organ Damage
utero-placenta IUGR
Hematological Epistaxis, DIC like features,
hemoconcentration
CNS Cerebral edema, cerebra...
CVS involvement:
• ↑afterload↑ed peripheral
resistance
•↓preload↓ed pregnancy induced
hypervolumia
•Pulmonary leak edemaal...
Hematological system
Thrombocytopenia
& other PL
abnormality:
• ↑ed PL activation
& degranulation,
• ↓ed life span.
• Core...
Renal system involvement:
 ↓ed renal perfusion :(d/t ↓ed blood volume & ↑ed
afferent arteriolar pr.)
 ↓ed GFR : d/t
 gl...
Hepatic involvement:
Periportal
hemorrhagic
necrosis
hematoma
formation
Stretch/Rupture
epigastric pain
Brain involvement:
Acute severe HTN
cerebrovascular
overregulation
Vasospasm
Parenchymal ischemia
Cytotoxic edema
sudden ↑...
Lungs involvement:
High SBP
↑ed arteriolar pr
↑ed extravasation of blood into
alveoli + rupture of arteriole
Pulmonary ede...
PREECLAMPSIA PREDICTION
 There are many test during early pregnancy—
or across pregnancy—of various biological,
biochemic...
Endothelial Dysfunction/Oxidant
Stress
Feto-Placental unit Endocrine
Dysfunction
Renal Dysfuntion Misc
Placental Perfusion...
Trials of different preventive methods
and their outcomes
Sibai et al. Lancet 365:785-99, 2005.
Provocative
Pressure Tests
Three tests have been extensively
evaluated to assess the blood pressure
rise in response to a ...
1.Roll-over test
After resting in the left lateral
position turning to a supine
position induces a rise in
diastolic pres...
2.Hand-grip test
 Isometric (sustained) contraction of
striated muscles is known to cause
general sympathetic activation ...
3. Angiotensin II sensitivity
Sensitivity to infused angiotensin II: is
increased may be due to alteration in
vascular smo...
• is most promising, but currently, none of them
is completely suitable for clinical use. (Conde-
Agudelo, 2014; Kleinrouw...
uterine artery DOPPLER
In preeclamptic mother:
Showing early diastolic NOTCH
Decreased EDF
(due to high resistance)
In nor...
Urinary assays
a. Micro-albuminuria: detected by
radioimmunoassay before albuminuria can
be detected by the ordinary metho...
Urinary assays
c.Kallikrein/creatinine ratio: is reduced
in patients who develop PIH later on
if compared to the increased...
Blood tests
 a. Plasma urate: serial increase is a
warning of PIH before appearance
of other clinical features.
 b.Plate...
PREVENTION
 Prepregnancy
• Weight loss to ideal BMI
• Control of glucose in diabetes
• Control of BP in CHTN (diet, exerc...
History -special points
• Patient Particulars: Age young or >35 yrs, nulliparity, low
SES -risk factors
• Chief Complaints...
Physical Examination:
● Obesity/BMI >35 kg/m2
● Weight (serial measurements): Gain in wt at the rate of >500gs a week or
2...
Obstetric Examination:
Nothing special is found except features
of IUGR, oligohydramnios in some
cases.
Maternal Investigations:
Tests may be abnormal even when BP elevation is minimal.
• Urine dipstick testing for proteinuria...
Diagnosing Preeclampsia-Eclampsia:
• Blood pressure ≥ 140/90 mm of Hg (at
or after 20 weeks of gestation) on 2
occasions a...
Foetal Investigations:
• Cardiotocograph (CTG)
• Ultrasound scan (USS) assessment
of:
o fetal growth
o amniotic fluid volu...
Differential Diagnosis
Pre-existing hypertension
New/gestational hypertension
Pre-eclampsia
Eclampsia
Exacerbation of...
N.B: Grades of proteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3,
4+=10
Hypertensive
Disorders in
Pregnancy
Gestational
...
Indicators of severity of Pre-eclampsia
ABNORMALITIES NONSEVERE SEVERE
Blood pressure ≥140/90mmHg but
<160/110mmHg
≥160/11...
MANAGEMENT
Definitive treatment: DELIVERY!
Based on:
AOG
Severity of PE
Maternal / Fetal condition
NONSEVERE PE: MANAGEMENT
Deliver at ≥37 weeks of
gestation
Labor induction encouraged
For Nonsevere - controlled disease :
There after induction may be done at
term depending on cervical condition
Can be mana...
What is EXPECTANT MANAGEMENT?
NO
YES
Neither forced nor
restricted
EXPECTANT ANTEPARTUM MANAGEMENT OF
NONSEVERE PREECLAMPSIA
 Inpatient vs outpatient care
Close maternal monitoring upon d...
EXPECTANT ANTEPARTUM MANAGEMENT
OF NONSEVERE PREECLAMPSIA
 Laboratory follow – up
platelet count, serum creatinine,
seru...
EXPECTANT ANTEPARTUM MANAGEMENT
OF NONSEVERE PREECLAMPSIA
 Assessment of fetal growth
Sonographic estimation of fetal we...
But wait…can antihypertensives be used in
expectant management???
• In non-severe Pregnancy hypertension – No clear
Eviden...
Fetal
considerations
Prematurity
Stillbirth
Newborn
asphyxia
Maternal
considerations
Worsening of
disease
Complications
Hospitalisation???
• Gestational HTN : only if severe
HTN
• Preeclampsia :
 If diastolic pressure≥ 100mm of Hg OR,
there ...
INTRAPARTUM MANAGEMENT
 Intrapartum monitoring
 Fluids
monitored closely to avoid
excessive administration,
since women...
DELIVERY CARE
• For any HDP, vaginal delivery should be
considered unless a CS is required for the
usual obstetric indicat...
PES: MANAGEMENT
Deliver regardless of gestational age
 if proteinuria ( ≥5 grams) is the
only criteria for severe diseas...
For early onset severe preeclampsia:
• Controversy regarding termination in
early onset disease
• But there is no benefici...
suspected
severe
preeclampsia
at < 34 weeks
Acute Management of PES
Set 1: Labetalol first protocol
•Notify OB provider when patient presents with severe HTN (systoli...
Acute Management of PES
 Set 2: Hydralazine first protocol
 • Notify OB provider when patient presents with severe HTN (...
TARGET BP
 130 to 150 mm Hg systolic and 80 to 100
mm Hg diastolic OR reduce MAP by no
more than 25% over 2hrs
 Cerebral...
WOMEN WHO FAIL TO RESPOND TO
FIRST LINE AGENTS
 Emergent consultation with anesthesia, maternal
fetal medicine or critica...
Seizure Prophylaxis
MgS04 given to mild / severe PE
Loading dose: 4-6 g, slow IV
push, over 15-20 mins
Continuous infu...
MgS04 Toxicity
1. Impaired breathing(@8-10meq/L)
2. Arrythmia and Asystole ( @10-13 mEq/L)
3. Decreased/absent deep tendon...
WHAT If magnesium toxicity is suspected???
Administration of 10mL of 10% calcium gluconate (1 g in total) as
a slow intrav...
For severe-uncontrolled disease:
LUCS OR In case of very severe uncontrolled disease
elective LUCS may be done without ind...
Postpartum Management
 NSAIDs
for pain control should be avoided in
women with poorly controlled
hypertension, oliguria,...
IMMEDIATE REMOTE
MATERNAL FETAL
● IUGR
● IUD
● Asphyxia
●Prematurity
During Pregnancy During Labour During
puerperium●Ecla...
HELLP Syndrome
This is an acronym for Hemolysis, Elevated Liver
enzymes, and Low Platelet count.
It is a rare multisystem ...
HEMOLYSIS
(due to
passage of
RBCs
through
partially
obstructed
vessel)
s)
HEPATIC
DYSFUNCTION
(due to
intravascular
fibrin...
Diagnosis
Hemolysis (Hallmark of
the triad)
Elevated Liver Enzymes Low Platelet Count
 LDH>600IU/L  Liver Enzymes  (<10...
HELLP Syndrome
Initiate IV Dexamethasone:
 Only for dangerously low platelet counts
<50,000/uL
 The 2013 Task Force does...
Usual Time of Onset
Relation to delivery Percentage
Antepartum 72
Post_partum 28
 ≤48 hours 80
 >48 hours 20
Gestational...
SUPERIMPOSED PREECLAMPSIA
ON CHRONIC HYPERTENSION
New onset proteinuria in
hypertensive women but no
proteinuria before 2...
ECLAMPSIA
 Generalized tonic-clonic seizure in a
patient with Preeclampsia not attributed
to any other cause.
 If seizur...
D/D ECLAMPSIA
Epilepsy,
Intracranial
haemorrhage/thrombosis,
Meningitis,
Cerebral malaria,
Amniotic fluid embolism
ca...
PATHOGENESIS OF SEIZURES
1. Cerebral overregulation in
response to high systemic blood
pressure
vasospasm of cerebral art...
PATHOGENESIS OF SEIZURES
2. Loss of autoregulation of cerebral
blood flow in response to high systemic
pressure
E.g., hyp...
MANAGEMENT
Iinitial Mx: Maintenance of airway
patency and prevention of
aspiration
Gravida rolled onto her left side
Pr...
Management of severe hypertension,
if present
Prevention of recurrent seizures
Evaluation for prompt delivery
definiti...
Management of Eclampsia :
Prompt delivery of fetus to achieve cure
Avoidance of diuretics & hyper osmotic agents
Limitatio...
to control convulsion
“It is the most effective drug
to control even recurrent
seizures without any central
nervous system...
Dosages
→Paralysing agent & Intubation
→Amobarbital 250mg I.V over 3 min
In case of uncontrolled recurrent seizure (10-15%...
• Duration : 24 hrs from last convulsion
or from delivery which one is longer.
116
MATERNAL FETAL
●Asphyxia
●Prematurity
●Hypoxia & IUD
Injuries Systemic
●Tongue bite
●Injuries due
to fall
●Bed sore
●PULMO...
CHRONIC HYPERTENSION IN
PREGNANCY
Hypertension before pregnancy /
Diagnosed before 20 weeks of
pregnancy not due to gesta...
Chronic HTN & Pregnancy
 Etiology :
1. Essential HTN (Most Common)
2. Secondary HTN :
1. Genetic: Glucocorticoid remediab...
Thank you…
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
Hypertensive Disorders in Pregnancy
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Hypertensive Disorders in Pregnancy

Hypertensive Disorders in Pregnancy,PIH , GHTN, Preeclampsia, Eclampsia, HELLP Syndrome,Chronic Hypertension

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Hypertensive Disorders in Pregnancy

  1. 1. Hypertensive Disorders in Pregnancy Dr. Jograjiya G.R. Post Graduate Student ESI-PGIMSR, Basaidarapur, New Delhi.
  2. 2. INTRODUCTION  It is associated with severe maternal obstetric complications.  Incidence is 5-10%.  The most frequent cause of iatrogenic prematurity.  Preterm delivery  Intrauterine growth restriction (IUGR)  Perinatal death  Maternal cerebrovascular accidents  Placental abruption
  3. 3. Hypertension in Pregnancy  Systolic B.P. ≥ 140 mmHg  and/or  Diastolic B.P. ≥ 90 mmHg  Documented on two occasions  At least 6 hours apart  Not more than 7 days apart  Readings should be confirmed using appropriate measurement technique, and should be remeasured after 10-15 minutes of rest.  Other Criteria (Not part of definition currently)  SBP increased by 30mmHg  DBP increased by 15mmHg  Mean Arterial Pressure increased by 20mmHg
  4. 4. SEVERITY HYPERTENSION  Non-severe hypertension: SBP 140-159 mmHg or DBP 90-109 mmHg. Mild: SBP 140-149 mmHg or DBP 90-99mmHg. Moderate: SBP 150-160 mmHg or DBP 100-110 mmHg.  Severe hypertension: SBP > 160 mm Hg or DBP > 110 mmHg or both.
  5. 5. How to Measure Blood Pressure  Sitting Position  Patient Relaxed  Arm well supported  Measured in right arm  Cuff at heart level  Proper cuff size (80% of arm circumference)  Slow deflation of bladder (2mmHg/s)  From start of Korotkoff I to end of Korotkoff V
  6. 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. 7. What is Significant Proteinuria in Pregnancy Total protein in 24 hours urine > 300mg Protein : Creatinine ratio in random sample > 0.1
  8. 8. Calcification and Definitions
  9. 9. Classification 2. Pre- eclampsia 4. Eclampsia 3. Preeclampsia superimposed on chronic hypertension 5. Chronic hypertension with pregnancy 1. Gestational hypertension
  10. 10. GESTATIONAL HYPERTENSION New onset of hypertension after 20 weeks of gestation without proteinuria or other features of preeclampsia, followed by return of B.P. to normal within 12 weeks post-partum. This terminology replaces the term “Pregnancy Induced Hypertension.”
  11. 11. Gestational HTN: DIAGNOSIS  Determine the severity of hypertension  Measure protein excretion 24-hour urine collection  Evaluate for signs/symptoms of severe preeclampsia  Perform laboratory evaluation +/- end - organ involvement
  12. 12. Gestational HTN: DIAGNOSIS CRITERIA FOR MILD GESTATIONAL HYPERTENSION Blood Pressure > 140 to < 160 mm Hg, systolic > 90 to < 110 mm Hg, diastolic Proteinuria < 300 mg per 24-hr collection Platelet count > 100,000/mm3 Liver enzymes Normal Maternal symptoms Absent IUGR / Oligohydramnios Absent
  13. 13. Gestational HTN: MANAGEMENT  Mild Gestational HTN Managed as outpatients (weekly antepartum visits) Daily fetal movement/kick counting NST + AFI OR BPS Fetal growth monitoring every 3-4 weeks No antihypertensive therapy No antenatal corticosteroids Deliver patients no later than their EDD
  14. 14. Gestational HTN: MANAGEMENT Severe Gestational HTN SBP ≥160 mmHg or DBP ≥110 mmHg is treated with antihypertensive agents > 34 wks AOG  DELIVER! < 34 wks AOG  give steroids
  15. 15. Gestational HTN: Risk of Progression to Preeclampsia 15-25% risk Women with early onset of gestational hypertension are more likely to progress to preeclampsia than women with late onset
  16. 16. Gestational HTN: RECURRENCE Prevalence: 22 - 47 % (2nd pregnancy) tends to recur with subsequent pregnancies
  17. 17. Gestational HTN: LONG-TERM PROGNOSIS associated with development of HTN later in life associated with development of diseases related to hypertension (CVD, CKD,DM)
  18. 18. PREECLAMSIA  New onset of hypertension after 20 weeks of gestation along with properly documented proteinuria or end-organ dysfunction symptoms, followed by return of B.P. to normal within 12 weeks post-partum. Preeclamsia Gestational Hypertension Proteinuria
  19. 19. Note it……………………..  Preeclampsia can also occur without proteinuria, with end- organ dysfunction manifestations.  Edema is no longer considered a specific diagnostic criterion for preeclampsia.
  20. 20. Risk Factors Genetic Age & parity Partner factors Pregnancy Factors Underlying Medical Conditions Others Risk Factors
  21. 21. Risk Factors: Cont. Genetic 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
  22. 22. Risk Factors: Cont. Pregnancy Factors 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 • Hyperhomocysteinemia , • Autoimmune disease • Antiphospholipid antibodies, • Thrombophilia
  23. 23. PATHOPHYSIOLOGY
  24. 24. 2 stage model for preeclampsia Stage 2 Maternal syndrome (HTN, proteinuria, Endothelial dysfunction) Stage1 Reduced placental implantation ???
  25. 25. Reduced placental implantation –Stage-1 PREDISPOSING FACTORS: Abnormal implantation Association with microvascular diseases (diabetes, hypertension etc.)  Association with large placentas (hydrops, multiple gestation, hydatidiform mole)
  26. 26. Net effect Replacement of endothelial lining & muscular arterial wall by trophoblast cells Distended tortuous spiral arteries Low resistence, low pressure, high flow system
  27. 27. ETIOLOGICAL FACTORS Placental hypoxia Immunological factors Placental enzymes Genetic factors (MTHFR, F5,) Oxidative stress
  28. 28. What causes maternal syndrome Stage 2 Maternal syndrome (HTN, proteinuria, Endothelial dysfunction) Stage1 Reduced placental implantation What gets into maternal circulation
  29. 29. Maternal Syndrome stage-II Not just hypertension and proteinuria But also involves different end organs
  30. 30. Physiology of maintain uteroplacental flow in Normal pregnancy  Placenta releases angiotensinase  destruction of angiotensin-II(a potent vasoconstrictor) BP stabilized  Vascular synthesis of PGI-2 and NO in excess  vasodilation  BP stabilized & uteroplacental flow maintains  Release of VEGF  restores uteroplacental flow
  31. 31. Normal balance of agonist & anta-gonistic factors: 1.vasodialator & vasoconstrictor 2. angiogenic and antiangiogenic factors
  32. 32. 1.vasodialator & vasoconstrictor vasodialator NO PGI-2 vasoconstrictor Angiotensin- II Endothelin-I Thromboxane A2 placenta Syncytiotrophoblast & endothelium
  33. 33. 2. angiogenic and antiangiogenic factors Angiogenic factor • VEGF • TFG-beta • PlGF Antiangiogenic factor • sFlt-1 • sEng
  34. 34. Gestational Hypertension
  35. 35. Basic mechanism of different organ damage Increased vasoconstriction Decreased organ perfusion Increased endothelial dysfunction – capillary leak, oedema, Pulmonary oedema, proteinuria. Activation of coagulation: DIC, low platelets Haemoconcentration
  36. 36. Multisystem Features Of Preeclampsia Hypertension Proteinuria Eclampsia HELLP syndrome Intra-uterine growth restriction Multi-organ disease Cerebral vessels Fetus Liver Systemic blood vessels Kidneys
  37. 37. Organ Damage utero-placenta IUGR Hematological Epistaxis, DIC like features, hemoconcentration CNS Cerebral edema, cerebral hge seizures Heart Subendothelial hge , focal necrosis & hge, cardiomyopathy, heart failure Lungs Pulmonary edema, hemorrhagic brochopneumonia Kidneys glomerular endotheliosis, oliguria liver Subcapsular hge, ischaemiaperiportal necrosis, HELLP
  38. 38. CVS involvement: • ↑afterload↑ed peripheral resistance •↓preload↓ed pregnancy induced hypervolumia •Pulmonary leak edemaalveolar endothelial damage & ↓ed plasma oncotic pr •hemoconcentration & ↑ed hematocrit ↓ed blood volume than normal pregnancy(16% vs 50%): Heart failure ↓cardiac output
  39. 39. Hematological system Thrombocytopenia & other PL abnormality: • ↑ed PL activation & degranulation, • ↓ed life span. • Corelates well wth disease severity. Intravascular hemolysis • endothelial damage & altered fluidity of erythrocyte membrane d/t change in serum lipid content → ↑ed LDH, spherocytosis, reticulocytosis • microangiopathic hemolysis ↑ed coagulation & fibrinolysis • Feature like DIC • Release of thromboplastin • ↓fibrinogen • AT-III • plasminogen
  40. 40. Renal system involvement:  ↓ed renal perfusion :(d/t ↓ed blood volume & ↑ed afferent arteriolar pr.)  ↓ed GFR : d/t  glomerular capillary endotheliosis  Endothelial dysfunction + mesangial swelling + BM disruption  (but podocyte disruption minimal)  Oliguria  ↑ed creatinine level  ↑ed uric acid
  41. 41. Hepatic involvement: Periportal hemorrhagic necrosis hematoma formation Stretch/Rupture epigastric pain
  42. 42. Brain involvement: Acute severe HTN cerebrovascular overregulation Vasospasm Parenchymal ischemia Cytotoxic edema sudden ↑↑SBP exceeds normal range of cerebrovascular autoregulation Forced vasodilation + hyperperfusion Vasogenic edema
  43. 43. Lungs involvement: High SBP ↑ed arteriolar pr ↑ed extravasation of blood into alveoli + rupture of arteriole Pulmonary edema, hemorrhagic brochopneumonia
  44. 44. PREECLAMPSIA PREDICTION  There are many test during early pregnancy— or across pregnancy—of various biological, biochemical, and biophysical markers implicated for preeclampsia prediction.  The most predictive investigative procedures are cumbersome, time-consuming and with poor sensitivity and with poor positive predictive value for preeclampsia.  The efficacy of the preventive methods is questionable too  Currently, no screening tests are predictably reliable, valid, and economical (Kleinrouweler, 2012).
  45. 45. Endothelial Dysfunction/Oxidant Stress Feto-Placental unit Endocrine Dysfunction Renal Dysfuntion Misc Placental Perfusion/ Vascular Resistance related Tests Uterine Artery Doppler Velocimetry AT- III ANPFree fetal DNA Adapted from Conde-Agudelo and associates (2009)
  46. 46. Trials of different preventive methods and their outcomes Sibai et al. Lancet 365:785-99, 2005.
  47. 47. Provocative Pressure Tests Three tests have been extensively evaluated to assess the blood pressure rise in response to a stimulus.
  48. 48. 1.Roll-over test After resting in the left lateral position turning to a supine position induces a rise in diastolic pressure of 20 mmHg or more is a positive test indicative of tendency to develop pre-eclampsia. Perform at 28 to 32 weeks pregnancy.
  49. 49. 2.Hand-grip test  Isometric (sustained) contraction of striated muscles is known to cause general sympathetic activation and hence increase systemic arterial pressure in healthy adults. The patient compresses an inflated sphygmomanometer cuff for a 3-minutes period at maximal and then at 50% of maximal voluntary contraction. An increase in diastolic pressure >20 mmHg at 28-32 weeks’ gestation is associated with an increased incidence of GHTN and eclampsia.
  50. 50. 3. Angiotensin II sensitivity Sensitivity to infused angiotensin II: is increased may be due to alteration in vascular smooth muscle A II receptors. Sensitivities of all above three tests to range from 55 to 70 percent, and specificities approximated 85 percent. (metaanalysis, Conde-Agudelo and associates 2014)
  51. 51. • 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… Uterine Artery Doppler Velocimetry (abnormal flow resistance/ diastolic notch in 2nd/ 3rd trimester)
  52. 52. uterine artery DOPPLER In preeclamptic mother: Showing early diastolic NOTCH Decreased EDF (due to high resistance) In normal mother
  53. 53. Urinary assays a. Micro-albuminuria: detected by radioimmunoassay before albuminuria can be detected by the ordinary methods. The drawback is that not all proteinuric pre- eclampsia are preceded by this phase. Sensitivities ranging from 7 to 90% and specificities between 29 and 97 % (Conde- Agudelo,2014). b. 24 hours urinary calcium excretion: is lower in women with pre-eclampsia than normotensive pregnant women.
  54. 54. Urinary assays c.Kallikrein/creatinine ratio: is reduced in patients who develop PIH later on if compared to the increased ratio in normal pregnancy. Kallikrein is a blood pressure reducing agent. d. Prostaglandins metabolites: The end metabolite of prostacyclin is decreased while thromboxane B2 (the metabolite of thromboxane A2) is increased in urine of pre-eclamptic women.
  55. 55. Blood tests  a. Plasma urate: serial increase is a warning of PIH before appearance of other clinical features.  b.Platelet count: a reduction occurs early in pre-eclampsia.  c. Anti-thrombin - III activity: begin to decline as much as 13 weeks prior to the development of clinical manifestations of pre-eclampsia.
  56. 56. PREVENTION  Prepregnancy • Weight loss to ideal BMI • Control of glucose in diabetes • Control of BP in CHTN (diet, exercise)  Low dose aspirin 75 mg in High risk patient (from 12 wks) once a day  Calcium 500mg twice a day.  Not recommended • Vitamins C & E • Dietary salt restriction • Anti-HTN therapy to prevent preeclampsia
  57. 57. History -special points • Patient Particulars: Age young or >35 yrs, nulliparity, low SES -risk factors • Chief Complaints: Swelling of legs or other parts of body (face, abdominal wall, vulva, or whole body and tightness of the ring on the finger.) Severe disease -Headache, visual changes, nausea, vomiting, abdominal or epigastric pain, and oliguria, insomnia, vaginal bleeding, seizures. • Present Obstetric History: Onset, Duration, Severity of Htn/Proteinuria and H/o drug intake • Past Obstetric History: H/o any hypertensive disorder of pregnancy with week of onset. Also note the interval since last pregnancy, gestational age at delivery. Any foetal complications. • Past History: of pre-existing hypertension, renal disease, diabetes, thrombophilia, or thyroid disorder. • Family History: of Htn, Preeclampsia, Diabetes, CVD
  58. 58. Physical Examination: ● Obesity/BMI >35 kg/m2 ● Weight (serial measurements): Gain in wt at the rate of >500gs a week or 2.5kgs a month in the later months of pregnancy may be the earliest sign of preeclampsia. ● Oedema (all sites): has to be pathological, meaning visible pitting edema demonstratable over the ankles after 12 hrs bed rest. ● Pulse ● B.P.: ○ right arm, sitting/supine, arm at level of heart, cuff length=1.5 times of arm circumference, diastolic BP is the disappearance of Korotkoff sounds (phase V) ○ taken on 2 occasions at least 6 hrs apart for confirmation of diagnosis. ● CVS examination: auscultation for heart rate, rhythm, splitting of S2, murmurs. ● Ophthalmic examination: retinal haemorrage, nicking of veins, arteriole/vein ratio 3:1 from 3:2, papilloedema ● Deep tendon reflexes: hyperreflexia/presence of clonus
  59. 59. Obstetric Examination: Nothing special is found except features of IUGR, oligohydramnios in some cases.
  60. 60. Maternal Investigations: Tests may be abnormal even when BP elevation is minimal. • Urine dipstick testing for proteinuria o Quantitation by laboratory methods if ≥1+ on dipstick testing o Urinary ACR(albumin-creatinine ratio) to detect significant proteinuria (≥30mg/mmol) o 24 hour urine collection is not necessary in routine clinical management • Routine Blood Examination: TLC, DLC, Peripheral Smear, BT, CT, Hb% • Serum Urea, creatinine, electrolytes including lactate dehydrogenase (LDH) and uric acid. • Liver function tests (LFT) -AST, ALT >70 IU/l  • Skiagram of chest –PA view, Pulmonary Capillary Wedge Pressure (PCWP), Brain Natriuretic Peptide (BNP)  for detection of pulmpnary oedema
  61. 61. Diagnosing Preeclampsia-Eclampsia: • Blood pressure ≥ 140/90 mm of Hg (at or after 20 weeks of gestation) on 2 occasions at least 6 hours apart during bed rest. (160/90 mm of Hg is severe disease) • accompanied by one or more of: o significant proteinuria -urinary dipstick 1+ -random urinary protein/creatinine ratio ≥ 30 mg/mmol -24 hour urine excretion ≥300 mg/24 hrs o renal involvement -serum creatinine ≥ 90 mmol/L or -oliguria (<400 ml in 24 hrs) o haematological involvement -platelet count <1 lakh o liver involvement -raised AST, ALT (>70 IU/l) -severe upper abdominal pain o neurological involvement -severe headache -persistent visual disturbances -hyperreflexia with sustained clonus -convulsions (eclampsia) -stroke o pulmonary oedema o fetal growth restriction o placental abruption
  62. 62. Foetal Investigations: • Cardiotocograph (CTG) • Ultrasound scan (USS) assessment of: o fetal growth o amniotic fluid volume (AFV) o umbilical artery flow (Doppler)
  63. 63. Differential Diagnosis Pre-existing hypertension New/gestational hypertension Pre-eclampsia Eclampsia Exacerbation of underlying renal disease/Superimposed pre-eclampsia- eclampsia SLE
  64. 64. N.B: Grades of proteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3, 4+=10 Hypertensive Disorders in Pregnancy Gestational HTN ● BP ≥ 140/90mmHg ●No evidence of underlying cause of HTN ●No associated symptoms ●Comes to normal within 12 wks of delivery Pre- eclampsia Non Severe Severe Eclampsia PreEclamsia + Convulsion ± Coma N.B: Pre-eclampsia is principally a syndrome of signs and when symptoms appear it is usually late.
  65. 65. Indicators of severity of Pre-eclampsia ABNORMALITIES NONSEVERE SEVERE Blood pressure ≥140/90mmHg but <160/110mmHg ≥160/110mmHg Proteinuria ≤2+ ≥3+ Oliguria Absent <400ml/day Headache Absent Present Visual disturbances Absent Present Platelet count Normal Thrombocytopenia (<100,000/mm3) HELLP syndrome Absent May be present ALT,AST >70 IU/L LDH>600 IU/L Bilirubin >1.2g/L Serum transaminases(AST,ALT) Normal (<40 IU/L) Elevated Serum Creatinine Normal Elevated Epigastric pain Absent Present Fetal growth restriction Absent Obvious Pulmonary oedema Absent present
  66. 66. MANAGEMENT Definitive treatment: DELIVERY! Based on: AOG Severity of PE Maternal / Fetal condition
  67. 67. NONSEVERE PE: MANAGEMENT Deliver at ≥37 weeks of gestation Labor induction encouraged
  68. 68. For Nonsevere - controlled disease : There after induction may be done at term depending on cervical condition Can be managed expectantly till term at home/hospital and continued till term. 74
  69. 69. What is EXPECTANT MANAGEMENT? NO YES Neither forced nor restricted
  70. 70. EXPECTANT ANTEPARTUM MANAGEMENT OF NONSEVERE PREECLAMPSIA  Inpatient vs outpatient care Close maternal monitoring upon diagnosis of preeclampsia is important to establish disease severity and the rate of progression Hospitalization is useful for making these assessments and facilitates rapid intervention in the event of rapid progression Outpatient care is a cost-effective option for women with stable mild preeclampsia after initial dx evaluation
  71. 71. EXPECTANT ANTEPARTUM MANAGEMENT OF NONSEVERE PREECLAMPSIA  Laboratory follow – up platelet count, serum creatinine, serum AST 1-2x/wk, assess disease progression  Assessment of fetal well-being daily fetal movement count twice weekly fetal NST with AFI or  twice weekly BPS UMA Doppler indices evaluation
  72. 72. EXPECTANT ANTEPARTUM MANAGEMENT OF NONSEVERE PREECLAMPSIA  Assessment of fetal growth Sonographic estimation of fetal weight done to look for growth restriction and oligohydramnios at the time of diagnosis of PE , repeated every 3 weeks if the initial examination is normal  Antenatal corticosteroids < 34 weeks AOG
  73. 73. But wait…can antihypertensives be used in expectant management??? • In non-severe Pregnancy hypertension – No clear Evidence of benefit other than to reduce The Frequency of Episodes of Severe hypertension • May Adversely Effect Fetal Growthvelocity
  74. 74. Fetal considerations Prematurity Stillbirth Newborn asphyxia Maternal considerations Worsening of disease Complications
  75. 75. Hospitalisation??? • Gestational HTN : only if severe HTN • Preeclampsia :  If diastolic pressure≥ 100mm of Hg OR, there is proteinuria OR, there is fetal compromise. 37 completed weeks of gestation.
  76. 76. INTRAPARTUM MANAGEMENT  Intrapartum monitoring  Fluids monitored closely to avoid excessive administration, since women with severe disease are at risk of pulmonary edema and significant third-spacing
  77. 77. DELIVERY CARE • For any HDP, vaginal delivery should be considered unless a CS is required for the usual obstetric indications. • Antihypertensives : continued throughout labour to maintain BP < 160/110 mmHg . • 3rd Stage : actively managed with 10 units IM, particularly in the presence of thrombocytopenia or coagulopathy. (I-A) • Ergometrine should NOT be given
  78. 78. PES: MANAGEMENT Deliver regardless of gestational age  if proteinuria ( ≥5 grams) is the only criteria for severe disease  managed as nonsevere PE mild fetal growth restriction with reassuring Doppler velocimetry  treat conservatively *  severe hypertension  treat conservatively * NOTE: * remote from term
  79. 79. For early onset severe preeclampsia: • Controversy regarding termination in early onset disease • But there is no beneficial role for mother, as well as perinatal mortality is also high instead of conservative management • So… 85 termination is seriously considered
  80. 80. suspected severe preeclampsia at < 34 weeks
  81. 81. Acute Management of PES Set 1: Labetalol first protocol •Notify OB provider when patient presents with severe HTN (systolic ≥ 160 mmHg or diastolic > 110 mmHg) • Initiate appropriate fetal surveillance • Labetalol 20 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Labetalol 40 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Labetalol 80 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Hydralazine 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then: • Emergency consultation with maternal fetal medicine (MFM), anesthesia, internal medicine, critical care specialist. • Give additional antihypertensive medication per specific order. • Once the aforementioned BP thresholds are achieved, repeat BP measurement every 10 minutes for 1 hour, then every15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for 4 hours. • Institute additional BP timing per specific order.
  82. 82. Acute Management of PES  Set 2: Hydralazine first protocol  • Notify OB provider when patient presents with severe HTN (systolic ≥ 160 mmHg or diastolic ≥ 110 mmHg)  • Initiate appropriate fetal surveillance  • Hydralazine 5 or 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then:  • Hydralazine 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then:  • Labetalol 20 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then:  • Labetalol 40 mg IV over 2 min and;  • Obtain emergency consultation with MFM, anesthesia, internal medicine, critical care specialist.  • Give additional antihypertensive medication per specific order.  • Once the aforementioned BP thresholds are achieved, repeat BP measurement every 10 minutes for 1 hour, then every 15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for 4 hours  • Institute additional BP timing per specific order.
  83. 83. TARGET BP  130 to 150 mm Hg systolic and 80 to 100 mm Hg diastolic OR reduce MAP by no more than 25% over 2hrs  Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation.
  84. 84. WOMEN WHO FAIL TO RESPOND TO FIRST LINE AGENTS  Emergent consultation with anesthesia, maternal fetal medicine or critical care for second line management decisions, which can include labetalol or nicardipine by infusion pump, and nitroprusside for extreme emergencies.(ACOG 2013)  Sodium nitroprusside to be used rarely when other agents fail, at 0.25 μg/kg/min to a maximum of 5 μg/kg/min. Nitroprusside should be used for the shortest amount of time possible, due to the risk of fetal cyanide poisoning and increased intracerebral pressure with worsening cerebral edema.
  85. 85. Seizure Prophylaxis MgS04 given to mild / severe PE Loading dose: 4-6 g, slow IV push, over 15-20 mins Continuous infusion: 1-2 g/hr OR 5g IM into each buttock (total 10 g) followed by 5 g IM, alternate buttocks ever 4h continued for 24 hours after last convulsion or delivery.
  86. 86. MgS04 Toxicity 1. Impaired breathing(@8-10meq/L) 2. Arrythmia and Asystole ( @10-13 mEq/L) 3. Decreased/absent deep tendon reflex (Hyporeflexia at 4 mEq/L, loss of patellar reflex at 7-10 mEq/L) 4. Shock (>13 mEq/L) • For a maintenance dose following must be present - Serum Mg level 4-7meq/l(twice daily) Having Patellar reflex Urine output >30ml/hr RR>12/min
  87. 87. WHAT If magnesium toxicity is suspected??? Administration of 10mL of 10% calcium gluconate (1 g in total) as a slow intravenous push. Serum magnesium level obtained. Magnesium infusion should be discontinued, supplemental oxygen administered,
  88. 88. For severe-uncontrolled disease: LUCS OR In case of very severe uncontrolled disease elective LUCS may be done without induction Preinduction Cervical ripening with prostaglandin followed by induction Termination is considered 95 If failed
  89. 89. Postpartum Management  NSAIDs for pain control should be avoided in women with poorly controlled hypertension, oliguria, renal insufficiency, or thrombocytopenia  patient controlled fentanyl or remifentanil analgesia or epidural.  Monitor VS q 2h while on MgS04  Treat PES
  90. 90. IMMEDIATE REMOTE MATERNAL FETAL ● IUGR ● IUD ● Asphyxia ●Prematurity During Pregnancy During Labour During puerperium●Eclampsia(2%) (more in acute cases) ●Accidental hemorrhage ●Oliguria ●Diminished vision ●HELLP Syndrome ●Cerebral hemorrhage ●ARDS ● Eclampsia ● Postpartum hemorrhage ●Eclampsia( in < 48hrs of delivery) ●Shock ●Sepsis ●Residual hypertension ●Recurrent pre- eclampsia ●Chronic Renal Disease • Abruptio placentae
  91. 91. HELLP Syndrome This is an acronym for Hemolysis, Elevated Liver enzymes, and Low Platelet count. It is a rare multisystem disorder that complicates pregnancy with lab evidences of micro- angiopathic hemolysis, hepatic dysfunctioning & thrombocytopenia. It is a complication mostly associated with Pre- eclampsia but can also be diagnosed (rarely though) in the absence of these disorders. Incidence 20% of women with severe preeclampsia.
  92. 92. HEMOLYSIS (due to passage of RBCs through partially obstructed vessel) s) HEPATIC DYSFUNCTION (due to intravascular fibrin deposition & sinosoidal obst.) Decreased Liver blood flow HELLP Syndrome THROMBO- CYTOPENIA (due to platelet aggregation & diposition in the sites of endothhelial damage)
  93. 93. Diagnosis Hemolysis (Hallmark of the triad) Elevated Liver Enzymes Low Platelet Count  LDH>600IU/L  Liver Enzymes  (<100,000/cu.mm)  Low serum haptoglobin  High serum bilirubin (>1.2 mg/dl) High ALT & AST (>70 IU/L)  Abnormal PBS (Schistocytes {helmet cells} , burr cells {Echinocytes})  Later-low Hb% • ●Epigastric /Right Upper Quadrant pain • ●Nausea, Vomiting1. Clinical Features: 2. Lab Investigation:
  94. 94. HELLP Syndrome Initiate IV Dexamethasone:  Only for dangerously low platelet counts <50,000/uL  The 2013 Task Force does not recommend for HELLP syndrome  Antepartum: Dex 10mg q12 hrs  Postpartum: Dex 10+10+5+5 @ 0,12,24,36 hrs
  95. 95. Usual Time of Onset Relation to delivery Percentage Antepartum 72 Post_partum 28  ≤48 hours 80  >48 hours 20 Gestational Age (Weeks) Percentage 21-27 10 28-36 70 >37 20
  96. 96. SUPERIMPOSED PREECLAMPSIA ON CHRONIC HYPERTENSION New onset proteinuria in hypertensive women but no proteinuria before 20 weeks' gestation A sudden increase in proteinuria or blood pressure or platelet count < 100,000/L in women with hypertension and proteinuria before 20 weeks' gestation
  97. 97. ECLAMPSIA  Generalized tonic-clonic seizure in a patient with Preeclampsia not attributed to any other cause.  If seizures occur beyond 48-72 hours postpartum causes may be more likely other than eclampsia.  occurs in 2 to 3 percent of severely preeclamptic women not receiving anti-seizure prophylaxis Eclampsia Preeclampsia Seizure/ Convulsion/ Coma
  98. 98. D/D ECLAMPSIA Epilepsy, Intracranial haemorrhage/thrombosis, Meningitis, Cerebral malaria, Amniotic fluid embolism can mimic eclampsia.
  99. 99. PATHOGENESIS OF SEIZURES 1. Cerebral overregulation in response to high systemic blood pressure vasospasm of cerebral arteries underperfusion of the brain localizedischemia/infarction cytotoxic (intracellular) edema
  100. 100. PATHOGENESIS OF SEIZURES 2. Loss of autoregulation of cerebral blood flow in response to high systemic pressure E.g., hypertensive encephalopathy Hyperperfusion endothelial damage vasogenic (extracellular) edema
  101. 101. MANAGEMENT Iinitial Mx: Maintenance of airway patency and prevention of aspiration Gravida rolled onto her left side Protect from trauma Supplemental O2 (8-10L/min via face mask)
  102. 102. Management of severe hypertension, if present Prevention of recurrent seizures Evaluation for prompt delivery definitive treatment of eclampsia is delivery, irrespective of gestational age
  103. 103. Management of Eclampsia : Prompt delivery of fetus to achieve cure Avoidance of diuretics & hyper osmotic agents Limitation of I.V fluid Intermittent antihypertensive to control BP judiciously Control of convulsion by MgSO4 (IM/IV route) Protection & supporting care during convulsion Protection in a railed cot Protection of airway & prevention of tongue bite Correction of hypoxia & acidosis Managed in Eclampsia room. 113
  104. 104. to control convulsion “It is the most effective drug to control even recurrent seizures without any central nervous system depression to mother & fetus” 114 Magnesium sulphate
  105. 105. Dosages →Paralysing agent & Intubation →Amobarbital 250mg I.V over 3 min In case of uncontrolled recurrent seizure (10-15%) : →additional 2-4g of 20% solution IV @ <1g/min →4gm of 20% solution IV slowly(@ <1g/min) + 10g of 50% solution deep IM in upper & outer quadrant of buttock by a wide bore needle then 5g of 50% solution IM 4hrly similarly IM regime (Pritchard protocol):1955 →4 gm loading in 100ml of IVF over 15-20 min followed by 2-3g/hr in 100 ml IVF as maintenance I.V regime (Sibai protocol):1990 IM doses are as active as IV doses in controlling seizures 115
  106. 106. • Duration : 24 hrs from last convulsion or from delivery which one is longer. 116
  107. 107. MATERNAL FETAL ●Asphyxia ●Prematurity ●Hypoxia & IUD Injuries Systemic ●Tongue bite ●Injuries due to fall ●Bed sore ●PULMONARY: edema, pneumonia, ARDS, embolism ●CARDIAC: acute left ventricular failure ●RENAL: renal failure ●HEPATIC: necrosis, subcapsular hematoma ●CNS: cerebral hemorrhage, edema(vasogenic) Vision ●Diminished vision due to retinal detachment or occipital lobe ischemia Hematology ●Low platelet count ●Disseminated Intravascular Coagulation Postpartum ●Shock ●Sepsis ●Psychosis
  108. 108. CHRONIC HYPERTENSION IN PREGNANCY Hypertension before pregnancy / Diagnosed before 20 weeks of pregnancy not due to gestational trophoblastic disease. Hypertension diagnosed after 20 weeks but persistent after 12 weeks postpartum
  109. 109. Chronic HTN & Pregnancy  Etiology : 1. Essential HTN (Most Common) 2. Secondary HTN : 1. Genetic: Glucocorticoid remediable aldosteronism, Liddle Syndrome 2. Renal : Parenchymal, Renovascular 3. Endocrine : Primary hyperaldosteronism, cushing syndrome, Pheochromocytoma 4. Vascular : Aortic coarctation, Estrogen use 5. Others
  110. 110. Thank you…

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