3.

1 Method and Steps in Finding Information

We are trying to solve the problem with a group discussion. First, we identify the
problem and search the keywords. After that, we asked some questions to our tutor
that may occur to patients like doing anamnesis. Then, we look for theories that
associated with these problem in accordance with evidence-based learning. We make
an early concept mapping and an early hypothesis for these problems. We make
learning issue to compared several theories or medical science associated with these
problems to find out more about what the disease may be suffered by the patient or we
can say this the initial diagnosis. We discussed the theory and after that, we create the
final hypothesis and final concept maping. This concept mapping is made to process
the problem and how to solve it and to get a final diagnosis that will describe in more
details in this report.

1. Search the references that related to learning issues from internet, journals,
and text books.
2. Open web browser and type the keyword.
3. The search engine and web address that we used are:

www.google.com
www.scholar.google.com
www.ncbi.nlm.nih.gov
www.sciencedirect.com
www.who.com
www.medlineplus.gov
www.medscape.com

3.2 Answer of Learning Issue 2

3.2.1. Anatomy Changes in Pregnancy and Embriology& Fetal Growth
 Anatomy Changes in Pregnancy
Uterus
Changes in size, shape, and position. The phenomenal uterine growth in the
first trimester is stimulated by high levels of estrogen and progesterone. By 7
weeks of gestation, the uterus is the size of a large hen’s egg; by 10 weeks of
gestation is the size of an orange, and by the 12 weeks of gestation it is the
size of a grapefruit. After the third month, uterine enlargement is primarily the
result of mechanical pressure of the growing fetus.
As the uterus enlarges, it also changes in shape and position. At the conception
the uterus is shaped like an upside-down pear. During the second trimester, as
the muscular walls strengthen and become more elastic, the uterus becomes
sphericalor globular. Later, the uterus becomes larger and more ovoid and
rises out of the pelvis into abdominal cavity.
As the uterine grows, it may be palpated above the symphisis pubis between
twelfth and fourteenth weeks of pregnancy. The uteris rises gradually to the
level of the umbilicus at 22 to 24 weeks of gestation and nearly reaches the
xiphoid process at term. Between weeks 38-40, fundal height drops as the
fetus begins to descend and engage in the pelvis.

The uterus normally rotates to the right as it elevates, probably because of the
presence of the rectosigmoid colon on the left side, but the extensive
hypertrophy (enlargement) of the round ligaments keeps the uterus in the
midline. Eventually the growing uterus touches the anterior abdominal wall
and displaces the intestines to either side of the abdomen. At approximately 6
weeks of gestation, softening and compressibility of the lower uterine segment
occur, this called as Hegar Sign. This results in exaggerated uterine
anteflexion during the first 3 months of pregnancy. In this position, the uterine
fundus presses on the urinary bladder, causing the woman to have urinary
frequency.

Vagina and Vulva

Pregnancy hormones prepare the vagina for stretching during labor and birth
causing the vaginal mucosa to thicken, the connective tissue to loosen, the
smooth muscle to hyperthrophy, and the vaginal vault to lengthen. Increased
vascularity results in a violet-bluish color of the vaginal mucosa and cervix.
The deepened color, termed as Chadwick sign, may be evident as the early
sixth noted at the eighth week of pregnancy. Leukorrhea is a white or slightly
gray mucoid discharge with a faint musty odor. This copious mucoid fluid
occurs in response to cervical stimulation by estrogen and progesterone. The
mucus fills the endocervical canal, resulting in the formation of the mucous
plug (operculum). The operculum acts as a barrier against bacterial invasion
during pregnancy. External structures of the perineum are enlarged during
pregnancy because of an increase in vasculature, hypertrophy of the perineal
body, and deposition of fat.

Breasts
Fullness, heightened sensitivity, tingling, and heaviness of the breasts begin in
the early weeks of gestation in response to increased levels of estrogen and
progesterone. Nipples and areolae become more pigmented, secondary pinkish
areolae develop, extending beyond the primary areolae, and nipples become
more erectile. Hyperthrophy of the sebaceous (oil) glands embedded in the
primary areolae, called Montgomery tubercles, may be seen aroud the nipples.
Placenta

Placenta is an organ that connects the developing fetus to the uterine wall
(endometerium) to allow nutrient uptake, thermo -regulation, waste
elimination, and gas exchange via the mother's blood supply; to fight against
internal infection; and to produce hormones which support pregnancy. Human
placenta develops from two sources Fetal component- Chorionic frondosum
Maternal component- decidua basalis Placental development begins at 6 weeks
and is completed by 12 th week. The umbilical cord contains the blood vessels
that link the fetus to the placenta. Fetal blood is carried to the placenta in two
umbilical arteries. While traveling through the placenta, the blood picks up
nutrients and oxygen and gives up carbon dioxide and metabolic waste.
Restored blood is carried from the placenta to the fetus in a single umbilical
vein.
Vascular Architecture
MATERNAL
Under the initial hormonal influences of the corpus luteum, the spiral arteries
of the uterus become elongated and more extensively coiled. In the area
beneath the developing conceptus, the compression and erosion of the decidua
induces lateral looping of the already convoluted spiral arteries. These vessels
under the placenta gain access to the intervillous spaces.
The intervillous space is a large cavernous expanse that develops from the
fusion of the trophoblastic lacunae and the erosion of the decidua by the
expanding blastocyst. This space, which is essentially a huge blood sinus, is
bounded by the chorionic plate and the decidua basalis (i.e., the maternal or
basal plate). Folds in the basal plate form septa that separate the space into 13
to 30 anatomic compartments known as lobules. Each lobule contains
numerous villous trees that are also known as cotyledons or placentones.
 Although tightly packed with highly branched villous trees, the intervillous
space of the mature placenta can accommodate approximately 350 mL of
maternal blood
FETAL
Two coiled arteries bring fetal blood within the umbilical cord toward the
placenta. On the placental surface, these arteries divide into chorionic arteries
that ultimately supply the vessels of the 50 villous trees located in the placental
At the base of each villous tree, the chorionic arteries are considered the main
villous stem or truncal arteries (first-order vessels), which in turn branch into
four to eight ramal or cotyledonary arteries (second-order vessels); as they
pass toward the maternal plate, they further subdivide into ramuluschorii
(thirdorder vessels) and finally, terminal arterioles. 4 The terminal arterioles
lead through a neck region into a bulbous enlargement where they form two to
four narrow capillary loops. Here the large endothelial surface area and the
near absence of connective tissue allow optimal maternal-fetal exchange .The
venous end of the capillaries loops, narrows, and returns through the neck
region to the collecting venules, which coalesce to form the larger veins in the
stem of the villous trees. Each villous tree drains into a large vein, which, as it
perforates the chorionic plate, becomes a chorionic vein. All of the venous
tributaries course toward the umbilical cord attachment site, where they empty
into one umbilical vein that delivers blood to the fetus.

 Embryo and Fetal Growth

Germinal Stage (1 to 10 days)
a. Conception:
Conception is the meeting of ovum and sperm. However, for the occurrence of
a conception, there are two events that must occur first, are ovulation and
insemination. Ovulation is the collapse of the ovum from the follicles in the
ovary. Insemination is the emulsification of the male urethra into the woman's
vagina. several million sperm that enter the female reproductive tract every
time ejaculation of semen. By moving the tail, and with the help of the
surrounding muscular contractions, sperm travel through the uterus and into
the fallopian tube at a rate of 1 foot / hour. Sperm live for several days. If
ovulation occurs during the day, the ovum will be fertilized as soon as it leaves
the ovary.
b. Zygote formation
Once the sperm enters the ovum, its tail is released, and its head enlarges to
form male pronucleus. The nucleus ovum is a female pronucleus. The two
nuclei, with each of their 23 chromosomes, unite and form the first cell, which
then divides into millions. Each of these cells contains 46 chromosomes. All
these cells form new individuals.
c. Cleavage
The zygote undergoes cleavage with an interesting process called mitosis for
24 hours after conception. The zygote nucleus contains 46 chromosomes. This
 chromosome extends in pairs, each of which is elongated separately and then
divided into two, forming two identical forms of 46 chromosomes for the two
new cells formed from the first cell.
d. Morula becomes blastula
The ovum cleavages and cleavages again for about 12-15 hours following a
slow motion towards the fallopian tube. Immediately, the ovum is shaped like
a marbles, or morula. About 6 days later, when the ovum reaches the uterine
cavity, there is a major change in it. Cells form themselves into the outer layer
and groups of inner cells that protrude into the cavity. The liquid fills the space
between these layers and groups. This structure is now called blstoderm, or
blastula.
e. Implantation
As the blastula rolls into the uterine cavity, it loses its outer membrane called
the pelluside zone, then the blastula prepares to undergo oxidation or
implantation, in the endometrium. The outer layer of the cell, the tropoblast
secretes proteolytic enzymes, which dissolve some of the endometrium.
Tropoblast cells absorb the the enzyme.
f. Endometrial Nest
With the passage of time the oxidation occurs, the mother's uterus reaches the
premenstrual stage of secretion and is rich in vascularization. This condition is
a good thing for the setting of the ovum, which resembles a small parasite. The
endometrium is now called decidua basalis. Normally the implantation
location is next to the anterior or posterior uterine fundus.

Embryonic Stage (10th day to 8th week)

a. Embryonic Disc
There are three layers which lines between the yolk sac and the amniotic
cavity. These two layers form embryonic disc. From the outer layer into the
ectoderm, mesoderm, endoderm. Ectoderm will become the skin, the nervous
system and the sense organs. Mesoderm will form musculoskeletal, circulatory
and genitourinary systems. Endoderm will become the respiratory system and
urinary tract. All body systems are the result of folding an embryonic complex
in one layer of tissue to another.
b. Growth of corionic vesicles
The embryo develops from the stalk body in the amniotic cavity. The
membrane, the amnion, coats the cavity, which normally contains a fluid
called amniotic fluid, in which the embryo floats safely. The second
membrane, chorion is completely covered by the outer layer of the villi. All of
these structures are buried under the uterine decidua and are now called
chorionic vesicles. Because of the size of the embryo and chorion, both grow
toward the uterine cavity, pushing aside the decidua that covers it. Chorionic
villi on the side also disappear, leaving only villi at the place of implantation.
This area will become the placenta.
c. Growth of umbilicus and placenta
 Chorionic protrusions increase and branch out, are inserted into large maternal
veins or sinusis. each bulge is covered by millions of microscopic villi
containing blood capillaries. The capillaries unite to form larger veins until
they finally unite to form a very large vein, the umbilical vein. Fetal blood is
channeled back to the placenta through two umbilical arteries. In 1% infan
only has one umbilical artery, most of these babies fail to live or have severe
abnormalities.
The placenta consists of the maternal part (decidua basalis) and the fetal part
(chorionic villi). Maternal surface is redder and divided into several parts
(cotyledons). The fetal surface is covered with an amniotic membrane and a
smooth and gray membrane surface with vascular protrusions. Usually the axis
comes from the center of the placenta. In the weight of the placenta about 500
grams. The placenta gets older with term, and there will be several dead tissue
areas, called infarcts.

3.2.2. Physiological Changes in Pregnancy

 Haemotological changes

Plasma vol increases progressively throughout normal pregnancy. Increase 50%

occurs by 34weeks gestation and is proportional to the birthweight of the baby.
Because the expansion in plasma volume is greater than the increase in red
blood cell mass, there is a fall in haemoglobin concentration, haematocrit and
red blood cell count. Despite this haemodilution, there is usually no change in
mean corpuscular volume (MCV) or mean corpuscular haemoglobin
concentration (MCHC).
The platelet count tends to fall progressively during normal pregnancy,
although it usually remains within normal limits. In a proportion of women (5–
10%), the count will reach levels of 100–150 × 109 cells/l by term and this
occurs in the absence of any pathological process.
Pregnancy cause two- to three- fold increase in the requirement for iron, not
only for haemoglobin synthesis but also for the fetus and the production of
certain enzymes. There is a 10- to 20- fold increase in folate requirements and a
two-fold increase in the requirement or vit B12.
Changes in the coagulation system during pregnancy produce physiological
state (in preparation for haemostasis following delivery). The concentrations of
certain clotting factors, particularly VIII, IX and X, are increased. Fibrinogen
levels rise significantly by up to 50% and fibrinolytic activity is decreased.
Concentrations of endogenous anticoagulants such as antithrombin and protein
S decrease.

 Cardiac Changes

Changes in the cardiovascular system in pregnancy are profound and begin

early in pregnancy, such that by eight weeks’ gestation, the cardiac output has
already increased by 20%. The primary event is probably peripheral
vasodilatation. This is mediated by endothelium-dependent factors, including
nitric oxide synthesis, upregulated by oestradiol and possibly vasodilatory
prostaglandins (PGI2). Peripheral vasodilation leads to a 25–30% fall in
systemic vascular resistance, and to compensate for this, cardiac output
increases by around 40% during pregnancy. This is achieved predominantly via
an increase in stroke volume, but also to a lesser extent, an increase in heart
rate. The maximum cardiac output is found at about 20–28 weeks’ gestation
An increase in stroke volume is possible due to the early increase in ventricular
wall muscle mass and end-diastolic volume (but not end-diastolic pressure)
seen in pregnancy. The heart is physiologically dilated and myocardial
contractility is increased. Although stroke volume declines towards term, the
increase in maternal heart rate (10–20 bpm) is maintained, thus preserving the
increased cardiac output. Blood pressure decreases in the first and second
trimesters but increases to non-pregnant levels in the third trimester.
Although both blood volume and stroke volume increase in pregnancy,
pulmonary capillary wedge pressure and central venous pressure do not
increase significantly. Pulmonary vascular resistance (PVR), like systemic
vascular resistance (SVR), decreases significantly in normal pregnancy.
Although there is no increase in pulmonary capillary wedge pressure (PCWP),
serum colloid osmotic pressure is reduced by 10–15%. The colloid osmotic
pressure/pulmonary capillary wedge pressure gradient is reduced by about
30%, making pregnant women particularly susceptible to pulmonary oedema.
Pulmonary oedema will be precipitated if there is either an increase in cardiac
pre-load (such as infusion of fluids) or increased pulmonary capillary
permeability (such as in pre-eclampsia) or both.
Labour is associated with further increases in cardiac output (15% in the first
stage and 50% in the second stage) Uterine contractions lead to an auto-
transfusion of 300–500 ml of blood back into the circulation and the
sympathetic response to pain and anxiety further elevate the heart rate and
blood pressure. Cardiac output is increased between contractions but more so
during contractions.
Following delivery there is an immediate rise in cardiac output due to relief of
the inferior vena cava obstruction and contraction of the uterus, which empties
blood into the systemic circulation. Cardiac output increases by 60–80%,
followed by a rapid decline to pre-labour values within about one hour of
delivery. Transfer of fluid from the extravascular space increases venous return
and stroke volume further.
Normal findings on ECG in pregnancy that may partly relate to changes in the
position of the heart include:
 atrial and ventricular ectopics
 Q wave (small) and inverted T wave in lead III
 ST-segment depression and T-wave inversion in the inferior
 and lateral leads
  left-axis shift of QRS.

 Adaptive Changes in Renal Vasculature

The primary adaptive mechanism in pregnancy is a marked fall in systemic

vascular resistance (SVR) occurring by week six of gestation. The 40% fall in
SVR also affects the renal vasculature.
Despite a major increase in plasma volume during pregnancy, the massive
decrease in SVR creates a state of arterial under-filling because 85% of the
volume resides in the venous circulation.
Relaxin, a peptide hormone produced by the corpus luteum, decidua and
placenta, plays an important role in the regulation of haemodynamic and water
metabolism during pregnancy. Serum concentrations of relaxin, already elevated
in the luteal phase of the menstrual cycle, rise after conception to a peak at the
end of the first trimester and fall to an intermediate value throughout the second
and third trimester. Relaxin stimulates the formation of endothelin, which in turn
mediates vasodilation of renal arteries via nitric oxide (NO) synthesis.

 Changes in Renal Anatomy and Function

As a consequence of renal vasodilatation, renal plasma flow and glomerular

filtration rate (GFR) both increase, compared to non-pregnant levels, by 40–65
and 50–85%, respectively. In addition, the increase in plasma volume causes
decreased oncotic pressure in the glomeruli, with a subsequent rise in GFR.
Vascular resistance decreases in both the renal afferent and efferent arterioles
and therefore, despite the massive increase in renal plasma flow, glomerular
hydrostatic pressure remains stable, avoiding the development of glomerular
hypertension. As the GFR rises, both serum creatinine and urea concentrations
decrease to mean values of about 44.2 μmol/l and 3.2 mmol/l, respectively.
The increased renal blood flow leads to an increase in renal size of 1–1.5 cm,
reaching the maximal size by mid-pregnancy. The kidney, pelvis and calyceal
systems dilate due to mechanical compressive forces on the ureters.
Progesterone, which reduces ureteral tone, peristalsis and contraction pressure,
mediates these anatomical changes.The increase in renal size is associated with
an increase in renal vasculature, interstitial volume and urinary dead space.
There is also dilation of the ureters, renal pelvis and calyces, leading to
physiological hydronephrosis in over 80% of women.
There are also alterations in the tubular handling of wastes and nutrients. As in
the non-pregnant state, glucose is freely filtered in the glomerulus. During
pregnancy, the reabsorption of glucose in the proximal and collecting tubule is
less effective, with variable excretion. About 90% of pregnant women with
normal blood glucose levels excrete 1–10 g of glucose per day. Due to the
increases in both GFR and glomerular capillary permeability to albumin, the
fractional excretion of protein may increase up to 300 mg/day and protein
excretion also increases. In normal pregnancies the total protein concentration in
urine does not increase above the upper normal limit. Uric acid excretion also
increases due to increased GFR and/or decreased tubular reabsorption.

 Body Water Metabolism

Arterial under-filling in pregnancy leads to the stimulation of arterial

baroreceptors, activating the RAA and the sympathetic nervous systems. This
results in a non-osmotic release of AVP from the hypothalamus. These changes
lead to sodium and water retention in the kidneys and create a hypervolaemic,
hypo- osmolar state characteristic of pregnancy.
Extracellular volume increases by 30–50% and plasma volume by 30–40%.
Maternal blood volume increases by 45% to approximately 1 200 to 1 600 ml
above non-pregnant values. By the late third trimester the plasma volume
increases by more than 50–60%, with a lower increase in red blood cell mass,
and therefore plasma osmolality falls by 10 mosmol/kg. The increase in plasma
volume plays a critical role in maintaining circulating blood volume, blood
pressure and uteroplacental perfusion during pregnancy.
Activation of the RAA system leads to increased plasma levels of aldosterone
and subsequent salt and water retention in the distal tubule and collecting duct. In
addition to the increased renin production by the kidneys, ovaries and
uteroplacental unit produce an inactive precursor protein of renin in early
pregnancy.
In middle and late pregnancy there is a four-fold increase in vasopressinase, an
aminopeptidase produced by the placenta. These changes enhance the metabolic
clearance of vasopressin and regulate the levels of active AVP. In conditions of
increased placental production of vasopressinase, such as pre-eclampsia or twin
pregnancies, a transient diabetes insipidus may develop.As a consequence of this
volume expansion, the secretion of atrial natriuretic peptides increases by 40% in
the third trimester, and rises further during the first week postpartum. The levels
of natriuretic peptides are higher in pregnant women with chronic hypertension
and pre-eclampsia.

 Respiratory Changes

There is a significant increase in oxygen demand during normal pregnancy. This

is due to a 15% increase in metabolic rate and a 20% increased consumption of
oxygen. There is a 40-50% increase in minute ventilation, mostly due to an
increase in tidal volume, rather than in the respiratory rate. This maternal
hyperventilation causes arterial pO2 to increase and arterial pCO2 to fall, with
compensatory fall in serum bicarbonate to 18-22 mmol/l (table 1).
A mild fully compensated respiratory alkalosis is therefore normal in pregnancy
(arterial pH 7.44). Diaphragmatic elevation in late pregnancy results in decreased
functional residual capacity but diaphragmatic excursion and therefore vital
capacity remain unaltered. Inspiratory reserve volume is reduced early in
pregnancy, as a result of increased tidal volume, but increases in the third
trimester, as a result of reduced functional residual capacity. Peak expiratory flow
rate (PEFR) and forced expiratory volume in one second (FEV1) are unaffected
may by pregnancy. Pregnancy may also be accompanied by a subjective feeling of
breathlessness without hypoxia. This is physiological and is most common in the
third trisemeter but may start at any time during gestation. Usually, the
breathlessness is occur at rest or while talking and may paradoxically improve
during mild activity.

3.2.3. Gestational Hypertension

Hypertension is the most common medical problem encountered during

pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during
pregnancy are classified into 4 categories, as recommended by the National High
Blood Pressure Education Program Working Group on High Blood Pressure in
Pregnancy: 1) chronic hypertension, 2) preeclampsia-eclampsia, 3) preeclampsia
superimposed on chronic hypertension, and 4) gestational hypertension (transient
hypertension of pregnancy or chronic hypertension identified in the latter half of
pregnancy). The difference betweet these categories is in the time and she’s
proteinuria or not.
This terminology is preferred over the older but widely used term pregnancy-induced
hypertension (PIH) because it is more precise.Gestational hypertension, formerly
known as pregnancy-induced hypertension (PIH), is the new onset of hypertension
after 20 weeks of gestation (Mammaro et al., 2009).
The pathophysiology of gestational hypertension is unknown, but in the absence of
features of preeclampsia, the maternal and fetal outcomes are usually normal.
Gestational hypertension may, however, be a harbinger of chronic hypertension later
in life.
A cohort study that covered over 13,000 pregnancies by Egeland et al found that
gestational hypertension and preeclampsia share several preconception risk factors,
some of which could be modified to reduce the risk of adverse pregnancy outcomes.
The baseline risk factors shared among gestational hypertension and preeclampsia
were: family history of diabetes mellitus, a women's own diabetes status prior to
conception, a high total cholesterol/high-density lipoprotein cholesterol ratio (>5),
overweight and obesity, and elevated blood pressure status.
The diagnosis requires that the patient have:
 Elevated blood pressure (systolic ≥ 140 or diastolic ≥ 90 mm Hg, the latter
measured using the fifth Korotkoff sound)
 Previously normal blood pressures
 No protein in the urine
 No manifestations of preeclampsiaeclampsia.
Also known as transient hypertension, gestational hypertension is actually diagnosed
retrospectively when the patient does not develop preeclampsia and if blood pressure
returns to normal by the 12-week postpartum visit. Fifty percent of women diagnosed
with gestational hypertension between 24 and 35 weeks develop preeclampsia. The
diagnosis of gestational hypertension mandates increased surveillance. Women who
progress to severe gestational hypertension based on the degree of blood pressure
elevation have worse perinatal outcomes than do women with mild preeclampsia, and
require management similar to those with severe preeclampsia.
Treatment
a. Non pharmacological therapeutic approach
Lifestyle interventions, such as weight loss and a reduction in salt intake, are of
proven benefit in non-pregnant hypertensive patients (Kattah and Garovic, 2013).

b. Pharmacologic treatment of hypertension in pregnancy

Pharmacologic therapy during pregnancy may prevent progression to severe
hypertension and maternal complications (such as heart failure and cerebrovascular
events) while improving fetal maturity by permitting prolongation of pregnancy.
During both induction and titration of anti-hypertensive medications, fetal well-being
and safety should be closely monitored by several methods that are available in daily
clinical practice (Kattah and Garovic, 2013).

A – Controlled human studies show no risk, B- No evidence of risk in studies, C-

*

Risk cannot be ruled out, D- Positive evidence of risk

3.2.4. Pre-eclampsia
I. Definition
 The International Society for the Study of Hypertension in Pregnancy
defines preec-lampsia as hypertension of at least 140/90 mmHg on two
separate occasions < 4 hours apart accompanied by significant proteinuria
of at least 0.3 g in a 24-hour collection of urine (or .30 mg/mmol
protein/creatinine ratio), arising de novo after the 20th week of gestation
in a previously normotensive woman and resolving completely by the 6th
postpartum week.
Preeclampsia complicates 2%–8% of pregnancies and occurs most
commonly during the second half of pregnancy. While overall rates of
preeclampsia remain static, rates of severe preeclampsia appear to have
increased over recent decades. Preeclampsia is responsible for
approximately 15% of all direct maternal deaths in the UK. Furthermore,
the condition increases perinatal mortality, largely through iatrogenic
prematurity, by five-fold.
II. Clinical presentation and workup findings
Clinical and laboratory tests are intended to define and determine the
severity of pre-eclampsia. Headaches, tinnitus, phosphene signals, visual
disorders, brisk tendon reflexes, and vigilance disorders are related to
cerebral edema; oliguria to acute renal failure; uterine contraction, vaginal
bleeding to placental abruption; vomiting to HELLP syndrome; band-like
epigastric pain to subcapsular hepatic hematoma; and dyspnea to cardiac
failure.
Eclampsia, the major neurological complication of pre-eclampsia, is
defined as a convulsive episode or any other sign of altered consciousness
arising in a setting of pre-eclampsia, and which cannot be attributed to a
pre-existing neurological condition. Clinical examination should include
resting blood pressure measurement using an appropriate cuff, and
screening for weight gain, edema (including signs of acute pulmonary
edema and cerebral edema), cardiomyopathy, and acute renal failure. The
fetus should be assessed by electrocardiotocography.
Laboratory tests include: a complete blood count with platelets, hapto-
globin, and lactate dehydrogenase; a blood smear to test for schistocytes;
bilirubin, aspartate transaminase, and alanine transaminase in order to
identify potential HELPP syndrome; electrolyte, urea, and creatinine
assessment to check for acute renal failure or uremia; 24-hour proteinuria;
prothrombin, activated thrombin time, and fibrinogen (microangiopathic
hemolytic anemia); blood group; and irregular antibody screening.
Other examinations include fetal ultrasound with Doppler velocimetry
of the umbilical, cerebral, and uterine arteries, estimation of fetal weight,
assessment of fetal well-being by Manning score, and examination of the
placenta.
Although the definition of severe pre-eclampsia varies,1,21,22 several
components of this definition are usually accepted: maternal systolic
blood pressure >160 mmHg or diastolic blood pressure >110 mmHg;
 maternal neurological disorders such as persistent headaches, phosphene
signals, tinnitus, and brisk, diffuse, polykinetic tendon reflexes, eclampsia,
acute pulmonary edema, proteinuria >5 g/day, oliguria, 500 cc/day,
creatinine .120 µmol/L, HELLP syndrome, thrombocytopenia,
100,000/mm3, and fetal criteria, especially intrauterine growth retardation,
oligohydramnios, or fetal death in utero.
Mild pre-eclampsia is defined as diastolic blood pressure >90 mmHg
measured on two occasions at least 6 hours apart, combined with
proteinuria (two or more occurrences of protein on dipstick, .300 mg total
protein in a 24-hour urine collection, or a protein creatinine ratio .30
mg/mmol)
III. Risk Factors of Pre-eclampsia
Early identification of preeclampsia (and if possible, prevention) is a core
tenet of adequate management. The National Institute for Health and Care
Excellence (NICE) recommends that women at high risk of preeclampsia
be identified before week 13 of gestation and low-dose aspirin
commenced until 36 weeks’ gestation. There are many conditions and
health risk behaviors that are thought to predispose to preeclampsia; these
are summarized in Table 1. High-risk women include those with
preexisting hypertension, chronic kidney disease, insulin-dependent
diabetics, and women with previous early onset preeclampsia.

Administration of low-dose aspirin to women at moderate-to-high risk has

been shown to be beneficial and reduces the incidence of preeclampsia by
approximately 15%.18 Preeclampsia is more common in primigravida women
and the risk of preeclampsia increases the greater the interval between
pregnancies. Age greater than 40 years of age increases risk (relative risk
[RR]: 1.96, 95% confidence interval [CI]: 1.34–2.87), as does a previous
history of preeclampsia (RR: 7.19, 95% CI: 5.85–8.83), pre-pregnancy obesity
 (RR: 2.47, 95% CI: 1.66–3.67), and women who become pregnant with donor
eggs, embryo donation, or donor insemination.
Other risk factors include diabetes (RR: 3.56, 95% CI: 2.54–4.99),
preexisting hypertension (RR: 1.38, 95% CI: 1.01–1.87), those with a family
history of preeclampsia (RR: 2.90, 95% CI: 1.70–4.93), and women suffering
from medical conditions such as antiphospholipid syndrome (RR: 9.72, 95%
CI: 4.34–21.75). In addition, it appears that various paternal factors can
increase the risk of a pregnancy being complicated by preeclampsia.
Preeclampsia is in itself a risk factor for both early and late complications
affecting mother and baby. Preeclampsia may be complicated by seizures
(eclampsia; 2–3 vs 40–90 cases/10,000 births in Europe and developing
countries, respectively), pulmonary edema, placental abruption (1%–4%),
oligohydramnios, and fetal growth restriction (up to 30%). Long-term effects
on offspring include an increased risk of stroke and hypertension.21–23 In
addition to the long-term health implications for offspring, women with
preeclampsia have 3.7 times higher risk of developing hypertension later in
life, 2.2 times increased risk of coronary heart disease, and 1.8 times higher
risk of stroke.

3.2.5. Eclampsia
I. Definition
Eclampsia is a uniquely pregnancy-related disorder that manifests as new
onset of generalized tonic colonic seizures. It typically occurs after 20 weeks of
concluded gestation, although it may occur sooner with plural gestations or molar
pregnancies, and may additionally occur in the 6-week postpartum window. It
represents the severe end of the preeclampsia spectrum. Preeclampsia spectrum
includes symptoms of the central nervous system (CNS), for example, severe
headaches or vision changes, and may involve hepatic abnormalities (such as
elevated liver transaminases with right upper quadrant/epigastric discomfort),
elevated blood pressures, and also may include thrombocytopenia, renal
abnormalities, and pulmonary edema. In developed countries, resultant maternal
mortality may be as high as 1.8%, and in the developing countries, it may be as
high as 14%.
II. Etiology
The etiology of the disorder remains elusive. The placenta seems to have a
prime role in its etiology. An increase in placental mass, as in plural pregnancies,
increases the risk for the preeclampsia-eclampsia spectrum, as does placental
edema that occurs in pregnancies complicated by fetal hydrops. Molar
pregnancies that impact placental architecture also have a higher risk of the
complication.
III. Pathophysiology
Some have suggested hypertension causes breakdown of the autoregulatory
mechanisms of cerebral circulation inducing endothelial dysfunction that
concludes in cytotoxic edema and expression of a generalized seizure.
 Inflammation of the cerebrum seems to play a role in the pathophysiology. In
some scenarios, it may be associated with posterior reversible encephalopathy
syndrome due to posterior circulation's inability to autoregulate itself in response
to acute hypertension.
IV. Sign And Symptom
The warning signs of imminent eclampsiaare :
1. Systolic blood pressure of 160 mmHg or more on two occasions six hours
apart when the patient is on bed rest;
2. Proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative
assay;
3. Oliguria or anuria;
4. Cerebral or visual disturbances;
5. Pulmonary edema or cyanosis; and Epigastric/right hypochondriac pain,
impaired liver function, and thrombocytopenia and coagulation disorders.
V. Features of eclampsiaincludes :
 Seizure or postictal state (100%)
 Headache (80%), usually frontal
 Generalized edema (50%)
 Vision disturbance (40%), such as blurred vision and photophobia
 Right upper quadrant abdominal pain with nausea (20%)
 Amnesia and other mental status changes
VI. History and Physical Diagnosis
There may history of worsening headaches with vision changes such as blurred
vision or “spots.” Hypertension and proteinuria may be present or absent.
Impending eclampsia may have clonus. Eclampsia is a clinical diagnosis that is
described by the occurrence of new-onset generalized tonic-clonic seizures in a
woman with preeclampsia; however, on occasion, it may be the first
presentation of preeclampsia. Clinical findings may include posterior
reversible encephalopathy syndrome (due to vasogenic edema predominantly
localized in the posterior cerebral hemispheres), which include a headache,
confusion, visual symptoms, and seizure.
VII. Risk Factor
 Nulliparity
 Family history of preeclampsia, previous preeclampsia and eclampsia
 Poor outcome of previous pregnancy, including intrauterine growth
retardation, abruptio placentae, or fetal death
 Multifetal gestation, hydatid mole,fetal hydrops
 Teen pregnancy
 Primigravida
 Patient older than 35 years
 Lower socioeconomic status
 Obesity
 Chronic hypertension
  Renal disease
 Thrombophilias-antiphospholipid antibody syndrome
 Antithrombin deficiency
 Vascular and connective tissue disorders
 Gestational diabetes
 SLE
VIII. Prognosis
Patients should be monitored closely because recurrent attack of seizure may
increase risk of morbidity. Most significant maternal complication of eclampsia is
permanent CNS damage from recurrent seizures or intracranial bleeding. The
fetus should also be monitored because the baby is born premature (Ross, 2017).
IX. Treatment/Management
Acute care is prioritized to maintain the airway, prevent aspiration, and
prevent maternal injury. The patient should be shifted onto her left side and once
the seizures have concluded maternal oxygenation is optimized with the
supplemental oxygen of 8 to 10 liters per minute administered via a
nonrebreathing face mask to treat hypoxemia that occurs from hypoventilation
during the seizure activity.
Magnesium sulfate is a treatment of choice to prevent recurrent seizures;
however, approximately 10% of will have a repeat a seizure despite magnesium
sulfate therapy. Recurrent seizures require surveillance for rhabdomyolysis,
metabolic acidosis, aspiration pneumonia and neurogenic pulmonary edema.
Magnesium sulfate remains superior for recurrent seizure activity (an additional 2
gm bolus can be considered in those already on magnesium sulfate therapy), but
the addition of intravenous lorazepam 2mg intravenously over 3 to 5 minutes may
also be considered. The initial loading bolus of magnesium sulfate is 4 gm to 6 gm
intravenously over 15 to 20 minutes with a maintenance dose of 1 gm to 3 gm an
hour, depending on renal function. Blood levels of magnesium are monitored
every four hours and targeted at four mE/L to -7 mE/L or 5 mg/dl to 9 mg/dl.
Urine output is closely monitored. Should magnesium sulfate toxicity occur
calcium, gluconate 1 gm intravenously can be administered.
Management of severe hypertension is the next focus of patient care. A
preferred agent for treatment of severe hypertension is intravenous labetalol
(initial dose of 20 mg and for recalcitrant severe hypertension follow-up dose of
40 mg and 80 mg every 15 minutes). Maintaining systolic blood pressure between
140 mm HG to 160 mmHg and diastolic blood pressure between 90 mmHg to
105 mmHg are targeted treatment goals.
Fetal bradycardia lasting 3 to 5 minutes is a common finding during and
immediately after the seizure and does not indicate emergency cesarean delivery.
Stabilization of the mother by stabilizing the seizure activity and correction of
maternal hypertension if present and oxygen to treat hypoxemia and hypercarbia
is the mainstay of initial supportive therapies are part of fetal intrauterine fetal
resuscitation. However, if the fetal heart rate strip does not improve after 15
 minutes of maternal and fetal resuscitative interventions then a differential
diagnosis of occult abruption should be considered, and emergent cesarean
delivery may be indicated. Eclampsia represents an absolute contraindication to
expectant management. Once the maternal-fetal condition is stabilized, delivery
should be accomplished labor induction. This is a particularly reasonable option
after 32 weeks of gestation. It may be an option at early gestations with a
favorable Bishop score; however, long induction-delivery intervals are best
avoided with a clear end-point for delivery to be concluded within 24 hours.
3.3 Analysis
3.4 Final Hypothesis
3.5 Group Opinion
3.6 Final Concept Mapping
3.7 Conclusion

Pregnant women, 8 months came to the hospital with complaints of swelling in the
right and left lower extremities. In the vital sign has blood pressure of 170/100
mmHg, while before pregnancy the blood pressure is 110/70 mmHg. In complete
urine examination, proteinuria +3 is obtained. Based on these data we diagnose
patients suffering from severe pre-eclampsia.

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