Dr. Gitanjali presented a case of a 36-year-old primigravida woman at 38 weeks and 2 days of pregnancy who presented with raised blood pressure of 200/150 mmHg. She was diagnosed with chronic hypertension, superimposed preeclampsia, anemia, fetal growth restriction, and hypothyroidism. Despite treatment with antihypertensive medications, her blood pressure remained elevated. She underwent an emergency cesarean section under spinal anesthesia and delivered a baby. Her case highlights the importance of monitoring and managing the multiple complications that can arise in hypertensive disorders of pregnancy.

1. Case on HDP
Dr Gitanjali
Moderator- Dr Kakade sir
1

2.  Patient Mrs. khan Salamat 36 years old Primigravida with 9 months of amenorrhea came to
Bharati hospital referred from a private practioner in view of raised BP i.e of 200/150mmhg
 At presentation she complained of headache and blurring of vision since 1 day
 Headache was localized in the occipital region, throbbing type, not relieved on rest
 No c/o nausea, vomiting, epigastric pain etc
 No c/o pain in abdomen, pv discharge
 Fetal movements well appreciated
2

3.  Menstrual history->
LMP- not known
PMH- 4-5 days/28-30days/RMF
AGA- 38 weeks 32days (BUSG @ 12 weeks 3 days on 13/7/20)
EDD- 26/1/21
 Obstetric history-
 Married since 1 year, On consanguineous marriage
G1- present pregnancy, spontaneous conception, Registered at a private practioner.
 diagnosed with increased BP at 3rd month of amenorrhoea -> was started on Tab Labetalol 100mg bd
 Diagnosed with Hypothyroidism since 3rd month of amenorrhoea->was started on Tab Thyrox 25 mcg
OD
3

4.  Antihypertensives were stepped to Tab Nefidepine Retard 20mg Bd together with Tab Labetalol
100mg BD since 1 month
 H/o anemia present -> was given 5 injection Iron Sucrose 15 days back
 Past history- NAD
 Family history- Mother and Father are Hypertensives on treatment
4

5.  Patient was seen in EMD
 GENERAL PHYSICAL EXAMINATION
Height-154 cm Weight- 80kg BMI-33 kg/m2
Afebrile,
P-84bpm;pallor +, bilateral pedal oedema + , U/a- 4+
DTR- BRISK
BP-200/150mmHg in right brachial artery
INJ labetalol 10mg iv given , INJ MGSO4 4gm iv given Repeat BP 150/100mmhg (in 10 minutes)
RS-airway entry equal on both sides, no basal crepitations,
CVS-S1 S2 normal
5

6.  PER ABDOMEN EXAMINATION-
INSPECTION-
Abdomen longitudinally ovoid
Linea nigra,stria gravidarum seen,abdominal wall oedema +
PALPATION-
Uterus- 34 WK period of geststion,Relaxed
6

7. Fundal grip-soft,non ballotable part s/o breech
Lateral grip-Irregular, knob like structure on right side s/o limbs; smooth, curved shaped structure on
left side s/o back
Pawlik grip-hard,globular,ballotable structure s/o head
Pelvic grip-hands converging-head not engaged
AUSCULTATION-
FHS +,regular,148bpm on left spinoumbilical line
 Pv-cervix soft, posterior, os closed ,uneffaced
7

8.  Diagnosis-Primigravida with 38 weeks 2 days pregnancy with chronic hypertension with
superimposed preeclampsia with anaemia with FGR with hypothyroidism with impending
eclampsia in Hypertensive emergency.
 Patient was shifted to LR for further management after starting zuspan regimen
 In LR -> Foleys catherization done, Her BP was 220/140mmhg -> INJ Labetalol 20mg iv given-
 BP repeated after 15 mins , which was 190/120mmhg IN Labetalol 40 mg given  Repeat
BP after 20 min was 190/120mmhg
8

9.  Capsule Nifedepin 10 mg given  Repeat BP after 20 mins was 220/150mmhg  Cap Nifedepine 10mg repeated -
BP was 170/110mmhg after 10 minutes
 1 PCV was issued ivo anaemia (HB=8.8 %) and , patient was shifted for Emergency LSCS
 On table was 140/90 mmhg -> LScs was done under spinal anaesthesia.
 LSCS done uneventfully -> Patient was shifted to Icu for further management.
9

10. Investigations
 Hb/TLC/Plt- 8.7/9300/2.04
 TB/DB- 0.2/0.1
 SGOT-17, SGPT- 10
 T.PROTEIN-3.46, SERUM ALBUMIN-1.82
 ALP-297
 PT-10.7, APTT-26.7, INR-0.91
 Sr. Cr- 0.64, Na/K/cl- 130/4.5/109
 LDH-439
 BSL R-100
 Usg-> single live intrauterine pregnancy of 34 weeks 6 days, AFI-9-10cm, EFW-2.4kg,FGR+
 Gestosis score in my patient=9
10
Age-1
Anaemai-1
BMI>30 -1
Primigravida-1
Hypothyroidism-2
Chronic HTN-3
Total-9

11. 11

12. Discussion
 Hypertensive disorders in pregnancy (HDP) are the spectrum of disorders ranging from already
existing chronic hypertension in the index pregnancy to complex multisystem disorder like
preeclampsia leading to the complications like eclampsia, HELLP syndrome, acute renal failure,
pulmonary edema, stroke and left ventricular failure.
12

13. Classifications-
 Gestational hypertension: Blood pressure =/> 140/90 mmHg, detected beyond 20 weeks of
gestation and returns to normal within 42nd postpartum day and is not associated with any other
features of preeclampsia.
 Chronic hypertension: Known case of hypertension or a case of hypertension detected before 20
weeks of gestation in absence of neoplastic trophoblastic disease and multiple pregnancies.
 Preeclampsia: It is a multisystem inflammatory disorder beyond 20 weeks of pregnancy with
significant proteinuria characterized by de novo onset of hypertension (BP =/>140/90 mmHg).
 More recently, atypical variant of preeclampsia is recognized which is accompanied by
neurological, hematological, hepatic, renal manifestations or fetal growth restriction, in absence
of proteinuria
 Eclampsia: It is occurrence of seizures in association with preeclampsia. It can also occur as
atypical eclampsia.
 Superimposed Preeclampsia: It is the occurrence of preeclampsia in women with chronic
hypertension.
 (Blood pressure reading should be reconfirmed after 4-6 hours before classifying a patient in
particular group.)
13

14.  Preeclampsia can be further classified as non severe and severe.
 It can also be classified as early onset and late onset as below.
 Non severe preeclampsia: Blood pressure =/>140/90 mm Hg and <=/ 160/110 mm Hg
 No premonitory symptoms and a normal HDP lab parameters
 Severe preeclampsia: Blood pressure > 160/110 mm Hg with/without premonitory symptoms with
/ without abnormal HDP laboratory parameters.
 Or Blood pressure >/=140/90 mm Hg with premonitory symptoms and /or abnormal HDP
laboratory parameters.
14

15.  Premonitory symptoms: Headache, blurring of vision, vomiting, right upper quadrant pain,
sudden excessive weight gain and severe edema.
 Abnormal HDP lab: Low platelets, elevated liver enzymes, elevated serum creatinine, and
abnormal coagulation profile.
15

16.  Early onset preeclampsia: Onset of proteinuric hypertension is before 34 weeks of pregnancy.
 The maternal complications are more severe.
 Low birth weight, fetal growth restriction and iatrogenic prematurity are common.
 Late onset preeclampsia: Onset of proteinuric hypertension is after 34 weeks of pregnancy.
 The maternal complications are less severe. Low birth weight and fetal growth restriction is less
common.
16

17. What is HDP gestosis score
 Primary clinical assessment for screening and prediction of preeclampsia can be objectively
performed by ‘easy to use’ HDP-Gestosis score.
 Process of risk scoring:
 This score involves all the existing and emerging risk factors in the pregnant woman.
 Score 1, 2 and 3 is allotted to each clinical risk factor as per its severity in development of
preeclampsia.
 With careful history and assessment of woman a total score is obtained time to time.
 When total score is =/> 3; pregnant woman should be marked as ‘At risk for Preeclampsia’.
17

18. 18

19. Prevention of Preeclampsia
 All ‘at risk ’women should be started with Aspirin 75-150 mg
 Dose-The optimum dose of aspirin is unclear; studies have used 60-75-100-150 mg.
 Low-dose aspirin has a good maternal and fetal safety profile.
 Aspirin for this indication should be started even earlier than 12 weeks.
 Mechanism-> Defective placentation is considered as the causative factor of preeclampsia. Early
aspirin balances the levels of thromboxane A2 and prostacyclin which will maintain adequate
uteroplacental blood flow and improve placentation without increasing the risks of adverse
maternal and perinatal outcomes. Therefore, it appears safe to use low-dose aspirin as a
prophylaxis to prevent preeclampsia throughout pregnancy until 2 days prior to delivery or
cesarean section.
 Along with aspirin, calcium 1-1.5 gm10 daily (in low calcium intake group) is to be started.
19

20. Diagnosis
1. Blood pressure measurement is the most important clinical test to diagnostic HDP.
• The position of the pregnant mother especially after 20 weeks of gestation should be either in the
sitting position or left lateral position with the zero level at the level of the heart.
20

21. 2)Proteinuria
• Significant proteinuria is urinary excretion of > 300 mg protein in a 24-hour period.
• Once significant proteinuria is established, further quantification is not required as proteinuria does
not have prognostic value from management point of view.
• However, if proteinuria is absent, pregnant woman with hypertension still requires frequent
monitoring.
The HDP Gestosis scientific group recommends the following methods till further research findings
are out –
o Urinary dipstick method (Visual / by automated device)
o Spot urine protein: creatinine ratio
• Significant proteinuria: can be assessed by urinary dipstick: >/= 2+ Or urinary protein: creatinine
ratio >/= 30 mg/mmol.
• Urinary dipstick method is quick and allows women with negative result to return home quickly. It
also helps quick assessment of severe proteinuria.
• The results of spot protein: creatinine also would be available within 2 - 4 hours.
• The gold standard of assessing proteinuria is 24-hour urine protein assessment.
21

22. Laboratory Investigations -When blood pressure reading of a pregnant woman is =/> 140/90 mmHg
(or known case of chronic hypertension visits first time to the antenatal clinic), following investigations
are advisable to assess severity of the disease.
•Baseline HDP lab
 Urine albumin- by dipstick method or urine protein: creatinine ratio ✓ Complete blood count:
Platelet count and anaemia assessment
 Liver enzymes- Alanine aminotransferase (ALT), Aspartate transaminase (AST), Lactate
Dehydrogenase (LDH).
 Serum bilirubin
 Serum creatinine
 Serum uric acid
 Additional laboratory investigations
 Coagulation profile (when platelet count is < 1,00000 /mm3 )
 Serum electrolytes (in severe disease),
22

23.  Ultrasonography
 • Maternal ultrasonography (USG abdomen and pelvis)
 Following things are suggested to be assessed in addition to obstetric evaluation:
 Liver: sub-capsular hematoma, hepatomegaly.
 Kidney: signs of renal causes of hypertension, other changes in renal parenchyma
 Ascites and pleural effusion: as other worsening signs of preeclampsia.
 Fetal surveillance and placental morphology (Obstetric USG with doppler)
 Fetal biometry, amniotic fluid volume (AFI), uterine artery doppler and umbilical artery doppler
should be performed at the first diagnosis of preeclampsia.
 In confirmed preeclampsia or in cases of fetal growth restriction, serial evaluation of fetal growth,
AFI, uterine artery umbilical artery doppler is recommended.
 More frequent ultrasound measurements and color doppler study are needed if there is a high
resistance or absent or reversed end-diastolic flow in uterine artery with appropriate further
management.
 Placental location, morphology and any evidence of placental bed hemorrhage, abnormal
adherence and presence of sinusoids should be documented. 23

24.  Fundoscopy
 ✓ Fundoscopy may be required to differentiate chronic and new onset disease and to diagnose
papilledema/ hemorrhages as these have ominous prognosis.
24

25.  Medical management –
 World Organization Gestosis recommends that a systolic BP of =/>140 and/or a diastolic BP of
=/>90 mm Hg warrants antihypertensive therapy.
 Target range of Blood Pressure to be kept: Systolic < =140
 Diastolic <= 90 mmhg
25

26.  Labetalol: 200 - 1200 mg / day in 2 divided doses It is accepted as the first line and effective
medication during pregnancy. Preferred medication when baseline pulse is >100/min It is
contraindicated in asthma, CCF, DM and cases of bradycardia.
 Nifedipine- 20-120 mg / day of slow releasing preparations in 2-3 divided doses Preferred
medication when baseline pulse is < 100/min .Maternal adverse effects include tachycardia,
palpitations, headaches, and facial flushing.
 Methyldopa : 500-2000 mg per day orally in 2-3divided doses. Methyl dopa is the most time
tested and safe anti-hypertensive. Nowadays it is not routinely available. Drug is to be
discontinued in postpartum period to avoid postpartum depression.
 Drugs contraindicated in pregnancy: ACE inhibitors, ARBs, ß- blockers and diuretics.
26

27. 27

28.  Delivery decision
 Gestational Hypertension: Pregnancy can be continued till the term
 Mild Preeclampsia: To be delivered at 37 completed weeks.
 Severe Preeclampsia: To be delivered after 34 completed weeks.
 Eclampsia: Should be delivered once mother is stabilized after MgSO4.
 Labor induction with appropriate method can be carried out safely.
 Cesarean section is done for obstetric indications only.
 Delivery decision should be carefully decided after assessing maternal and fetal risks.
 Corticosteroids
 Corticosteroids are recommended in all women delivering before 34 completed weeks and in case of elective
cesarean delivery before 38 completed weeks.
 Intramuscular dexamethasone: 6 mg 12 hourly 4 doses or
 Intramuscular betamethasone: 12 mg 24 hourly 2 doses can be used for reducing neonatal respiratory
distress.
 Even a single dose of steroid at least an hour prior to delivery can reduce the neonatal respiratory distress
syndrome remarkably
28

29.  Management of eclampsia -Eclampsia is a situation needs to follow the principles of ABCD of
critical management.
 Principles of management of eclampsia “Call for help”
 timely additional help is essential for effective management
 A: Airway: Lateral decubitus position, mouth gag and neck extension Avoid injury to the mother
 B: Breathing: Nasal oxygen and suction Pulse oximeter: oxygen saturation >96%
 C: Circulation: IV access for maternal resuscitation Laboratory investigations are sent.
 Crystalloids: Ringer Lactate or Normal Saline 80 ml/hr.
 Control of convulsions: Magnesium sulphate-Loading and maintenance dose. Catheterization:
Foley’s catheter is inserted.
 Control of blood pressure: With anti-hypertensives
 Corticosteroids: For gestational age < 34 weeks
 D: Delivery: Baby should be delivered once mother is stabilized
29

30. 30

31.  Management after stabilization ->
 Deliver the patient after stabilization in the situations like eclampsia, HELLP, severe preeclampsia,
chronic hypertension with superimposed preeclampsia and if gestational age is more than or equal to
34 weeks.
 Vaginal delivery may be considered if attainable in reasonable amount of time.
 In case of preterm pregnancy, expectant management can be considered with individual assessment
and antenatal steroids and rationale use of antihypertensive medications with close supervision.
 Intrapartum management: It is preferable to conduct delivery in a well-equipped birthing centre with
facility of obstetrical expertise and accessible obstetric high dependency and/or critical care units with
blood bank, anesthesiologist, neonatologist and a transfer facility.
 Mode of delivery: It depends upon the urgency to deliver, cervical Bishop’s score, gestational age,
severity of FGR and doppler study findings in the umbilical artery
31

32.  Induction of labor: Induction of labor should be offered to mothers eligible for vaginal delivery.
 Prostaglandins (PGs) (dinoprostone gel, suppositories or tablets) can be used for induction.
 Misoprostol may be used in patients remote from term.
 Mechanical dilatation of the cervix with Foley’s balloon or vaginal hygroscopic dilators may be
considered.
 Augmentation of labor is to be done only with oxytocin
32

33.  Caesarean delivery: Severe FGR or REDF in the umbilical artery on color Doppler or any
obstetric contraindication for vaginal delivery or failure of induction may make cesarean delivery
a preferred choice.
 Fluid Management: Inappropriate use of fluids can cause pulmonary edema and maternal death.
 Intrapartum fetal monitoring: Close monitoring of the fetus with continuous or intermittent Doppler
device or EFM (electronic fetal heart monitoring) is preferred. Laboratory investigations may be
repeated when required.
33

34.  Preventing PPH: Active management of third stage of labour and prophylactic administration of
oxytocics in case of cesarean delivery should be followed in all cases.
 It is safe to use oxytocin 5 U bolus equally diluted over 2-3 minutes or prostaglandin (PG)
injections.
 PG can be used also as misoprostol sublingual, transrectal or transvaginal. Average blood loss
of labour may not be well tolerated by these patients due to hemoconcentration.
 Underlying endothelial dysfunction, hypertension and use of magnesium sulphate may make the
mother more susceptible to PPH.
 The use of fluids should be judicious. Recommendation is 80 ml/hr or1ml/kg/hr as overinfusion
can cause pulmonary edema in these women.
34

35.  Post-delivery management-> It involves close vigilance for eclampsia, PPH, HELLP, pulmonary
edema, cardiovascular, cerebrovascular events and thrombo-embolic complications.
 Continued postpartum surveillance has to be the norm to prevent additional morbidity as gestosis
can develop post-delivery.
 During the hospital stay, blood pressure should be closely monitored for first 48 hours post
delivery.
 Postpartum use of NSAIDs should be avoided.
 Antihypertensive therapy is recommended for persistent BP of SBP > 150 and DBP > 100 mm
Hg.
 Persistent BP of >= 160 SBP and or DBP of >=110 mm Hg should be treated within one hour and
magnesium sulphate considered for seizure prophylaxis
35

36.  Thank you
36

37.  Discussion

38.  Gestational hypertension
 Pre eclampsia and eclampsia syndrome .
 Chronic hypertension
 Pre eclampsia superimposed on chronic hypertension .
Classification of HDP

39.  Defined as blood pressure 140mmhg (systolic)and 90 mmhg
(diastolic) without proteinuria on atleast 2 occasions,at least 4
hours apart after 20 th week of gestation in women known to be
normotensivebefore pregnancy .
GESTATIONAL HYPERTENSION

40. CHRONIC HYPERTENSION
 Chronic hypertension in pregnancy is defined as
hypertension before pregnancyor before 20 th week of
gestation ,on more than one occasion at least 4-6 hours
apart
 Systolic Bp of 140 mmhg or greater ,or diastolic Bpof 90
mmhg or greater or both .
 Persistent hypertension for 12 weeks postpartum is also
retrospectively described as chronic hypertension .

41.  It is best described as pregnancy specific syndrome that
can affect virtually every organ system .
 Defined as Bp ->140/90mmhgtaken 2 ocassion 4-6hours
apart taken in sitting position with proteinuria .
 Appearance of proteinuria with hypertension is an
important diagnostic criteria .
visual dipstick test.
Trace- 0.15to0.3g/I
1+= 0.3g/l
2+=1g/l
3+=3g/l
According to new guidelines – Proteinuria is not a specific
marker of pre eclampsia .
PRE-ECLAMPSIA

42. 1)DIASTOLIC BP
2)SYSTOLIC BP
3)PROTEINURIA
4)HEADACHE
5)VISUAL
DISTRUBANCE
6)UPPER
ABDOMINAL PAIN
7)OLIGURIA
8)CONVULSION
<110mmhg
<160mmmhg
<5 G/24 hr
not present
not present
not present
not present
not present
not present
ABNORMALITY NON SEVERE (mild) SEVERE
>110mmhg
>160mmhg
>5 G/24 hr
present
present
present
present
present
present

43. 8) SERUM CREAT
9)THROMBOCYTOPE
NIA (<100,000/UL)
10)SERUM
TRANSAMINASE
ELEVATION
11)FETAL GROWTH
RESTRICTION
12)PULMONARY
EDEMA
13)GESTATIONAL
AGE
Not elevated
absent
minimal
absent
absent
late
elevated
present
marked
present
present
early

44.  It is diagnosed when one or more features ofpreclampsia (e.g elevated
liver enzymes ,low platelets , proteinuria ) develop for first time during
pregnancy after 20 weeks in a women with pre existing chronic
hypertension .
PRE-ECLAPSIA SUPERIMPOSED ON
CHRONIC HYPERTENSION

45.  Incidence of pre eclampsia in nulliparous ranged from
3 to 10 %.
 In multipara ranged from 1.4 to 4 %
 Young and nulliparous women are vulnearble to
developing pre eclampsia .
Incidence

46.  Couple related risk factor :
Primipaternity.(exposure of chronic villi for the firsttime)
Limited sperm exposure
Pregnancyafter donar insemination ,donar egg , donar
embryo .
 Maternal or pregnancy related risk factor :
Extremes of age ( teenage / elderly primigravida )
Smoking
Obesity and insulin resistance/ gestationaldiabetes
Multifetal pregnancies.
Pre eclampsia in previous pregnancy.
RISK FACYTOR FOR PRE ECLAMPSIA

47. Maternal low birth weight .
Family history of pre eclampsia .
 Pre existing medical disease :
Pre gestational diabetes ,
Chronic hypertensiveor renal disease .
Maternal immunological disease.
Pre existing thrombophilia , anti phospholipidsantibody
syndrome .

48.  Stage1 – abnormal placentation .
(faulty endovascular trophoblastic remodeling ).
 Stage 2 – clinical syndrome .
Pre existing maternal condition that are also manifest by
endothelial cell activation or inflammation .
TWO STAGE DISORDER HYPOTHESIS

49. ETIOPATHOGENESIS
 Markers of placental dysfunction
 Abnormal trophoblastic invasion. Vasospam .
 Immunological factor .
 Endothelial cell activation /coagulation activation .
Increased pressor response .
Angiogenic – anti- angiogenic proteins .
 Genetic multifactorial disorder

51.  Fibronectin - fibronectin is a high molecular
weight glycoprotein that has important role in all
cellular adhesions and is component of connective
to tissue and basement membranes .increased level
of fibronectin preeceds clinical signs of pre
eclampsia and useful for prediction of disease.
MARKER OF PRE ECLAMPSIA

52. Symptoms
• Headache- mild to severe and intermittent to constant.
Pain may be frontal or occipital , may be pulsatile or dull
Headache may arise from cerebrovascularhyperperfusion .
• Eye symptoms:scotoma ,transientperceptionof brightor black spot –
can lead to diplopia ,blurred vision and in severe cases complete
blindness , visual symptoms can be cause by vasospams and due to
occipital vasogenic oedema .
• Blindnesssecondaryto retinal ischaemia or infarctionis
called purtscherretinopathy.

53. • Epigastric or right upper quadrant pain:frequently
accompanies hepatocellular necrosis, ischemia, and edema that
stretches Glissoncapsule.
Severe form of disease – leads to HELLP SYNDROME.
Marked alteration in AST (aspartateaminotransferase),ALT-
(alanine aminotransferase)and LDH value .
• Diminished urinary output—Urinary output of less than 400 ml
in 24 hours is the alarming symptoms.
• Edema - Swelling of the leg , hands , face , abdomen .

54. Signs
• Abnormal weight gain:
A rapid gain in weight of more than 5 lb a month or more than 1 lb a week in later month
of pregnancyis significant.
• Rise of blood pressure
• Edema
• Proteinuria .

56. LABORATORY FINDINGS
 Laboratory changes reflect the effectsof the disease on the renal ,hepatic,
hematological systems.
 Hematological abnormalities– Increase in
haemoglobin . Increase in hematocrit level.
Decrease in plasma fibrinogen level (<200 mg/dl) Platelet count – below
100,000/mm3.
 Liver function test .
Elevation in serum transaminase is most common . An AST or ALT levels of
about 70 IU/L is seen as significant as a level above 150 iu/l
associatedwith increase morbidity to the mother.

57. Serum bilirubin level – elevated bilirubin level (>1.2g/dl)
Lactate dehydrogenase – markerof hemolysis (increased Ldh >600
u/l).
Altered renal functions :
Serum creatnine (increase upto 1.2 mg /dl )
Increased blood urea nitrogen ( normal value in pregnancy is 15 mg /dl
Increased uric acid ( normal value upto 6 mg /dl)- hyperuricemia associated with renal
dysfunction,glomerular endothelosis and decreased tubular secretion)

58.  Opthalmic assessment :Retinal detachment.
Retinal ischaemia /infarction Occipital lobe
vasogenic edema . Retinal arteryocclusion
Ultrasonography :
FTS SCREENING .
 Low PAPP-A levels associated with development of pre eclampsia
 uterine artery doppler usg is the best available test for early detection of pre eclampsia
of placental origin .
Doppler study at 11-13 weeks demonstrated that impedance to blood
flow is increased in pregnancies which subsequently develop hypertensive disorders-
correlation with BETA-hcg and PAPP-A .

59.  At 20 weeks , uterine artery doppler is a part of initial evaluation–
disapperance of diastolic notching .
 Umbilical artery doppler provides as assessment of placental-
umbilical circulation .
 An abnormally elevated umbilical artery PI with absent diastolic flow and reversed
diastolic flow – worsening indicator of resistance to blood flow in fetal side of of placental
circulation .
 MCA ( middle cerebral artery )-brain sparing effect – indicated by low PI (pulsality index)
 CP RATIO- cerebroplacental ratio .
 Calculated by MCA(S/D RATIO)/UA (S/D RATIO) .
 If cp ratio >1 – no brain sparing effect .
 If cp ratio<1 - brain sparing effect present

60. • Dietary modification (according to BMI ).
• Low salt diet
• Calcium supplement
• Fish oil supplement
• Exercise
• Antioxidants
• Antithrombotic agents
• Low dose aspirin (50-150 daily)
• Low dose aspirin plus low molecular weight heparin
PREVENTION

61. REST
 In left-lateral position as muchas possible.
 It lessen the effectsof vena caval compression.
 Increases the renal bloodflow→diuresis
 Increases the uterine bloodflow →improvesthe placental perfusion
 Reduces the blood pressure.

62. • According toBMI
Should containadequate amount of daily protein (about 100 gm). Total calorie
approximate1600 cal/day.
Usual salt intakeis permitted.
Fluids need not be restricted

63. MANAGEMENT
• CONTROL OVER HYPERTENSION
• PREVENTION OF CONVULSION
• TREATMENT ARELATED TO COMPLICATION

64. Drug MOA route Action Dose on set
of
action
Side effect
Labetel
olo
(1st
line of
manag
ement)
(c)
Alpha 1
and
non
selectiv
e beta1
blocker
Iv/oral Decrea
sing
PVR
with
little or
no
effect
on
cardiac
output
Initial
i/v
dose-
20 mg
,max-
220
mg/hr.
Oral
dose-
100
mg
i/v
route- 5
mins .
Oral
route-
20 mins
Maternal
hypotension .
Bradycardia
Nifidepi
ne
(C)
CCB Oral Decrea
se PVR
10-20
mg
Max-
120
mg
/day
Can be
repeate
d in 30
minutes
Hedache
Palpitation
Flushing
ANTI- HYPERTENSIVE DRUGS

65. drug MOA Route Action Dose Onset
of
action
s/e
Hydralaz
ine
(c)
Arterial
Vasodilat
i/v Rapid
lowering
of blod
pressure
Act
directly
on
arterial
smooth
muscles
.
5-10 mg Can be
repeated
every 20
mins
Duration
1-4 hrs
Maternal
tachycar
dia .
palpitati
on
Methyldo
pa
(B)
Centrally
Acting
sympath
olytic
i/v Smooth
muscle
relaxant
500-750
mg .
Maintain
1-2 gm
4-6 hrs .
Duration
- 12-24
hrs
Drowsin
ess
Headach
e
Lack of
energy

66.  Magnesium sulfate is effectiveanti- convulsant and is used as neuro prophylaxis.
 During labour and delivery more chances of convulsion to develop ,women with pre
eclampsia and eclampsiausually given mgso4 during labour and for 24 hrs post partum .
 It can be given intravenous route and intra muscular route .
 Mechanism of action–
1)reduced pre synaptic release of neuro transmitter glutamate . 2)blockade of glutamergic N-
methyl –d-aspartate
(NMDA)receptor.
3)improve calcium buffering by mitochondria 4)blockage of calcium entry via voltage
gated channel.
MGSO4

67.  CONTINOUS INTRAVENOUS INFUSION
:(ZUSPAN REGIME)
 GIVE 4 TO 6 gm loading dose of magnesium sulfate diluted in 100 ml iv fluid over 15-
20mins.
 Begin 2g/hr in 100 ml iv maintenance infusion . Some recommends 1 g/dl .
 INTERMITTENT INTRAMUSCULAR INJECTION (PITCHARDS
REGIME)
 10 gm of 50% magnesium sulphate , ½ (5g) injected deeply in upper outer quadrant of
each buttock .
 If convulsion persist after 15 mins , give up 2 gm more intravenously as a 20 % solution
not to exceed 1 gm /min . If the woman is large , upto 4 g may be
given .

68.  Pulse ,BP monitoring 1 hrly.
 Respiratory rate
 urine output 1 hrly
 Deep tendonreflexes
 premonitory signs and symptoms.
 Monitoring for magnesium toxicity.
 Urine output should be at least 30 ml /hr , 400 ml/24 hrs.
 Deep tendon reflex should be present .
 Respiratory rateshould be >14 breaths /min
 Pulse oximetry should be >equal to96%
MONITORING OF ZUSPAN REGIMEN

69. Magnesium toxicity .
 Normal serum magnesium level is 4- 7 meq /L .,4.8to8.4 mg
/dl , 2 to 3.5 mmol/l.
 Magnesium is cleared totally by renal excretion.serum
creatinine levels must be measured to detect GFR .
 Serum magnesium level- at which toxicity.
 8-10 meq/l- patellar reflex absent.
 >10 meq/l –breathing become weakend.
 >12 meq/l – respiratoryarrest /respiratoryparalysis .

70. Antidote of Magnesium toxicity .
1 gm intravenously calcium gluconate or calcium chloride.
 Fetal and neonatal effects .
Magnesium sulphate is protective effect against development of cerebral palsy in
very low birth weight newborn

71.  Eclampsia
 HELLP syndrome .
 Pulmonary oedema
 Reversible cerebral vasoconstriction syndrome .
 Acute renal failure
 Abruption placentae
 Visual disorders .

72. Outpatient management – not severe
features (fetal and maternal assessment)
 FETALASSESSMENT :
Fetal growth assessment every 3-4weeks AFI assessment
weekly.
Antenatal testing 1-2 times per week.
 MATERNAL ASSESSMENT :
Labs weekly .
Atleast 1 visit per week inclinic
Bp and symptoms assessment arerecommended serially

73.  Decision regarding management based on gestationalage
and result from following evaluation.
Maternal- bp recording , proteinuria ,premonitory sign and symptoms ,PIH labs
status.
Fetal- EFW/ANTENATAL TESTING(BPP,NST).
 CANDIDATE FOR EXPECTANT MANAGEMENT : Pre eclampsia without
severe features <37 weeks . controlled blood pressure.
normal biochemical and pre eclampsia marker.

74.  Mode of delivery determined after considering presentation of fetus ,fetal condition ,
maternal condition
, gestational age, laboratory markers .
 Vaginal delivery is generally preferred.

75. WEEKS OF PREGNANCY TIMING OF BIRTH
BEFORE 34 WEEKS continuous survillance unless
there are indication for
blanned birth .off intravenous
mgso4 and a course of
antenatal corticosteroid in line
with nice guidelines on
preterm labor and birth .
FROM 34 TO 36 +6 WEEKS Continous survillance unless
indication for planned early
birth
37 weeks on wards Offer planned birth within 24-
48 hours

76.  Patient should be monitored closely with Bp measurement at least four times aday
for first 2 days followed by once daily for next 2 weeks or more till they are off anti
hypertensive and blood pressure normalize .
 Same anti – hypertensive treatment should be continued in post partum period
.dosage can be reduced once bp falls below 130/80 mmhg .
 Anti – hypertensive can be stopped once bp become normal for
atleast 48 hrs
 Careful for the omnious signs.
 Careful evaluation of intake and output and chest auscultation is necessary in
postpartum period .

77.  Cardivascular –
Chronic hypertension .
Ischaemic heart disease .
Athersclerosis
Coronary arterycalcification
Cardiomyopathy
Thromboembolism
 Neurovascular
Stroke
Retinal detachment
Diabetic retinopathy

78.  Metabolic – Type 2 diabetes
Metabolic syndrome
Dyslipidemia Obesity
 Renal
Glomerulardysfunction
Proteinuria.
 Central nervous system
White matter lesion Cognitive
dysfunction Retinopathy

79.  THANK YOU