Chronic Hypertension and

Preeclampsia
Hipertensi Kronik Preeklampsia
- <20 minggu - >20 minggu
- Tidak hilang 12 - Disertai
minggu proteinuria
postpartum
• Hipertensi Kronik
– Hipertensi yang didapatkan sebelum kehamilan,
dibawah 20 minggu umur kehamilan, dan hipertensi
tidak menghilang setelah 12 minggu pasca persalinan.
• Preeklampsia
– Hipertensi dan proteinuria yang didapatkan setelah
umur kehamilan 20 minggu
• Hipertensi kronik (superimposed preeklamsi)
– Hipertensi kronik yang disertai proteinuria
• Hipertensi gestational
– Timbulnya hipertensi pada kehamilan yang tidak
disertai proteinuria hingga 12 minggu
pascapersalinan. Bila hipertensi menghilang setelah
12 minggu persalinan, maka dapat disebut juga
“Hipertensi Transien”
Hypertensive Disease Associated with
Pregnancy
Preeclampsia
 Associated with:
 Proteinuria.
 Thrombocytopenia.
 Impaired liver function.
 New onset renal insufficiency.
 Pulmonary edema.
 New onset cerebral or visual distrubances.
Hypertensive Disease Associated with
Pregnancy
Chronic Hypertension
 Predates the pregnancy.
 Diagnosed before the 20th week or present before
the pregnancy.
Hypertensive Disease Associated with
Pregnancy
Chronic Hypertension with Superimposed
Preeclampsia
 Hypertension predates the pregnancy.
 Features of preeclampsia noted after 20 weeks.
Hypertensive Disease Associated with
Pregnancy
Gestational Hypertension
 Hypertension after 20 weeks.
 Absence of proteinuria.
 Absence of systemic findings noted with
preeclampsia.
Faktor resiko
 Old classification New classification

Name Severe preeclampsia Preeclampsia with severe features

BP BP > 160 or > 110 (6 hr) BP > 160 or > 110 (4 hrs apart)
Platelets < 100,000 < 100,000
Liver increased LFTs increased LFTs
RUQ/epigastric pain RUQ/epigastric pain
Renal creatinine not used creatinine > 1.1 mg or doubling
oliguria not used
> 5000 mg protein not used
Lungs pulmonary edema pulmonary edema
CNS persistent HA persistent HA
visual changes persistent visual changes
Fetus growth restriction not used
 Pre-eclampsia Pre-existing
(chronic)
Hypertension
Parity usually usually
primigravida multigravida.
Past History of pre-eclampsia of hypertension in
may be present between
pregnancies.
Hypertension after the 20th week before pregnancy,
of pregnancy during the first 20
(except in vesicular weeks and persists
mole) and after 6 weeks
disappears within 6 postpartum.
weeks postpartum
Proteinuria If present, it If present, it
develops after develops before
hypertension hypertension due
to underlying renal
disease.
 Pre-eclampsia Pre-existing (chronic)
Hypertension
Hyperreflexia may be present. absent.

Fundus Examination Normal or retinal vessels Sclerotic changes.

spasm, oedema, exudate
and papilloedema (oedema
of the optic disc).
Serum Uric Acid Its increase is not Its increase is propotionate
proportionate to serum to serum creatinine
creatinine
 Pathophysiology
• Vasospasm
• Uterine vessels
• Hemostasis
• Prostanoid balance
• Endothelium-derived factors
• Lipid peroxide, free radicals and antioxidants
 Pathophysiology
Vasospasm
◦ Predominant finding in gestational hypertension
and preeclampsia
 Uterine vessels
 Hemostasis
 Prostanoid balance
 Endothelium-derived factors
 Lipid peroxide, free radicals and antioxidants
 Pathophysiology
 Vasospasm

Uterine vessels
◦ Inadequate maternal vascular response to
trophoblastic mediated vascular changes
◦ Endothelial damage
 Hemostasis
 Prostanoid balance
 Endothelium-derived factors
 Lipid peroxide, free radicals and antioxidants
 Pathophysiology
 Vasospasm
 Uterine vessels

 Hemostasis
◦ Increase platelet activation resulting in consumption
◦ Increased endothelial fibronectin levels
◦ Decreased antithrombin III and α2-antiplasmin levels
◦ Allows for microthrombi development with resultant
increase in endothelial damage
 Prostanoid balance
 Endothelium-derived factors
 Lipid peroxide, free radicals and antioxidants
 Pathophysiology
 Vasospasm
 Uterine vessels
 Hemostasis

Prostanoid balance
◦ Prostacyclin (PGI2):Thromboxane (TXA2) balance
shifted to favor TXA2
◦ TXA2 promotes:
 Vasoconstriction
 Platelet aggregation
 Endothelium-derived factors
 Lipid peroxide, free radicals and antioxidants
 Pathophysiology
 Vasospasm
 Uterine vessels
 Hemostasis
 Prostanoid balance

Endothelium-derived factors
◦ Nitric oxide is decreased in patients with
preeclampsia
 As this is a vasodilator, this may result in vasoconstriction
 Lipid peroxide, free radicals and antioxidants
 Pathophysiology
 Vasospasm
 Uterine vessels
 Hemostasis
 Prostanoid balance
 Endothelium-derived factors

Lipid peroxide, free radicals and antioxidants

◦ Increased in preeclampsia
◦ Have been implicated in vascular injury
 Pathophysiologic Changes
• Cardiovascular effects
• Hematologic effects
• Neurologic effects
• Pulmonary effects
• Renal effects
• Fetal effects
 Pathophysiologic Changes
Cardiovascular effects
◦ Hypertension
◦ Increased cardiac output
◦ Increased systemic vascular resistance
 Hematologic effects
 Neurologic effects
 Pulmonary effects
 Renal effects
 Fetal effects
 Pathophysiologic Changes
 Cardiovascular effects

 Hematologic effects
◦ Volume contraction/Hypovolemia
◦ Elevated hematocrit
◦ Thrombocytopenia
◦ Microangiopathic hemolytic anemia
◦ Third spacing of fluid
◦ Low oncotic pressure
 Neurologic effects
 Pulmonary effects
 Renal effects
 Fetal effects
 Pathophysiologic Changes
 Cardiovascular effects
 Hematologic effects

Neurologic effects
◦ Hyperreflexia
◦ Headache
◦ Cerebral edema
◦ Seizures
◦ Findings of PRES on radiologic imaging
 Pulmonary effects
 Renal effects
 Fetal effects
 Pathophysiologic Changes
 Cardiovascular effects
 Hematologic effects
 Neurologic effects

Pulmonary effects
◦ Capillary leak
◦ Reduced colloid osmotic pressure
◦ Pulmonary edema
 Renal effects
 Fetal effects
 Pathophysiologic Changes
 Cardiovascular effects
 Hematologic effects
 Neurologic effects
 Pulmonary effects

Renal effects
◦ Decreased glomerular filtration rate
◦ Glomerular endotheliosis
◦ Proteinuria
◦ Oliguria
◦ Acute tubular necrosis
 Fetal effects
 Renal Effects
• Decreased glomerular filtration rate
• Glomerular endotheliosis
• Proteinuria
• Oliguria
• Acute tubular necrosis
 Pathophysiologic Changes
 Cardiovascular effects
 Hematologic effects
 Neurologic effects
 Pulmonary effects
 Renal effects

Fetal effects
◦ Placental abruption
◦ Fetal growth restriction
◦ Oligohydramnios
◦ Fetal distress
◦ Increased perinatal morbidity and mortality
Management
 Treatment
• Prophylactic
• Curative
 Prophylactic
• Proper antenatal care:
– To detect the high risk patients who may develop PIH through
the screening tests.
– Early detection of cases who have already developed PIH and
examine them more frequently.
• Low dose aspirin:
– It inhibits thromboxane production from the platelets and the
AII binding sites on platelets.
– A low dose (60 mg daily) selectively inhibits thromboxane due to
higher concentration of such a low dose in the portal circulation
than systemic affecting the platelets when they pass through
the portal circulation. The Prostacyclin production from the
systemic vessels will not be affected.
 Curative
• Delivery of the foetus and placenta is the only
real treatment of pre-eclampsia. As the
conditions are not always suitable for this, the
treatment aims to prevent or minimize the
maternal and foetal complications (see
before) till reasonable maturation of the
foetus.
 General measures:
Observation:

Maternal: Foetal:

• blood pressure twice daily. • daily foetal movement

• urine volume and count,
proteinuria daily, • serial sonography,
• oedema daily, • non-stress and stress test if
• body weight twice weekly, needed.
• fundus oculi once weekly,
• blood picture including
platelet count, liver and
renal functions particularly
serum uric acid on
admission.
 Medical treatment
• Antihypertensives:
– decrease the maternal cerebral and cardiovascular complications but do not affect the foetal
outcome.
– Alpha-methyl-dopa (Aldomet):
• It reduces the central sympathetic drive.
• Dose: 250-500 mg every 6-8 hours up to a maximum dose of 4 gm/day. Its effect appears after 48
hours.
• A loading single dose of 2 gm may act within 1-2 hours.
• Side effects: headache, athenia and nightmares.
– Hydralazine (Apresoline):
• It is a vasodilator, increases renal and uteroplacental blood flow.
• Dose: 20 mg slowly IV initially followed by 5mg every 20 min. until diastolic blood pressure is 100-110
mmHg. This regimen is used for severe and acute hypertension. Oral hydralazine can be used in the
chronic situation as a second line treatment in a dose of 25-75 mg/ 6 hours.
• Side effects: tachycardia, headache, flushing, nausea and vomiting.
– Calcium channel blockers (Nifedipine):
• It is a vasodilator acting by blocking the Ca influx into smooth muscle cells.
• It can be given sublingually (acts within 10 minutes) or orally (acts within 30 minutes) in a dose of 10-
20 mg 2-3 times daily.
• The higher the starting blood pressure the greater is the hypotensive effect.
• Side effects: headache and flushing.
 Obstetric measures
• Timing of delivery
• Method of delivery
• Intrapartum care
• Postpartum care
 Timing of delivery: Severe pre-eclampsia is usually treated
conservatively till the end of the 36th week to ensure reasonable
maturation of the foetus. Indications of termination before 36th
week include:
Foetal: deteriorating placental Maternal: deteriorating maternal
function as judged by: condition as judged by:

– intrauterine growth – blood pressure is sustained

retardation, or exceeds 180/110
– oligohydramnios, mmHg,
– reduced foetal – urine proteinuria > 5
movements, gm/24 hours,
– abnormal foetal heart – oliguria,
patterns, or – evidence of DIC, or
– failing biochemical results. – imminent or already
developed eclampsia.
 Method of delivery:

– Vaginal delivery may be commenced in vertex

presentation by:
• amniotomy + oxytocin if the cervix is favourable.
• prostaglandin vaginal tablet (PGE2) if the cervix is not
favourable.
– Caesarean section is indicated in:
• Foetal distress.
• Late deceleration occurs with oxytocin challenge test.
• Failure of induction of labour.
• Other indications as contracted pelvis, and
malpresentations.
 Intrapartum care:

– Close monitoring of the foetus is indicated.

– Proper analgesia to the mother.
– Anti-Hypertensives may be given if needed.
– 2nd stage of labour may be shortened by forceps.
 Postpartum care:

– Methergin (Ergometrine) is better avoided as it

may increase the blood pressure.
– Continue observation of the mother for 48 hours.
– Anti- hypertensive drugs are continued in a
decreasing dose for 48 hours.