Hypertension in pregnancy By Dr ahmad

1. Hypertension in pregnancy
AHMAD ALI
KHAN
08-014
BATCH I

2. Hypertension :
 High blood pressure is said to be present if bp is
persistently at or above 140/90 mmHg.

3. May belong to one of the following
 Gestational hypertension (occurring solely because of pregnancy)
 Chronic hypertension (hypertensive from before the pregnancy)
 Chronic hypertension (incidentally becoming apparent first time in
pregnancy

4. Gestational hypertension
 Pregnancy induced hypertension
 (Gestational hypertension is usually defined as having a blood pressure higher
than 140/90mm hg without the presence of protein in the urine and diagnosed
after 20 weeks of gestation)
 Pre eclampsia
 (Pre-eclampsia is gestational hypertension (blood pressure greater than
140/90) plus proteinuria (>300 mg of protein in a 24-hour urine sample).
Severe preeclampsia involves a blood pressure greater than 160/110, with
additional medical signs and symptoms)
 Eclampsia
 (This is when tonic-clonic seizures appear in a pregnant woman with high blood
pressure and proteinuria)

5. Pathophysiology
 Disease of pregnancy.
 Exact aetiology is unknown
 According to the current concept it is a disease of wide spread
endothelial damage
 Occurs from placental pathology and its signs are due to secondary
involvement of other organ system

6. PRIMARY PLACENTAL PATHOLOGY
 two lesions have been identified
1- Lack of secondary wave of trophoblastic invasion:
 Normally the spiral arteries undergo physiological changes
these are
 cytotrophoblast of placenta that breaks down the endothelium, internal
elastic lamina& muscular coat of vessel
 these are replaced by fibrinoid converting the vessel to sinusoids.

7.  In pre eclampsia only half to 2/3rd of arteries undergo these changes.
 This leads to restriction in placental blood flow
 which becomes evident with advancing gestation.
 More over they remain sensitive to vasomotor stimulus.

9. 2-Acute atherosis :
 The second lesion is called acute atherosis. ,which is characterized by
aggregates of fibrin, platelets & lipid laden macrophages
 It is seen in spiral arteries the basal arteries and the decidua parietalis
.
 These lasions partly or completely block the Vessels
 leading to ischaemia of fetal placenta giving rise to infarcts patchy
necrosis & intracellular damage to syncytiotrophoblast

10. Secondary influences :
 Maternal effects:
 the abnormal placentation& production of products of inflammation effect wide range
of organs
 Maternal organ involvement :
 Cardiovascular system :
(rise in bp because of ↑ vascular resistance & may lead to severe hypertension)
 Renal system:
 first tubular dysfunction leading to hyperurecemia
 then gromerular dysfunction leading to proteinuria exceeding 5 grams /24hrz.
 Proteinuria leads to hypoalbumenaemia
 this leads to lower colloid osmotic pressure & generalized edema,ascites,pleural
effusion pulmonary & cerebral edema .

11.  Liver:
 periportal and subcapsular haemorrhage , periportal fibrin deposition
 areas of infarction and necrosis
 Excessive haemorrhage may lead to rupture shock and maternal death .
 Blood :
 activation of coagulation and fibrinolytic system.
 In severe cases it may lead to DIC & microangiopathic haemolytic anemia
 HELLP syndrome :
 (haemolysis ,elevated liver enzymes and low platelet count)
 Occurs in later part of pregnancy.
 The common symptoms are epigastric or right hypochondral pain, nausea ,
 vomiting and visual disturbance
 Respiratory system :
 pulmonary edema & adult respiratory distress syndrome

12. Fetal effects :
Malnourished
Growth restriction
May die in utero

13.  Risk factors : May be maternal & fetal
 MATERNAL :
 Primigravidity
 Age less than 20 & more than 35
Previous pre eclampsia & its family history
Obesity
Pregnancy with a new partner
Chronic hypertension
Diabetes
Chronic renal disease
Hypothyroidism
Migrane

14. Fetal / placental factors :
Large placenta
Prolonged pregnancy
Multiple pregnancy
Hydatidiform mole
Chromosome anomaly

15. Management :
 The women is hypertensive when the bp is persistenly high at two consective readings when taken 4 or more hours
apart.
 To determine the type of hypertension & where it is preeclampsia the extict of the disease
 The steps are:
 History
 Examination
 Investigations (maternal & fetal)
 maternal
↓
Proteinuria ( ↑300mg/24 hrs)
Renal function test (urea ↑7mmol/l & creatinine ↑100mmol/l indicate severe disease)
LFTs
Coagulation profile (platelet count, fibrinogen level, thrombin time & fibrinogen
degradation products)
 Fetal → ultrasound

16.  FURTHER MANAGEMENT :
Hypertension alone
Hypertension with proteinuria
Hypertension with proteinuria and symptoms

17. Hypertension alone :
focus on antihypertensive therapy and salt intake
↓
Antihypertensive therapy
↓ ↓
emergency long term antihypertensives
↓ ↓
Hydralazine Methyl dopa
Nefidipine Diuretics
Labetalol etc
 Salt intake :
Should consume salt to taste but refrain from added salt

18.  Hypertension with proteinuria:
 should be admitted to hosp on the same day
↓
Management in hospital
 Daily observations ( urea, symptoms, kick count
chart etc )
Twice week observations ( cardiotocography twice a
week)
Weekly observations (uric acid, urea, creatinine, LFT,
ultra sound at 2 weeks interval)

19.  Conservative management should be culminated in the favour of delivery when:
 Pregnancy reaches term
 Maternal bp Cannot be controlled
 Platelet count falls below 50 ×109
/L
 Creatinine rises above 120mmol/L
 Women develops symptoms
 Evidence of liver damage
 Urinary protein loss exceeds 3g/24 hrs
 Fetus is seriously compromised

20.  Hypertension with proteinuria & symptoms (fulminating preeclampsia)
:
↓
Management on following lines
 Hospital admission
 High level of care
 Fluid management ( to avoid oliguria)
 Drug therapy (prophylactic anti convulsants like magnesium
sulphate & antihypertensives)

21.  Management of labour & delivery :
 Mode of delivery
→ vaginal delivery is the route of choice
→ pre eclampsia at times makes vaginal delivery risky
→ while managing pre eclampsia one should have low
threshold for c sec
 Induction of labour
→ spontaneous labour carries best outcome
→ prostaglandins must be used with caution & patient
must be watched
properly

22.  Oxytocin
→used for induction & augmentation of labour
→may lead to myocardial failure in patients with compromised
cardiac function
 Fetal monitoring
 Intstrumental delivery (not an indication but can be used)
 Caesarean section
→ choice of anesthesia is important as GA poses specific problems in
pre eclamptic patients.

23. Management of eclampsia :
 Two phases :
 General measures
 Specific measures
 General measures :
 Placed flat in the left lateral position & tight clothes are loosened
 Air ways , breathing & circulation is maintained
 IV line is taken preferably with a wide bore needle on both sdes
 Foley,s catheter is passed for comfort of patient & measuring output

24.  Specific measures :
Anticonvulsant drugs ( Diazepam is drug of choice,Mg sulpate &
phenytoin to prevent recurrence
 Diazepam ( 10mg IV initially. Dose is repeated with every fit
to a total of 50mg)
 Magnesium sulphate
↓
Loading dose of 4g given IV over 4 minutes & 10g IM(5g each
buttock). Dose of 2g IV over 2 min is repeated if convulsions
persist after 15 min . followed by maintainence dose of 5g IM
every 4 hrs on alternate buttock
 Phenytoin ( IV dose of 18mg/kg at rate of 50 mg /min

25. Antihypertensive therapy
 IV labetalol & Hydralazine
Dilivery :
After seizures & hypertension are controlled fetal well
being can be assessed & delivery is made
C section is recommended in the following
↓
 all deeply unconscious patients until delivery is imminent
 uncooperative patients due to restlessness
 vaginal delivery is unlikely to occur within 6-8 hrs of
first fit
 obstetrical indication for C section
 fetal distress

26. Thank you !!!