Severe preeclampsia
IDENTITY OF PATIENTS
I. History
I.1 Identification of Patients
Name: Mrs. L
Age: 43 years
Education: Junior High school
Religion: Hindu
Occupation: Swasta
Tribe / Nation: Dayak / Indonesia
Address: Kereng bangkirai
Taheta Palangkaraya
I.2 Complaints
-Main complaints: Swelling
-History Disease Now: Os come with swelling of the
hands, feet and tingling of hands and feet from one
month ago. Os claimed to have been pregnant for 7 to
25 weeks' gestation. During this os no history of high
blood pressure, only in this pregnant high blood
pressure, there is heartburn, pastures eyes blurred (-), a
history of seizures (-), Small bowel movements (+) like
tea, nausea (-) , vomiting (-), cough (-), shortness of
breath (-), abdominal contraction (-), blood mucus (-),
water out from vaginal (-), fetal movements (+), ANC
(-), ultrasound ( -) History of trauma (-), History of
Operations (-), Fever (-).
Continues...
Thorax:
Pulmo: I: symmetrical shape, retraction (- / -), symmetrical
breathing motion
P: fremitus touch symmetric
P: sonor / resonant
A: vesicular breath sounds, ronkhi - / -, wheezing - / Cor :
I: ICTUS cordis (-)
P: thrill (-)
P: Right limit ICS II LS dextra, left LMK ICS IV
A: S1 S2 regular single, Murmur (-), Gallop (-)
Abdomen: Convex, BU (+) Normal, timpani, Pain Press (-)
Extremities:
Above: warm, pitting edema (+ / +), no deformity, CRT <2 '
Below: warm, pitting edema (+ / +), no deformity, CRT <2 '
b. Obstetrics Status
1. Examination outside
Inspection: abdomen looks convex
Palpation:
Leopold 1: TFU 2 fingers above the umbilicus (McD
25 cm)
Leopold 2: Back Left
Leopold 3: Head of Presentation
Leopold 4: Not signed The pelvic
Auscultation: FHR: (+) 135 x / minute
2. Examination in
Inspekulo and Vaginal toucher not done
Diagnose
G7P6A0, Age Pregnancy 25 weeks, not
inpartu, a fetals intra-uterine single
life, head presentation with severe
Preeclampsia
The treatment
follow up
CHAPTER II
Preeclampsia - Eclampsia
Hypertension after 20 weeks
gestation
Proteinuria > than 300 mg/dl or +1
dipstick
Convulsions: eclampsia
Preeclampsia
Incidence: 5 - 8% of all pregnancies.
Etiology remains elusive.
Major cause for maternal and perinatal
mortality and morbidity.
To date no treatment for prevention (baby
ASA or calcium) or cure, except delivery.
However, the maternal benefits must be
weighed against the neonatal risks of
preterm delivery.
Preeclampsia
Definition = New onset of hypertension and
proteinuria after 20 weeks gestation.
Systolic blood pressure 140 mmHg OR diastolic blood
pressure 90 mmHg
Proteinuria of 0.3 g or greater in a 24-hour urine
specimen
Preeclampsia before 20 weeks, think MOLAR
PREGNANCY!
Categories
Mild Preeclampsia
Severe Preeclampsia
Eclampsia
Occurrence of generalized convulsion and/or coma in the
setting of preeclampsia, with no other neurological
condition.
Preeclampsia
Severe Preeclampsia must have one of the
following:
Symptoms of central nervous system dysfunction = Blurred
vision, scotomata, altered mental status, severe headache
Symptoms of liver capsule distention = Right upper
quadrant or epigastric pain
Nausea, vomiting
Hepatocellular injury = Serum transaminase concentration
at least twice normal
Systolic blood pressure 160 mm Hg or diastolic 110 mm
Hg on two occasions at least six hours apart
Thrombocytopenia = <100,000 platelets per cubic
milimeter
Proteinuria = 5 or more grams in 24 hours
Oliguria = <500 mL in 24 hours
Severe fetal growth restriction
Pulmonary edema or cyanosis
Cerebrovascular accident
Blood pressure of 160 mm Hg systolic or higher or 110 mm Hg diastolic or higher on two occasions at
least 6 hours apart while the patient is on bed rest
Proteinuria of 5 g or higher in a 24-hour urine specimen or 3+ or greater on two random urine samples
collected at least 4 hours apart
Thrombocytopenia
ACOG,Practice Bull.2002
Etiology
1. abnormal trophoblast invasion of the
blood vessels of the uterus.
2. immunological intolerance between
maternal and fetoplacental tissue.
3. Maladaptation mother against
cardiovascular changes or changes in the
inflammatory response of normal
pregnancy.
4. Factor nutritional deficiencies.
5. Genetic factors
Nulliparity
Preeclampsia in a previous pregnancy
Age >40 years or <18 years
Family history of pregnancy-induced hypertension
Chronic hypertension
Chronic renal disease
Antiphospholipid antibody syndrome or inherited
thrombophilia
Vascular or connective tissue disease
Diabetes mellitus (pregestational and gestational)
Multifetal gestation
High body mass index
Male partner whose previous partner had preeclampsia
Hydrops fetalis
Unexplained fetal growth restriction
Pathophysiology
Preeclampsia - Pathophysiology
May be initiated by placental factors that
enter the maternal circulation and cause
endothelial dysfunction resulting in
hypertension and proteinuria.
Recently, soluble fms-like tyrosine kinase 1
(sFlt-1) an antiangiogenic protein has been
found to be increased in preeclampsia
(Maynard et al.J Clin Invest 2003)
Angiogenic Factors
Endothelium
+ VEGF
+ PIGF
- sFlt1
Preeclampsia - Pathophysiology
sFlt-1 acts by binding to placental growth
factor(PGF) and vascular endothelial growth
factor (VEGF), preventing the interaction with
endothelial receptors on the cell surface and
inducing endothelial dysfuntion.
Exogenous administration of sFlt-1 in pregnant
rats induces hypertension, proteinuria, and
glomerular endotheliosis.
Circulating Angiogenic
Factors and the Risk of
Preeclampsia
Circulating angiogenic
factors
Increased levels of sFlt-1 and
reduced levels of PIGF predict
the subsequent development
of preeclampsia
Preeclampsia - Pathophysiology
Soluble Endoglin (CD105), a cell receptor
for transforming growth factor-beta (TGF), has been localized to both placental
syncytiotrophoblasts and endothelial cells.
The primary role include angiogenesis,
endothelial cell differentiation and
regulation of vascular tone through
endothelial nitric oxide synthetase (enos)
Preeclampsia - Pathophysiology
Soluble endoglin as a second
trimester marker for preeclampsia
Soluble endoglin elevated in patients
destined to develop severe earlyonset preeclampsia
Circulating angiogenic
factors
Increase
sFlt-1
Increase Endoglin
Decrease
PGIF
Preeclampsia: Management
Mild: 140/90, +1 proteinuria. Management:
conservative, bedrest, deliver if close to term
Severe: Significant HTN, proteinuria
(>5g/24hrs) or any systemic manifestation
of the disease. Management: Consider
delivery
Eclampsia: Delivery
Patholog
y
Spasm of
vessels
Vessel
stenos
is
Higher
periphery
resistance
Blood
pressur
e
elevate
Injury of
endotheliocyte
Proteinuri
a
Edem
a
Hypertensi
on
Preeclampsia superimposed on
Chronic Hypertension
Affects 10-25% of patients with chronic
HTN
Preexisting Hypertension with the following
additional signs/symptoms:
New onset proteinuria
Hypertension and proteinuria beginning prior
to 20 weeks of gestation.
A sudden increase in blood pressure.
Thrombocytopenia.
Elevated aminotransferases.
Treatment of Preeclampsia
Definitive Treatment = Delivery
Major indication for antihypertensive
therapy is prevention of stroke.
Diastolic pressure 105-110 mmHg or
systolic pressure 160 mmHg
Evaluation of Hypertension in
Pregnancy
History
ID and Complaint
HPI (S/S of Preeclampsia)
Past Medical Hx, Past
Family Hx
Past Obstetrical Hx, Past
Gyne Hx
Social Hx
Medications, Allergies
Prenatal serology, blood
work
Assess for Hypertension
in Pregnancy risk factors
Physical
Vitals
HEENT = Vision
Cardiovascular
Respiratory
Abdominal =
Epigastric pain, RUQ
pain
Neuromuscular and
Extremities = Reflex,
Clonus, Edema
Fetus = Leopolds,
FM, NST
Evaluation of Hypertension in
Pregnancy
Laboratory Tests
Management of Hypertension
in Pregnancy
Depends on severity of hypertension
and gestational age!!!!
Observational Management
Restricted activity
Close Maternal and Fetal Monitoring
BP Monitoring
S/S of preeclampsia
Fetal growth and well being (NST, and U/S)
Management of Hypertension
in Pregnancy
Medical Management
Acute Therapy = IV Labetalol, IV
Hydralazine, SR Nifedipine
Expectant Therapy = Oral Labetalol,
Methyldopa, Nifedipine
Eclampsia prevention = MgSO4
Contraindicated
antihypertensive drugs
ACE inhibitors
Angiotensin receptor antagonists
Management of Hypertension
in Pregnancy
Proceed with Delivery
Vaginal Delivery VS Cesarean Section
Depends on severity of hypertension!
May need to administer antenatal
corticosteroids depending on gestation!
Complications of
mother
Heart failure
Cerebrova- scular accident
Placenta abruption
DIC
Renal failure
HELLPS syndrome
Postpartum hemorrhage
Complications of
fetus
Fetus
FGR
fetal distress
fetal death
neonatal
asphyxia
HELLP SYNDROME
Is a severe form of pre-eclampsia
MANAGEMENT
CONT
BP CONTROL
Keep SBP between 140 -160 mm Hg and DBP
between 90 -110 mm Hg
?Why these levels: Avoid potential reduction in
either uteroplacental blood flow or cerebral
perfusion pressure.
Drugs:
Anti HPTs: Hydralazine, nifedipine, or labetalol
Diuretics are not used except in the presence of
pulmonary edema
MANAGEMENT: CONTROL
CONVULSIONS
I. An overview on MgSO4.
Mechanism:
Cerebral vasodilator reducing cerebral
vasospasm ischemia (brain).
Superior to other anti-convulsants used to
control and prevent fits;
Important part of mgt of eclampsia
Recurrence rate after MgSO4 = 10 -15%
MANAGEMENT CONT
MANAGEMENT
CONT
2. INTRAVENOUS 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
fits
MANAGEMENT
CONT
Treatment duration:
Continue for 24 hours after delivery or last
convulsion, whichever occurs first
MANAGEMENT
CONT
MANAGEMENT CONT
Management of labour
1st stage
Relieve pain: pethidine 25 mg iv every 2-4 hours
Augmentation of labour
Monitor FHR,
MANAGEMENT CONT
Management of labour
If there is delay perform C/S
Post delivery:
Continue observation for at least 48 hrs
post delivery
Record and monitor BP and urine output
for at least 48 hours after delivery,
Keep the pt in hospital until BP stabilizes,
Continue with aldomet PO until BP back
to normal
Thankyou