A comprehensive overview of hypertensive disorders in pregnancy with its complications and management. Mainly focused on gestational hypertension, preeclampsia and eclampsia.

1. Hypertensive
Disorders in
Pregnancy
Mohammad Sohail Khan
Tasbeeh ur Rehman
Ayub Medical College

2. 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

3. 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

4. Classification
Hypertension in
Pregnancy
Pregnancy Induced
Hypertension (PIH)
Preeclamsia-Eclampsia
Chronic Hypertension
Preeclamsia superimposed on
Chronic Hypertension

5. What is Significant Proteinuria in
Pregnancy
 Total protein in 24 hours urine >
300mg

6. Pregnancy Induced Hypertension
 New onset of hypertension after 20
weeks of gestation without
proteinuria, followed by return of
B.P. to normal within 6 weeks post-
partum.

7. Preeclamsia
 New onset of hypertension after 20
weeks of gestation along with properly
documented proteinuria, followed by
return of B.P. to normal within 6 weeks
post-partum.
Preeclamsia
Pregnancy
Induced
Hypertension
Proteinuria

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

9. 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 6 weeks postpartum

10. 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

11. Superimposed Preeclampsia On
Chronic Hypertension
 New onset proteinuria in hypertensive
women after 20 weeks' gestation
 A sudden increase in proteinuria or blood
pressure or platelet count < 100,000/L
after 20 weeks’ gestation in women with
hypertension and proteinuria before 20
weeks' gestation

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

13. 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

14. 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

15. PATHOPHYSIOLOGY

16. 2 stage model for
preeclampsia
Stage 2
Maternal syndrome
(HTN, proteinuria,
Endothelial
dysfunction)
Stage1
Reduced placental
implantation ???

17. Stage-1
Reduced placental implantation
–
 PREDISPOSING FACTORS:
 Abnormal implantation
 Association with microvascular diseases (diabetes,
hypertension etc.)
 Association with large placentas (hydrops, multiple
gestation, hydatidiform mole)

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

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

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

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

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

25. Physiology of maintained
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

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

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

28. 2. angiogenic and
antiangiogenic factors
VEGF
TFG-beta
PDGF
ANGIOGENIC ANTIANGIOGENIC
sFlt-1 (VEGFR-1)
VEGFR-2
Tie-1
Tie-2

31. Pathophysiology for different
organ damage

32. 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

33. 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

34. 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

35. 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

36. 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

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

38. 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

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

40. Diagnosis
of HDP

41. 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

42. 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

43. 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

44. 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

45. 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

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

47. 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.

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

49. 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
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.

50. Indicators of severity of Pre-eclampsia
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

51. 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

52. 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

53. 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.

54. 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)

55. 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, burr
cells)
 Later-low Hb%
• ●Epigastric /Right Upper Quadrant pain
• ●Nausea, Vomiting1. Clinical Features:
2. Lab Investigation:

56. Treatment

57. Can we predict whether a pregnancy would
be complicated with Hypertensive disorders?
Indirectly, YES…
Placental Perfusion/ Vascular
Resistance related Tests
Uterine Artery Doppler Velocimetry
Uterine Artery Doppler Velocimetry
(abnormal flow resistance/ diastolic notch in
2nd/ 3rd trimester)

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

59. Management of preeclampsia & PIH
After early diagnosis, further management
depends on …
Severity of disease
Fetal maturity
Condition of cervix

60. Treatment
proper

61. For mild - controlled disease :
Thereafter induction may be done at
term depending on cervical condition
Can be managed expectantly till term at
home/hospital and continued till term.
61

62. 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.

63. 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.

64. 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

65. But wait…can antihypertensives be
used in expectant management???
 In non-severe Pregnancy hypertension – No clear
Evidence of benefit other thanto reduce
The Frequency of Episodes of Severe
hypertension
 May Adversely Effect Fetal Growthvelocity

66. For severe-uncontrolled disease:
Caesarian Section OR In case of very severe uncontrolled
disease elective Caesarian Section may be done without
induction
Preinduction
Cervical ripening with prostaglandin/osmotic dilators
followed by induction
Termination is considered
66
If failed

67. 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…
67
termination is seriously considered

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

69. 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

70. 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
70

71. to control convulsion
“It is the most effective drug
to control even recurrent
seizures without any central
nervous system depression to
mother & fetus”
71
Magnesium
sulphate

72. 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
72

73. 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
73

74. 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,

75. Thank
You!!!