HYPERTENSIVE DISORDERS

IN PREGNANCY
Presented by,
Monisha U

INCIDENCE

Hypertensive disorders of pregnancy in India-5.38%

Preeclampsia-44%
Eclampsia-40%
HEELP syndrome-7%

DEFINITION OF HYPERTENSION IN PREGNANCY

Hypertension in pregnancy is diagnosed either from an

absolute rise in blood pressure or from a relative rise above
measurements obtained at booking.
The convention for absolute value is a systolic>140 mm Hg
or a diastolic > 90 mm Hg.
The definition for a relative rise in blood pressure incorporates
either a rise in systolic pressure of > 30 mm Hg or rise in
diastolic pressure of >15 mm Hg above blood pressure at
booking.
Blood pressure must be elevated on at least two occasions and
measurements should be made with the woman seated and
using the appropriate cuff size.

NORMAL PHYSIOLOGICAL CHANGE IN BP DURING PREGNANCY

First trimester there is a fall in blood pressure

Blood pressure continues to fall until 22-24
weeks
Gradual increase in blood pressure until term
when pre-pregnancy levels are attained
Immediately after delivery blood pressure
usually falls, then increases

CLASSIFICATION OF
HYPERTENSION IN PREGNANCY

PRE-ECLAMPSIA
INCIDENCE
The incidence of pre-eclampsia in
hospital practice varies widely from
5-15%.
The incidence in primigravidae is
about 10% and in multigravidae 5%.

DEFINITION
Pre-eclampsia is a multisystem disorder of
unknown etiology characterized by
development of hypertension to the extent of
140/90 mm Hg or more with proteinuria after
the 20th week in a previously normotensive
and nonproteinuric woman.

DIAGNOSTIC CRITERIA FOR

PREECLAMPSIA
Hypertension
Edema
Protenuria

RISK FACTORS FOR PREECLAMPSIA

Primigravida : Young or elderly

Family history : (Hypertension, pre-eclampsia).
Placental abnormalities :
Hyperplacentosis : excessive exposure to chorionic villi
(molar pregnancy twins, diabetes)
Placental ischaemia.
Obesity : BMI > 35 kg/M2, Insulin resistance.
Pre-existing vascular disease.
New paternity.
Thrombophilias (anti phospholipid syndrome, protein C, S
deficiency, Factor V Leiden

Etiopathological factors for pre-elampsia

.

Failure of trophoblast invasion (abnormal

placentation)
Vascular endothelial damage.
Inflammatory mediators (cytokines).
Immunological intolerance between maternal and
fetal tissues.
Coagulation abnormalities .
Increased oxygen free radicals.
Genetic predisposition (polygenic disorder).
Dietary deficiency or excess.

ETIOPATHOGENESIS OF PRE-ECLAMPSIA

HYPERTENSION
EDEMA
PROTENURIA

Hypertension
Imbalance in different components of prostaglandins
Increased vascular sensitivity to the pressor agent
angiotensin-II.
Nitric oxide
Endothelin-1
Inflammatory mediators
Abnormal lipid metabolism
Imbalance of angiogenic and antiangiogenic proteins in
placental vascular bed
Others

Edema

Increased oxidative stress

Endothelial injury
Increased capillary permeability
Leaky capillaries

Protenuria
Spasm of the afferent glomerular
arteriole
Anoxic changes in the epithelium o
Increased capillary permiability
Incresed leakage of proteins

PATHOPHYSIOLOGY

Uteroplacental bed
Villi
Intervillous circulation
Kidney
Blood vessels
Liver
HELLP Syndrome

CLINICAL TYPES
Mild :
This includes cases of sustained rise of blood pressure of more than 140/90 mm Hg but
less than 160 mm Hg systolic or 110 mm Hg diastolic without significant proteinuria.
Severe :
(1)A persistent systolic blood pressure of > 160 mm Hg or diastolic pressure of > 110 mm Hg.
(2) Protein excretion of > 5 gm/24 hrs.
(3) Oliguria (< 400 ml/24 hr).
(4) Platelet count < 100,000/mrr
(5) HELLP syndrome
(6) Cerebral or visual disturbances.
(7) Persistent severe epigastric pain.
(8) Retinal haemorrhages, exudates or papilledema.
(9) Intrauterine growth restriction of the fetus.
(10) Pulmonary oedema.

CLINICAL FEATURES
ONSET :
The onset is usually insidious and the syndrome runs a slow
course.
On rare occasion, however, the onset becomes acute and follows
a rapid course.
SYMPTOMS:
Pre-eclampsia is principally a syndrome of signs and when
symptoms appear, it is usually late.
Mild symptoms :
Slight swelling over the ankles which persists on rising from the
bed in the morning or tightness of the ring on the finger is the
early manifestation of pre and even the whole body.

Alarming symptoms
(1) Headache
(2) Disturbed sleep
(3) Diminished urinary output
(4) Epigastric pain
(5) Eye symptoms

SIGNS

Abnormal weight gain

Rise of blood pressure
Oedema
Pulmonary oedema due to leaky
capillaries and low oncotic pressure.
Abdominal examination may reveal
evidences of chronic placental
insufficiency such as scanty liquor or
growth retardation of the fetus.

INVESTIGATIONS
Urine
Proteinuria is the last feature of preeclampsia .
It may be trace or at times copious that
urine becomes solid on boiling (10-15
gm/litre).
There may be few hyaline casts, epithelial
cells or even few red cells.
24 hours urine collection for protein
measurement is done.

Ophthalmoscopic examination :
In severe cases there may be retinal
oedema,
constriction of the arterioles,
alteration of normal ratio of vein :
arteriole diameter from 3 : 2 to 3 :1
and nicking of the veins where
crossed by the arterioles. There may
be haemorrhage.

 Blood values :
The blood changes are not specific and often
inconsistent.
A serum uric acid level (biochemical marker of
pre-eclampsia) of more than 4.5 mg/dl indicates
the presence of pre-eclampsia.
Blood urea level remains normal or slightly raised.
Serum creatinine level may be more than 1 mg/dl.
There may be thrombocytopenia and abnormal
coagulation profile of varying degrees.
Hepatic enzyme levels may be increased.

 Antenatal fetal monitoring:

Antenatal fetal well being
assessment is done by
clinical examination,
daily fetal kick count,
ultrasonography for fetal growth and
liquor pockets, cardio-tocography,
umbilical artery flow velocimetry and
biophysical profile.

COMPLICATIONS OF PRE-ECLAMPSIA

IMMEDIATE :
Maternal
During pregnancy:
(a) Eclampsia (2%) more in acute than in subacute
cases
(b) Accidental haemorrhage
(c) Oliguria and anuria
(d) Dimness of vision and-even blindness
(e) Preterm labour
(f) HELLP syndrome
(g) Cerebral haemorrhage
(h) Acute respiratory distress syndrome (ARDS).

 During labour :
(a) Eclampsia
(b) Postpartum haemorrhage may be related with coagulation
failure.
Puerperium :
(a) Eclampsia usually occurs within 48 hours
(b) ShockPuerperal vasomotor collapse is associated with
reduced concentration of sodium and chloride due to sudden fall
in corticosteroid level
(c) Sepsis due to increased incidence of induction, operative
interference and low vitality.
Fetal:
The fetal risk is related to the severity of pre-eclampsia,
duration of the disease and degree of proteinuria.

 The following hazards may occur,

(a) Intrauterine death due to spasm of uteroplacental circulation leading to accidental
haemorrhage or acute red infarction
(b) Intra-uterine growth restriction due -to
chronic placental insufficiency
(c) Asphyxia
(d) Prematurity either due to spontaneous
preterm onset of labour or due to preterm
induction.

REMOTE:
Residual hypertension
Recurrent pre-eclampsia
Chronic renal disease
Risk of placental abruption

SCREENING TESTS FOR PREDICTION AND PREVENTION OF PREECLAMPSIA

Doppler ultrasound
i Presence of diastolic notch
Absence of end diastolic
frequencies
Average mean arterial
pressure (MAP)
Fetal DNA
Roll over test:

PROPHYLACTIC MEASURES FOR PREVENTION OF PRE-ECLAMPSIA

Regular antenatal check up

Antithrombotic agents
Heparin or low molecular weight heparin .
Calcium supplementation (2 gm per day) .
Antioxidants, vitamins E and C and
nutritional supplementation with magnesium,
zinc, fish oil and low salt diet have been tried but
are of limited benefit.
Balanced diet rich in protein may reduce the
risk

MANAGEMENT OF PREECLAMPSIA
Objectives are:
(1) To stabilise hypertension and to
prevent its progression to severe preeclampsia
(2) To prevent the complications
(3) To prevent eclampsia
(4) Delivery of a healthy baby in
optimal time.
(5) Restoration of the health of the
mother in puerperium.

 Hospital or home treatment

Hospital management
Rest:
Diet:
Diuretics:
Antihypertensives :

FIRST LINE MANAGEMENT

1.Methyldopa
SECOND LINE AGENTS
1.Nifedipine
3.Oral Hydralazine
THIRD LINE AGENTS
4.Alpha and Beta adrenergic blockers
5.Thiazide Diuretics

PROGRESS CHART
Daily clinical evaluation for any symptoms(eg. Head
ache, epigastric pain, visual disturbances, oliguria)
Blood pressure: at least 4 times a day.
State of edema and daily weight record.
Fluid intake and urinary output.
Urine examination for protein daily and if present, to
estimate it amount in 24 hours urine
Blood for haematocrit, platelet count, uric acid,
creatinine and liver function test at least once a week .
Ophthalmoscopic examination on admission and to be
repeated, if necessary
Fetal wellbeing assessment.

DURATION OF
TREATMENT

(1) severity of pre-eclampsia,

(2) duration of pregnancy and
(3) response to treatment and
(4) condition of the cervix.

 METHODS OF DELIVERY :
Induction of labour
Caesarean section

 Induction of labour
Indications :

It is indeed difficult to lay down hard and fast rules for the indications
for induction.
(1) Aggravation of the pre-eclamptic features in spite of medical treatment
and/or appearance of newer symptoms such as epigastric pain
(2) Hypertension persists in spite of medical treatment with pregnancy
reaching 37 weeks or more (3) Acute fulminating pre-eclampsia irrespective of
the period of gestation
(4) Tendency of pregnancy to overrun the expected date.
Methods :

If the cervix is ripe, surgical induction by low rupture of the

membranes is the method of choice. Oxytocin infusion may be added. If the
cervix is unripe, prostaglandin (PGE2) gel 500 ug intracervical or 1-2 mg in
the posterior fornix is inserted to make the cervix ripe when low rupture of the
membranes can be performed. In severe pre-eclampsia, antihypertensive
drugs should be used during induction.

 Caesarean section
Indications :
(1) When an urgent termination is indicated and the
cervix is unfavourable (unripe and closed)
(2) Severe pre-eclampsia with a tendency to prolong
the induction delivery interval
(3) Associated complicating factors such as elderly
primigravidae, contracted pelvis, malpresentation etc.
The operation should be done by an experienced
surgeon with the help of an expert anaesthetist.
Epidural anaesthesia is preferred unless there is
coagulopathy.

MANAGEMENT DURING LABOUR :

The patient should be in bed.
Antihypertensive drugs are given if the blood pressure
becomes high.
Blood pressure and urinary output are to be noted frequently
so as to detect imminent eclampsia.
Prophylactic MgS04 is started when Systolic BP > 160 Diastolic
> 110, MAP > 125 mm Hg.
Careful monitoring of the fetal well being is mandatory.
Labour duration is curtailed by low rupture of the membranes
in the first stage; and forceps or ventouse in second stage.
Intravenous ergometrine following the delivery of the anterior
shoulder is withheld as it cause further rise of blood pressure.


PUERPERIUM :
The patient is to be watched closely for at least 48 hours, the period during
which convulsion usually occur.
Antihypertensive drug treatment should be continued if the BP is high
(systolic > 150 mmH ; -diastolic > 100 mmHg).
Oral nifedipine 10 mg at every 6 hours is given until BP remains below the
hypertensive levels for at least 48 hours.
Oral frusemide 20 mg a day for 5 days is also found to improve recovery and
reduce the need of antihypertensive drugs in severe pre-eclampsia
. Magnesium sulphate (for at least 24 hours and antihypertensive drugs may
be needed in women with severe hypertension and symptoms of acuft
fulminant pre-eclampsia during the postpartum period.
The patient is to be kept in the hospital, till the blood pressure is brought
down to a safe level and proteinuria disappears.
In breastfeeding women, labetalol, nifedipine or enalapril may used on
discharge. Methyldopa is avoided due to the risks of postpartum depression.

ACUTE FULMINANT PREECLAMPSIA

It is a clinical entity where the onset of
the preeclamptic manifestations is
acute, occurring de novo or there is
rapid deterioration in an established
case of preeclampsia with severe
hypertension over a short period of
time. There is a constant threat of
convulsion, cerebral hemorrhage,
cardiac failure or placental abruption.
All the features of severe preeclampsia
are intensified .

TREATMENT
Detected at home
the patient should be adequately
sedated by midazolam 1-2 mg IV, may
be repeated in 5-10 minutes time or
diazepam 10 mg IV (slow). She should
be shifted as gently as possible, with
an attendant doctor or a midwife, to
tackle the fit, if it occurs during the
journey to the hospital

 In the hospital, the patient is to be kept in eclampsia

room under close supervision. Prophylactic
anticonvulsant therapy is to be instituted urgently.
Administration of magnesium sulfate either IM or IV
regimen in a dose schedule as mentioned in the
treatment of eclampsia is recommended (MAGPIE Trial2002). The blood pressure is to be stabilized by
antihypertensive drugs given parenterally . First-line
antihypertensives are: a) Labetalol (IV) or b) Hydralazine
(IV). Response to treatment should be watched carefully
noting frequently the blood pressure, urinary output,
proteinuria and hematological parameters .

 Obstetric management:
As there is a constant threat of eclampsia, maternal
interest should always be considered. In cases with
pregnancy beyond 37th completed weeks or where the
condition fails to improve within a reasonable period
(say 6-8 hours), delivery should be seriously considered
irrespective of period of gestation (see table below).
Termination is done either by low rupture of the
membranes aided by oxytocin infusion or by Cesarean
section depending upon the severity of the condition
and state of the cervix. PGE2 gel may help in cervical
ripening. Corticosteroid is given if pregnancy is < 34
weeks.

ECLAMPSIA
DEFINITION
Pre eclampsia complicated with
convulsion and coma is called
eclampsia.
INCIDENCE
Eclampsia occurs antepartum in 3545%, intrapartum in 15-20% and post
partum in 35-45% of the cases.

 PATHOPHYSIOLOGY

Eclampsia is the severe form of pre

eclampsia, the biochemical changes
are similar although intensified than
those of pre eclampsia

 CAUSES OF CONVULSION
The causes of cerebral irritation is not clear.
The irritation may be provoked by:
1)Anoxia spasm of cerebral vessels
increased cerebro vascular resistance
Fall in cerebral oxygen conception
anoxia
2)Cerebral edema
3)cerebral disrrhythmia

 ONSET OF FITS
AntepartumFits occurs before the
onset of labour -50%
Intrapartum(30%)- Fits occurs first
time during the first stage of labour
Postpartum(20%)-Fits occurs for the
first time in puerperium usually
within 48 hours of delivery.

PHASES/CLINICAL FEATURES

The typical eclamptic seizure is described in four phases:

Initial prodromal phase
There may be an aura , followed by convulsive movements that begin around the mouth.

Tonic phase

The entire body becomes rigid, the face becomes contorted. The arms are flexed
and the fists are clenched, respiration ceases, this phase lasts for 15 to 20sec.
Clonic phase

Jerky movements then appear starting from the facial muscles to involve the
entire body, there is frothing of the sputum at the mouth. The patient is prone to injury
and may often be cyanosed. Duration is approximately 1 min.
Recovery phase

The movements slowly subside, stertorous respiration then resumes and the
patient passes into a coma of variable duration.

 DIAGNOSIS

The diagnosis of eclampsia is

usually clear when women present with
seizures, hypertension and proteinuria.the
presence of hemoconcentration, elevated
liver enzymes, elevated LDH and
thrombocytopenia help to establish the
correct diagnosis when high bloodpressure
and proteinuria are not present.

MANAGEMENT
PREDICTION AND PREVENTION

Use of antihypertensive drugs

,prophylactic anticonvulsant therapy
and timely delivery are important
steps
Close monitoring during labour and
24 hours postpartum is also
important in prevention of
eclampsia..Magpie trial showed
prophylactic use of magnesium
sulphate lowers the risk of

FIRSTAID TREATMENT OUTSIDE HOSPITAL

Important steps in management are
All materal records and a detailed summary should be sent with
the patient
BP should be stabilized and convulsions should be arrested
Magnesium sulphate(4 gm iv loading dose with 10 gm IM) is
given.
Labetalol 20 mg is given to control hypertension
Diuretics is given to controll pulmonary edema
Diazepam if used should be given 5 mg slowely over 1 minute
period to avoid apnea or cardiac arrest
One medical personnel or trained midwife should accompany
the patient in the ambulance equipped to prevent
injury,recurrent fits and to clear air passage

THE PRINCIPLES OF MANAGEMENT

Maintain airway breathing and circulation

Oxygen administration
Arrest convulsions
Ventilatory support
Prevention of injury
Hemodynamic stabilization
Organize investigations
Deliver by 6-8 hours
Prevention of complications
Post partum care

GENERAL MANAGEMENT (MEDICAL AND NURSING)

*Supportive care:
(i) to prevent serious maternal injury
from fall,
(ii) prevent aspiration,
(iii) to maintain airway and
(iv) to ensure oxygenation.

 Detailed history is to be taken from the relatives.

Examination:

Once the patient is stabilized, a thorough but quick

general, abdominal and vaginal examinations are made.
Monitoring:

Half hourly pulse, respiration rate and blood

pressure
Fluid balance:
Antibiotic:

SPECIFIC MANAGEMENT
Anticonvulsant regime:
Magnesium sulfate is the drug
of choice

 Other regimens are:

(1) Lytic cocktail (Menon1961) using chlorpromazine,
promethazine and pethidine.
(2) Diazepam (Lean) and
(3) Phenytoin. Compared to other regimes,
magnesium sulfate has got the following
benefits:
(i) it controls fits effectively without any depression
effect to the mother or the infant,
(ii) reduced risk of recurrent convulsions (9%)
(iii) significantly reduced maternal death rate (3%)
and (iv) reduced perinatal mortality rate.

 Antihypertensives and diuretics;

if the blood pressure remaps more than 160/110 mm Hg,
antihypertensive drugs should be administered.
First line of antihypertenOve drugs are: labetalol and hydralazine
(ACOG-2011).
Target level of BP is SBP; 140-160 mm Hg and D 90-100 mm Hg.
Labetalol 20 mg IV is given.
Repeat doses may be needed after an interval of 10 minute.
Alternatively hydralazine 5 or 10 mg IV is given.
Repeat dose may be needed if no response occursa.icr 20 minutes
time.
Presence of pulmonary edema requires diuretics.
In such cases, the potent one (furosemide) should be administered
in doses of 20-40 mg intravenously and to be repeated at intervals.

 Management during fit:

(a) In the premonitory stage, a mouth gag is
placed in between the tecih to prevent tongue
bite and should be removed after the clonic
phase is over,
(b) The air passage is to be cleared off the
mucus with a mucus sucker. The patient's head is
to be turned to one side and the piL;:w is taken
off. Raising the foot end of the bed, facilitates
postural drainage of the upper respiratory tract.
(c)Oxygen is given until cyanosis disappears.

 INDICATIONS FOR INTUBATION

Patient remains unconscious in post
seizure period
Signs of aspiration
Persistent hypoxia
Seizure are not controlled

Treatment of complications;
Prophylactic use of antibiotics markedly reduces the complications like
pulmonary and puerperal infection.
Pulmonary edema; Furosemide 40 mg IV followed by 20 g of mannitol IV
reduces pulmonary edema and also prevents adult respiratory distress
syndrome.Pulse oximeteris very useful to monitor such a
patient.Aspiration of the mucus from the tracheobronchial tree by a
suction apparatus is done.
Heart failure: Oxygen inhalation, parenteral lasix and digitalis are used.
Anuria: The treatment should be in the line as formulated in the chapter
of anuria .Dopamine infusion (1 jug/kg) is given with oliguria when CVP is
above 8 mm Hg. It is often surprising that urine output returns to normal
following delivery.
Hyperpyrexia: It is difficult to bring down the temperature as it is central
in origin. However, cold sponging and antipyretics may be tried.
Psychosis:Chlorpromazine or Eskazine (trifluoperazine) is quite effective.

OBSTETRIC MANAGEMENT:
During pregnancy:
In majority of cases with antepartum
eclampsia, labor starts soon after
convulsions. But when labor fails to
start, the management depends on
whether the fits are controlled or not
and
(ii) the maturity of the fetus. The
decision to deliver is made once the
woman is stable.

 i Fits controlled:
Baby mature:Delivery should be done,
(a) If the cervix is favorable and there is no
contraindication of vaginal delivery, surgical
induction by low rupture of the membranes is done.
Oxytocin drip may be added, if needed, (b) When
the cervix is unfavorable, cervical ripening with
PGE2 gel or pessary could be achieved before ARM.
(c) If the cervix is unfavorable and/or there is
obstetric contraindication of vaginal delivery,
cesarean section is done.

 Baby premature (<37 weeks):

Delivery is recommended in a set up with
neonatal intensive care unit (NICU). The underlying
disease process of preeclampsia and eclampsia
persists until the woman delivers. At times the
disease process may flare up. Moreover, there lies
the risk of recurrent convulsions and IUFD. Steroid
therapy is given when pregnancy is less than 34
weeks . Conservative management at very
early pregnancy may improve perinatal outcome
but this must be carefully balanced with maternal
well-being

 Baby dead:
The preeclamptic process gradually subsides and
eventually expulsion of the fetus occurs. Otherwise
medical method of induction is started .
Fits not controlled:
If the fits are not controlled with anticonvulsant within a
reasonable period (6-8 hours), termination of pregnancy
should be done. If vaginal examination indicates a quick
response to induction, low rupture of the membranes is
done. Oxytocin infusion maybe added. The uterus
responds well to oxytocin in such cases. In presence of
unfavorable factors, cesarean section gives a quick
response.

 During labor:
In the absence of any contraindication to vaginal delivery,
as soon as the labor is well established, low rupture of the
membranes is to be done to accelerate the labor. The
dose schedule of antihypertensive and anticonvulsant
drugs maybe increased to quieten the patient. Second
stage should be curtailed by forceps, ventouse or
craniotomy, if the baby is dead. Prophylactic intravenous
ergometrine or syntometrine following the delivery of the
anterior shoulder should not be given as it may produce
further rise of blood pressure. Instead, 10 units of oxytocin
IM or IV slowly should be given. One should remain
vigilant about postpartum hemorrhage and shock.

Indications of cesarean section:

Uncontrolled fits in spite of therapy,
(ii) Unconscious patient and poor prospect of vaginal delivery,
(iii) Obstetric indications (malpresentation).
Follow-up and prognosis: Patient should be followed up in
the postnatal clinic by 6 weeks time. Persistence of
hypertension, proteinuria and abnormal blood biochemistry
necessitates further investigation and consultation with a
physician. Further pregnancy should be deferred till they are
controlled.
Recurrence risk varies between 2% and 25%. The risk of
preeclampsia and eclampsia to the daughter of an eclampsia
patient is about 25% and 3%, respectively.

 Atypical preeclampsia is defined as the development of preeclampsia

(even eclampsia) without fulfilling the standard definition or criteria
(hypertension or proteinuria). The common presentations are:
Early onset preeclampsia/eclampsia less than 20 weeks
Late postpartum preeclampsia, eclampsia more than 48 hours
postpartum
Women with gestational hypertension or gestational proteinuria
presenting with symptoms of
(a) Preeclampsia
(b) Thrombocytopenia
(c) Elevated liver enzymes.
Women with atypical preeclampsia and who have other diagnostic
criteria of severe preeclampsia should be treaed as if they have severe
preeclampsia. Patients are also treated with parenteral MgS0 4.

 Status eclampticus:
Thiopentone sodium 0.5 g dissolved in
20 mL of 5% dextrose is gibn intravenously
very slowly. The procedure should be
supervised by an expert anesthetist. If the
procedfails, use of complete anesthesia,
muscle relaxant and assisted ventilation
may be employed.In unresponsive
cases, cesarean section in ideal
surroundings may be a life saving attempt.

COMPLICATIONS OF PRE ECLAMPSIA AND ECLAMPSIA

HELLP SYNDROME
Haemolysis , elevated liver enzymes and low platelet
count(HELLP) syndrome is a rare complication of severe pre
eclampsia and may occur in 3-4% of the patients with
severe pre eclampsia and eclampsia.The pathophysiology
of HELLP syndrome is similar to that of pre eclampsia with
microvascular damage, platelet activation and vasospasm.
Criteria for the diagnosis of HELLP syndrome
Hemolysis :
Schistocytes in the blood smear
Bilirubin 1.2mg/dl
Absent plasma haptoglobin

Elevated liver enzymes:

AST 72 IU/L
LDH 600 IU/L
Low platelet count:
Platelets < 100,000/mm3
Management
The diagnosis of HELLP syndrome is an indication for
immediate delivery if the pregnancy is 34 weeks or any
gestational age if pulmonary edema, renal failure, placental
abruption, severe liver dysfunction or bleeding non reassuring
fetal status or uncontrolled hypertensionis present. All the
other cases require administration of magnesium sulphate,
steroids for the prevention of intraventricular bleeding and
RDS.

PULMONARY EDEMA
ACUTE RENAL FAILURE
ABRUPTIO PLACENTA
INTRACRANIAL BLEEDING
VISUAL DISORDERS

GESTATIONAL HYPERTENSION
DEFINITION
A sustained rise of blood pressure to
140/90mmhg or more on atleast two
occasions 4 or more hours apart
beyond the 20th week of pregnancy
or during the first 24 hours after
delivery in a previously normotensive
women is called gestational
hypertension

 INCIDENCE
It is the most frequent of hypertensive
conditions of pregnancy with a
prevalence between 6 and 15% in
nulliparas and 2-4% in multiparas.

 TYPES
Early gestational hypertension :
gestational hypertension before 30
weeks frequently is severe ,
advances to pre eclampsia
Late gestational hypertension:
gestational hypertension after 34
weeks is usually a beningn condition
that rarely becomes severe ,
progresses to pre eclampsia.

PATHOPHYSIOLOGY
Early gestational hypertension
It is due to poor placentation with
placental ischemia and
hemodynamic changes charecterized
by the vasoconstriction and
decreased urinary output.
Late gestational hypertension
It is due to the poor maternal
adaptation to the physiologic
changes of pregnancy.

 CLINICAL FEATURES
Edema : is excessive accumulation of fluid
with demonstrable pitting edema over the
ankle greater than 1+ after 12 hours in bed or
gain in weight of 2kg or more in a week due to
influence of pregnancy.
Proteinuria : it is the presence of protein of
more than 0.3 gm in the 24 hours urine during
or under influence of the pregnancy in the
absence of hypertension , edema or renal
infection.

 DIAGNOSIS
Uterine artery Doppler velocimetry
was used for the prediction of the
gestational hypertension.

MANAGEMENT
Gestational hypertension without risk factors

The weekly assessment of patients with

gestational hypertension and no risk factors
include a systematic review of the maternal and
fetal status. Maternal review includes the levels of
blood pressure , the presence or absence of
symptoms suggestive of end organ damage and
presence of proteinuria. From the fetal side the
review includes the daily charting of fetal
movements and measurement of the uterine
fundal height.

 Gestational hypertension with

risk factors
Women with systolic pressure
160mmhg and diastolic pressure
110mmhg require treatment with
anti hypertensive agents. The
treatment is with antihypertensives
and beta blockers. The beta blocker
used is labetalol.

 Delivery

The route of delivery in women

depends on the results of the digital
pelvic examination . if the cervix is
unripe and the cervical length is
2.5cm it is better to deliver by
caesarean and if the cervix is ripe
vaginal delivery will be the best
option.

CHRONIC HYPERTENSION IN
PREGNANCY
Chronic hypertensive disease (CHD) is defined
as the presence of hypertension of any cause
antedating or before the 20th week of
pregnancy and its presence beyond the 12
weeks after delivery. The condition poses a
difficult problem as regards the diagnosis and
management when seen for the first time,
beyond the 20th week of pregnancy.
Overall incidence is 2-4% of which 90% are
due to essential hypertension.

The high risk factors for CHD are:

Age (> 40 years),
(ii) Duration of hypertension (>15 years)
(iii) Level of BP (>160/110 mm of Hg),
(iv) Presence of any medical disorder
(renovascular), and
(v) Presence of thrombophilias. Majority of
women with CHD are low risk and have
satisfactory maternal and fetal outcome
without any antihypertensive therapy.

ESSENTIAL HYPERTENSION IN
PREGNANCY
The diagnostic criteria are:
(1) Rise ofblood pressure to the extent of 140/90 mm Hg or
more during pregnancy prior to the 20th week (molar
pregnancy excluded),
(2) Cardiac enlargement on chest radiograph and ECG,
(3) Presence of medical disorders, and
(4) Prospective follow-up shows persistent rise ofblood
pressure even after 42 days following delivery. However,
confusion in the diagnosis arises when the case is first
seen in later months of pregnancy, especially when the
pre-pregnant level of blood pressure remains unknown.
Differential diagnosis with preeclampsia, gestational
hypertension and essential hypertension are given below.

EFFECTS OF PREGNANCY ON
THE DISEASE
(1) There may be a midpregnancy fall ofblood
pressure in about 50%. However, the blood pressure
tends to rise in the last trimester which may or may
not reach its previous level,
(2) In 50%, the blood pressure tends to rise
progressively as pregnancy advances,
(3) In about 20%, it is superimposed by
preeclampsia evidenced by rise ofblood pressure to
the extent f 30 mm Hg systolic and 15 mm Hg
diastolic associated with edema and/or proteinuria,
(4) In 30%, there is permanent deterioration of the
hypertension following delivery.

EFFECT OF THE DISEASE ON PREGNANCY:

Maternal risk:
In the milder form, the maternal risk remains unaltered
but in the severe form or when superimposed by
preeclampsia, the maternal risk is ^fleh increased.
Fetal risk:
Due to chronic placental insufficiency, the babies are
likely to be growth retarded. Preterm forth is high. In the
milder form, with the blood pressure less than 160/100
mm Hg, the perinatal loss is about 10 %.When Bp
exceeds 160/100 mmhg.,the perinatal loss increases by
3 to 4 times and when complicated by pre eclampsia ,it
increases further.Risk of placental abruption is high(0.510%)

MANAGEMENT:
The principles of management are:
(1) To stabilize the blood pressure to
below 160/100 mm Hg,
(2) To prevent superimposition of
preeclampsia,
(3) To monitor the maternal and fetal
well-being,
(4) To terminate the pregnancy at the
optimal time.

GENERAL MANAGEMENT
In mild cases with blood pressure less than 160/100
mm Hg,
adequate rest (physical and mental),
low-salt diet are all that are needed.
The check up should be more frequent 1-2 weeks
interval up to 28 weeks and thereafter weekly.
In severe cases or in cases of superimposed
preeclampsia
the patients should be hospitalized and are placed
in the treatment protocol as described under
preeclampsia.

Antihypertensive drugs:
Routine use of antihypertensive drug is
not favored.
Thus, antihypertensive drugs
(methyldopa, labetalol, nifedipine or
hydralazine) should be used only when
the pressure is raised beyond 160/100
mm Hg, to prevent target organ damage
(stroke, renal or cardiac failure).

OBSTETRIC MANAGEMENT:
In mild cases, spontaneous labor is
awaited.
In severe or complicated cases, the
aim is to try to continue the
pregnancy to at least 34 weeks
otherwise up to the 37th week to
attain fetal maturity and then to
terminate the pregnancy.