hypertensive disorders of pregnancy features ACOG 2013 guidelines

1. Presenter : Sumit Gupta
Moderator : Prof. Anjan Trikha

2. Introduction
Incidence : 5-7% of all pregnancies.
Maternal and perinatal mortality & morbidity:
50-60,000 deaths/year
Developed countries: Leading cause of prematurity
Pregnancy Induced Hypertension
Hypertensive disorders of pregnancy

3. Classification
Ist classified in 1972 by ACOG
National High Blood Pressure Education Program: 2000
Recent: ACOG 2013.
Preeclampsia & Eclampsia:
Chronic Hypertension.
Chronic Hypertension with superimposed Preeclampsia
Gestational Hypertension

4. Preeclampsia: Not a triad
Hypertension:
After 20 wks, MC near term
SBP> 140 or DBP>90
SBP>160 or DBP>110 → Initiate treatment
Proteinuria:
24 hour excretion>300mg in 24 hours.
Single sample: Urine protein: Creatinine >3.0
 As good as 24 hr sample.
Dipstick test: +1 reading. False +ve
 Used only when other tests aren’t available.
Edema
Non specific. “Physiological in pregnancy”
Korotkoff 5
2 readings 4
hours apart

5. Preeclampsia
Preeclampsia without Proteinuria,
 Hypertension with
Thrombocytopenia (<100000).
S. Cr>1.1 or 2X of previous value w/o any renal
disease
Pulmonary edema
Elevated AST/ALT (2X the normal value).
S/s of intracranial or visual abnormalities.

6. Severe preeclampsia
Severe preeclampsia
 SBP>160 or DBP>110.
Thrombocytopenia (<100000).
S. Cr>1.1 or 2X previous value w/o any renal disease
Pulmonary edema
 Rt upper quadrant pain, Elevated AST/ALT (2X the
normal).
S/s intracranial or visual abnormalities.
Mild preeclampsia
 “Preeclampsia without severe features”.

7. Chronic Hypertension
Chronic Hypertension
Hypertension diagnosed either before conception or
before 20 weeks pregnancy
Gestational hypertension persisting 12 weeks
postpartum.
Chronic hypertension with superimposed
preeclampsia
Preeclampsia
 Incidence 4-5 times more in Hypertensive.
 Worse prognosis
 Both mother and child.

8. Chronic Hypertension
Chronic hypertension with superimposed
preeclampsia
New onset Proteinuria
 After 20 weeks in known hypertensive (<20 weeks).
No Proteinuria
 Thrombocytopenia (<100000).
 S. Cr>1.1 or 2X previous value.
 Pulmonary edema
 Rt upper quadrant pain or Elevated AST/ALT (2X the normal)
 Sudden worsening of hypertension or need to ↑ t/t in
previously controlled patient.

9. Gestational Hypertension
Gestational Hypertension
New onset ↑BP after 20 weeks
No proteinuria
Transient nature (if not→?? Chr. HTN)
Enhanced surveillance : Risk of HTN ↑ ↑.
“Late” or post partum hypertension
Normotensive during gestation.
Mild HTN post partum (2weeks-6months)
Labile BP
Normalizes upto 1 year.

10. Risk Factors
Demographic factors
Age>35 years(2X than 20-29 years).
Ethnicity: African Americans, Hispanic
 Severe hypertension→ require intense therapy.
Genetic factors
Previous history of Preeclampsia(7X more likely)
 Multiple affected pregnancies.
 Family history for Preeclampsia(2-4X more)
History of placental abruption, IUGR or IUD

11. Risk Factors
Medical Conditions
Obesity ↑BMI 5-7kg/m2 ↑ 2X risk
Chronic Hypertension
Diabetes Mellitus
Chronic renal disease, APLA syndrome, SLE
Obstetric
Multiple Gestation, H. mole
Behavioral
Cigarette smoking protective
 ↓ 30-40%. Dose related effect.
Physical activity protective
Partner related risk factors
Nulliparity.

12. Pathophysiology
 Normal pregnancy
Cytotrophoblast of embryo invade the
spiral arteries of pregnant uterus
Remodeling of smooth muscle of uterine
arteries S Spiral artery diameter ↑
Intervillous space has very low resistance
to blood flow and remodeled arteries
Nonresponsive to vasoconstrictors

13. Pathophysiology
Preeclampsia
Asymptomatic First
stage
Abnormal placental
implantation
Symptomatic Second
stage
Release of angiogenic
factors into
Maternal circulation

14. Asymptomatic first stage
Abnormal placental implantation
Cytotrophoblast of embryo invade the
spiral arteries of pregnant uterus
Remodeling of smooth muscle of uterine
arteries S spiral artery diameter ↑
Intervillous space has very low resistance
to blood flow and remodeled arteries
Nonresponsive to vasoconstrictors
Incomplete cytotrophoblastic
invasion
of spiral arteries
No remodeling of spiral
arteries and diameter
remains small . Exaggerated
response to vasopressors
Superficial Placentation
↓ placental perfusion,
placental infarcts, IUGR
Placental ischemia gradually

15. Abnormal placental implantation
 Complex interplay of vascular, environmental, genetic
and immune factors.
Immune factors.
 ↓ NK cells &↑ macrophages and chemokines in placenta.
 NK cells facilitate trophoblastic invasion.
 Macrophages
 ↑ ↑ inflammation: inhibits placentation.
 HLA C and HLA DR are associated with ↑ risk.

16. Abnormal placental implantation
Angiotensin receptor-1 Antibodies.
Act as agonist and ↑ sensitivity to angiotensin II
 Defective remodeling of placenta vasculature
 Block trophoblastic invasion.
 ↑production of reactive oxygen species.
 ↑ Sflt-1 (Receptor for VEGF)
Hypertension and proteinuria.
Oxidative stress
Cause atherosclerosis and atherosis

17. Symptomatic second stage
Release of angiogenic factors into
Maternal circulation

18. Symptomatic second stage
 Endothelial dysfunction:
Key event
Placental hypoxia → antiangiogenic substances released
into maternal circulation.
 Soluble fms like tyrosine kinase-1(sFlt-1) and Soluble endoglin
(sEng)
 Antagonize angiogenesis
 Bind to and ↓ VEGF and PIGF.

19. Symptomatic second stage

20. Maternal Syndrome Preeclampsia:
multisystem disorder
•AIRWAY
•Pharyngolayngeal edema
•Tracheal diameter ↓ ↓
•Difficulty in direct
laryngoscopy
•Subglottic edema
• Airway obstruction
PULMONARY
•Pulmonary edema
•3% of preeclampsia.
•More in elderly
multigravida, superimposed
Chr. HTN or oliguria
↓ Plasma oncotic
pressure
↑ Vascular permeability.
•Excess iv fluids.
CVS
•Vasospasm
•SVR and BP ↑ ↑
•↑ Sensitivity to
catecholamines
•Hyper dynamic circulation
↑ C.O
•Misleading CVP
measurement
•High risk: ↓ LV
function, ↓ ↓SVR
HEPATIC
•Rt hypochondrium and epigastric
pain.
•D/t sub capsular hematoma
•Periportal hemorrhage and
sinusoidal
fibrin deposits.
•HELLP syndrome
• Spont. Hepatic rupture

21. Maternal Syndrome Preeclampsia.
CNS
•Severe headache, hyper
excitability,
•Loss of cerebral auto
regulation, vasogenic
edema
•Cerebral hemorrhage and
edema
•PRES: Posterior
Reversible
Encephalopathy
Syndrome.
•Eclampsia: Seizures
OPTHALMOLOGICAL
•Scotoma, blurred vision
and amaurosis
•Retinal arteriolar spasm
•Bilateral retinal
detachment
RENAL
•“Glomerular capillary
endotheliosis”
Most Characteristic lesion.
•GFR ↓ (↑ in N pregnancy).
•Proteinuria( ∆stic criteria)
•Uric acid ↑ ( early detection).
•Oliguria
Occurs late & correlates with
severity.
•Renal failure
HEMATOLOGICAL
•Thrombocytopenia: MC
hematological abn
•Severe disease or HELLP.
•Severe disease:
Hypercoagulable.
(↓ Blood Volume & ↑
Viscosity)
•Mild disease: hypocoagulable

22. Fetal Syndrome Preeclampsia
Leading cause of
IUGR
Preterm labor
NICU admission
 IUD → DIC & PPH
in mother

23. Prophylaxis
Prevents imbalance b/w thromboxane & prostacyclin.
Modest risk reduction (15-20%) but no S/E.
No. Needed To Treat
 Low risk 500 Vs High risk NNT: 50
Started in late Ist trimester
 H/o Preeclampsia causing preterm delivery<34 weeks.
 Preeclampsia in > 1 pregnancy.
Low dose Aspirin 60-80 mg

24. Prophylaxis
Believed to reduce oxidative stress.
No benefit in multicentre trials
Benefit in females with calcium deficiency
 1.5-2g in patients with low base line intake or high risk.
No benefit in females with adq. calcium intake.
No Benefit.
Diuretics: no benefit
Vitamin C(1000mg) and E(400 IU)
Calcium supplementation.
Dietary salt restriction

25. Prophylaxis
No benefit in pregnant patients
Risk of DVT ↑
Exercise : 30 min or more
 Protective
 Improves uterine blood flow, placental angiogenesis and
endothelial function
Bed rest and no physical activity

26. Investigations
Initial evaluation:
CBC with Plt. Count
S. Creatinine level
LFT (AST, ALT, and S.bil.)
Uric acid
 Marker of severity
 Detects disease early.
Urine analysis
 24 hr Urine protein
 Urine protein to creatinine ratio.
Danger signs → Headache, Unusual change in vision, ↓Urine,
epigastric/ labor pain Hospitalize
Severe Preeclampsia
repeated daily
Mild Preeclampsia:
Repeated weekly
Proteinuria
Not evaluated again if
+ve for preeclampsia

27. Investigations
Fetal evaluation
USG evaluation for fetal weight
Amniotic fluid index(AFI)
Daily fetal movement count(DFMC)
NST & BPP
 Gestational Hypertension: Weekly NST
 Preeclampsia: Bi Weekly NST
Umbilical artery Doppler:
 Screening: no benefit
 Indicates severity of IUGR
↓ DFMC /Fundal Ht<3cm
(Prompt NST & AFI)

28. Investigations.
Coagulation profile
Platelet count >100,000: Not needed.
Plt. Count<100,000: PT and aPTT.
 Additional studies
 DIC Risk: Abruptio, liver disease, HELLP
Induction of labor: platelets repeated 6 hrly.

29. Management
Anti HTN drugs
Only if BP>160/110mmHg
No benefit if BP>140/90 but<160/110
 ↓progression to severe HTN.
 Risk of fetal growth retardation
 No change in maternal or fetal mortality or prematurity.
First line drugs: Methyldopa, Labetalol
Second line drugs: Hydralazine, Nifedipine,.
C/I: Ace inhibitors or ARBS

30. Anti Hypertensive drugs
Labetalol
• 100mg BD
• S/E: CHF,
Asthma
• Discontinue
:liver
dysfunction
Methyldopa
• 250 mg TDS
• S/E: dry
mouth,
somnolence,
sedation
Nifedipine
• 10-30 TDS
• S/E: Edema,
• headache,
allergic
hepatitis
Atenolol
• 50-100mg
OD
• S/E: Heart
Block, IUGR

31. Anti Hypertensive drugs.
For Emergency Control.

32. Management.
 Observe for 24-48 hours
Corticosteroids if gestational age <34 weeks.
Monitor: USG, FHR, investigations and danger signs
daily.
MgSO4 for severe preeclampsia.
Oral anti HTN drugs
C/I to expectant management → delivery
Eclampsia
DIC
Pulmonary edema
Uncontrolled HTN
Non Viable fetus
Abnormal fetal test results
Abruptio placentae
IUD

33. Management.
 Deliver after 48 hrs with corticosteroids
Persistent symptoms
HELLP
IUGR, Severe oligohydramnios
 USG Doppler: Reversal of flow
Labor
 Significant Renal dysfunction

34. Management
Route of delivery
Vaginal delivery in all
 Unless Cesarean is indicated.
Corticosteroids
All patients between 24- 34 weeks of gestation
Beneficial in HELLP syndrome
Fetal lung maturity.
Dexamethasone or Betamethasone
Seizure prophylaxis
Severe Preeclampsia & Eclampsia
MgSO4

35. Long term outcome
↑ Risk of
Chronic Hypertension
DM
Ischemic Heart disease.
 AHA: Preeclampsia risk factor for cardiovascular disease.
Renal failure.
↑ Risk for
Recurrent Preeclampsia
Preeclampsia with IUGR or Preterm Birth
ADVICE
BP, FBS, Lipids and
BMI yearly
Aerobic Exercise
5 days/ week -30min.
Avoid Tobacco

36. Complications
Cerebrovascular accident
 ↑ risk of intracerebral and subarachnoid hemorrhage.
↑ ↑ risk with DIC or HELLP
Loss of cerebral autoregulation → Vasogenic edema
Systolic BP better than DBP or MAP at predicting
adverse events
Majority are Hemorrhagic (93%) and occur in post
partum

37. Complications
Pulmonary edema
3% cases of preeclampsia
More in elderly multigravida or women with
superimposed preeclampsia
Presents in 2-3 days after delivery
T/t underlying cause (sepsis, cardiac failure)
 O2, Fluid restriction, diuretics
 Rapid Resolution

38. Complications
Renal Failure
Rare complication
HELLP and severe preeclampsia
Majority Pre-renal or Intra-renal (ATN)
 Resolution completely
 B/L cortical necrosis
 High maternal mortality and morbidity
 DIC, HELLP, Abruptio placentae, IUD, Sepsis etc
Abruptio placentae:
2% of preeclampsia (3X risk);
Chronic Hypertension.

39. Eclampsia
New onset seizures or unexplained coma in a
Preeclamptic patient
During pregnancy or postpartum.
No preexisting neurological disorder.
0.1-5.9/10,000 pregnancies
Most Commonly
Intrapartum or 48Hrs after delivery
Late Eclampsia: 48Hrs after delivery to 4 wks
postpartum

40. Eclampsia
Risk factors
Young nullipara
Multifetal & Molar pregnancy
Preexisting Hypertension, renal or cardiac disease.
SLE or non immune hydrops
Maternal Complications:
Pulmonary aspiration, pulmonary edema, Cerebrovascular
accident, venous thromboembolism, ARF or death
Fetus
IUGR, Prematurity

41. Eclampsia
Signs or symptoms
80% premonitory symptoms.
 MC Headache or Visual disturbances.
 Photophobia, Right upper quadrant pain, Hyperreflexia
 Seizures abrupt onset
 Facial twitching →Tonic phase (15-20 seconds).
 Generalized clonic phase →apnea for 1 minute.
 Postictal state with variable period of coma .
Poor neurocognitive outcome
Usually temporary ( focal motor deficit, blindness etc).
Can be permanent as well

42. HELLP syndrome
Variant of severe preeclampsia
Maternal mortality ↑↑ (DIC, pulmonary edema, APH,
Liver failure etc.)
Sibai’s criteria
Hemolysis
•Abn Periph. Blood
smear
MAHA(Schistocytes
&BURR cells)
•↑ S. bilirubin>1.2mg%
•↑S. LDH>600IU/L
Low platelets
•Platelet count
<100,000/cumm
Elevated liver
enzymes
•↑AST>70IU/L
•↑LDH>600IU/L

43. HELLP syndrome
Not candidates for expectant management
Seizures: IV magnesium
Anti HTN: BP>160/110 mmHg.
Corticosteroids for fetal lung maturity.
Platelets:
Spontaneous bleeding or platelet count <20,000.
 Sub capsular hematoma d/t liver rupture
Serial USG/MRI
Surgery/ Embolization.

44. Thank
YOU

45. Seizure prophylaxis
MgSO4
↓ Risk for
 Eclampsia
 Maternal death
 Abruptio placentae.
No benefit
 Maternal morbidity
 Fetal/neonatal outcome.
 Preeclampsia w/o severe disease.
↑ Risk
 Hypotension
 Muscle weakness
 Respiratory depression.

46. Seizure prophylaxis
MOA
↓peripheral vascular resistance
NMDA agonist ↑ seizure threshold
Protects blood brain barrier
Dose:
 4-6gm over ½ hour f/b infusion of 1-2gm/hr
For caesarean
 2hr before procedure.
 Continued till 12 hrs postpartum.

47. MgSO4 toxicity
1.5-2.0 meq/l : normal plasma level
4.0-8.0 meq/l :therapeutic range
5.0-10.0 meq/l: p-q interval prolong, wide QRS
10.0 meq/l : loss of deep tendon reflexes
15.0 meq/l :Respiratory paralysis
25.0 meq/l : cardiac arrest
ANTIDOTE – CALCIUM Gluconate

48. Eclampsia
Airway
• Left lateral position, jaw thrust.
• Bag and mask ventilation.
• Avoid Oropharyngeal airway,
• Nasopharyngeal airway
Breathing
• Continue Bag and mask ventilation.
• Apply pulse oximeter and monitor SpO2
Circulation
• Secure IV access
• Monitor BP and ECG

49. Stop convulsions
MgSO4
4-6g IV over 20 min
1-2g/hr IV maintenance
2g iv over 10 min for recurrent seizures
Antihypertensive therapy
 Labetalol or Hydralazine
Induction of labor