Notes for undergraduates and postgraduates in OBS gyne

1. PRE-ECLAMPSIA
DR.PRIYA SAXENA

2. Classification of hypertensive disorder of
pregnancy
 Gestational hypertension
 Preeclampsia
 Eclampsia
 Chronic hypertension
 Preclampsia superimposed on chronic hypertension

3. PREECLAMPSIA
 Preeclampsia is a multiorgan disorder
 Significant hypertension associated with any organ damage is called
preeclampsia

4. TYPES OF PREECLAMPSIA
 Preeclampsia without severe features:SBP-140-160 and/or DBP 90-110mmhg
confirmed by repeated examination 4hrs apart
 Severe preeclampsia :SBP>/=160mmhg and/or >/=110mmhg

5. SEVERE PREECLAMPSIA
 Any one or more of the following conditions:
 SBP>/= 160 or DBP>/=110 mm of Hg
 Thrombocytopenia
 Impaired liver function
 Progressive renal insufficiency
 Pulmonary edema
 New onset cerebral or visual disturbances

6. RISK FACTORS
 Primiparity
 Age<18 years
 Advanced maternal age(>35years)
 High BMI(>35kg/m2)
 Multiple pregnancy
 Hydatidiform mole
 Rh isoimmunization
 Polyhydramnios
 Maternal medical problems(diabetes,hypertension,renal disease,connective tissue
disorders,antiphospholipid antibody syndrome)

7.  Past h/o preeclampsia
 Family h/o preeclampsia
 Race
 Low socioeconomic status
 Environmental factors

8. PATHOPHYSIOLOGY
 In preeclampsia invasion of spiral arteries by cytotrophoblast is incomplete i.e. the
second wave of trophoblastic invasion is absent;there is insufficient remodelling of
spiral arteries;thus spiral arteries remain constricted and blood flow through the
placenta is restricted,this ultimately lead to placental ischemia.

9. TWO STAGE THEORY
 Stage1-origin in placenta:release of anti-angiogenic factors
 Stage2-maternal endothelial dysfunction

10. BASIC PATHOLOGY OF
PREECLAMSIA
 Vasoconstriction of arterioles which occurs throughout the maternal body
 The vascular changes and hypoxia of the surrounding tissue leads to
haemorrhage,necrosis and other pathological changes in various organ systems
 Preeclampsia creates a functional derangement of multiple organ systems such as
cns,haematological,hepatic,renal and cardiovascular system

11. CENTRAL NERVOUS SYSTEM
 Arteriolar vasoconstriction
 Cerebral ischemia,infarction and edema
 When the mean arterioral pressure exceeds 120mm hg,cerebral auto regulation fails
resulting in cerebral edema,peticheal,intracranial hemorrhages (pontine)
 Symptoms include:headaches(occipital),mental confusion,drowsiness,convulsions

12. HEPATIC SYSTEM
 Vasospasm,ischemia,endothelial damage,fibrin deposition
 Subcapsular hemorrhages
 Periportal necrosis,hepatic rupture
 Symptoms include:nausea,vomiting,rt hypochondriac tenderness,elevated liver enzymes

13. ENDOCRINE SYSTEM
 Microhemorrhages and necrosis occur in endocrine glands like pituitary,pancreas and
adrenal gland also

14. CARDIOVASCULAR SYSTEM
 Cardiac output and peripheral vascular resistance is increased
 hypovolemia and have less tolerance for blood loss associated with delivery
 Clinical features:weight gain,edema,Hb>12g/dl,creatinine >0.8 mg%
 Vascular hallmark of preeclampsia:hemoconcentration
 Rarely myocardial,subendocardial hemorrhages,necrosis may occur-left ventricular
failure-dyspnea,edema of legs and chest pain

15. PLACENTA
 Endothelial damage-acute athetosis of decidual arterioles-placental
hypoperfusion,infarcts-chronic placental insufficiency-oligohydramnios,IUGR,fetal
distress,fetal demise
 Placental thrombosis and infarction can also lead to abruptio placentae

16. RETINAL CHANGES
 Retinal arteriolar vasospasm,hemorrhages,exudates-loss of retinal sheen,V-A ratio
increase to 2:1(later 3:1),maculopapular edema,retinal detachment-blurred
vision,scotomna,temporary blindness

17. COAGULATION SYSTEM
 Platelets activated in placental microcirculation of placenta,kidney and liver-fibrin
increase,factorVII,factor VIII,FDP increase-fibrin platelet deposition in placental,liver
and kidney arterioles-hypercoagulibility,DIC,HELLP syndrome-bleeding from various
sites,shock,death

18. INCREASED CAPILLARY
PERMEABILITY
 Endothelial dysfunction-leaking of proteins into extra vascular space,decrease plasma
oncotic pressure (causes fluid to shift from intravascular to extravascular
compartment)–tissue and clinical edema,hemoconcentration

19. PREDICTION OF PREECLAMPSIA
 Biochemical markers:
 sFIT1/PIGF ratio>38
 PAPP-A decrease,PP13 decrease
 Inhibin-A increase
 Role of doppler ultrasound:persistence of diastolic notch of uterine artery after 22weeks
predicts development of preeclampsia later on;B/L notching is more concerning

20.  Diastolic notch of the uterine artery is no longer used for prediction of preeclampsia.
 Pulsatility index>95 percentile(2.35)of uterine artery-faulty trophoblastic invasion of
uterine artery
 95th centile for mean uterine artery doppler PI at 18-24 weeks is 1.14 and is usually
preferred

21. UTERINE ARTERY PI
 11-13wks-2.35(TA) and 3.1(TV)
 20-24wks-1.44(TA) and 1.58(TV)
 30-34wks-1.17(TA)

22. MATERNAL INVESTIGATIONS
 CBC(neutrophilia)
 Peripheral smear
 Urine for proteinuria
 24 hr urine for proteinuria and creatinine clearance
 LFT(AST,ALT),LDH,S.Bilirubin
 Coagulation profile
 Renal function tests
 Serum creatinine and uric acid

23. FETAL SURVEILLANCE
 NST,DFMC
 Biophysical profile
 Usg:fetal biometry
 Fetal Doppler flow studies

24. DEFINITIVE TREATMENT
 Delivery of the fetus and placenta

25. TREATMENT OF PRETERM
PREECLAMPSIA
 Expectant management in a tertiary care hospital

26. CONTRAINDICATIONS TO
CONSERVATIVE MANAGEMENT
 Severe headache
 Epigastric or rt upper quadrant pain
 Eclampsia,oliguria/renal failure
 Pulmonary edema
 Hypoxia
 Hepatocellular injury
 Altered mental status

27. MANAGEMENT OF SEVERE
PREECLAMPSIA
 Administer corticosteroids to improve FLM
 Stabilize mother by controlling BP
 Seizure prophylaxis
 Daily lab evaluation for HELLP syndrome and renal failure
 After 48hrs:
 Patient stabilises-continue expectant management
 Severe hypertension continues-proceed to delivery

28. MANAGEMENT STRATEGY
 Stabilise the patient (BP control)
 Seizure prevention
 Delivery at 34/37 weeks
 Postpartum (BP) surveillance

29. BP Control
 Drugs commonly used are:
 Labetalol
 Alpha methyl dopa
 Nifedipine

30. TREATMENT OF HYPERTENSIVE
CRISES:
 Drugs commonly used are:
 Labetalol
 Hydralazine
 Nifedepine

31. ANTIHYPERTENSIVES USED IN
PREECLAMPSIA
Drug Mechanism Dosage
Alphamethyl dopa Central and peripheral
antiadrenergic action
250-500mg tid or qid
Labetalol Adrenoceptor antagonists
(alpha and beta blockers)
100mg tid or qid
Nifedipine Calcium channel blocker 10-20mg bid
Hydralazine Vascular smooth muscle
relaxant
10-25mg bid

32. DRUGS IN MANAGEMENT OF
HYPERTENSIVE CRISES
Drug Dose schedule Maximum dose
Labetalol 10-20mg iv every 10
minute
300mg iv
Hydralazine 5 mg iv every 30 minute 30mg iv
Nifedipine 10-20mg oral,can be
repeated in 30 minute
240mg/24hr
Nitroglycerin
Sodium nitroprusside
5 microgram /minute
0.25-5
microgram/kg/minute iv

33. TIME OF DELIVERY
 Preeclampsia without severe features:37weeks
 Severe preeclampsia or severe GH:34 weeks

34. LABOR AND DELIVERY
 Deliver in a tertiary care hospital with NICU
 First stage:
 Intrapartum EFM
 Injectable antihypertensives
 Second stage:
 Cut short with outlet forceps or vacuum assisted delivery
 Third stage:
 Active management
 Methergin contraindicated

35. ANAESTHETIC CONSIDERATIONS
 Women who require cesarean delivery should continue MgSO4 infusion
 Administration of neuraxial anesthesia (spinal or epidural) is recommended
 Routine invasive monitoring is not needed

36. POSTPARTUM SURVEILLANCE
 Close BP monitoring in hospital for 72 hrs
 Outpatient monitoring for 6 weeks postpartum

37. MATERNAL COMPLICATIONS IN
PREECLAMPSIA
 Short term:
 Placental abruption
 Preterm labor
 Pulmonary edema
 Rupture of liver due to hematoma
 HELLP syndrome
 DIC
 Acute renal failure
 Eclampsia
 Operated vaginal delivery

38.  Cesarean section
 Long term:
 Recurrent preeclampsia
 Chronic hypertension
 Cardiovascular disease
 Metabolic syndrome

39. FETAL COMPLICATIONS
 Short term:
 Fetal growth restriction
 Prematurity
 Intrauterine death
 Hypoxic ischemic encephalopathy
 Perinatal mortality

40.  Long term:
 Cerebral palsy
 Other neurological disorders