Gestational Hypertension-Me

El Housseiny Fatmé, SDC
PIH, PRE- ECLAMPSIA AND

ECLAMPSIA
Objectives
At the end of this session you will be able to:

1. Outline diagnostic features of pre-eclampsia
2. Classify pre-eclampsia according to severity
3. Outline risk factors for pre-eclampsia
4. Outline maternal and fetal complications of
pre-eclampsia.
5. Describe the management of pre-eclampsia
and eclampsia.
Introduction
 Synonyms: Toxemia of pregnancy, pre-eclampsia,

pregnancy induced hypertension.
 Pre-eclampsia commonly manifests after the 20th week
of pregnancy.
 Prevalence of pre-eclampsia: varies from one place to
another
 Severe pre-eclampsia and eclampsia
 Are serious and potentially fatal
 Third commonest cause of maternal mortality
Definitions:
 Gestational hypertension / pregnancy induced

hypertension (PIH): sustained BP ≥ 140/90 mmHg
 Preeclampsia is a hypertensive disorder of

pregnancy developing after 20 weeks gestation
and characterized by edema, vasospasms of the
arteries and proteinuria.
 Eclampsia is an extension of preeclampsia and is

characterized by seizures.
Considerations or BP measurements:
 Proper cuff size

 Measurement taken while patient is seated
 Two consecutive abnormal measurements
recorded at least 6 hours apart are required to
confirm the PHI.
Risk factors:
 Young maternal age
 Nulliparity: 85% of pre-eclampsia occur in primigravida.
 Increased placental tissue for gestational age: Hydatiform
moles, twin pregnancies
 Family history of pre -eclampsia
 Diabetes mellitus
 Renal diseases,
 Chromosomal abnormality in the fetus (eg, trisomy).
Worrisome signs for pre-eclapmsia development
 Rapid increase of weight during the latter ½ of pregnancy
 An upward trend in diastolic BP even while still within normal
range
Patho-physiology:
 There are several theories and etiologic

mechanisms.
 Vasospasm theory: Most favored theory
 Vasospasms → vasoconstriction → resistance →
arterial BP
 Eclampsia:
Cerebral arterial vasospasm → cerebral edema or
infarction and/or cerebral hemorrhage
Investigations
 Urine analysis
 Proteinuria
 A 24-hour urine collection
 Quantity of urine and protein
 Uric acid level:
 GFR and creatinine clearance decrease →in ↑uric acid
levels.
 LFT – Transaminases
Classification of pre eclampsia :
ACCORDING TO SEVERITY
1. Mild pre-eclampsia
2. Moderate pre-eclampsia
3. Severe pre-eclampsia
4. Mild Pre eclampsia

Diagnostic Features
 Systolic BP is 140 -160 mmHg
 Diastolic BP is 90 – 100 mmHg
 Proteinuria up to ++
2. Moderate pre-eclampsia
Symptoms
 Severe & persistent occipital or frontal headaches
 Visual disturbance: blurred vision, photophobia
 Epigastric and/or right upper-quadrant pain
Signs
 Diastolic BP > 11ommHg, systolic BP > 160mmHg
 Proteinuria +++ or more
 Altered mental status
 Hyper-reflexia
 Oliguria
HELLP syndrome
 Severe form of pre eclampsia :

 Affects approx 10% of women with severe
preeclampsia and 30-50% of women with
eclampsia.
 Characterized by:
 Hemolysis,
 Elevated liver enzymes
 Low platelet count.
 Increased mortality rate and DIC

Maternal Complications:
 CVS
 Haemoconcentration (cause: vasoconstriction and
vascular permeability)
 Hamatological changes – HELLP → DIC
 Kidneys
 acute RF
 Proteinuria – due to ⇈permeability to large
protein,
 Oliguria – both renal perfusion and GFR decrease .
Maternal Complications:
Brain
 Cerebral edema
 Infarction, cerebral hemorrhage
 Blindness: Due to -?retinal artery vasospasms and
retinal detachment
 Fever 39ºC: a grave sign, may be a consequence of
intracranial hemorrhage.
 Coma – may be a result of CVA
RS :
 Pulmonary oedema and cyanosis
MAJOR CAUSES OF MATERNAL DEATH
 Cerebrovascular accident (CVA)
 Pulmonary oedema
 Cardiac failure,
 Renal failure
Fetal complications
 IUFD,
 IUGR
 Increased prenatal morbidity
 Placental abruption
 Fetal growth restriction
 Fetal distress
MANAGEMENT OF MILD - MOD PRE ECLAMPSIA
 Sequential work ups,

 Antihypertensives: Aldomet,
 Fetal movements monitoring,
 Plan delivery at 38/40 Gestational age
 Manage as severe pre-eclampsia If not responding to treatment
Education:
 Bed rest at home,
 Schedule antenatal clinic every 2 weeks up to 32 wks and weekly
thereafter
 Advice the mother to come to the health facility in case of severe
headache, blurred vision, nausea or upper abdominal pain.
Criteria for Treatment
 Diastolic BP > 105-110

 Systolic BP > 200
 Avoid rapid reduction in BP
 Do not attempt to normalize BP
 Goal is DBP < 105 not < 90
MANAGEMENT OF SEVERE PRE ECLAMPSIA AND
ECLAMPSIA
 Keep airway clear

 Control convulsions
 Control BP: Keep BP between 140 -160 /90 -110 mm Hg
 Control fluid balance
 Antibiotics
 Investigations
 Deliver the mother
Indications for Delivery
 Worsening BP
 Non-reassuring fetal condition
 Fetal lung maturity
 Favorable cervix
Medical BP control:
 Anti HPTs: Hydralazine, nifedipine, or labetalol

 Diuretics are not used except in the presence of
pulmonary edema
Hypertensive Emergencies
 Fetal monitoring
 IV access
 IV hydration
 The reason to treat is maternal, not fetal
 May require ICU
Nursing Care Focus
 Assisting the woman in obtaining prenatal care

 Helping her cope with therapy
 Caring for acutely ill woman
 Know what signs/symptoms to monitor for and
when to intervene
 Administering medications as prescribed
Acute Medical Therapy
 Labetalol
 Nifedipine
 Nitroprusside
 Diazoxide
 Clonidine
Key Steps Using Vasodilators
 250-500 cc of fluid, IV
 Allow time for drug to work
 Avoid over treatment
Labetalol
 Dose: 20mg, then 40, then 80 every 20

minutes, for a total of 220mg
 Onset: 1-2 minutes
 Duration: 6-16 hours
 Side effects: hypotension
 Mechanism: Alpha and Beta block
Nifedipine
 Dose: 10 mg po, not sublingual

 Side effects: chest pain, headache,
tachycardia
 Mechanism: CA channel block
Clonidine
 Dose: 1 mg po
 Side effects: unpredictable, avoid rapid
withdrawal
 Mechanism: Alpha agonist, works centrally
Seizure Prophylaxis
 Magnesium sulfate
 4-6 g bolus
 1-2 g/hour
 Monitor urine output
 With renal dysfunction, may require a lower
dose
Overview on MgSO4:
 Mechanism:
 Cerebral vasodilator → reducing cerebral
vasospasm → ↓ischemia (brain).
 Superior to other anti-convulsants used :
 Important part of mgt of eclampsia
 Improves maternal and fetal outcome
MgSO4 regimen:
i. Loading dose
MgSO4 4 g (i.e. 20mls of 20% solution) +
200mls NS I.V over 5 minutes
ii. Maintenance dose
MgSO4 4 g (i.e. 20ml of 20% solution) IN
500ml NS 4 hourly for 24 hrs after the last
seizure
MgSO4 regimen: (cont’d)
Recurrent seizure:
 Therapeutic dose may not have been reached
 Give 2g (i.e. 10ml of 20% solution) i.v. over 5
minutes
Treatment duration:
Continue for 24 hours after delivery or last
convulsion, whichever occurs first
MgSO4 side effects:
 loss of deep tendon reflexes,

 respiratory depression
 Respiratory arrest.
Thus, before repeating MgSO4, ensure that;

 RR ≥ 16/min
 Patellar reflexes are present
 Urinary output is at least 30ml per hour over 4 hours
 Otherwise withhold or delay MgSO4
 Keep antidote ready
 In case of respiratory arrest: Assist ventilation and administer
calcium gluconate

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El Housseiny Fatmé, SDC

PIH, PRE- ECLAMPSIA AND

At the end of this session you will be able to:

 Synonyms: Toxemia of pregnancy, pre-eclampsia,

 Gestational hypertension / pregnancy induced

 Preeclampsia is a hypertensive disorder of

 Eclampsia is an extension of preeclampsia and is

 Proper cuff size

 There are several theories and etiologic

4. Mild Pre eclampsia

 Severe form of pre eclampsia :

 Increased mortality rate and DIC

 Cerebrovascular accident (CVA)

 Sequential work ups,

 Diastolic BP > 105-110

 Keep airway clear

 Anti HPTs: Hydralazine, nifedipine, or labetalol

 Assisting the woman in obtaining prenatal care

 Dose: 20mg, then 40, then 80 every 20

 Dose: 10 mg po, not sublingual

 loss of deep tendon reflexes,

Thus, before repeating MgSO4, ensure that;

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