Hypertension in preg

1. Hypertensive disorders of
pregnancy
Moderator: Dr. Asmita
Presented by : Dr. Divya

2. INTRODUCTION
► Hypertensive disorders represent one of the common medical
complication of pregnancy affecting between 7–15% of all gestations
and account for approximately a quarter of all antenatal admissions.
► The most frequent cause of iatrogenic prematurity.
► Preterm delivery
► fetal growth restriction (FGR)
► Perinatal death
► Maternal cerebrovascular accidents.

3. DEFINITIONS
□ Systolic B.P. ≥ 140 mmHg
and/or
□ Diastolic B.P. ≥ 90 mmHg(Korotkoff V)
□ documentation on at least two occasions 4 to 6 hours apart
□ within a maximum of a week period
□ Other Criteria (Not part of definition currently)
□ SBP increased by 30mmHg
□ DBP increased by 15mmHg
□ MAP Increased by 20mmHg

4. Concept of “Delta Hypertension”
□ ‘Delta hypertension’ introduced by macdonald-wallis in 2012.
□ A sudden rise in mean arterial pressure in later half of pregnancy which
may predispose the affected female to pre-eclampsia even if her blood
pressure still < 140/90 mm hg, thus she is considered to be
“normotensive.”
□ Some of these women will go on to have obvious pre eclampsia , and
some even develop eclamptic seizures or HELLP (hemolysis, elevated
liver enzyme levels, low platelet count) syndrome while still
normotensive.

5. As per the NICE guidelines (for the purpose of management) hypertension
is further divided as per the severity :-
□ Mild hypertension: Systolic blood pressure 140– 149 mmHg, diastolic
blood pressure 90–99 mmHg.
□ Moderate hypertension: Systolic blood pressure 150– 159 mmHg,
diastolic blood pressure 100–109 mmHg.
□ Severe hypertension: Systolic blood pressure 160 mmHg or greater,
diastolic blood pressure 110 mmHg or greater

6. Measure Blood Pressure
□ At every visit
□ Sitting or in left lateral recumbent position
□ Patient Relaxed (after a 10minutes Or longer rest period)
□ Measured in right arm
□ Arm supported in horizontal position
□ Cuff at level of the heart
□ Proper cuff size (80% of arm circumference)
□ Slow deflation of bladder (2mmHg/s)
□ From start of Korotkoff I to end of Korotkoff V

7. Normal Blood Pressure changes in Pregnancy
► Normal pregnancy is characterized by
▪ Increased plasma volume (preload)
▪ Increased cardiac output
▪ Decreased peripheral vascular resistance (PVR)
► Decreases during the first trimester Reaching its lowest point at 20 weeks.
Physiologic decrease in mean blood pressure during the second trimester .
► Returns to pre-pregnancy levels during the third trimester.

8. CLASSIFICATION OF HYPERTENSIVE DISORDERS IN
PREGNANCY
□ 1. Preeclampsia and eclampsia syndrome
□ 2. Chronic hypertension of any etiology
□ 3. Preeclampsia superimposed on chronic hypertension
□ 4. Gestational hypertension

9. PRE-ECLAMPSIA

10. Pre-eclampsia
► Hypertension (≥140/90 mmHg) on 2 occasions 4 hours apart after 20 weeks gestation)
+
► Proteinuria
≥300mg/24 hr or
Protein creatinine ratio ≥ 0.3mg/dl or
Dipstick 2+(used only if other quantitative methods not available)
OR
► Thrombocytopenia – Platelets < 100,000×109/µl
► Renal insufficiency – creatinine >1.1 mg% or doubling of baseline (no prior renal disease)
► Liver involvement – Serum transaminase levels (AST or ALT) twice normal)
► Pulmonary edema
► Cerebral Symptoms – Headache, Visual, disturbances, convulsions

11. Note it……………………..
► Preeclampsia can also occur without proteinuria, with end
organ dysfunction manifestations.
► Edema is no longer considered a specific diagnostic
criterion for preeclampsia.

12. Proteinuria in Pregnancy
□ It is defined as the urinary excretion of 300 mg/dl or more of
protein in 24 hours urine collection
or
□ urine protein/ creatinine ratio of >30 mg/mmol.
□ This usually correlates with >30 mg/dl (>1+ by qualitative
estimation using reagent strips) in at least two random urine
samples collected 4 to 6 hours apart, with no evidence of urinary
tract infection
□ visual dipstick test ,Approximate equivalence is Trace = 0.15 to
0.3 g/l, 1+ = 0.3 g/l, 2+ = 1g/l, 3+ = 3g/l

13. Risk Factors for Preeclampsia
Maternal or pregnancy related risk factors
► Extremes of age (<18 or >35years)
► primigravida
► Obesity and insulin resistance/gestational diabetes
► Smoking
► Multifetal pregnancies
► Molar pregnancies
► Preeclampsia in previous pregnancy
► Family history of preeclampsia

14. Pre-existing medical disease:
► Pre-gestational diabetes
► Chronic hypertensive or renal disease
► Maternal immunological disease /SLE
► Preexisting thrombophilia, antiphospholipid antibody syndrome, protein C, S deficiency,

15. Criteria for Severe Preeclampsia
□ Blood pressure of ≥160 mmHg systolic or ≥110 mmHg diastolic, recorded on
at least 2 occasions at least 4 hours (unless antihypertensive therapy is initiated
before this time).
□ Thrombocytopenia
□ Impaired liver function as indicated abnormally elevated liver enzyme
□ severe persistent right upper quadrant or Epigastric pain unresponsive to
medication
□ Renal insufficiency
□ New onset headache unresponsive to medication.
□ Pulmonary edema
□ visual disturbances

16. PATHOPHYSIOLOGY OF
PRE-ECLAMSIA

17. ETIOLOGY
An imposing number of mechanisms have been proposed to explain
the cause of preeclampsia.
Those currently considered important include:
1.Placental implantation with abnormal trophoblastic invasion of
uterine vessels
2.Immunological maladaptive tolerance between maternal, paternal
(placental), and fetal tissues
3.Maternal maladaptation to cardiovascular or inflammatory changes
of normal pregnancy
4.Genetic factors including inherited predisposing genes and
epigenetic influences.

18. PATHOPHYSIOLOGY OF PRE-ECLAMSIA

19. ► Normally there is invasion of the endovascular trophoblasts into the walls of the spiral arterioles of the
uteroplacental bed.
► Endovascular trophoblasts invades up to decidual segments in the first trimester (10–12 weeks) .
► Another wave of trophoblasts invades up to the myometrial segments in the second trimester (16–18
weeks)
► This process replaces the endothelial lining and the muscular arterial wall by fibrinoid formation.
► The spiral arterioles become distended, tortuous and funnel-shaped.
► This physiological change transforms the spiral arterioles into a low resistance, low pressure, high flow
system.
► Preeclampsia
□ Defective implantation is characterized by incomplete invasion of the spiral arteriolar wall by
extravillous trophoblasts.
□ Failure of the second wave of endovascular trophoblast migration.
□ This results in a small-caliber vessel with high resistance to flow.
□ Reduction of blood supply to the fetoplacental unit

20. Reduced placental implantation –Stage-1

21. Physiology of maintain uteroplacental flow in Normal pregnancy:-
□ Placenta releases
vasoconstrictor)
angiotensinase destruction of angiotensin-II(a potent
BP stabilized.
□ Vascular synthesis of PGI-2 and NO in excess
stabilized & uteroplacental flow maintains
vasodilation BP
□ Release of VEGF restores uteroplacental flow

22. Etiological factors
□ Increase vascular sensitivity to angiotensin II.
□ Imbalance between prostacyclin and thromboxane A2
□ Inhibition of Nitric Oxide synthesis- increases main arterial pressure
□ Increase oxygen free radicals
□ Inflammatory mediators
□ Vit E, C, Antioxidant and micronutrient deficiency
□ Endothelin-1

23. ► Angiogenic and antiangiogenic factors:-
► Angiogenic imbalance describes excessive amounts of antiangiogenic
factors, which are worsening hypoxia at the uteroplacental interface.
► Angiogenic factor
• VEGF
• PLGF
► Antiangiogenic factor
► • sFlt-1(soluble fms- like tyrosine kinase I)
► • sEng( Soluble edoglin)

24. Pathogenesis
Changes in Mother:-
► Vasospasm Resistance to blood flow arterial hypertension.
► Release of Angiotensin II contract endothelial cell damage inter
subendothelial deposition of platelets and
endothelial cell leaks
fibrinogen.
► Vascular changes local hypoxia hemorrhage and necrosis of tissue
end organ disturbances in mother.
fetal compromise growth
Fetus:-
► Reduced uteroplacental perfusion
retardation, oligohydramnios, IUD.
► Placenta :- Placental infarction, calcification, abruptio placentae

25. Basic mechanism of different organ damage
► Increased vasoconstriction
► Decreased organ perfusion
► Activation of coagulation DIC, low platelets
► Hemoconcentration
► Increased oxidative stress → endothelial injury → increased capillary - permeability.
decreased blood osmotic pressures edema
► PROTEINURIA: Spasm of the afferent glomerular arterioles → anoxic change to the
endothelium of the glomerular tuft → glomerular endotheliosis → increased capillary
permeability → increased leakage of proteins.
► Tubular reabsorption is simultaneously depressed.
► Albumin constitutes 50–60% and a-globulin constitutes 10–15% of the total proteins
excreted in the urine.

26. PATHOLOGICAL CHANGES
Cardiovascular System
Increased cardiac after load caused by-Hypertension , endothelial injury,
extravasation- especially in lungs (pulmonary edema)
□ Hemodynamic Changes
Marked reduction in cardiac output
Increased peripheral resistance
□ Blood Volume
Hemoconcentration
Increased vascular permeability
Patients is sensitive to vigorous fluid therapy, even sensitive to blood loss at
delivery.

27. Haematological Changes
► Thrombocytopenia- Platelets count <100,000, delivery is indicated because platelet count
continues to decrease
► HELLP Syndrome- Hemolysis, Elevated Liver enzyme, Low Platelets count.
► Coagulation failure occurs when associated consumptive coagulopathy like Placental
abruption, profound hemorrhage.
► Hemoconcentration

28. Kidney
□ Decrease glomerular filtration
□ Decrease renal perfusion
□ Increase plasma uric acid concentration
□ Increased plasma creatinine level (>0.5 mg/dl)
□ Proteinuria >300 mg dl/24 hrs .
□ Renal failure- tubular necrosis- oliguria, anuria
Liver
□ Alteration in hepatic function test
□ Periportal hemorrhagic necrosis in periphery of liver lobule- Increased serum liver
□ enzymes.
□ Hepatic rupture
□ Sub-capsular hemorrhage- abdominal pain and hepatic hemorrhage.
□ HELLP syndrome

30. Brain-
► Hypertension is responsible for
► Oedema
► Hyperemia
► Thrombosis
► Haemorrhage
► Confusion and coma
Eye-
► Retinal haemorrhage, papilioedema
► Retinal detachment- retinal ischemia and infarction
► Visual loss- cortical blindness
► Prognosis is good, changes usually return to normal within a week.
Lung-
► Pulmonary edema, hemorrhagic brochopneumonia

32. immediate Remote
Maternal Fetal
During
labour
During
puerperium
●Residual hypertension
●Recurrent preeclampsia
●Chronic Renal Disease
• Abruptio placentae
● IUGR
● IUD
● Asphyxia
●Prematurity
COMPLICATION OF PRE-ECLAMPSIA
During
pregnency
●Eclampsia(2%) (more in acute
cases) puerperium
●Accidental hemorrhage
●Oliguria
●Diminished vision
●HELLP Syndrome
●Cerebral hemorrhage
●ARDS
Eclampsia
● Postpartum
hemorrhage
●Eclampsia(
in < 48hrs
of delivery)
●Shock
●Sepsis

33. PREDICTION OF PRE-ECLAMPSIA
► Various biological markers implicated in the preeclampsia syndrome have been measured to
help predict its development.
► Although most have been evaluated in the first half of pregnancy
► some have been tested as predictors of severity in the third trimester.
► Role over test- 28-32 wks lateral to supine DBP >20mmHg.
► Angiotensin II infusion Test- 28-32 wks rise of 20 mm of Hg DBP ,with < 8 ng/kg/min
► Mid trimester Mean arterial Pressure- >90 mm of Hg in 2nd trimester
► Doppler ultrasound- Persistent of diastolic notch at 18-24 wks.
► Currently, no screeningtests for preeclampsiaare predictablyreliable, valid, and economical.

34. Uterine artery doppler velocimetry
► Increased impedance to flow in the uterine arteries as indicated by:
► Diastolic Notch in uterine artery waveform
► Increase in uterine artery pulsatility index above the 95th percentile.
► The first two trimesters might provide ,indirect evidence of this process and thus serve as a
predictive test for preeclampsia.
► Sensitivity of abnormal Ut A Doppler predicting pre-eclampsia 20%to 60%.
► Recently lot of research being conducted on ut A doppler at 11-13 week.
► Demonstrated that impedance to flow is increase in pregnancies and that particularly marked
for early pre-eclampsia.

35. In normal mother In preeclamptic mother:
Showing early diastolic NOTCH
Decreased EDF
(due to high resistance)

36. Fetoplacental unit dysfunction
► Increased Human chorionic gonadotrophin(hCG), Alpha-fetoprotein,
Estriol.
► Low Inhibin A
► Low Pregnancy associated plasma protein A.
Renal Function Tests
► Hyperuricemia
► Isolated gestational proteinuria
► hypocalciuria

37. Endothelial Dysfunction and Oxidative Stress
► Increased Fibronectins level, Endothelin, C – reactive protein.
► Hyper homocysteine
► serum levels of VEGF and PLGF
► fms- like tyrosine kinase receptor(sFlt-1)
► Flt-1/PlGF ratio in women admitted near 37 weeks’ gestation
Other Markers
▪ cell-free DNA (c f DNA)
▪ Antithrombin

38. Prevention
► Various strategies used to prevent or modify preeclampsia severity have been
evaluated.
► Dietary and Lifestyle Modifications
► low-salt diet
► Regular exercise during pregnancy is linked to a lower risk of developing
preeclampsia.
► Calcium supplementation, (1-2 gm/day) in high-risk women lowered the risk
for preeclampsia
▪ Decrease intracellular ion
▪ Smooth muscle relaxant
▪ Decrease responsiveness to pressure stimuli

39. ► Antioxidants-
Vit. C,D, E (reduce oxidative stress)
► Statins were proposed to prevent preeclampsia because they stimulate
hemoxygenase-1 expression, which inhibits sFlt-1 release. Preliminary animal
data suggest that statins may prevent hypertensive disorders of pregnancy.
► Metformin inhibits hypoxicinduciblefactor1α by lowering mitochondrial electron
transport chain activity. It reduces sFlt-1 and sEng activity and thus has potential
to prevent preeclampsia.
► Antithrombotic Agents Aspirin, (low oral doses of 50 to 150 mg daily)
▪ effectively inhibits platelet thromboxane A2 biosynthesis .
▪ Prevents platelets aggregation

40. MANAGEMENT
Basic aim of management-
► Termination of pregnancy at appropriate time only curative
treatment.
► Birth of alive and healthy baby.
► Complete restoration of health of mother.

41. History -special points
► Patient Particulars: Age young or >35 yrs, primiparity
► 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 fetal complications.
• Past History: pre-existing hypertension, renal disease, diabetes, thrombophilia, or thyroid
disorder.
• Family History: HTN, Preeclampsia, Diabetes, CVD
Women should be made aware of symptoms which she needs to report immediately like pain in
the abdomen, uterine contractions, bleeding per vagina or decreased fetal movement.

42. Physical Examination:
► Obesity/BMI >35 kg/m2
► Weight (serial measurements): Gain in weight at the rate of >500gms a week or 2.5kgs a month
in the later months of pregnancy may be the earliest sign of preeclampsia.
► edema (all sites): has to be pathological, meaning visible pitting edema demonstratable over
the ankles after 12 hrs bed rest.
► Pulse, blood pressure , temperature
► CVS examination: auscultation for heart rate, rhythm, splitting of S2,murmurs
► Chest auscultation for added sound.
► Ophthalmic examination: retinal haemorrage , papilloedema.

44. Treatment
► Definitive treatment: DELIVERY!
Based on:-
► Gestational age of the fetus.
► Severity of PE.
► Maternal / Fetal condition.

45. Care to be taken
► Frequent antenatal visit
► Reduced activity is beneficial
► Absolute bed rest is not necessary
► Adequate protein and calories should be given
► Sodium and fluid intake should be adequate

46. Expectant antepartum management of non-severe
preeclampsia
maternal evaluation:-
► Measure BP-4 times per day
► Measure body weight- weekly
► Daily urine dipstick evaluation of protein in urine
► Proteinuria in a 24 hr. specimen every week
► CBC with platelet count, LDH, AST, ALT twice per week
► Inquire in each contact about fetal movements, development of
scotoma, headache, epigastric pain.

47. ► Fetal surveillance includes:
► 1. Daily fetal movement count
► 2. FHR monitoring (NST)one to two times per week with liquor
assessment (AFI)weekly.
► 3. Fetal biometry every 3 weeks
► 4. Umbilical and cerebral Doppler fortnightly/weekly if associated with
growth restriction.

49. Control of blood pressure
Anti-hypertensive drug therapy
► To prolong pregnancy to get better fetal outcome
► To reduce blood pressure in severe hypertension.
► Sudden fall in blood pressure must be avoided.
► The NICE clinical guidelines suggest treating moderate hypertension (BP 150/100 mm hg )and
above with antihypertensives with aim to keep BP 150/80–100 range.
► As per ACOG 2019,Women with severe gestational hypertension BP >160/100 mm hg require
treatment with antihypertensive agent.
Drugs
► Methyl dopa- 250 mg 8 hrly – 2 gm/day orally
► Hydralazine- 5 mg I.V. stat. 5 mg ½ hrly.
► Nifedipine- 10 mg 6 hrly – 20 mg/4 hrly orally
► Labetalol- initial dose 100 mg twice daily. Maintenance dose 200-400 mg twice daily,orally.
► ACE inhibitor are contraindicated during pregnancy

50. Hospitalisation???
► Gestational HTN : only if severe HTN
► Preeclampsia :
✔ If diastolic pressure≥ 100mm of Hg
OR
✔ there is fetal compromise.
37 completed weeks of gestation.

51. Delivery care
► Induction of labour and vaginal delivery should be attempted in women with mild
preeclampsia.
► Continue pregnancy till 37weeks
► Labour induction is usually carried out by prostaglandins as majority of these women
are primigravidas with an unripe cervix due to their early gestational age.
► Third stage can be actively managed with oxytocin or prostaglandins to prevent
postpartum haemorrhage.
► Epidural analgesia/anaesthesia is the procedure of choice in labour and caesarean
delivery.
► Ergometrine should NOT be given

52. Initial Recommended Management of Severe PE
► Immediate hospitalization
► Detailed history taken to assess severity – Headache, visual disturbance, epigastric
pain, rapid weight gain, bleeding P/V or labor
► Detailed examination done for – edema, brisk reflexes & clonus, Chest auscultation
for basal crepts , fetal growth & well being
► IV magnesium sulfate started to prevent convulsions
► Anti hypertensive medication administered to lower BP ( iv Labetalol plus oral
nifedipine)
► Aim is to keep systolic BP between below 150 and diastolic BP between below 100
mm Hg
► Corticosteroids given between 26-34 weeks gestation.

53. Indications for delivery in preeclampsia
Maternal indications-
□ BP persistently 160/100 or greater despite treatment
□ Progressive deterioration in liver function
□ Progressive deterioration in renal function(serum creatinine >1.1mg/dl or twice baseline)
□ Suspected abruptio placentae, vaginal bleeding in the absence of placenta previa.
□ Persistent severe headaches refractory to treatment
□ visual changes, motor deficit or altered sensorium.
□ Persistent severe epigastric pain, nausea or vomiting
□ Stroke
□ Pulmonary edema

54. □ Eclampsia
□ HELLP SYNDROME
□ Myocardial infarction
Fetal
□ Abnormal fetal testing
□ Fetal death
□ Fetus without expectation of survival at the time of maternal diagnosis (lethal
anomaly, extreme prematurity)
□ Persistent reversed end diastolic flow in the UA

55. Indications for delivery in women <34 weeks’ gestation managed
expectantly
Corticosteroid Therapy for Lung Maturation and Delivery after Maternal
Stabilization:
□ Uncontrolled severe hypertension
□ Eclampsia
□ Pulmonary edema
□ Placental abruption
□ Disseminated intravascular coagulation
□ Non reassuring fetal status
□ Fetal demise

56. Corticosteroid Therapy for Lung Maturation—Delay Delivery 48 hr If
Possible:
□ Preterm ruptured membranes or labor
□ Thrombocytopenia <100,000/μL
□ Hepatic transaminase levels twice upper limit of normal
□ Fetal-growth restriction
□ Oligohydramnios
□ Reversed end-diastolic Doppler flow in umbilical artery
□ Worsening renal dysfunction

57. Expectant Management of Severe Preeclampsia Less than 34 Weeks
□ Hospitalization
□ Daily weight
□ Daily input and output
□ Antihypertensive treatment (labetalol, nifedipine)
□ Betamethasone (two 12 mg doses 24 hours apart)
□ Laboratory every other day or more frequently if needed:
□ AST, ALT, LDH, platelet count, creatinine, bilirubin,
□ 24-hour urinary protein.
□ Daily fetal movement count
□ Weekly to as frequently as daily NST depending upon fetal growth status and liquor
□ Umbilical and middle cerebral Doppler twice every week
□ Amniotic fluid volume twice every week
□ Ultrasound for fetal growth every 2 weeks.

58. Management of severe preeclampsia.

59. Antihypertensives for Hypertensive emergency
Drug Starting dose Maximum dose Comments
Labetalol 20 mg IV every 15min
Dose doubled to 40-80
mg according to effect
220 mg Avoid in Asthma, CHF,
cardiac conduction
abnormality
Hydralazine 5mg iv Or Im, followed
by 5-10 mg every 20
-40 min
20 mg Tachycardia, persistent
headache
Nifedipine(immediate
release)
10-20 mg orally,
repeat in 20 minutes if
needed then 10-20 mg
every 2-6 hours.
180 mg Tachycardia, palpitation
headache
Do not use sublingual

60. Prevention of convulsion
► Anti-convulsant drug therapy- in severe pre-eclampsia to prevent convulsion
► Guidelines for Intramuscular Magnesium Sulfate Administration (PRITCHARD
REGIME)
► Intravenous loading dose (only in patients with eclampsia):
▪ Give 20 mL of 20% magnesium sulfate (4 g) slow intravenous in 3–5 minutes at a rate not exceeding 1
g/min
► Intramuscular loading dose:
▪ 10 mL of 50% magnesium sulfate (5 g) deep intramuscular in the upper outer quadrant of each buttock
using a 20 gauge needle.
▪ The intramuscular injection should immediately follow the intravenous loading dose in patient with
convulsions.
▪ Patients without convulsions may receive only the intramuscular loading dose.
► Maintenance dose:
▪ Give 5 g magnesium sulfate (10 mL of 50% solution) deep IM injection in alternate buttock every 4 hours.

61. Guidelines for Intravenous Magnesium Sulfate Administration
► Loading dose:
▪ Give 30 mL of 20% magnesium sulfate (6 g) in 100 mL of normal saline over 15–20
minutes.
► RCOG guidelines recommend a lower dose of 4 g as loading.
► Maintenance dose:
▪ Add 20 g of magnesium sulfate (four 10 mL amps of 50% solution) to 1000 mL of normal
saline solution and give intravenously at a rate of 100 mL/hour (2 g/ hour).
► RCOG guideline recommends 1g/hour maintenance dose.

62. Monitoring for magnesium toxicity:
► Urine output should be at least 30 mL/hour or 100 mL in 4 hours
► Deep tendon reflexes should be present
► Respiration rate should be > 14 breaths/minute
► Pulse oximetry should be >96%
► THERAPEUTIC RANGE 4-8mEq/L
► Any change in these indices makes it necessary to re evaluate the rate of
administration
► Magnesium sulfate is discontinued 24 hours after delivery or after last
convulsion.
► Disappearance of the patellar reflex is important because it is the first sign of
impending toxicity.
► An excellent marker of magnesium toxicity is pulse oximetry.

63. MgS04 Toxicity
► Patellar reflexes disappear at level of 7 mEq /L
► respiratory paralysis and respiratory arrest follow10 mEq /L or higher levels
► Cardiac arrest at 25mEq/L
Management
► stop magnesium sulfate and monitor hourly.
► Estimate of serum magnesium and creatinine level.
► Give antidote- Calcium gluconate 1 gm IV 10 ml of 10% solution over 10 min
► Forced diuresis
► Mechanical ventilation if respiratory paralysis(>15 meq/lit)

64. Obstetrical management
Termination of Pregnancy
Indications
► Patient develops signs of imminent eclampsia
► Severe pre-eclampsia does not respond to conservative treatment.
► Eclampsia
Method of Termination
► Induction of labour at term if favorable cervix.
► LSCS in unfavorable cervix or other indication.

65. > 37 weeks-
► Termination of pregnancy.
► Induction of labour as per the bishop score.
> 34-< 37 weeks-
► Treatment should be individualized-
► BP controlled- explain maternal and fetal adverse effect to relatives.
► Regular fetal and maternal surveillance.
► Terminate at 37 weeks.
► BP uncontrolled, worsening clinical and biochemical parameters- terminate
the pregnancy.

66. >24- <34 weeks
► corticosteroid coverage
► BP controlled- continue maternal and fetal surveillance- terminate at 37
weeks.
► BP uncontrolled, worsening clinical and biochemical parameters-
terminate the pregnancy.
< 24 weeks-
► Fetal salvage difficult- terminate the pregnancy.

67. Post-Partum period management
► Closely monitored postpartum with blood pressure measurement at least four times a
day for the first 2 days .
► Once daily for next 2 weeks or more till they are off antihypertensive and the blood
pressure normalizes.
► Dose of antihypertensive is usually reduced once bp falls below 130/80 mm hg.
► Methyl dopa is discontinued- causes post-partum depression.
► Ace inhibitor may be started- if required
► Patient must be counseled for recurrence in future pregnancy or develop hypertension in
later life.
► Women with persistent hypertension /or proteinuria at 6 week postpartum should be
evaluated by medical specialist.

68. ECLAMPSIA

69. INTRODUCTION
► Convulsive state of pre-eclampsia is called eclampsia.
► Pre-eclampsia is complicated by generalized tonic and clonic convulsions and coma .
► The hospital incidence in India ranges from 1 in 500 to 1 in 30.
► The frequency of timing of eclampsia reported in literature ranges from:-(mostly third
trimester)
□ 38–53% antepartum(Mostly occurs in the third trimester (90%).
□ 15–20% intrapartum
□ 11–44% in the postpartum period.(within 48–72 hours of delivery , Fits occurring beyond
48 hours but less than 4 weeks after delivery is considerd as late postpartum eclampsia.)
► Eclampsia occurring before 20 weeks is usually associated with molar pregnancy.
► Most postpartum eclampsia occurs within the first 48 hours of delivery.

70. 1. Cerebral overregulation in respons
P
ea
to
th
hio
gh
ge
sy
n
st
e
es
m
ii
s
c blood pressure
▪ Vasospasm of cerebral arteries
▪ Under perfusion of the brain
▪ anoxia
2. Loss of autoregulation of cerebral blood flow in response to high systemic pressure
▪ Hypertensive encephalopathy
▪ Hyper perfusion
▪ Endothelial damage
▪ Vasogenic (extracellular) edema
► An explanation for the onset of seizures:-
▪ seizures are the result of an abnormal autoregulatory response consisting of exaggerated
vasoconstriction and ischaemic changes with rupture of the vascular endothelium and
pericapillary haemorrhages with development of foci of abnormal electrical discharges that
generalize, and cause convulsions

71. Cerebral Pathology-
► Cortical and sub- cortical edema
► Infarction
► Hemorrhage
► Hypoxia, ischaemia (occipital and parietal occipital region).

73. Clinical Features
► Eclamptic convulsions are consist of four stages:-
▪ Premonitory stage:
❖ Twitching of muscles of face, tongue, limbs.
❖ Eyeballs rolled or turned to one side become fixed
❖ Its last for 30 sec
▪ Tonic stage:
❖ Whole body goes into a tonic spasm (opisthotonos )
❖ Limbs flexed, hands clenched
❖ Respiration ceases, tongue protrudes out ,cyanosis appears.
❖ This stage last for 30 sec

74. ▪ Clonic stage:-
❖ 1-4 min
❖ frothing, tongue bite, stertorous breathing,
❖ Cyanosis gradually disappear
▪ Stage of coma:
❖ Following fits patient passes in stage of coma
▪ Status eclampticus : -
❖ Multiple recurring fits at varying intervals

76. Fetal heart rate tracing shows fetal bradycardia following an intrapartum
eclamptic convulsion. Bradycardia resolved and beat-to-beat variability returned
approximately 5 minutes following the seizure.

77. Maternal and Perinatal Outcome
► Major maternal complications
► placental abruption (7–10%)
► DIC (7–11%)
► HELLP syndrome (9.7–20%)
► acute renal failure (5–9%)
► pulmonary oedema (3–5%)
► aspiration pneumonia(2–3%)
► cerebral haemorrhage and cardiopulmonary arrest (2–5%).
► The most common causes of maternal death are intracranial bleeding and
acute renal failure secondary to abruption placentae.

78. Perinatal outcome
Perinatal mortality- 30-50%
► Pre maturity- spontaneous, induced
► Intra uterine asphyxia- Infarction, retro-placental, haemorrhage spasm
► fetal growth restriction(FGR)
► Trauma
► The most common causes of perinatal death are prematurity and fetal
asphyxia
► Perinatal morbidity is substantial and correlates strongly with
preterm birth, abruptio placentae, FGR.

79. Differential diagnosis
► Epilepsy
► Hysteria
► Encephalitis
► Meningitis
► Puerperal cerebral thrombosis
► Poisoning
► Cerebral malaria
► PRES(Posterior reversible encephalopathy syndrome )
► Intracranial tumor

80. Diagnosis
► The diagnosis of eclampsia when women present with seizures, hypertension and
proteinuria.
► Hypertension is the hallmark for the diagnosis of eclampsia.
► Hypertension may be severe (20–54% of cases) or mild (30–60% of cases).
► 15% of the cases, hypertension and proteinuria may not be present.
► In the majority of cases, the onset of convulsions is preceded by persistent occipital or
frontal headache(throbbing in nature) ,visual symptoms, epigastric or right upper quadrant
pain or altered mentation.
► Sudden death may occur during or after a seizure which is often due to massive cerebral
haemorrhage.
► Sublethal intracranial haemorrhage may present as haemiplegia.
► Hyperthermia following seizure is ominous as it is suggestive of cerebral haemorrhage.
(seen more often in older women with underlying chronic hypertension).

81. ► Two syndrome that present similarly and may overlap with eclampsia :-
► Posterior reversible encephalopathy syndrome (PRES)
▪ Constellation of neurological symptoms complex visual deficit, seizure, headache, and
altered sensorium.
▪ The diagnosis of PRES made by the documentation of vasogenic oedema and
hyperintensities in the posterior aspect of brain on MRI.
► Reversible cerebral vasoconstriction
▪ Presents with thunderclap headache and less commonly focal neurological deficit related to
brain edema, stroke, or seizure and characterised by reversible multifocal narrowing of
arteries of brain.
► Treatment of both syndromes includes medical control of hypertension, antiepileptic
drugs and long term neurological follow up.

82. Management
► Basic principles of management of eclampsia fall under three major
categories:
► Control of convulsion
► Control of hypertension
► Delivery of the fetus

83. ► Control of Convulsion
► Maintain airway, breathing and circulation
► To decrease the risk of aspiration the patients should be placed in the lateral decubitus
position and oral secretions or vomitus are suctioned if needed
► Oxygen administration 8-10 L/min.
► Magnesium sulfate is the drug of choice in treatment of eclampsia
► If the patient has an IV line a 6 g loading dose of magnesium sulfate should be given over 20
minutes, to be followed by a maintenance dose of 2 g/hour infusion.
► If another seizure occurs when the patient is on maintenance dose of magnesium sulfate an
additional 2 g bolus of magnesium sulfate should be given over 5 minutes.
► If another seizure occurs, give phenobarbital 300 mg IV over 5 minutes.
► In refractory cases, intubation may be necessary.

84. ► Treatment of Hypertension
▪ Treating severe hypertension helps prevent congestive heart failure and cerebral
hemorrhage and also has an important role in the treatment and prevention of seizures.
▪ The first line antihypertensive drug is labetalol (IV boluses of labetalol 20 mg initially
then 40 mg and then 80 mg at 15-minute intervals until blood pressure is in the desired
range) or nifedipine(10-mg initial immediate-release oral dose to be followed in 20 to 30
minutes with 10 to 20 mg if necessary).
▪ The goal should be to maintain systolic blood pressure between 140 and 160 mmHg and
diastolic blood pressure between 90 and 105 mmHg.
► Fluid Therapy
► Lactated Ringer solution is administered routinely at a rate between 60 and 125 mL per hour,
unless fluid loss is unusual from vomiting, diarrhea, or diaphoresis, or, more likely, excessive
blood loss with delivery .
► To maintain urine output above 30 ml per hour.

85. Delivery of the Fetus
► Delivery is the only definitive treatment for eclampsia.
► The mode of delivery should be decided depending on the fetal presentation.
► Caesarean delivery may be indicated:-
► Presence of prolonged fetal bradycardia, unripe cervix, gestational age ,< 30 weeks, FGR.
► inadequate blood pressure control and poor progress in labour.
► The anaesthesia of choice for eclamptic patients:-
► regional, spinal or epidural.
► The only contraindication to regional block anaesthesia is a platelet count <50,000/mm3.
► When general anaesthesia is necessary, administration of labetalol before endotracheal
intubation is important to avoid the significant elevation of blood pressure.

86. Long-Term Prognosis
► The seizure characteristics of eclampsia are acute and transient and
long-term neurologic deficits are rare in patients adequately treated.
► However, approximately 35% of patients who develop eclampsia will
have preeclampsia in a subsequent pregnancy.

87. Some Long-Term Consequences in Women with Preeclampsia
Syndrome
Cardiovascular
► Chronic hypertension
► Atherosclerosis
► Cardiomyopathy
Ischemic heart disease
Coronary artery calcification
Thromboembolism
Neurovascular
► Stroke Retinal detachment
► Diabetic retinopathy

88. Metabolic
► Type 2 diabetes
► Dyslipidemia
Metabolic syndrome
Obesity
Renal
► Glomerular dysfunction Proteinuria
Central nervous system
► White-matter lesions
► Retinopathy
Cognitive dysfunction

89. Other Regimens
► Lytic cocktail- Is a combination of chlorpromazine, promethazine and
pethidine
► Diazepam
► Phenytoin - in1000mg, iv infusion in one hour, 500mg oral after 10
hrs .

90. HELLP Syndrome
► He-hemolysis
► EL-elevated liver enzymes
► LP-low platelets

91. Criteria for the Diagnosis of HELLP Syndrome
► Haemolysis
► Abnormal peripheral blood smear (burr cells, schistocytes)
► Elevated bilirubin > 1.2 g/dL
► Low serum haptoglobin
► Increased LDH . twice the upper limit of normal (> 600 U/L)
Elevated liver enzymes
► Elevated AST, ALT > twice the upper limit of normal ( >72 IU/L)
► Low platelet count (< 100,000/mm3)

92. classification
► The Mississippi classification categorizes the severity of HELLP syndrome into
three categories according to maternal platelet count.
▪ Class I (severe thrombocytopenia): platelet count below 50,000/mm3
▪ Class II (moderate thrombocytopenia): platelet count between 50,000 and
100,000/mm3
▪ Class III (AST >40 IU/L, mild thrombocytopenia): platelet count between 100,000
and 150,000/mm3
► Tennessee System also classifies HELLP :-
▪ complete syndrome if there is presence of all three parameters abnormal (AST/ALT,
LDH, Platelets)
▪ incomplete syndrome if there are one or two of the three as abnormal.

93. ► Maternal Morbidity Associated with HELLP Syndrome
► Abruptio placenta 10–15%
► Disseminated intravascular coagulation 10–15%
► Pulmonary oedema 6–8%
► Acute renal failure 5–8%
► Adult RDS 1–2%
► Death 1%

94. Management of HELLP syndrome
► Immediate hospitalisation
► Stabilize mother
► Antihypertensive
► Anti-seizure prophylaxis
► Correct coagulation abnormalities.
► Immediate delivery if the pregnancy is ≥ 34 weeks or at any gestational age:-
▪ pulmonary oedema
▪ renal failure
▪ placental abruption
▪ severe liver dysfunction or bleeding
▪ non reassuring fetal status
▪ uncontrollable hypertension is present.
► Women selected for steroid treatment .
► Very close monitoring required until delivery and in postpartum period with lab tests at least 12 hours
intervals.
► Plasmapheresis for those patients who follow relentless course of deterioration despite the
conventional therapy.

95. Mississippi protocol
► The Mississippi protocol, which includes high doses of dexamethasone in
Combination with antihypertensives and magnesium sulphate, is usually used for
planned delivery within 48 hours After diagnosis of HELLP syndrome to prevent
severe maternal morbidity.
► Partial HELLP syndrome occurring during the periviable period, which were
treated with a modified Mississippi Protocol.
► The modified Mississippi protocol involved administration of three-day,
high-dose dexamethasone Followed by long-term, low-dose prednisolone (10 mg
/day).
► The modified Mississippi protocol contributed to Prolongation of pregnancy (8,
10, and 16 days), and may be a promising therapeutic option especially for
Periviable HELLP/partial HELLP syndrome

96. CHRONIC HYPERTENSION

97. CHRONIC HYPERTENSION AND PREGNANCY
► Chronic hypertension complicates about 0.5–3% of all pregnancies.
► Chronic hypertension in pregnancy is defined as hypertension before
pregnancy or before the 20th week of gestation, on more than one
occasion, at least 4–6 hours apart.
► Persistence of hypertension for 12 weeks postpartum is also
retrospectively described as chronic hypertension

98. ► Essential hypertension is diagnosed when there is no apparent underlying cause for chronic
hypertension. (It is responsible for 90% of cases of chronic hypertension in pregnancy).
► Secondary hypertension may be caused by renal parenchymal disease or scarring,
renovascular disease, endocrine disorders or coarctation of aorta(10% of cases).
► Chronic hypertension in pregnancy is subclassified as:
► Mild hypertension: Systolic blood pressure of 140– 159 mmHg or Diastolic blood pressure
of 90–109 mmHg.
► Severe hypertension: Systolic blood pressure of 160 mmHg or greater or diastolic blood
pressure of 110 mmHg or greater.

99. Etiology of Chronic Hypertension
□ Primary or essential hypertension
□ Secondary hypertension
□ Renal
□ Renal parenchymal disease (glomerulonephritis, reflux nephropathy, adult polycystic
disease)
□ Renovascular hypertension (renal artery stenosis)
□ Endocrine
□ Diabetes with vascular involvement
□ Thyrotoxicosis
□ Pheochromocytoma
□ Primary aldosteronism
□ Cushing syndrome

100. Collagen vascular disease
□ Systemic lupus erythematosus
□ Scleroderma
Others
□ Aortic coarctation
□ Increased intracranial pressure

101. Complications
Maternal complications
□ Superimposed preeclampsia
□ Placental abruption
□ Congestive cardiac failure
□ Malignant hypertension
□ Cerebrovascular accidents
□ Renal damage and failure
Fetal complication
□ Abortions
□ Fetal growth restriction,
□ Premature births
□ Fetal demise

102. ► Adverse fetal and maternal outcome are directly proportional to the duration of
hypertension, severity of hypertension, associated end organ damage and presence of
superimposed preeclampsia.
Risk factor for developing superimposed pre-eclampsia
□ Presence of renal disease
□ Age(>40 years)
□ Long duration of hypertension (>15 years)
□ Bp (>160/110 mmhg)
□ Presence of thrombophilia
□ Diabetes mellitus
□ Connective tissue disorders
□ Coarctation of aorta

103. MANAGEMENT
Pre-conceptional care:-
□ Evaluated aetiology and severity of hypertension
□ Identify possible presence of end organ disease
□ Coexistence of other medical disease
□ Counsel the patient accordingly.
□ The history and physical examination should be directed to determine the duration of
disease.
□ History of antihypertensive medications
□ The presence of signs or symptoms suggestive of secondary hypertension or end organ
damage.
□ A detailed obstetric history of outcomes in previous pregnancies including presence of
hypertension, development of superimposed preeclampsia or abruption, preterm or sga fetus
and neonatal morbidity and mortality

104. ► Pre pregnancy counseling will be useful to introduce:-
► Lifestyle modifications
► Weight loss for obese women.
► Avoiding alcohol and smoking.
► Adequate control of hypertension,
► Medications reviewed and changes made in the antihypertensive drugs that are unsafe
in pregnancy.
► They should be made aware that pregnancy can exacerbate their condition with
potential for causing renal failure, cardiac failure or even death.
► Such patients if still plan to conceive should be managed in a tertiary care center under
a maternal fetal medicine specialist and in conjunction with a medical specialist.

105. Investigations for Chronic Hypertensives Presenting Prior to
20 Weeks of Gestation
All patients
□ Establish baseline blood pressure values
□ Complete blood count with platelets
□ Establish baseline renal function tests (serum creatinine, Blood urea
nitrogen, serum uric acid, serum electrolytes)
□ Complete urinalysis for microscopy for (albumin, sugar , WBC, RBC and
casts)
□ Urine culture and sensitivity
□ Spot urine for protein/creatinine ratio for screening or
□ 24-hour urine protein

106. □ ECG and echocardiography
□ Ophthalmic examination (fundus)
□ Glucose tolerance test
Selected patients
□ Renal ultrasound, renal doppler flows (if feasible as in early pregnancy)
□ Fasting free plasma metanephrine or 24-hour urine metanephrine
□ Serum potassium levels or plasma renin activity

107. General Care during Pregnancy
► They should have prenatal clinic visits very 2 weeks until 32 or 34 weeks and then every week
until the end of pregnancy.
□ Blood pressure measurement along with home bp monitoring
□ Monitoring maternal weight
□ Monitoring for signs of superimposed preeclampsia
□ Assessment for proteinuria using dipstick test or spot urine protein /creatinine ratio
□ Lab tests (renal function, urine microscopy, complete blood count if worsening hypertension or
proteinuria)
□ Fetal growth and well-being assessment includes:-
• A baseline ultrasonography for dating and 18–20 weeks anatomical survey.
• Surveillance with ultrasound for fetal growth, liquor and uterine and umbilical artery doppl
monitoring is necessary at 28–30 weeks.

108. • nonstress test twice weekly or biophysical profile biweekly (after 34 weeks or earlier)
and umbilical artery Doppler in patients with fetal growth restriction (ACOG guideline
).
□ Severity Assessment
► Chronic hypertension in pregnancy is subclassified (ACOG 2012, NICE 2010,
SOMANZ 2008)
• Mild hypertension: Systolic blood pressure of 140–159 mmHg or Diastolic blood
pressure of 90–109 mmHg.
• Severe hypertension: Systolic blood pressure of 160 mmHg or greater or diastolic
blood pressure of 110 mmHg or greater.

109. Nonpharmacologic Therapy
► Restricted non-strenuous activity with extra 1–2 hours of rest in a day.
► Dietary sodium intake low as it can reduce blood pressure.
► They should avoid a large weight gain by limiting caloric intake to only
that is necessary to cover their needs.
► Low dose aspirin(81 mg) between 12 to 28 weeks of gestation (
optimally before 16 weeks) and to continue therapy until delivery.
[As per ASPREE trial the dosage of aspirin should be 150 mg to be given
preferably at night time form 12 to 36 week]

110. Antihypertensive Therapy
► As per ACOG pregnant women with hypertension in the blood pressure range of
150–160/100–110 mm hg should be treated with antihypertensives.
► Blood pressure to be kept lower than 150/100 mm hg.
► In pregnant women with end organ damage secondary to chronic hypertension (left
ventricular hypertrophy or renal insufficiency)
▪ It is recommended that antihypertensive treatment should be given to maintain blood
pressure in the normal range, lower than 140/90 mm hg
▪ Reducing the risk of further end organ damage.
► Labetalol or nifedipine are recommended antihypertensive drugs.

111. Delivery
► Women with chronic hypertension with no maintenance antihypertensive medications
and additional maternal and fetal complications delivery after 38-0/7 weeks.
► If patients on maintenance antihypertensive medications no other complications delivery
after 37-0/7 weeks of gestation.
► Women with severe acute hypertension that not controlled with medications or who
develop superimposed pre- eclampsia with severe features should be delivered upon
diagnosis at 34- 0/7 weeks gestation or more.
► The incidence of caesarean is high because of the development of complications and the
need to delivery prematurely.
► Continuous fetal monitoring should be done in labour.
► Epidural analgesia is ideal for labour.
► Antihypertensives need to be continued in labour to keep blood pressure below 150/100
mm hg.

112. Management of chronic hypertension during pregnancy.

113. Postnatal managment
► Postnatal women with mild chronic hypertension must be monitored with blood
pressure daily for the first 2 days after birth
► At least once between day 3 and day 5 and as per clinical indication.
► High risk women with chronic hypertension should be monitored more closely for the
first 48 hours because of the risk of hypertensive encephalopathy, pulmonary oedema
and renal failure.
► BP may remain unstable for one to two weeks after delivery and may require increase
in medications.
► Diuretic therapy can be used in patients with evidence of circulatory congestion or
pulmonary oedema.

114. ► Continue antenatal antihypertensive treatment after birth with an aim to keep blood
pressure lower than 140/90.
► Need for long term antihypertensive treatment can be reviewed at 2 weeks after the
birth.
► Methyldopa during pregnancy
▪ Stopped within 2 days of birth
▪ Restarted on the pre-pregnancy antihypertensive regime.
► All chronic hypertensives should be called for a medical review at postnatal 6–8
weeks with the pre-pregnancy medical specialist.

115. GESTATIONAL HYPERTENSION

116. 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.
□ Gestational hypertension is the most frequent of the
hypertensive disorders of pregnancy with prevalence
between 6 - 15% in nulliparous and 2–4% in
multiparous.

117. Criteria to Identify High-Risk Women with
Gestational Hypertension
□ Blood pressure >150/100mm hg
□ Gestational age less than 30 weeks
□ Evidence of end-organs damage (elevated serum
creatinine, liver enzymes, LDH, decreased platelet
count)
□ Oligohydramnios
□ Fetal growth restriction
□ Abnormal uterine and/or umbilical Doppler velocimetry

118. Gestational HTN: MANAGEMENT
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

119. Gestational HTN: MANAGEMENT
Gestational HTN without risk factors
Managed as outpatients (weekly antepartum visits)
► The weekly assessment of patients with gestational hypertension and
no risk factors must include a systemic review of the maternal and
fetal status.
► From the maternal side:-
► Assessment of the levels of blood pressure at home.
► The presence or absence of symptoms suggestive of end-organ damage
(blurred vision, epigastric pain, headache) and Presence of proteinuria.
► From the fetal side:-
► daily charting of fetal movements.
► measurement of the uterine fundal height.

120. ► Fetal growth monitoring every 3-4 weeks
► Amniotic fluid assessment at least once weekly
► Expectant management up to 37-0/7 weeks gestation is recommended.
Gestational HTN with risk factors
► Require admission to the hospital for further evaluation and treatment.
► The objectives of care are the pharmacologic control of their blood pressure.
► The blood pressure should be measured at intervals of no longer than 6 hours
► The early detection of preeclampsia, end-organ damage, and fetal decompensation.
► The initial evaluation :-
► 24-hour urine collection for protein.
► complete blood count, platelet count, lactate dehydrogenase (LDH) and liver enzymes ,Urea,
creatinine , electrolytes at presentation then weekly
► PT (prothrombin time), PTT (partial thromboplastin time) if platelets count abnormal.
► NST and fetal movement count.
► ultrasound for fetal growth, amniotic fluid volume, umbilical and cerebral Doppler every 2 weeks
and weekly cardiotocography (CTG).

121. ► Women with systolic blood pressure >160 mmHg and/or diastolic blood pressure >110
mmHg require treatment with antihypertensive agents.
► The recent NICE guidelines on hypertension in pregnancy suggests need to treat moderate
hypertension (BP 150/100 mmHg) and above.
► Aim to keep diastolic blood pressures between 80–100 mm hg and systolic BP less than 150
mm hg.
► Expectant management is terminated when hypertension cannot be controlled or there is
evidence of end-organ damage.

122. Long-Term Prognosis
□ The risk of recurrence of gestational hypertension ranges between
16–47%.
□ Chance of the patient developing preeclampsia in future pregnancy is
low (2–7%).

123. Thank you