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1. Mengapa tangan, kaki dan mukanya edem ?

Fluid and Electrolyte Changes


In women with severe preeclampsia, the volume of extracellular
fluid, manifest as edema, is usually much greater than that of
normal pregnant women. The mechanism responsible for
pathological fluid retention is thought to be endothelial injury.
In addition to generalized edema and proteinuria, these women
have reduced plasma oncotic pressure. This reduction creates a
filtration imbalance and further displaces intravascular fluid
into the surrounding interstitium.
Electrolyte concentrations do not differ appreciably in
women with preeclampsia compared with those of normal pregnant
women. This may not be the case if there has been vigorous
diuretic therapy, sodium restriction, or administration of
free water with sufficient oxytocin to produce antidiuresis.
Following an eclamptic convulsion, the serum pH and bicarbonate
concentration are lowered due to lactic acidosis and
compensatory respiratory loss of carbon dioxide. The intensity
of acidosis relates to the amount of lactic acid produced and the
rate at which carbon dioxide is exhaled.

PATHOPHYSIOLOGY
Hypertension in pregnancy affects the mother and newborn
to varying degrees. Given the characteristic multisystem
effects, it is clear that several pathophysiologic
mechanisms are involved (Fig. 16.1). The predominant pathophysiologic
finding in preeclampsia and gestational hypertension
is maternal vasospasm. Several potential causes for maternal
vasospasm have been postulated:
1. Vascular changes: Instead of noting the physiologic
trophoblast-mediated vascular changes in the uterine
vessels (decreased musculature in the spiral arterioles
leads to the development of a low-resistance, lowpressure,
high-flow system), inadequate maternal vascular
response is seen in cases of preeclampsia and/or
intrauterine fetal growth restriction. Endothelial damage
is also noted within the vessels.
2. Hemostatic changes: Increased platelet activation
with increased consumption in the microvasculature is
noted during the course of preeclampsia. Endothelial
fibronectin levels are increased and antithrombin III
and 2-antiplasmin levels are decreased, reflecting endothelial
damage. Low antithrombin III levels are permissive
for microthrombi development. Endothelial
damage is then thought to promote further vasospasm.
3. Changes in prostanoids: Prostacyclin (PGI2) and
thromboxane (TXA2) are increased during pregnancy,
with the balance in favor of PGI2. In patients who
develop preeclampsia, the balance shifts to favor TXA2.

Again, PGI2 functions to promote vasodilatation and


decrease platelet aggregation, and TXA2 promotes vasoconstriction
and platelet aggregation. Because of this
imbalance, vessel constriction occurs.
4. Changes in endothelium-derived factors: Nitric
oxide, a potent vasodilator, is decreased in patients with
preeclampsia and may explain the evolution of vasoconstriction
in these patients.
5. Lipid peroxide, free radicals, and antioxidant release:
Lipid peroxides and free radicals have been implicated
in vascular injury and are increased in pregnancies complicated
by preeclampsia. Decreased antioxidant levels
are also noted.
These five mechanisms, in any combination or permutation,
are thought to contribute to the following common pathophysiologic
changes seen in patients with preeclampsia:
1. Cardiovascular effects: Elevated blood pressure is seen
as the result of potential vasoconstriction as well as an
increase in cardiac output.
2. Hematologic effects: Plasma volume contraction
may develop, with risk of rapid onset hypovolemic
shock, if hemorrhage occurs. Plasma volume contraction
is reflected in increased hematocrit values.
Thrombocytopenia/disseminated intravascular coagulation
may also develop from microangiopathic hemolytic
anemia. Involvement of the liver may lead to
hepatocellular dysfunction and further evolution of
coagulopathy. Third spacing of fluid may be noted,
because of increased blood pressure and decreased
plasma oncotic pressure.
3. Renal effects: Decreased glomerular filtration rate
(increasing serum creatinine) and proteinuria (urine
protein levels greater than 300 mg per 24 hours) develop
secondary to atherosclerotic-like changes in the renal
vessels (glomerular endotheliosis). Uric acid filtration is
decreased; therefore, elevated maternal serum uric acid
levels may be an indication of evolving disease.
4. Neurologic effects: Hyperreflexia/hypersensitivity may
develop. In severe cases, grand mal (eclamptic) seizures
may develop.
5. Pulmonary effects: Pulmonary edema may occur and
can be related to decreased colloid oncotic pressure,
pulmonary capillary leak, left heart failure, iatrogenic
fluid overload, or a combination of these factors.
6. Fetal effects: Decreased intermittent placental perfusion
secondary to vasospasm is thought to be responsible
for the increased incidence of intrauterine growth
restriction (<10% estimated fetal weight for gestational
age), oligohydramnios, and increased perinatal
mortality of infants born to mothers with preeclampsia.
An increased incidence of placental abruption is
also seen. With the stress of uterine contractions during
labor, the placenta may be unable to adequately
oxygenate the fetus. This may result in signs of intrapartum
uteroplacental insufficiency. Specifically, a nonreassuring
fetal-heart-rate pattern may necessitate
cesarean delivery.

Presumably because of vasospastic changes, placental size and function


are decreased. The results are progressive fetal hypoxia
and malnutrition, as well as an increase in the incidence of
intrauterine growth restriction and oligohydramnios.

Obstetrics and Gynecology


SIXTH EDITION
American College of Obstetrics and Gynecology (ACOG)
2. Mengapa pasien mengeluhkan pusing, mual, dan pandangan kabur?

1. Headache and scotomata are thought to arise from


cerebrovascular hyperperfusion that has a predilection for
the occipital lobes. According to Sibai (2005) and Zwart
and associates (2008), 50 to 75 percent of women have
headaches and 20 to 30 percent have visual changes preceding
eclamptic convulsions. The headaches may be mild to
severe and intermittent to constant. In our experiences,
they are unique in that they usually improve after magnesium
sulfate infusion is initiated.
2. Convulsions are diagnostic for eclampsia.
3. Blindness is rare with preeclampsia alone, but it complicates
eclamptic convulsions in up to 15 percent of women
(Cunningham and colleagues, 1995). Blindness has been
reported to develop up to a week or more following
delivery (Chambers and Cain, 2004). There are at least two
types of blindness as discussed subsequently.
4. Generalized cerebral edema may develop and is usually manifest
by mental status changes that vary from confusion to
coma. This situation is particularly dangerous because fatal
supratentorial herniation may result.

Visual Changes and Blindness


Scotomata, blurred vision, or diplopia are common with severe
preeclampsia and eclampsia. These usually abate with magnesium
sulfate therapy and/or lowered blood pressure. Blindness is
less common, is usually reversible, and may arise from three potential
areas. These are the visual cortex of the occipital lobe, the
lateral geniculate nuclei, and retina. In the retina, lesions may
include ischemia, infarction, and detachment.
Occipital blindness is also called amaurosisfrom the Greek
dimming. Affected women usually have evidence of extensive occipital
lobe vasogenic edema on imaging studies. Of 15 women
cared for at Parkland Hospital, blindness lasted from 4 hours to
8 days, but it resolved completely in all cases (Cunningham and
associates, 1995). Rarely, extensive cerebral infarctions may result
in total or partial visual defects (Fig. 34-14).
Blindness from retinal lesions caused by either retinal
ischemia or infarction is also called Purtscher retinopathy (Fig.
34-15). Moseman and Shelton (2002) described a woman with
permanent blindness due to a combination of infarctions in the
retina as well as in the lateral geniculate nucleus bilaterally. In
many cases of eclampsia-associated blindness, visual acuity improves,
but if caused by retinal artery occlusion, vision may be
permanently impaired (Blodi and associates, 1990; Lara-Torre
and colleagues, 2002).
Finally, retinal detachment may also cause altered vision, although
it is usually unilateral and seldom causes total visual
loss. Occasionally, it coexists with cortical edema and accompanying
visual defects. Asymptomatic serous retinal detachment is

relatively common and is obvious by examination (Saito and


Tano, 1998). Surgical treatment is seldom indicated, the prognosis
generally is good, and vision usually returns to normal
within a week.

3. Mengapa tidak teraba bagian kecil2 dari janin dan bagian yang berdenyut,
pada sarung tangan di dapatkan cairan+?
4. Mengapa bbnya naik cukup drastis? berapa Normal kenaikan BB pada ibu
hamil?
5. Apa hubungan antara gejala dengan tanda vital TD?
6. Apakah efficement 25% di umur 8 bulan normal / tidak, dan mengapa?
7. Apa px laboratorium dan penunjang yang dianjurkan dokter?
8. Mengapa dokter memberikan mgso4 pada pasien dan bagainama cara
kerjanya?
9. DD? (preeklamsi, eklamsi, KPD, DMG) (patofsiologi)

CLASSIFICATION
Various classifications of hypertensive disorders in pregnancy
have been proposed. Box 16.1 presents a commonly
used classification. Because hypertensive disorders in pregnancy
represent a spectrum of disease, classification systems
should be used as a guide only.

Chronic Hypertension

Chronic hypertension is defined as hypertension present before


the 20th week of pregnancy or hypertension present before pregnancy.
The categories of hypertension in pregnancy and
the blood pressure (BP) criteria used to define each are as
follows:
Mild hypertension: Systolic pressure of 140180 mm Hg
or diastolic pressure of 90100 mm Hg or both
Severe hypertension: Systolic pressure of 180 mm Hg or
diastolic pressure of 100 mm Hg
A major risk with chronic hypertension is the development
of preeclampsia or eclampsia later in the pregnancy, which
is relatively common and difficult to diagnose. The acute
onset of proteinuria and worsening hypertension in women
with chronic hypertension is suggestive of superimposed

preeclampsia

Gestational Hypertension
Hypertension that develops after 20 weeks of gestation in the absence
of proteinuria and returns to normal postpartum is termed
gestational hypertension. Gestational hypertension develops
in 5% to 10% of pregnancies that proceed beyond the
first trimester, with a 30% incidence in multiple gestations,
regardless of parity. Maternal morbidity is directly
related to the severity and duration of hypertension.
Approximately 25% of women with gestational hypertension
develop superimposed preeclampsia or eclampsia. It is
often difficult to distinguish between preeclampsia and
gestational hypertension when a patient is seen late in
pregnancy with an elevated blood pressure level. In such
cases, it is always wise to assume that the findings represent
preeclampsia and treat accordingly.

Preeclampsia
Preeclampsia is the development of hypertension with proteinuria
and edema after 20 weeks of gestation. This condition can
occur earlier in the presence of gestational trophoblastic
disease (see Chapter 41, Gestational Trophoblastic
Neoplasia). Risk factors for preeclampsia are in Box 16.2.
The criteria for diagnosis of preeclampsia are:
Blood pressure of 140 mm Hg systolic or 90 mm Hg
diastolic that occurs after 20 weeks of gestation in a
woman with previously normal blood pressure
Proteinuria, defined as urinary excretion of 0.3 g protein
or higher in a 24-hour urine specimen
Severe preeclampsia is characterized by one or more of
the following:
Blood pressure 160 mm Hg systolic or 110 mm Hg
diastolic on two occasions at least 6 hours apart while
the patient is on bed rest Marked proteinuria (generally 5 g per 24-hour urine
collection, or 3or more on two dipstick of random
urine samples collected at least 4 hours apart)
Oliguria 500 mL in 24 hours
Cerebral or visual disturbances such as headache and
scotomata (spots before the eyes)
Pulmonary edema or cyanosis
Epigastric or right-upper-quadrant pain (probably caused
by subcapsular hepatic hemorrhage or stretching of
Glisson capsule)
Evidence of hepatic dysfunction
Thrombocytopenia
Intrauterine fetal growth restriction (IUGR)
These changes illustrate the multisystem involvement associated
with preeclampsia. Severe preeclampsia is an indication
for delivery, regardless of gestational age or maturity.

Eclampsia
Eclampsia is the additional presence of convulsions (grand mal
seizures) in a woman with preeclampsia that is not explained
Most cases of eclampsia occur within 24 hours of delivery,
but approximately 3% of cases are diagnosed between 2 and
10 days postpartum.

HELLP Syndrome

HELLP syndrome is the presence of hemolysis, elevated liver


enzymes, and low platelet count.
HELLP syndrome, like severe preeclampsia, is an indication
for delivery to avoid jeopardizing the health of the woman.
This syndrome is now appreciated as a distinct clinical entity,
occurring in 4% to 12% of patients with severe preeclampsia
or eclampsia. Criteria for diagnosis are:
Microangiopathic hemolysis
Thrombocytopenia
Hepatocellular dysfunction

10.Faktor resiko dari DD?

11.Bagaimana cara penegakan diagnosis?

EVALUATION
The history and physical examination are directed toward
detection of pregnancy-associated hypertensive disease
and its signs and symptoms. A review of current obstetric
records, if available, is especially helpful to ascertain
changes or progression in findings. Visual disturbances, especially
scotomata, or unusually severe or persistent headaches
are indicative of vasospasm. Right-upper-quadrant pain may
indicate liver involvement, presumably involving distention
of the liver capsule. Any history of loss of consciousness
or seizures, even in the patient with a known seizure
disorder, may be significant.
The position of the patient influences blood pressure. It is
lowest with the patient lying in the lateral position, highest
when the patient is standing, and at an intermediate
level when she is sitting. The choice of the correct-size
blood pressure cuff also influences blood pressure readings,
with falsely high measurements noted when normal-sized
cuffs are used on large patients. Also, during the course
of pregnancy, blood pressure typically declines slightly in
the second trimester, increasing to prepregnant levels as
gestation nears term (Fig. 16.2). If a patient has not been
seen previously, there is no baseline blood pressure against
which to compare new blood pressure determinations,
thereby making the diagnosis of pregnancy-related hypertension
more difficult.

The patients weight is compared with her pregravid


weight and with previous weights during this pregnancy,
with special attention to excessive or too-rapid weight gain.
Peripheral edema is common in pregnancy, especially in
the lower extremities.
Indeed, the puffy-faced, edematous, hypertensive pregnant
woman is the classic picture of preeclampsia. Careful
blood pressure determination in the sitting and supine
positions is necessary. Funduscopic examination may detect
vasoconstriction of retinal blood vessels indicative of
similar vasoconstriction of other small vessels. Tenderness
over the liver, attributed partly to hepatic capsule distension,
may be associated with complaints of right-upperquadrant
pain. The patellar and Achilles deep tendon
reflexes should be carefully elicited, and hyperreflexia
noted. The demonstration of clonus at the ankle is especially
worrisome.
The maternal and fetal laboratory evaluations for
pregnancy complicated by hypertension are presented
in Table 16.1 and demonstrate, by the wide range of tests,
the multisystem effects of hypertension in pregnancy.
Maternal liver dysfunction, renal insufficiency, and coagulopathy
are significant concerns and require serial evaluation. Evaluation
of fetal well-being with ultrasonography, and a nonstress
test and/or biophysical profile are important.

12.Penanganan dokter selanjutnya?

Preeclampsia
The severity of the preeclampsia and the maturity of the
fetus are the primary considerations in the management of
preeclampsia. Care must be individualized, but there are
well-accepted general guidelines.
The mainstay of management for patients with mild
preeclampsia is rest and frequent monitoring of mother and fetus.
Testing for suspected fetal growth restriction or oligohydramnios
and twice-weekly nonstress tests, biophysical profiles, or both, are
commonly employed and should be repeated as indicated, according
to maternal condition. Testing is recommended twice
weekly for suspected fetal growth restriction or oligohydramnios.
Ultrasound examination for fetal growth and
amniotic fluid assessment is recommended every 3 weeks.
Daily fetal movement assessment also may prove useful.
Hospitalization is often initially recommended for
women with new-onset preeclampsia. After maternal and
fetal conditions are serially assessed, subsequent management
may be continued in the hospital, at a day-care unit,
or at home on the basis of the initial assessment.
For the patient with worsening preeclampsia or the patient
who has severe preeclampsia, management is often best accomplished
in a tertiary-care setting. Daily laboratory tests and
fetal surveillance may be indicated. Stabilization with magnesium
sulfate, antihypertensive therapy (as indicated),
monitoring for maternal and fetal well-being, and delivery
by either induction or cesarean delivery are required.
For almost a century, magnesium sulfate has been

used to prevent and to treat eclamptic convulsions. Other


anticonvulsants, such as diazepam and phenytoin, are
rarely used because they are not as efficacious as magnesium
and because they have potential adverse effects on
the fetus. Magnesium sulfate is administered by intramuscular
or intravenous routes, although the latter is far more common.
In 98% of cases, convulsions will be prevented. Therapeutic
levels are 4 to 6 mg/dL with toxic concentrations having predictable
consequences (Table 16.2). Frequent evaluations of
the patients patellar reflex and respirations are necessary
to monitor for manifestations of rising serum magnesium
concentrations. In addition, because magnesium sulfate
is excreted solely from the kidney, maintenance of urine
output of at least 25 mL/hour will help avoid accumulation
of the drug. Reversal of the effects of excessive magnesium
concentrations is accomplished by the slow intravenous
administration of 10% calcium gluconate, along
with oxygen supplementation and cardiorespiratory support,
if needed.
Antihypertensive therapy is initiated if, on repeated
measurements, the systolic blood pressure is 160 mm Hg
or if diastolic blood pressure exceeds 105 to 110 mm Hg.
Hydralazine is often the initial antihypertensive medication
of choice, given in 5- to 10-mg increments intravenously
until an acceptable blood pressure response is
obtained. A 10- to 15-minute response time is usual. The
goal of such therapy is to reduce the diastolic pressure to the 90to 100-mm Hg range. Further reduction of the blood
pressure may impair uterine blood flow to rates that are
dangerous to the fetus. Labetalol is another agent used to
manage severe hypertension (Table 16.3).
Once anticonvulsant and antihypertensive therapies are
established in patients with severe preeclampsia or eclampsia,
attention is directed toward delivery. Induction of labor is
often attempted, although cesarean delivery may be needed
either if induction is unsuccessful or not possible, or if the
maternal or fetal status is worsening. At delivery, blood
loss must be closely monitored, because patients with preeclampsia
or eclampsia have significantly reduced blood
volumes. After delivery, patients remain in the labor and
delivery area for 24 hours (longer if the clinical situation
warrants) for close observation of their clinical progress
and further administration of magnesium sulfate to prevent
postpartum eclamptic seizures. Approximately 25%
of eclamptic seizures occur before labor, 50% occur during
labor, and 25% occur in the first 24 hours after delivery.
Usually, the vasospastic process begins to reverse itself in
the first 24 to 48 hours after delivery, as manifested by a
brisk diuresis.

Apa Yang menyebabkan disfungsi endotel ? (terutama d daerah bifucartio)


Endotel yang mana yang mengalami disfungsi ?

Usia >35th

Kaki bengkak
Nyyeri kepala
Pandangan
kabur

Tanda vital :
180/110mmhg

Px fisik :

Px leopold :

Kenaikan 25kg, edem


ekstremitas, reflek
fisiologis +

TFU 25 cm

DD
(preeklamsia,eklams
ia, hipertensi kronik,
DMG, KPD)
Px. Darah rutin, protein urin,
gula darah
Px. Radiologi : USG,
cardiotografi

penatalaksanaa
n

Djj 11-11-12