6.HYPERTENSIVE_DISORDERS_IN_PREGNANCY.pdf

Obstetrics

1. HYPERTENSIVE
DISORDERS IN
PREGNANCY
Dr. Mohammed Alrasheed
UofK, MBBS

2. Definition
Hypertension (HTN) during pregnancy is diagnosed with a systolicBP 140mm
Hg or more and/or diastolicBP of 90mm Hg or more, measured at 2
occasions at least 4 hours apartafter a period of rest

3. Classification of hypertensive disorder during pregnancy
1.Gestational hypertension: hypertension alone firstoccurring> 20weeks gestation
2.Preeclampsia: hypertension + Proteinuriafirst occurring > 20weeks gestation
3.Eclampsia: preeclampsia + grand mall seizures
4.Chronic hypertension: hypertension alone diagnosed beforepregnancy or < 20
weeks gestation
5.Superimposed PE: Preeclampsia developing on top of chronic HTN

4. Table of contents
01
04
02
03
Gestational
Hypertension
Outline
Type of
Miscarriage
Risk Factors

5. Gestational Hypertension
(Pregnancy-induced hypertension)
01

6. Definition:
-BP (>/=140/90) > 20 weeks of gestationin the absenceof proteinuria or other
markers of pre-eclampsia.
-BP usually returns to pre-pregnancy limits within 6wks of delivery
Risk factor:
1.Firstpregnancy
2.Age > 40, BMI > 35
3.Multiplepregnancy
4.Medicalcondition: autoimmune disease, CKD, DM
5.Gestation hypertension in previouspregnancy
6.Family historyof gestational hypertension

7. Diagnosis:
-G-HTN usually notassociated with specific symptomsapart from mild recurrent
headachesencountered in some patients.
Laboratory tests:
-Urine analysis: absentproteinuria
-RFT: normal
-LFT: normal
-CBC: normal
-Preeclampsia (PE) should be always and repeatedly ruled out, since 15 –30%of
cases with G-HTN may develop PE later in pregnancy.

8. Management:
1.Conservative management: life style modification, close observation on
repeated antenatal care visits and repeated urine analysis to rule out PE.
2.Antihypertensive drugs; are only indicated with increasing BP levels
(160/110)
a.Oral Labetalolis the drug of choice
b.Methyldopaoral is an alternative
●Fetal surveillance: proper evaluation of fetal wellbeing including daily fetal
movement count (DFMC), non-stress test (NST) and repeated US

9. Chronic hypertension
during pregnancy
02

10. Definition:
-Hypertension before pregnancyor the development of hypertension < 20 weeks
gestation.
Risk factor:
1.Obesity
2.advanced maternal age
3.positive family history
4.Diabetes mellitus, chronic nephritis, and systemic lupus erythematosus

11. Management principle
-History, examination, and laboratory tests to differentiate Essential from
secondary hypertension and to exclude superimposed PE and IUGR.
-Treatment should aimfor BP levels not <120/80 to avoid decrease uteroplacental
perfusion leading to iatrogenic induced IUGR
-Treatment of BP protects women from the adverse effects of ↑ BP but does not
alter the course of pre -eclampsia.

12. Antihypertensive drugs and pregnancy:
-Methyldopa: has long been considered the safest oral antihypertensivedrug used
during pregnancy.
-Nifedipineand Labetalol; are safeand highly efficient as well.
-B-blockingagents; are not recommendedas they may be associated with IUGR
-Diureticsare not recommendedfor possible associated plasma volume reduction
-ACEIare contraindicatedas they may be associated with fetal renal agenesis,
oligohydramnios, and IUFD

14. Chronic hypertension
during pregnancy
02

15. Risk Factors
1.Previousand recurrent pregnancy loss, especially > 2successive abortions.
2.Medical disorders; as severe thyroiddisorders, uncontrolled DM, and SLE.
3.Psychosocial stress, and domestic violence.
4.Infectionsas Mycoplasma, Listeria and Toxoplasma
5.Heavy smokingand regular alcoholintake.
6.Maternal age > 35years.
7.Morbid maternal obesity(BMI > 35)

16. Preeclampsia
03

17. Definition:
❑Hypertensionand proteinuriaoccurring for the first timein the second
half of pregnancy (>20 weeksgestation).
❑It may complicate 3-7%of all pregnancies, especially cases with high risk
factors

18. Diagnostic Criteria Of PE
1.Sustainedelevation of the BPto 140/90mm Hg or moreon twooccasions
4 hoursapart
2.Proteinuria:
o> 300 mg in a 24-hour urine collection
o+2 or more on a dipstick test
oAlbumin /creatinine ratio of > 30
3.In absence of proteinuriaPE can be also diagnosed if new onset
hypertension > 20 weeks is associated with a recent organ dysfunction
manifested by one or more of the following;
oThrombocytopenia (platelets < 100.000)
oElevated serum liver transaminases (AST & ALT > twice the norms)
oRising serum creatinine, CNS symptoms, DIC and pulmonary edema

19. Risk Factors
1.Primigravida:: PE occurs 8 timesmore frequently in first than in
subsequent pregnancies
2.Extremes ofage (> 40, < 20)or Obesity(BMI > 30)
3.Previous historyof PE or Eclampsia
4.Family historyof PE or Eclampsia
5.Multifetalpregnancy and molarpregnancy with abnormal placentation
6.Pre-existing medical conditions: chronic hypertension, diabetes, renal
disease, SLE, antiphospholipid syndrome, thrombophilia

20. Pathophysiology
-The origin of PE is considered multifactorialwith inadequate
uteroplacental perfusionbeing central to its development leading to
placental ischemiaand hypoxia.
-During a normal pregnancy, cytotrophoblastic invasion of myometrial
spiral vessels renders these vessels widerand less responsiveto
vasoconstrictor substances →increaseduteroplacental blood flow.

22. Pathophysiology
❑In PE there is inadequatecytotrophoblastic invasionof the myometrial
spiral arterioles will preventthe development of a high-flow, low-
resistanceuteroplacental circulationand leads to uteroplacentalischemia
→Vascular endothelial cell damage →release of secondary mediators
responsible for;
1.Local and systemic vasospasm
2.Vascular endothelial dysfunction
3.Activation of the coagulation system
❑Diffuse vasospasm is potentiated by an increasein the vasoconstrictive
PGLs (thromboxane & PGL F2) and a decreasein the vasodilatorPGLs
(prostacyclin & PGL E2).

23. Pathophysiology
-Decreased Organ Perfusion;
oUtero-placental unit: IUGR and oligohydramnios
oKidneys: Decreased GFR, proteinuria, oliguria
oLiver: Sub-capsular liver hemorrhage and necrosis
oCNS: Cerebral oedema, Retinal hemorrhage
oBlood vessel: edema, Petechial hemorrhage, platelet thrombosis and
DIC in severe cases.

24. Clinical Picture:
❑PE is a disease of signsrather than symptoms,
❑PE is graded into
1.mild PE
2.severe PE.

25. Mild PE
❑Sign
*Hypertension> 140/90 mm Hg
*Proteinuria; > 300 mg/24hr. or dip stick test 2+, or ACR> 30
*lower limb edema
*Normal or mild changesin CBC, LFT and RFT functions
❑Symptoms: No symptoms, once pre-eclampsia become symptomatic this
indicates severity

26. Severe PE
❑Sign
*Hypertension: >/=160/110
*Proteinuria; > 300 mg/24hr.
*Serum Creatinine > 1.1 mg/dlor doublingof baseline values
*Oliguria < 750 ml/24hr.
*Elevated Liver Enzymes: AST & ALTincreased > twicetheir normal values
*Thrombocytopenia: Platelet count < 100,000.
*Facialedema.
*Pulmonaryedema on CXR
*Epigastric/RUQtenderness
*Sign of cerebral irritability: Papilledema, Hyperreflexia, clonus
*Fetal growth restriction on ultrasound, particularly if <36wks.

27. Severe PE
❑Symptoms
*Headaches, Blurred vision
*Dyspnea
*Nausea and vomiting
*Epigastricpain or right upper quadrantpain: due to stretch of liver
capsule

28. Investigations
1.CBC:↑Hb due to hemoconcentration, Thrombocytopenia, Anemia if
HELLP syndrome occurs
2.LFT:AST & ALT increased > twice their normal values
3.RFT:↑ Urea and creatinine.
4.Coagulation profile: ↑PT and ↑ APTT
5.LDH:a marker for hemolysis
6.Urine analysis:Proteinuria: >300mg protein/24h
7.Abdominal US:Fetus viable or not, Liquor volume (oligohydramnios due to
IUGR)

29. Complications Of Severe PE
❑Progression to eclampsia
❑Cerebral hemorrhage,Pulmonary edema, Acute kidney injury,
Subcapsular liver hematoma(risk of rupture), DIC
❑Placental abruption
❑HELLP syndrome: hemolysis, elevated liver enzymes, and low platelets
❑Oligohydramnios, IUGR and IUFD

30. Management Of Preeclampsia
❑The only definitivecure for PE is termination of pregnancy. Once the
placenta is delivered a rapid decline in most of the signs and symptoms of
PE will occur.
❑The goal of management of PE will be to preventmaternal complications
of severe PE while minimizingthe neonatal hazards of prematurity.

31. Management Of Preeclampsia
Outpatient management of pre-eclampsia
▪Criteria
a.Asymptomatic.
b.BP 140 –150 systolic and 90 –100 diastolic and can be controlled
c.Noor low(1+/<300mg/24h) proteinuria
▪Management:
a.Follow up every 2 weeksfor BP and urine.
b.Weeklyreview of bloodbiochemistry.
c.Warnabout development of symptoms.

32. Management Of Preeclampsia
Mild–moderate pre-eclampsia:
▪Criteria:
a.Nomaternal complications.
b.BP <160systolic and <110diastolic
c.significant proteinuria: (2+, >300mg/24h, ACR> 30)

33. Management Of Preeclampsia
Mild–moderate pre-eclampsia:
▪Management:
1.Hospital admission
2.4-hourly BP, 24h urine collection for protein.
3.Daily urinalysis
4.Daily fetal assessment with CTG.
5.Regular blood tests every 2–3 days unless symptoms or signs worsen
6.If BP increases (>160 systolic or >110 diastolic or MAP > 125)
antihypertensive therapy should be started (Medication does not
cure the condition, but aims to prevent hypertensive complications
of pre-eclampsia)

34. Management Of Preeclampsia
Severe pre-eclampsia:
▪Criteria:
a.BP ≥160systolic or ≥110diastolic Plus
b.significant proteinuria (≥1g/24hor ≥2+on dipstick) OR
c.Maternal complicationsoccur.

35. Management Of Preeclampsia
▪Management:
1. BP stabilizedwith antihypertensive medication
*must aimfor <160 systolic and <110 diastolic
*Initially use oral nifedipine10mg: can be given twice 30min apart.
*Start maintenance therapy, usually labetalol(first line) or
methyldopaif asthmatic
2. Fluid restriction: up to 1 ml/kg/hrto prevent pulmonary oedema
3. Seizure prophylaxis: MgSO4 loading 4gram IV and maintenance dose
1g/h

36. Management Of Preeclampsia
4. Enhancement of lung maturity: IM betamethasone or dexamethasone 24 mg in 24
hours for minimizing risks of prematurity
5. CTG monitoringof fetus until condition stable.
6. Ultrasound of fetus:
*evidence of IUGR, estimate weight if severely preterm
*assess condition using fetal and umbilical artery Doppler.
7. Terminationof pregnancy

37. Indications for termination:
1.Worseningthrombocytopenia or coagulopathy.
2.Worseningliver or renal function.
3.Severematernal symptoms, especially epigastric pain with abnormal LFTs.
4.Refractorypre-eclampsia, (resistance to 3 drugs on maximum dose)
5.Fetal compromisedetected by pathological CTG or reversed umbilical
artery flow.
6.HELLPsyndrome or eclampsia.
7.Placental abruption
8.Gestation age > 37 weeks
9.MAP > 125

38. Type of delivery
❑Induction of laborby lV oxytocin in cases with favorable Bishop score(>7),
no fetal distress, no severe IUGR
❑Elective CSin cases with severe PE, or fetal distress,severe IUGR, HELLP
syndrome

39. Prediction Of PE
❑There are No reliabletests available for the prediction of PE, or its course
and severity
❑Serum biomarkersas low level of pregnancy-associated protein-A (PAP-A)
in the 2nd trimester is associated with increased risk.
❑Uterine Artery Dopplerultrasound at 18-24weeks gestation may show
high resistance flow with diastolic notchingthat may identify up to 75% of
women at risk for PE later in pregnancy.
❑Raised uric acid, low platelets, and high Hb may help differentiate pre-
eclampsia from PIH before proteinuria occurs

40. Prevention PE
-Low Dose Aspirin(75mg PO) daily from 18-34 weeksgestation has been
shown to minimize the risk for recurrent PE and IUGR in high-risk cases
with a previous history of the disease.

41. ANY
QUESTION?

42. THANK
YOU