this presentation includes a brief account of various hypertensive disorders of pregnancy

1. Hypertensive
Disorders in
Pregnancy
By
Agnibho Mondal
Bismoy Mondal
Atrayo Law
Debtanu Banerjee
Debjit Ghosh

2. Incidence
 Hypertensive disorders are among the most
significant & still now unresolving problem
complicating almost one in ten pregnancies
 Responsible for 16% of Maternal Mortatlity in
developing countries
 Commonest cause of iatrogenic prematurity
accounting 15% of all premature births & 20%
of very LBW births

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
 Other Criteria (Not part of definition currently)
 SBP increased by 30mmHg
 DBP increased by 15mmHg
 Mean Arterial Pressure increased by 20mmHg

4. Classification
Hypertension in
Pregnancy
Gestational Hypertension
Preeclamsia-Eclampsia
Chronic Hypertension
Preeclamsia superimposed
on Chronic Hypertension

5. Normal Blood Pressure changes in
Pregnancy

6. What is Significant Proteinuria in
Pregnancy
Total protein in 24 hours urine >
300mg
Protein : Creatinine ratio in random
sample > 0.1

7. Gestational Hypertension
New onset of hypertension after 20
weeks of gestation without
proteinuria, followed by return of
B.P. to normal within 12 weeks post-partum.

8. Preeclamsia
 New onset of hypertension after 20
weeks of gestation along with properly
documented proteinuria, followed by
return of B.P. to normal within 12
weeks post-partum.
Preeclamsia Gestational
Hypertension Proteinuria

9. Eclampsia
 Generalized tonic-clonic seizure in a
patient with Preeclampsia not attributed
to any other cause.
Eclampsia Preeclampsia
Seizure/
Convulsion/
Coma

10. 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

11. 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

12. 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

13. Risk Factors
Genetic
Age & parity
Partner factors
Pregnancy Factors
Underlying Medical
Conditions
Others
Risk Factors

14. Risk Factors: Cont.
Genetic
Genetic
Predisposition
Family History
Race & Ethnicity
More Common in
black & Asians
Pregnancy by
ovum donation
Age &Parity
Teenage
pregnancy
Age>35 yrs
Long interval
between
pregnancy
Nulliparity
Partner Factors
Change of
partner
Limited sperm
exposure
Pregnancy by
donor
insemination
Partner fathered
an eclamptic
pregnancy

15. 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
Sickle cell disease
Others
Obessity
Psychological
stress & strain
Previous history of
preeclamsia

16. PATHOPHYSIOLOGY:

18. 2 stage model for
preeclampsia
Stage 2
Maternal syndrome
(HTN, proteinuria,
Endothelial
dysfunction)
Stage1
implantation ???
Reduced placental

19. 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)

22. Net effect
Replacement of endothelial lining & muscular
arterial wall by fibrinoid formation
Distended tortuous spiral arteries
Low resistence, low pressure high flow system

23. uterine artery DOPPLER
In preeclamptic mother:
Showing early diastolic NOTCH
Decreased EDF
(due to high resistance)
In normal mother

24. ETIOLOGICAL FACTORS
 Placental hypoxia
 Immunological factors
 Placental enzymes
 Genetic factors (MTHFR, F5,)
 Oxidative stress
 ???????????????????

25. What causes maternal
syndrome
Stage 2
Maternal syndrome
(HTN, proteinuria,
Endothelial
dysfunction)
Stage1
implantation ???
Reduced placental
What gets into maternal circulation??????

26. Maternal Syndrome
stage-II
 not just hypertension and
proteinuria
 But also involves different end
organs

27. 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

28. Normal balance of agonist &
anta-gonistic factors:
1.vasodialator &
vasoconstrictor
2. angiogenic and
antiangiogenic factors

29. 1.vasodialator & vasoconstrictor
vasodialator
NO
PGI-2
vasoconstrictor
Angiotensin-
II
Endothelin-I
placenta
Syncytiotrophoblast
& endothelium

30. 2. angiogenic and
antiangiogenic factors
Angiogenic
factor
•VEGF
•TFG-beta
•PlGF
Antiangiogenic
factor
• sFlt-1
• sEng

33. Pathophysiology for different
organ damage:

34. 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. Pathophysiology of different
organ damage:

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. CVS involvement:
• ↑afterload
↑ed peripheral
resistance
• ↓preload
↓ed pregnancy induced
hypervolumia
•Pulmonary leak edema
alveolar endothelial
damage & ↓ed plasma
oncotic pr
•hemoconcentration & ↑ed
hematocrit
↓ed blood volume than
normal pregnancy(16%
vs 50%):
Heart
failure
↓cardiac
output

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. 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. Hepatic involvement:
Periportal
hemorrhage
hematoma
formation
Rupture
epigastric pain

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. Lungs involvement:
High SBP
↑ed arteriolar pr
↑ed extravasation of blood into
alveoli + rupture of arteriole
Pulmonary edema,
hemorrhagic brochopneumonia

44. Diagnosis
of HDP

45. 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 2+
-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

46. HELLP Syndrome:
-Hemolysis:
● LDH > 600 U per L
● Abnormal PBS showing schistocytes,
burr cells.
● Serum bilirubin ≥ 1.2 mg/dL
-Elevated Liver enzymes:
● AST and ALT >70 IU/l
-Low Platelet count:
● <1 lakh/cubic mm

47. 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

48. Physical Examination:
● Obesity/BMI>35 kg/m2
● Weight (serial measurements): Gain in wt at the rate of >1 lb a week or
>5 lbs 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 (in all 4 limbs)
● 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

49. 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

50. Obstetric Examination:
Nothing special is found except features of IUGR, oligohydramnios in some
cases.

51. Maternal Investigations:
Tests may be abnormal even when BP elevation is minimal.
• Urine dipstick testing for proteinuria
o Quantitation by laboratory methods if ≥ 2+ 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

52. Foetal Investigations:
• Cardiotocograph (CTG)
• Ultrasound scan (USS) assessment of:
o fetal growth
o amniotic fluid volume (AFV)
o umbilical artery flow (Doppler)

53. Differential Diagnosis
 Pre-existing hypertension,
 New/gestational hypertension
 Pre-eclampsia
 Eclampsia
 Exacerbation of underlying renal disease/Superimposed pre-eclampsia-eclampsia
 SLE
 ΔΔ ECLAMPSIA
 -Epilepsy,
 -Intracranial haemorrhage/thrombosis,
 -meningitis,
 -cerebral malaria,
 -amniotic fluid embolism can mimic eclampsia.

54. There are several
indicators used to
assess the severity of
PIH
Blood pressure
Proteinuria
Other associated
abnormalities

55. Pregnancy
induced
Hypertension
N.B: Grades of proteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3,
4+=10
Gestational
HTN
● BP ≥ 140/90mmHg
●No evidence of
underlying cause of HTN
●No associated symptoms
●Comes to normal within
6 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.
Assessment of the severity of pre-eclampsia
is given in the next slide.

56. ABNORMALITIES NONSEVERE (mild) 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
Epigastric pain Absent Present
Fetal growth restriction Absent Obvious
Pulmonary oedema Absent present

57. IMMEDIATE REMOTE
MATERNAL
FETAL
● IUGR
● IUD
● Asphyxia
●Prematurity
●Residual hypertension
●Recurrent pre-eclampsia
●Chronic Renal Disease
• Abruptio placentae
During Pregnancy During Labour During
●Eclampsia(2%) (more in acute cases) puerperium
●Accidental hemorrhage
● Eclampsia
●Eclampsia(
●Oliguria
● Postpartum
hemorrhage
in < 48hrs
●Diminished vision
of delivery)
●HELLP Syndrome
●Shock
●Cerebral hemorrhage
●Sepsis
●ARDS

58. 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

59. HELLP Syndrome
This is an acronym for Hemolysis (H), Elevated Liver
enzymes (EL), and Low Platelet count (LP).
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.

60. 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)

61. Diagnosis
• ●Epigastric /Right Upper Quadrant pain
• ●Nausea, Vomiting 1. Clinical Features:
2. Lab Investigation:
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, burr
cells)
 Later-low Hb%

62. Usual Time of Onset
Relation to delivery Percentage
Antepartum 72
Post_partum 28
 ≤48 hours 80
 >48 hours 20
Gestational Age
(Weeks)
21-27 10
28-36 70
>37 20

63. Treatment

64. Can we predict whether a pregnancy would be
complicated with Hypertensive disorders?
Endothelial Dysfunction/Oxidant
Stress
Feto-Placental unit Endocrine
Dysfunction
Placental Perfusion/ Vascular
Resistance related Tests
Uterine Artery Doppler Velocimetry
Renal Dysfuntion Misc
AT- III
Free fetal DNA ANP
Adapted from Conde-Agudelo and
associates (2009)
Indirectly, YES…

65. How effective are they???
Uterine Artery Doppler Velocimetry
(abnormal flow resistance/
diastolic notch in 2nd/ 3rd
trimester)
• is most promising, but currently, none of them
is completely suitable for clinical use.
• As a result of these trials, some methods to
prevent Preeclampsia have been theorized…

66. Trials of different preventive methods
and their outcomes
Sibai et al. Lancet 365:785-99, 2005.

67. The investigative procedures are cumbersome,
time-consuming and
expensive…
The efficacy of the preventive
methods is questionable too…

68. MANAGEMENT OF
APftRer EearElyC diLagAnoMsis,P fuSrtIhAer m&an aPgIemHent
depends on …
Severity of disease
Fetal maturity
Condition of cervix

69. What is EXPECTANT MANAGEMENT?
NO
YES
Neither forced nor
restricted

70. Treatment
proper

71. For mild - controlled disease :
Can be managed expectantly till term at
home/hospital and continued till term.
Thereafter induction may be done at
term depending on cervical condition
71

72. 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.

73. When should we use antihypertensive
to control the BP???
• Acute management of
severe hypertension
(BP > 160/110: to
prevent stroke)
which may require
parenteral therapy.

74. What are the
options???
Acute
Hydralazine inj.:
now available
Labetalol
Injection
Nifedipine
capsule/Tablet
Long
term
Methyl Dopa
250 mg Tab.
Labetalol Tablet
100 mg
Nifedipine
5,10,20 mg

75. 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 Growth velocity

76. For severe-uncontrolled disease:
Termination is considered
Preinduction
Cervical ripening with prostaglandin/osmotic dilators followed by
induction
LUCS OR In case of very severe uncontrolled disease elective LUCS
may be done without induction
76
If failed

77. 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…
77
termination is seriously considered

78. Fetal
considerations
Prematurity
Stillbirth
Newborn
asphyxia
Maternal
considerations
– Worsening
of disease
Complications

79. 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 oxytocin 5
units IV or 10 units IM, particularly in the
presence of thrombocytopenia or
coagulopathy. (I-A)
• Ergometrine should NOT be given

80. Management of Eclampsia :
Managed in Eclampsia room.
Protection & supporting care during convulsion
Protection in a railed cot Protection of airway &
prevention of tongue bite
Correction of hypoxia &
acidosis
Control of convulsion by MgSO4 (IM/IV route)
Intermittent antihypertensive to control BP judiciously
Limitation of I.V fluid
Avoidance of diuretics & hyper osmotic agents
Prompt delivery of fetus to achieve cure
80

81. to control convulsion
“It is the most effective drug
to control even recurrent
seizures without any central
nervous system depression to
mother & fetus”
81
Magnesium
sulphate

82. Dosages
IM doses are as active as IV doses in controlling seizures
I.V regime (Sibai protocol):1990
→4 gm loading in 100ml of IVF over 15-20 min followed by
2-3g/hr in 100 ml IVF as maintenance
IM regime (Pritchard protocol):1955
→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
In case of uncontrolled recurrent seizure (10-15%) : →additional 2-4g of 20%
solution IV @ <1g/min
→Amobarbital 250mg I.V over 3 min
→Paralysing agent & Intubation
82

83. Some more about Magnesium
• Duration : 24 hrs from last convulsion or from delivery which one is
longer.(This is called Magnesium sulphate prophylaxis in severe
preeclampsia.)
• Features of toxicity:
i> Impaired breathing(@8-10meq/L)
ii>Arrythmia and Asystole ( @10-13 mEq/L)
iii>Decreased/absent deep tendon reflex
(Hyporeflexia at 4 mEq/L, loss of patellar reflex at 7-10 mEq/L)
iv> 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
83

84. WHAT If magnesium toxicity is suspected???
Magnesium infusion should be discontinued, supplemental oxygen
administered,
Serum magnesium level obtained.
Administration of 10mL of 10% calcium gluconate (1 g in total) as
a slow intravenous push.

85. Thank You!!!