This document discusses hypertensive disorders in pregnancy, including their classification, symptoms, pathogenesis, predictors, and management. It classifies hypertensive disorders into gestational hypertension, preeclampsia, eclampsia, preeclampsia superimposed on chronic hypertension, and chronic hypertension. It describes the symptoms and criteria for diagnosing each condition. It discusses the risk factors, preventive measures, pathological alterations, maternal and neonatal complications, and medical management for preeclampsia. The medical management involves monitoring, controlling blood pressure below certain thresholds, and delivering early if certain severe conditions develop.

1. HYPERTENSIVE DISORDERS IN PREGNANCY :
COMPLICATIONS & MANAGEMENT
PRESENTER: DR. SUMIT TYAGI
MODERATOR: DR.MANISH GOYAL

2. CLASSIFICATION
• GESTATIONAL HYPERTENSION ( PIH / TRANSIENT HYPERTENSION )
• PRE-ECLAMPSIA
• ECLAMPSIA
• PREECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION
• CHRONIC HYPERTENSION

3. GESTATIONAL HYPERTENSION
• BP > 140/90 mm Hg for the first-time during pregnancy after 20
weeks but no protein urea. This is transient hypertension and BP
becomes normal by 12 weeks postpartum.

4. PRE-ECLAMPSIA
• Hypertensive syndrome that occurs in pregnant women after 20 weeks’ gestation
consisting of new onset and persistent hypertension defined as systolic pressure >/= 140
mm Hg or diastolic BP >/= 90 mm HG take on at least 2 occasions >4 hours apart with any
of the following :
• URINE ANALYSIS
1. Proteinuria >300 mg/24 hours or persistentm30 mg/dl (1+ on dip stick ) in 2 random urine
samples collected at least 4 hours apart
2. Urine albumin: creatinine ratio > 8mg/dl
• Systemic involvement yes
1. Renal insufficiency : serum creatinine > 1.1 mg/dl
2. Liver involvement : elevated transaminases, right upper quadrant pain
3. Neurological complications
• Hematological complications

5. SEVERE PRE-ECLAMPSIA
• BP > 160/110 mm Hg
• Protein urea : 2 gm/24 hours or 2+ on dipstick
• Serum creatinine : >1.2 mg/dl
• Platelets < 1 lac/mm3
 Microangiopathic hemolysis
 Elevated SGOT/SGPT
 persistent headache or visual disturbances
 persistent epigastric pain due to hepatocellular necrosis, ischemia and oedema
leading to stretch in Glisson’s capsule

6. CHRONIC HYPERTENSION
• BP > 140/90 mmHg Before pregnancy or diagnose before 20 weeks
gestation or hypertension first diagnosed after 20 weeks gestation
and persistent after 12 weeks postpartum

7. Superimposed Preeclampsia on Chronic
Hypertension
• All chronic hypertensive disorders regardless of their cause
predisposed to the development of superimposed Preeclampsia or
Eclampsia
• Preeclampsia is accompanied by proteinuria

8. ECLAMPSIA
• Eclampsia is the occurrence of seizures in women with Pre-Eclampsia
when seizures cannot be attributed to other causes.
• seizures are grand mal type
• May appear before, during or after labour
• May develop more than 48 hours after delivery and may be
encountered up to 10 days postpartum

9. PATHOGENESIS
• Failure of normal invasion of trophoblast cells leads to mal adaptation
of maternal spiral arterioles
• Maladaptation of vessels Can interfere with normal villous
development leading to placental insufficiency and subsequently
hypoxia leading to foetal growth retardation and release of both
vasoconstrictors and vasodilators leading to increased perfusion of
vascular beds with endothelial damage and hypertension
• Vascular construction causes resistance to blood flow and accounts
for the development of arterial hypertension

10. PREDICTORS OF PRE-ECLAMPSIA
• Rollover test : Elevation of 20 mm hg or more in systolic BP after patient assume supine position after lying
lateral recumbent
• Elevated uric acid levels > 5.9 mg/dl
• Hypocalciuria
• Decrease urinary kallikrein excretion
• Increased cellular plasma fibronectin
• coagulation activation : Thrombocytopenia and platelet aggregation appear to be an integral feature of pre-
eclampsia excessive platelet activation has been linked to maternal vasoconstriction, endothelial cell injury
placental infarction and transient renal dysfunction thromboxane A2 is released promoting vasospasm
further platelet aggregation and endothelial cell injury
• Immunological factors : TNF- alpha, Growth factors and interleukins increased
• Placental peptides: Increased corticotropin releasing hormone, ACTIVIN A, INHIBIN A
• Doppler velocimetry studies of the uterine artery : unreliable screening test as sensitivity is 78% with
positive predictive value of 28%

11. Risk factors of Pre-eclampsia
• HIGH RISK FACTORS
• Hypertension during last pregnancy
• Chronic renal disease
• SLE
• Anti-phospholipid syndrome
• Diabetes
• Chronic hypertension

12. Risk factors of Pre-eclampsia
• MODERATE RISK FACTORS
• First pregnancy
• Assisted reproduction
• Age 40 years or more
• Pregnancy interval of more than 10 years
• BMI of 35 kg per metre square or more
• Family history of pre-eclampsia
• Multiple pregnancies
• Vitamin d deficiency
• Low dietary calcium

13. PREVENTIVE MEASURES
• Aspirin 75 mg daily from 12 weeks of gestation till delivery for
patients with 1 high risk factor or >1 moderate risk factors
• Calcium supplementation >1 g daily during pregnancy may reduce
chances in low dietary calcium supplementation
• Adequate rest in 3rd trimester
• Reduction of workload and stress
• Controlled weight loss
• Exercise

14. PATHOLOGICAL ALTERATIONS
• 1. Cardiovascularchanges : Increase in cardiac afterload due to hypertension.
• 2. Haematological changes: Thrombocytopenia (platelet count less than
1,00,000/mm3), microangiopathichemolysis(due to intense vasospasm),decreased
clottingfactors,increasederythrocytedestruction,increasedfibrin degradation
products and deficiency of antithrombin III.
• 3. Endocrine changes: Increase in deoxycorticosteronein third trimesterdue to
conversionfrom plasma progesterone causes retention of sodium.
• 4. Fluid and electrolyte changes: Decreased plasma oncotic pressure which
leads to increased extracellular fluid with associated decrease in intravascular
volume.
• 5. Kidney: Oliguria is a result of reduced renal perfusion and glomerularfiltration.
Plasma uric acid and serum creatinineare elevated.There is proteinuria> 300 mg per 24
hours or more than 1 + on urinary dipstick test.
• Acute renal failure and renalcorticalnecrosis may develop in severe cases

15. PATHOLOGICAL ALTERATIONS
• 6. Liver: Increased liver enzymes. Epigastric and right hypochondriac pain
due to periportal haemorrhagic necrosis, which causeshepatic rupture or
subcapsular hematoma.
• 7. HELLP syndrome: Triad of Haemolysis, elevated liver enzymes and low
platelets.
• 8. Nervous system: Cerebral oedema, hyperaemia, focal thrombosis and
haemorrhage , visual disturbances due to retinal artery vasospasm. Increased
cerebral perfusion pressure may cause severe headaches.
• 9. Uterus and placenta: Incompletetrophoblastic invasion of spiral arteries
causes reduction in diameter of vessels as compared to normal. In
addition, vasospasm decreases placental perfusion leading to Intra Uterine
Growth Retardation

16. MATERNAL COMPLICATIONS
• Intracranial haemorrhage : leading cause of maternal death
• DIC
• Pulmonary oedema
• Congestive heart failure
• Placental abruption
• Acute renal failure
• Liver rupture
• Cerebrovascular accident
• Septic shock

17. NEONATAL COMPLICATIONS
• SHORT TERM COMPLICATION
• OLIGOHYDRAMNIOS
• FETAL GROWTH RETARDATION
• PRETERM BIRTH
• PREMATURITY WITH RESPIRATORY DISTRESS
• LOW APGAR SCORE
• NICU STAY & SMALL FORGE
• MECONIUM ASPIRATION
• INTRACRANIAL HEMORRHAGE
• INTRA UTERINE FETAL DEATH

18. NEONATAL COMPLICATIONS
• LONG TERM COMPLICATIONS
• CEREBRAL PALSY
• LOW IQ
• HEARING LOSS
• VISUAL IMPAIRMENT
• INSULIN RESISTANCE
• DIABETES MELLITUS
• HYPERTENSION
• CAD

19. MANAGEMENT OF PRE-ECLAMPSIA
• MEDICAL MANAGEMENT
• Early prenatal detection and prompt institution of therapy and corrective
measures.
• The timingof prenatal examinations :4 weeks until 28 weeks then every 2 weeks
until 36 weeks and weekly thereafter.
• Hospitalization is considered for women with new-onset hypertension, which is
persistent or worsening or development of proteinuria.
• Detailed systemic examination
• Daily scrutiny of headache,visual disturbance,epigastricpain and rapidweight gain.
• Weighton admissionand every day thereafter.

20. MANAGEMENT OF PRE-ECLAMPSIA
• Weight on admission and every day thereafter.
• Analysis for proteinuria on admission and at least every 2 days thereafter.
• Four hourly blood pressures monitoring in sitting position.
• Measurement of serum creatinine, complete blood count (CBC),
liver enzymes, platelets—frequency determined by the severity of
hypertension.
• Frequent foetal monitoring clinically or by USG.
• Ample but not excessive proteins and calories; and no salt or fluid
restriction in the diet

21. MANAGEMENT OF PRE-ECLAMPSIA
• ACE inhibitors, ARBs and chlorothiazideshave to stop these drugs and change over to other drugs
before they become pregnant as these drugs can cause congenitalmalformations.
• Blood pressure shouldbe controlledto below 160/110 mm Hg to prevent maternalmorbidity,
particularly from intracranial haemorrhage, encephalopathy, myocardial ischemia and
failure. Oral antihypertensiveinclude the following drugs:
• Beta blockers: Labetalol (300 mg to 2400 mg/day). combinedα and β blocker.50 mg over 1
minute f/b 20 mg/hr which can be increased by 20 mg every 20 min to a maximumdose of 160 mg
per hour.
• Methyldopa : It is α methylanalogue of dopa, the precursor of dopamine (DA) and NA. The α
methyl-NAis a selectiveα2 agonist formed in brain from methyldopaand acts oncentral α2
receptors to decrease efferent sympathetic activity.Antihypertensive effect develops over 4–6
hours and lasts 12–24 hours. Dose: 0.25–0.5 g BD–QID oral (max 4 g/day).

22. MANAGEMENT OF PRE-ECLAMPSIA
Nifedipine : Calcium channel blocker, it decreases peripheral vascular
resistance without compromisingcardiac output. Dose is 10 to 20 mg every 4 to 6
hourly.
Hydralazine : 5-10 mg slow iv injection or 200-300 mcg/min then 50-150 mcg/min
for maintainence control. Caution : acute porphyria, cor-pulmonale, idiopathic SLE,
severe tachycardia. Patient may need Fluid bolus along with titration of
antihypertensives.
SODIUM NITROPRUSIDE : use in refractory cases.
Alternative anti HTN agents : oral clonidine, GTN infusion
The target of blood pressure control in uncomplicated chronic hypertension is to
keep blood pressure less than 150/100 mm Hg. Do not lower diastolicblood pressure
below 80 mm Hg. In pregnant women with target-organdamage secondary to chronic
hypertension; aim is to keep blood pressure lower than 140/90 mm Hg.

23. CONDITIONS MANDATE FOR IMMEDIATE
DELIVERY
• Severe hypertension that persists after 24 to 48 hours
of treatment
• Progressive thrombocytopenia
• Liver dysfunction
• Progressive renal dysfunction
• Premonitory signs of eclampsia
• Evidence of foetal jeopardy
• Persistent headache or other neurologic sequelae of pre-
eclampsis

24. • Definitive treatment for pre-eclampsia and eclampsia is termination
of pregnancy.
• In uncomplicated pre-eclampsia, if women is near term, pregnancy is
allowed to continue under the close observation until the cervix is
more suitable for induction.
• In severe pre-eclampsia, before 34 weeks of gestation glucocorticoids
may be tried for lung maturity : betamethasone 12 mg IM 24 HOURS
apart in women between 24 and 34 weeks.

25. SIGNS OF IMPENDING ECLAMPSIA
• Headache
• Visual disturbance, such as blurring or flashing before the eyes
• Epigastric pain
• Oliguria
• Vomiting
• Sudden swelling of the face, hands or feet

26. Measures taken to prevent seizures
• Collaborative Eclampsia trial regimen for administration of MgSO4 :-
• ZUSPAN REGIMEN :-
• LOADING DOSE : 4-5 gm IV over 5 minutes followed by
• MAINTAINANCE DOSE : an infusion of 1 gm/hr maintained for 24 hours.
• If the woman had an eclamptic seizure, the infusion should be continued
foe 24 hours after the last seizure and should not be discontinued during
delivery.
• For recurrent seizures, further 2-4 gm MgSO4 given over 5 minutes.
• Measure serum Mg levels 4-6 hourly & maintain in between 4-7 meq per
litre.

27. • PRITCHARD REGIMEN :-
• Loading dose : 4 gm of 20 % MgSO4 slow IV followed by 5 gm of 50 %
IM in each buttock , total dose : 14 gm.
• Maintainance dose : 5 gm 50 % IM in alternate buttock 4 hourly.
• SIBAI REGIMEN :-
• LOADING DOSE : 6 gm MgSO4 IV over 20 minutes
• MAINTAINANCE DOSE: 2 gm/hour IV infusion

28. Monitoring & Management of MgSO4 Toxicity
• In therapeutic doses magnesium sulphate is associated with muscle weakness
due to decrease in the amount of acetylcholine released at motor nerve endings,
decreased action of acetylcholine on the motor end plate and reduction of
excitability of motor fibre membrane.
• Therefore, it increases the sensitivity of the mother to both the depolarizing
as well as non-depolarizing muscle relaxants.
• When a patient is started on MgSO4
• it is necessary to monitor:
• Patellar reflex (disappears when plasma magnesium level reaches 10 mEq/L;
warning impending Mg toxicity)
• Rate and depth of respiration (depressed at level above 10 mEq/L, respiratory
paralysis and arrest occurs above 12 mEq/L)

29. Monitoring & Management of MgSO4 Toxicity
• Urine output (Mg is cleared totally by renal excretion, when there is renal
insufficiency, plasma magnesium level needs to be checked 4-6 hourly and
dosage adjusted accordingly).
• Uterine effects: In high concentration MgSO4 depresses myometrial contractility
secondary to inhibition of intracellular free Ca++ concentration in the uterine cell
(seen at serum Mg level of 8–10 mEq/L).
• Neonatal effects: Magnesium crosses the placenta to achieve equilibrium in
foetal serum. Magnesium sulphate is associated with a minimal risk
of intracranial bleed and irregular bone deposits. It can cause a transient
reversible change in foetal heart rate and should not be considered as a sign of
foetal distress. The neonate may be depressed only if there is
severe hypermagnesemia at delivery.

30. Treatment
• Withhold MgSO4
• Administer Calcium gluconate, 1 g intravenously.
• For severe respiratory depression and arrest, prompt tracheal intubation and
mechanical ventilation is life-saving

31. Management of a patient with eclampsia on MgSO4 with
foetal distress who is posted for emergency LSCS
• Aspiration prophylaxis :-
• Pre-induction administration of nonparticulate antacid such as 0.3 M sodium citrate, 30 mL.
• Intravenous administration of histamine receptor blocking agent 40 minutes before induction. Eg
Ranitidine 100 mg
• Administration of metoclopramide 4 mg to decrease gastric volume 30–60 minutes before induction.
• Pre-oxygenation and denitrogenation with 100% oxygen over 3 minutes is preferred technique; however, if
not feasible; patient can be advised to take 8 vital capacity breaths of 100% oxygen in one minute.
• If blood pressure is high, rapid control of blood pressure can be achieved by:
• Hydralazine (5 mg IV aliquots up to a maximum of 20 mg)
• Labetalol (5–10 mg IV every 10 min)
• Oral nifedipine (sublingual nifedipine can cause rapid changes in placental circulation which may
compromise foetal condition)
• In resistant cases of Hypertension, sodium nitroprusside and glyceryl trinitrate can be used with
continuous arterial BP monitoring.

32. Management of a patient with eclampsia on MgSO4 with
foetal distress who is posted for emergency LSCS
• Crystalloid fluid bolus of 500 ml to prevent sudden hypotension
• CVP is indicated in patient with persistent oliguria and presence of pulmonary oedema for
fluid management in antepartum and postpartum period
• Anticipate difficult airway and keep small size tubes, gum elastic bougie, laryngeal mask
airway and difficult airway set ready
• plan for attenuation of response to laryngoscopy
• Crash induction with thiopentone sodium or propofol and succinylcholine after checking
the ability to ventilate if BP is high
• Use atracurium for maintenance of relaxation it is preferable to use a peripheral nerve
stimulator in intraoperative period.
• Use 2/3rd of the Mac value of inhalational agent to ensure adequate depth of
anaesthesia
• Watch for hemodynamic changes during delivery and removal of placenta.
• continue magnesium sulphate during intraoperative and post operative.

33. HELLP SYNDROME
• HELLP syndrome is a severe form of pre-eclampsia characterizedby:
• H-Hemolysis (abnormalperipheralblood smear, and an increasedbilirubinlevel of 1.2 mg/dL or
greater)
• EL - elevated liverenzymes (SGOT > 70 U/L, LDH > 600U/L)
• LP - low platelets (< 1, 00,000/mm
• It can occur antepartum or postpartum.
• Delivery represents the only definitive treatment of HELLP syndrome.
• Patient with HELLP syndrome have a high incidenceof seriousmaternal complicationsincluding
disseminatedintravascular coagulation, placentalabruption,need for bloodtransfusion, pleural
effusion, acute renal failure, and wound infection.
• After deliveryof placenta,recovery from HELLP syndrome can be expected to start
within 24–48 hours. These patients shouldbe monitored in the ICU or HDU. Steroids have no
role in management of HELLP syndrome

34. NEED FOR PLATELET TRANSFUSION IN HELLP
SYNDROME
• For a platelet count of 20K to 49K per mm3 with hemolysis, elevated
liver enzymes and low platelet syndrome, platelet transfusion is
recommended before LSCS.
• For a platelet count of 20K to 49K per mm3 with hemolysis, elevated
liver enzymes and low platelet syndrome, platelet transfusion should
be considered prior to vaginal delivery if there is :
1. Excessive active bleeding
2. Known platelet dysfunction
3. Rapidly falling platelet count
4. coagulopathy

35. Thank you