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Alternative Names Return to top

Premature separation of placenta; Ablatio placentae; Abruptio placentae; Placental abruption

Definition Return to top

Placenta abruptio is separation of the placenta (the organ that nourishes the fetus) from the site
of uterine implantation before delivery of the fetus.

Causes Return to top

The exact cause of a placetal abruption may be difficult to determine.

Direct causes are rare, but include:

• Abnormally short umbilical cord


• Injury to the belly area (abdomen) from a fall or automobile accident
• Sudden loss in uterine volume (can occur with rapid loss of amniotic fluid or the delivery
of a first twin)

Risk factors include:

• Advanced maternal age


• Cigarette smoking
• Cocaine use
• Diabetes
• Drinking more than 14 alcoholic drinks per week during pregnancy
• High blood pressure during pregnancy -- About half of placental abruptions that lead to
the baby's death are linked to high blood pressure
• History of placenta abruptio
• Increased uterine distention (as may occur with multiple pregnancies or abnormally large
volume of amniotic fluid)
• Large number of prior deliveries

Placenta abruptio, including any amount of placental separation prior to delivery, occurs in about
1 out of 150 deliveries. The severe form, which results in fetal death, occurs only in about 1 out of
500 to 750 deliveries.

Symptoms Return to top

• Abdominal pain
• Back pain
• Vaginal bleeding

Exams and Tests Return to top

Tests may include:

• Abdominal ultrasound
• Complete blood count
• Fibrinogen level
• Partial thromboplastin time
• Pelvic exam
• Prothrombin time

Treatment Return to top

Treatment may fluids through a vein (IV) and blood transfusions. The mother will be carefully
monitored for symptoms of shock and the unborn baby will be watched for signs of distress,
which includes an abnormal heart rate.

An emergency cesarean section may be necessary. If the fetus is very immature and there is only
a small placenta rupture, the mother may be kept in the hospital for close observation and
released after several days if the condition does not get worse

If the fetus is developed (matured) enough, vaginal delivery may be chosen if there is minimal
distress to the mother and child. Otherwise, a cesarean section may be the preferred choice.

Outlook (Prognosis) Return to top

The mother does not usually die from this condition. However, the following increase the risk for
death in both the mother and baby:

• Absence of labor
• Closed cervix
• Delayed diagnosis and treatment of placenta abruption
• Excessive blood loss resulting in shock
• Hidden (concealed) vaginal bleeding in pregnancy

Fetal distress appears early in the condition in about half of all cases. The infants who live have a
40-50% chance of complications, which range from mild to severe.

Possible Complications Return to top

Excessive loss of blood may lead to shock and possible death in the mother or baby. If bleeding
occurs after the delivery and blood loss cannot be controlled by other means, a hysterectomy
(removal of the uterus) may become necessary.

When to Contact a Medical Professional Return to top

Call your health care provider if you are in an auto accident, even if the accident is relatively
minor.

See your health care provider immediately, call your local emergency number (such as 911), or
go to the emergency room if you are pregnant and have symptoms of this condition. Placenta
abruptio can rapidly become an emergency condition that threatens the life of both the mother
and baby.

Prevention Return to top


Avoid drinking, smoking, or using recreational drugs during pregnancy. Get early and continuous
prenatal care.

Early recognition and proper management of conditions in the mother such as diabetes and high
blood pressure also decrease the risk of placenta abruptio.

References Return to top

Francois KE, Foley MR. Antepartum and postpartum hemorrhage. In: Gabbe SG, Niebyl JR,
Simpson JL, eds. Obstetrics - Normal and Problem Pregnancies. 5th ed. Philadelphia, Pa:
Elsevier Churchill Livingstone; 2007:chap 18.

Houry DE, Abbott JT. Acute complications of pregnancy. In: Marx J, ed. Rosen’s Emergency
Medicine: Concepts and Clinical Practice. 6th ed. St Philadelphia, Pa: Mosby Elsevier; 2006:chap
177.

., Inc. Placental abruption


From Wikipedia, the free encyclopedia

(Redirected from Abruptio placentae)


Jump to: navigation, search
Placental abruption
Classification and external
resources

ICD-10 O45.

ICD-9 641.2

DiseasesDB 40

MedlinePlus 000901

eMedicine med/6
emerg/12

MeSH D000037

Placental abruption (Also known as abruptio placentae) is a complication of


pregnancy, wherein the placental lining has separated from the uterus of the
mother. It is the most common cause of late pregnancy bleeding. In humans, it
refers to the abnormal separation after 20 weeks of gestation and prior to birth. It
occurs in 1% of pregnancies world wide with a fetal mortality rate of 20-40%
depending on the degree of separation. Placental abruption is also a significant
contributor to maternal mortality.

The heart rate of the fetus can be associated with the severity.[1]

Contents
[hide]

• 1 Lasting effects
• 2 Symptoms
• 3 Pathophysiology
• 4 Risk factors
• 5 Intervention
• 6 References

• 7 External links

[edit] Lasting effects


On the mother:

• A large loss of blood or hemorrhage may require blood transfusions and intensive
care after delivery.
• The uterus may not contract properly after delivery so the mother may need
medication to help her uterus contract. 'APH weakens, for PPH to kill'.
• The mother may have problems with blood clotting for a few days.
• If the mother's blood does not clot (particularly during a caesarean section) and
too many transfusions could put the mother into disseminated intravascular
coagulation (DIC), the doctor may consider a hysterectomy.
• A severe case of shock may affect other organs, such as the liver, kidney, and
pituitary gland.
• In some cases where the abruption is high up in the uterus, or is slight, there is no
bleeding, though extreme pain is felt and reported.

On the baby:

• If a large amount of the placenta separates from the uterus, the baby will probably
be in distress until delivery. It may die in utero, resulting in a Stillbirth.
• The baby may be premature and need to be placed in the newborn intensive care
unit. He or she might have problems with breathing and feeding.
• If the baby is in distress in the uterus, he or she may have a low level of oxygen in
the blood after birth.
• The newborn may have low blood pressure or a low blood count.
• If the separation is severe enough, the baby could suffer brain damage or die
before or shortly after birth.

[edit] Symptoms
• contractions that don't stop
• pain in the uterus
• tenderness in the abdomen
• vaginal bleeding (sometimes)

[edit] Pathophysiology
Trauma, hypertension, or coagulopathy, contributes to the avulsion of the
anchoring placental villi from the expanding lower uterine segment, which in turn,
leads to bleeding into the decidua basalis. This can push the placenta away from
the uterus and cause further bleeding. Bleeding through the vagina, called overt
or external bleeding, occurs 80% of the time, though sometimes the blood will
pool behind the placenta, known as concealed or internal placental abruption.

Women may present with vaginal bleeding, abdominal or back pain, abnormal or
premature contractions, fetal distress or death.

Abruptions are classified according to severity in the following manner:

• Grade 0: Asymptomatic and only diagnosed through post partum examination of


the placenta.
• Grade 1: The mother may have vaginal bleeding with mild uterine tenderness or
tetany, but there is no distress of mother or fetus.
• Grade 2: The mother is symptomatic but not in shock. There is some evidence of
fetal distress can be found with fetal heart rate monitoring.
• Grade 3: Severe bleeding (which may be occult) leads to maternal shock and
fetal death. There may be maternal disseminated intravascular coagulation. Blood
may force its way through the uterine wall into the serosa, a condition known as
Couvelaire uterus.

[edit] Risk factors


• Maternal hypertension is a factor in 44% of all abruptions.
• Maternal trauma, such as motor vehicle accidents, assaults, falls, or nosocomial
• Short umbilical cord
• Prolonged rupture of membranes (>24 hours)
• Retroplacental fibromyoma
• Maternal age: pregnant women who are younger than 20 or older than 35 are at
greater risk.
• Previous abruption: Women who have had an abruption in previous pregnancies
are at greater risk.
• some infections are also diagnosed as a cause

The risk of placental abruption can be reduced by maintaining a good diet


including taking folic acid, regular sleep patterns and correction of pregnancy-
induced hypertension.

[edit] Intervention
Placental abruption is suspected when a pregnant woman has sudden localized
uterine pain with or without bleeding. The fundus may be monitored because a
rising fundus can indicate bleeding. An ultrasound may be used to rule out
placenta praevia but is not diagnostic for abruption. The mother may be given
Rhogam if she is Rh negative.

Treatment depends on the amount of blood loss and the status of the fetus. If the
fetus is less than 36 weeks and neither mother or fetus are in any distress, then
they may simply be monitored in hospital until a change in condition or fetal
maturity whichever comes first.

Immediate delivery of the fetus may be indicated if the fetus is mature or if the
fetus or mother are in distress. Blood volume replacement and to maintain blood
pressure and blood plasma replacement to maintain fibrinogen levels may be
needed. Vaginal birth is usually preferred over caesarean section unless there is
fetal distress. Caesarean section is contraindicated in cases of disseminated
intravascular coagulation. Patient should be monitored for 7 days for PPH.
Excessive bleeding from uterus may necessitate hysterectomy if family size is
completed.

What is a miscarriage?

A miscarriage is the loss of a pregnancy during the first 20 weeks. It is usually your body's way of
ending a pregnancy that has had a bad start. The loss of a pregnancy can be very hard to accept.
You may wonder why it happened or blame yourself. But a miscarriage is no one’s fault, and you
can't prevent it.

Miscarriages are very common. About 1 in 4 pregnancies end in a miscarriage.1 It is also common
for a woman to have a miscarriage before she even knows that she is pregnant.

What causes a miscarriage?


Most miscarriages happen because the fertilized egg in the uterus does not develop normally. A
miscarriage is not caused by stress, exercise, or sex. In many cases, doctors don't know what
caused the miscarriage.

The risk of miscarriage is lower after the first 12 weeks of the pregnancy.

What are the common symptoms?

Common signs of a miscarriage include:

• Bleeding from the vagina. The bleeding may be light or heavy, constant or off and on. It can
sometimes be hard to know whether light bleeding is a sign of miscarriage. But if you have
bleeding with pain, the chance of a miscarriage is higher.

• Pain in the belly, lower back, or pelvis.

• Tissue that passes from the vagina.

How is a miscarriage diagnosed?

Call your doctor if you think you are having a miscarriage. If your symptoms and a pelvic exam do
not show whether you are having a miscarriage, your doctor can do tests to see if you are still
pregnant.

How is it treated?

No treatment can stop a miscarriage. As long as you do not have heavy blood loss, a fever,
weakness, or other signs of infection, you can let a miscarriage follow its own course. This can
take several days.

If you have Rh-negative blood, you will need a shot of Rhogam. This prevents problems in future
pregnancies. If you have not had your blood type checked, you will need a blood test to find out if
you are Rh-negative.

Many miscarriages complete on their own, but sometimes treatment is needed. If you are having
a miscarriage, work with your doctor to watch for and prevent problems. If the uterus does not
clear quickly enough, you could lose too much blood or develop an infection. In this case,
medicine or a procedure called a dilation and curettage (D&C) can more quickly clear tissue from
the uterus.

A miscarriage doesn't happen all at once. It usually takes place over several days, and symptoms
vary. Here are some tips for dealing with a miscarriage:
• Use pads instead of tampons. You will probably have vaginal bleeding for a week or so. It may
be like or slightly heavier than a normal period. You may use tampons during your next period,
which should start in 3 to 6 weeks.

• Take acetaminophen (Tylenol) for cramps. Read and follow all instructions on the label. You
may have cramps for several days after the miscarriage.

• Eat a balanced diet that is high in iron and vitamin C. You may be low in iron because of blood
loss. Foods rich in iron include red meat, shellfish, eggs, beans, and leafy green vegetables.
Foods high in vitamin C include citrus fruits, tomatoes, and broccoli. Talk to your doctor about
whether you need to take iron pills or a multivitamin.

• Talk with family, friends, or a counselor if you are having trouble dealing with the loss of your
pregnancy. If you feel very sad or depressed for longer than 2 weeks, talk to a counselor or your
doctor.

• Talk with your doctor about any future pregnancy plans. Most doctors suggest that you wait until
you have had at least one normal period before you try to get pregnant again. If you don't want
to get pregnant, ask your doctor about birth control options.

Miscarriage
From Wikipedia, the free encyclopedia

Jump to: navigation, search


Miscarriage
Classification and external
resources

ICD-10 O03.

ICD-9 634

MedlinePlus 001488

eMedicine topic list

MeSH D000022
Miscarriage or spontaneous abortion is the natural or spontaneous end of a
pregnancy at a stage where the embryo or fetus is incapable of surviving,
generally defined in humans at prior to 20 weeks of gestation. Miscarriage is the
most common complication of early pregnancy.[1] The medical term "spontaneous
abortion" is used in reference to miscarriages because the medical term
"abortion" refers to any terminated pregnancy, deliberately induced or
spontaneous, although in common parlance it refers specifically to active
termination of pregnancy.

Contents
[hide]

• 1 Terminology
• 2 Forms and types
• 3 Causes
o 3.1 First trimester
o 3.2 Second trimester
o 3.3 General risk factors
o 3.4 Correlations
• 4 Prevalence
• 5 Detection
• 6 Management
• 7 Pathology
• 8 Psychological aspects
• 9 ICD10 codes
• 10 See also
• 11 References

• 12 External links

[edit] Terminology
Very early miscarriages - those which occur before the sixth week LMP (since the
woman's Last Menstrual Period) are medically termed early pregnancy loss[2] or
chemical pregnancy.[3] Miscarriages that occur after the sixth week LMP are
medically termed clinical spontaneous abortion.[2]

In medical contexts, the word "abortion" refers to any process by which a


pregnancy ends with the death and removal or expulsion of the fetus, regardless
of whether it is spontaneous or intentionally induced. Many women who have had
miscarriages, however, object to the term "abortion" in connection with their
experience, as it is generally associated with induced abortions. In recent years
there has been discussion in the medical community about avoiding the use of
this term in favor of the less ambiguous term "miscarriage."[4]
Labour resulting in live birth before the 37th week of pregnancy is termed
"premature birth," even if the infant dies shortly afterward. The limit of viability at
which 50% of fetus/infants survive longterm is around 24 weeks, with moderate
or major neurological disability dropping to 50% only by 26 weeks.[5] Although
long-term survival has never been reported for infants born from pregnancy
shorter than 21 weeks and 5 days,[6] infants born as early as the 16th week of
pregnancy may sometimes live for some minutes after birth.[7]

A fetus that dies while in the uterus after about the 20-24th week of pregnancy is
termed a "stillbirth"; the precise gestational age definition varies by country.
Premature births or stillbirths are not generally considered miscarriages, though
usage of the terms and causes of these events may overlap.

[edit] Forms and types


The clinical presentation of a threatened abortion describes any bleeding seen
during pregnancy prior to viability, that has yet to be assessed further. At
investigation it may be found that the fetus remains viable and the pregnancy
continues without further problems. It has been suggested that bed rest improves
the chances of the pregnancy continuing when a small subchorionic hematoma
has been found on ultrasound scans.[8]

Alternatively the following terms are used to describe pregnancies that do not
continue:

• An empty sac is a condition where the gestational sac develops normally, while
the embryonic part of the pregnancy is either absent or stops growing very early.
Other terms for this condition are blighted ovum and anembryonic pregnancy.
• An inevitable abortion describes where the fetal heart beat is shown to have
stopped and the cervix has already dilated open, but the fetus has yet to be
expelled. This usually will progress to a complete abortion.
• A complete abortion is when all products of conception have been expelled.
Products of conception may include the trophoblast, chorionic villi, gestational
sac, yolk sac, and fetal pole (embryo); or later in pregnancy the fetus, umbilical
cord, placenta, amniotic fluid, and amniotic membrane.
• An incomplete abortion occurs when tissue has been passed, but some remains in
utero.[9]
• A missed abortion is when the embryo or fetus has died, but a miscarriage has not
yet occurred. It is also referred to as delayed miscarriage.

The following two terms consider wider complications or implications of a


miscarriage:
• A septic abortion occurs when the tissue from a missed or incomplete abortion
becomes infected. The infection of the womb carries risk of spreading infection
(septicaemia) and is a grave risk to the life of the woman.
• Recurrent pregnancy loss (RPL) or recurrent miscarriage (medically termed
habitual abortion) is the occurrence of three consecutive miscarriages. If the
proportion of pregnancies ending in miscarriage is 15%,[10] then the probability of
two consecutive miscarriages is 2.25% and the probability of three consecutive
miscarriages is 0.34%. The occurrence of recurrent pregnancy loss is 1%. [10] A
large majority (85%) of women who have had two miscarriages will conceive and
carry normally afterwards.

[edit] Causes
Miscarriages can occur for many reasons, not all of which can be identified.

[edit] First trimester

Most clinically apparent miscarriages (two thirds to three-quarters in various


studies) occur during the first trimester.[11][12]

Chromosomal abnormalities are found in more than half of embryos miscarried in


the first 13 weeks. A pregnancy with a genetic problem has a 95% chance of
ending in miscarriage. Most chromosomal problems happen by chance, have
nothing to do with the parents, and are unlikely to recur.[13] Genetic problems are
more likely to occur with older parents; this may account for the higher
miscarriage rates observed in older women.[14]

Another cause of early miscarriage may be progesterone deficiency. Women


diagnosed with low progesterone levels in the second half of their menstrual
cycle (luteal phase) may be prescribed progesterone supplements, to be taken
for the first trimester of pregnancy.[13] However, no study has shown that general
first-trimester progesterone supplements reduce the risk of miscarriage,[15] and
even the identification of problems with the luteal phase as contributing to
miscarriage has been questioned.[16]

[edit] Second trimester

Up to 15% of pregnancy losses in the second trimester may be due to uterine


malformation, growths in the uterus (fibroids), or cervical problems.[13] These
conditions may also contribute to premature birth.[11]

One study found that 19% of second trimester losses were caused by problems
with the umbilical cord. Problems with the placenta may also account for a
significant number of later-term miscarriages.[17]
[edit] General risk factors

Pregnancies involving more than one fetus are at increased risk of miscarriage.[13]

Uncontrolled diabetes greatly increases the risk of miscarriage. Women with


controlled diabetes are not at higher risk of miscarriage. Because diabetes may
develop during pregnancy (gestational diabetes), an important part of prenatal
care is to monitor for signs of the disease.[13]

Polycystic ovary syndrome is a risk factor for miscarriage, with 30-50% of


pregnancies in women with PCOS being miscarried in the first trimester. Two
studies have shown treatment with the drug metformin to significantly lower the
rate of miscarriage in women with PCOS (the metformin-treated groups
experienced approximately one-third the miscarriage rates of the control
groups).[18] However, a 2006 review of metformin treatment in pregnancy found
insufficient evidence of safety and did not recommend routine treatment with the
drug.[19]

High blood pressure and certain illnesses (such as rubella and chlamydia)
increase the risk of miscarriage.[13]

Tobacco (cigarette) smokers have an increased risk of miscarriage.[20] An


increase in miscarriage is also associated with the father being a cigarette
smoker.[2] The husband study observed a 4% increased risk for husbands who
smoke less than 20 cigarettes/day, and an 81% increased risk for husbands who
smoke 20 or more cigarettes/day.

Severe cases of hypothyroidism increase the risk of miscarriage. The effect of


milder cases of hypothyroidism on miscarriage rates has not been established.
Certain immune conditions such as autoimmune diseases greatly increase the
risk of miscarriage.[13]

Cocaine use increases miscarriage rates.[20] Physical trauma, exposure to


environmental toxins, and use of an IUD during the time of conception have also
been linked to increased risk of miscarriage.[21]

[edit] Correlations

Several factors have been correlated with higher miscarriage rates, but whether
they cause miscarriages is debated. No causal mechanism may be known, the
studies showing a correlation may have been retrospective (beginning the study
after the miscarriages occurred, which can introduce bias) rather than
prospective (beginning the study before the women became pregnant), or both.

Nausea and vomiting of pregnancy (NVP, or morning sickness) are associated


with a decreased risk of miscarriage. Several mechanisms have been proposed
for this relationship, but none are widely agreed on.[22] Because NVP may alter a
woman's food intake and other activities during pregnancy, it may be a
confounding factor when investigating possible causes of miscarriage.

One such factor is exercise. A study of over 92,000 pregnant women found that
most types of exercise (with the exception of swimming) correlated with a higher
risk of miscarriage prior to 18 weeks. Increasing time spent on exercise was
associated with a greater risk of miscarriage: an approximately 10% increased
risk was seen with up to 1.5 hours per week of exercise, and a 200% increased
risk was seen with over 7 hours per week of exercise. High-impact exercise was
especially associated with the increased risk. No relationship was found between
exercise and miscarriage rates after the 18th week of pregnancy. The majority of
miscarriages had already occurred at the time women were recruited for the
study, and no information on nausea during pregnancy or exercise habits prior to
pregnancy was collected.[23]

Caffeine consumption has also been correlated to miscarriage rates, at least at


higher levels of intake. A 2007 study of over 1,000 pregnant women found that
women who reported consuming 200 mg or more of caffeine per day
experienced a 25% miscarriage rate, compared to 13% among women who
reported no caffeine consumption. 200 mg of caffeine is present in 10 oz
(300 mL) of coffee or 25 oz (740 mL) of tea. This study controlled for pregnancy-
associated nausea and vomiting (NVP or morning sickness): the increased
miscarriage rate for heavy caffeine users was seen regardless of how NVP
affected the women. About half of the miscarriages had already occurred at the
time women were recruited for the study.[24] A second 2007 study of
approximately 2,400 pregnant women found that caffeine intake up to 200 mg
per day was not associated with increased miscarriage rates (the study did not
include women who drank more than 200 mg per day past early pregnancy).[25]

[edit] Prevalence
Determining the prevalence of miscarriage is difficult. Many miscarriages happen
very early in the pregnancy, before a woman may know she is pregnant.
Treatment of women with miscarriage at home means medical statistics on
miscarriage miss many cases.[26] Prospective studies using very sensitive early
pregnancy tests have found that 25% of pregnancies are miscarried by the sixth
week LMP (since the woman's Last Menstrual Period).[27][28] Clinical miscarriages
(those occurring after the sixth week LMP) occur in 8% of pregnancies.[28]

The risk of miscarriage decreases sharply after the 10th week LMP, i.e. when the
fetal stage begins.[29] The loss rate between 8.5 weeks LMP and birth is about
two percent; loss is “virtually complete by the end of the embryonic period."[30]

The prevalence of miscarriage increases considerably with age of the parents.


One study found that pregnancies from men younger than twenty-five years are
40% less likely to end in miscarriage than pregnancies from men 25-29 years.
The same study found that pregnancies from men older than forty years are 60%
more likely to end in miscarriage than the 25-29 year age group.[31] Another study
found that the increased risk of miscarriage in pregnancies from older men is
mainly seen in the first trimester.[32] Yet another study found an increased risk in
women, by the age of forty-five, on the order of 800% (compared to the 20-24
age group in that study), 75% of pregnancies ended in miscarriage.[33]

[edit] Detection
The most common symptom of a miscarriage is bleeding;[34] bleeding during
pregnancy may be referred to as a threatened abortion. Of women who seek
clinical treatment for bleeding during pregnancy, about half will go on to have a
miscarriage.[26] Symptoms other than bleeding are not statistically related to
miscarriage.[34]

Miscarriage may also be detected during an ultrasound exam, or through serial


human chorionic gonadotropin (HCG) testing. Women pregnant from ART
methods, and women with a history of miscarriage, may be monitored closely
and so detect a miscarriage sooner than women without such monitoring.

Several medical options exist for managing documented nonviable pregnancies


that have not been expelled naturally.

[edit] Management
Blood loss during early pregnancy is the most common symptom of both
miscarriage and of ectopic pregnancy. Pain does not strongly correlate with
miscarriage, but is a common symptom of ectopic pregnancy.[34] In the case of
concerning blood loss, pain, or both, transvaginal ultrasound is performed. If a
viable intrauterine pregnancy is not found with ultrasound, serial βHCG tests
should be performed to rule out ectopic pregnancy, which is a life-threatening
situation.[35][36]

If the bleeding is light, making an appointment to see one's doctor is


recommended. If bleeding is heavy, there is considerable pain, or there is a fever,
then emergency medical attention is recommended to be sought.

No treatment is necessary for a diagnosis of complete abortion (as long as


ectopic pregnancy is ruled out). In cases of an incomplete abortion, empty sac, or
missed abortion there are three treatment options:

• With no treatment (watchful waiting), most of these cases (65–80%) will pass
naturally within two to six weeks.[37] This path avoids the side effects and
complications possible from medications and surgery.[38]
• Medical management usually consists of using misoprostol (a prostaglandin,
brand name Cytotec) to encourage completion of the miscarriage. About 95% of
cases treated with misoprostol will complete within a few days.[37]
• Surgical treatment (most commonly vacuum aspiration, sometimes referred to as a
D&C or D&E) is the fastest way to complete the miscarriage. It also shortens the
duration and heaviness of bleeding, and is the best treatment for physical pain
associated with the miscarriage.[37] In cases of repeated miscarriage or later-term
pregnancy loss, D&C is also the best way to obtain tissue samples for pathology
examination.

[edit] Pathology
When looking for gross or microscopic pathologic symptoms of miscarriage, one
looks for the products of conception. Microscopically, these include villi,
trophoblast, fetal parts, and background gestational changes in the endometrium.
Genetic tests may also be performed to look for abnormal chromosome
arrangements.

[edit] Psychological aspects


Although a woman physically recovers from a miscarriage quickly, psychological
recovery for parents in general can take a long time. People differ a lot in this
regard: some are 'over it' after a few months, others take more than a year. Still
others may feel relief or other less negative emotions.

For those who do go through a process of grief, it is often as if the baby had been
born but died. How short a time the fetus lived in the womb may not matter for
the feeling of loss. From the moment pregnancy is discovered, the parents can
start to bond with the unborn child. When the child turns out not to be viable,
dreams, fantasies and plans for the future are disturbed roughly.

Besides the feeling of loss, a lack of understanding by others is often important.


People who have not experienced a miscarriage themselves may find it hard to
empathize with what has occurred and how upsetting it may be. This may lead to
unrealistic expectations of the parents' recovery. The pregnancy and miscarriage
are hardly mentioned anymore in conversation, often because the subject is too
painful. This can make the woman feel particularly isolated.

Interaction with pregnant women and newborn children is often also painful for
parents who have experienced miscarriage. Sometimes this makes interaction
with friends, acquaintances and family very difficult.[39]

[edit] ICD10 codes


Pregnancy-Induced Hypertension
The exact etiology of this disorder is unknown, with several theories being advanced.
Data have suggested that PIH may be the result of increased peripheral vascular resistance
secondary to generalized vasospasm when the vessels are no longer refractory to the effects
of pressor agents. New research proposes that elevated cardiac output and associated
hyperdynamic vasodilation during the first trimester result in damage to the endothelium with
compensatory vascular vasodilation. Regardless of the mechanisms, PIH is a chronic disease
process, with a decrease in placental perfusion occurring before the late sign of hypertension
is detected.
(This plan of care is to be used in conjunction with the Trimesters and the High-Risk
Pregnancy CPs.)
CLIENT ASSESSMENT DATA BASE
Circulation
Persistent increase in BP over pregravid or first-trimester baseline readings after 20 wk of
pregnancy (systolic elevation > 30 mm Hg, diastolic elevation > 15 mm Hg or a BP
> 140/90 mm Hg on two consecutive readings assessed at least 6 hr apart).
History of chronic hypertension.
Jugular venous distension.
Gallop rhythm may be present.
Pulse may be decreased.
May have spontaneous bruising, prolonged bleeding, or epistaxis (thrombocytopenia).
Elimination
Oliguria/anuria may be present.
Hematuria may be noted.
Food/Fluid
Nausea/vomiting.
Weight gain of 2+ lb in 1 wk, 4 lb or more per month (depending on length of gestation).
Malnourished (overweight or underweight by 20% or greater); poor protein/caloric intake.
Edema may be present, ranging from mild to severe/generalized; and may involve facies,
extremities, and organ systems (i.e., liver, brain).
Glycosuria (diabetes mellitus).
Neurosensory
Dizziness, frontal headaches.
Decreased responsiveness/somnolence.
Diplopia, blurred vision, or even loss of visual fields; scotomata (spots before eyes).
Hyperreflexia; clonus.
Convulsions—tonic, then tonic-clonic phases, followed by a period of loss of consciousness.
Funduscopic examination may reveal edema or vascular spasm.
Pain/Discomfort
Epigastric pain (right upper quadrant [RUQ] region)
Respiration
Respirations may be less than 14/min.
Bibasilar crackles may be present.
Dyspnea.
Safety
Rh incompatibility may be present.
Sexuality
Primigravida, multiple gestation, hydramnios, gestational trophoblastic disease (e.g.,:
hydatidiform mole), hydrops fetalis (Rh antigen-antibody)
Fetal movement may be diminished
Signs of abruptio placentae may be present (e.g., uterine tetany, tenderness)
Teaching/Learning
Adolescent (under age 15 yr) and older primigravida (age 35 yr or older) are at greatest risk
Family history of pregnancy-induced hypertension (PIH)
DIAGNOSTIC STUDIES
Supine Pressor Test (“rollover test”): May be used to screen for clients at risk for PIH,
28–32 wk gestation, although accuracy is questionable; an increase of 20–30 mm Hg in
systolic pressure or 15–20 mm Hg in diastolic pressure indicates a positive test.
Mean Arterial Pressure (MAP): 90 mm Hg at second trimester indicates PIH.
Hematocrit (Hct): Elevated with fluid shifts, or decreased in HELLP syndrome (hemolysis,
elevated liver enzymes, low platelet count).
Hemoglobin (Hb): Low when hemolysis occurs (HELLP syndrome).
Peripheral Smear: Distended blood cells or schistocytes in HELLP syndrome or intravascular
hemolysis.
Serum Platelet Counts: Less than 100,000/mm3 in disseminated intravascular coagulation
(DIC) or in HELLP syndrome, because platelets adhere to collagen released from damaged
blood vessels.
Serum Creatinine Level: Elevated above 1.0 mg/dL and blood urea nitrogen (BUN): Greater
than 10 mg/dL reflects severe renal involvement.
AST, LDH, and Serum Bilirubin Levels (indirect particularly): Elevated in HELLP
syndrome with liver involvement.
Uric Acid Level: Greater than 5 mg/100 mL. Helpful in distinguishing preeclampsia from
uncomplicated chronic hypertension.
Prothrombin time (PT), Partial Thromboplastin Time (PTT), Clotting Time: Prolonged;
fibronogen decreased, FSP and FDP positive when coagulopathy occurs (DIC).
Urine-Specific Gravity: Elevated, reflecting fluid shifts/vascular dehydration.
Proteinuria: By dipstick, may be 1+ to 2+ (moderate), 3+ to 4+ (severe), or greater than
500 mg/dL in 24 h.
Creatinine Clearance: Decreased in preeclampsia (before serum BUN/Creatinine elevated).
Urinary/Plasma Estriol Levels: Decline indicates reduced placental functioning. (Estroils
are not as useful a predictor as biophysical profile [BPP] because of the lag time between
fetal problem and test results.)
Human Placental Lactogen Levels: Less than 4 mEq/ml suggests abnormal placental
functioning (not frequently done n PIH screening).
Ultrasonography: At 20–26 weeks’ gestation and repeated 6–10 wk later, establishes
gestational age and detects IUGR.
Tests of Amniotic Fluid (lecithin sphingomyelin [L/S] ratio, phosphalidylglycerol
(PG), saturated phosphatidylcholine levels): Determine fetal lung maturity.
Biophysical Profile (BPP) (amniotic fluid volume, fetal tone, fetal breathing
movements [FMB], fetal movements, and fetal heart rate [FHR]
reactivity)/Nonstress Test (NST): Determines fetal risk/well-being.
CST: Assesses the response of the fetus to the stress of uterine contractions.
NURSING PRIORITIES
1. Monitor maternal, fetal, and placental status.
2. Prevent or reduce progressive fluid accumulation and other complications.
3. Promote positive maternal/fetal outcome.
4. Provide information to enhance self-care and therapeutic management.
DISCHARGE GOALS
(Inpatient care generally not required, unless fetal compromise or eclampsia develops, or
when labor process begins.)
If hospitalized:
1. Hemodynamically stable, free-of-seizure activity
2. Fetus active and in no distress
3. Condition, prognosis, therapeutic regimen understood
4. Participating in care with plan in place for home monitoring/management
NURSING DIAGNOSIS: Fluid Volume deficit [isotonic]
May Be Related To: Plasma protein loss, decreasing plasma colloid
osmotic pressure, allowing fluid shifts out of the
vascular compartment
Possibly Evidenced By: Edema formation, sudden weight gain,
hemoconcentration, nausea/ vomiting, epigastric pain,
headaches, visual changes, decreased urine output
DESIRED OUTCOMES/EVALUATION Verbalize understanding of need for close
CRITERIA—CLIENT WILL: monitoring of weight, BP, urine protein, and edema.
Participate in therapeutic regimen and monitoring, as
indicated.
Display Hct WNL and physiological edema with no
signs of pitting.
Be free of signs of generalized edema (i.e., epigastric
pain, cerebral symptoms, dyspnea, nausea/vomiting).
ACTIONS/INTERVENTIONS RATIONALE
Independent
Weigh client routinely. Encourage client to Sudden, significant weight gain (e.g., more than
monitor weight at home between visits. 3.3 lb (1.5 kg)/month in the second trimester or more
than 1 lb (0.5 kg)/wk in the third trimester) reflects
fluid retention. Fluid moves from the vascular to
interstitial space, resulting in edema.
Distinguish between physiological and pathological The presence of pitting edema (mild, 1+ to
2+;
severe,
edema of pregnancy. Monitor location and 3+ to 4+) of face, hands, legs, sacral area, or
abdodegree
of pitting. minal wall, or edema that does not disappear after 12
hr of bedrest is significant. Note: Significant edema
may actually be present in nonpre-eclamptic clients
and absent in clients with mild or moderated PIH.
Note signs of progressive or excessive edema Edema and intravascular fibrin deposition (in
(i.e., epigastric/RUQ pain, cerebral symptoms, HELLP syndrome) within the encapsulated liver
nausea, vomiting). Assess for possible eclampsia. are manifested by RUQ pain; dyspnea,
indicating
(Refer to ND: Injury, risk for maternal.) pulmonary involvement; cerebral edema, possibly
leading to seizures; and nausea and vomiting,
indicating GI edema.
Note changes in Hct/Hb levels. Identifies degree of hemoconcentration caused by
fluid shift. If Hct is less than 3 times Hb level,
hemoconcentration exists.
Reassess dietary intake of proteins and calories. Adequate nutrition reduces incidence of
prenatal
Provide information as needed. hypovolemia and hypoperfusion; inadequate
protein/calories increases the risk of edema
formation and PIH. Intake of 80–100 g of protein may
be required daily to replace losses.
Monitor intake and output. Note urine color, and Urine output is a sensitive indicator of
circulatory
measure specific gravity as indicated. blood volume. Oliguria and specific gravity of 1.040
indicate severe hypovolemia and kidney involvement.
Note: Administration of magnesium sulfate (MgSO4)
may cause transient increase in output.
Test clean, voided urine for protein each visit, or Aids in determining degree of severity/
daily/hourly as appropriate if hospitalized. progression of condition. A 2+ reading suggests
Report readings of 2+, or greater. glomerular edema or spasm. Proteinuria affects fluid
shifts from the vascular tree. Note: Urine
contaminated by vaginal secretions may test positive
for protein, or dilution may result in a false-negative
result. In addition, PIH may be present without
significant proteinuria.
Assess lung sounds and respiratory rate/effort. Dyspnea and crackles may indicate pulmonary
edema, which requires immediate treatment.
Monitor BP and pulse. (Refer to ND: Cardiac Elevation in BP may occur in response to
Output, decreased.) catecholamines, vasopressin, prostaglandins, and, as
recent findings suggest, decreased levels of
prostacyclin.
Answer questions and review rationale for Diuretics further increase state of dehydration by
avoiding use of diuretics to treat edema. decreasing intravascular volume and placental
perfusion, and they may cause thrombocytopenia,
hyperbilirubinemia, or alteration in carbohydrate
metabolism in fetus/newborn. Note: May be useful
in treating pulmonary edema.
Collaborative
Schedule prenatal visit every 1–2 wk if PIH is mild; Necessary to monitor changes more closely
for the
weekly if severe. well-being of the client and fetus.
Review moderate sodium intake of up to 6 g/day. Some sodium intake is necessary because
levels
Instruct client to read food labels and avoid foods below 2–4 g/day result in greater
dehydration in
high in sodium (e.g., bacon, luncheon meats, some clients. However, excess sodium may
hot dogs, canned soups, and potato chips). increase edema formation.
Refer to dietitian as indicated. Nutritional consult may be beneficial in determining
individual needs/dietary plan.
Place client on strict regimen of bedrest; Lateral recumbent position decreases pressure
encourage lateral position. onthe vena cava, increasing venous return
and circulatory volume. This enhances
placental and renal perfusion, reduces adrenal
activity, and may lower BP as well as account for
weight loss through diuresis of up to 4 lb in 24-hr
period.
Refer to home monitoring/day-care program, Some mildly hypertensive clients without
as appropriate. proteinuria may be managed on an outpatient basis if
adequate surveillance and support is provided and
the client/family actively participates in the
treatment regimen.
Replace fluids either orally or parenterally Fluid replacement corrects hypovolemia, yet must
via infusion pump, as indicated. be administered cautiously to prevent overload,
especially if interstitial fluid is drawn back into
circulation when activity is reduced. With renal
involvement, fluid intake is restricted; i.e., if output is
reduced (less than 700 ml/24 hr), total fluid intake is
restricted to approximate output plus insensible loss.
Use of infusion pump allows more accurate control
delivery of IV fluids.
When fluid deficit is severe and client is hospitalized:
Insert indwelling catheter if kidney output is Allows more accurate monitoring of output/renal
reduced or is less than 50 ml/hr. perfusion.
Assist with insertion of lines and/or monitoring Provides a more accurate measurement of fluid
of invasive hemodynamic parameters, such as volume. In normal pregnancy, plasma volume
CVP and pulmonary artery wedge pressure increases by 30%–50%, yet this increase does not
(PAWP). occur in the client with PIH.
Monitor serum uric acid and creatinine levels, Elevated levels, especially of uric acid, indicate
and BUN. impaired kidney function, worsening of maternal
condition, and poor fetal outcome.
Administer platelets as indicated. Clients with HELLP syndrome awaiting delivery of
the fetus may benefit from transfusion of platelets
when count is below 20,000.
NURSING DIAGNOSIS: Cardiac Output, decreased
May Be Related To: Hypovolemia/decreased venous return, increased
systemic vascular resistance
Possibly Evidenced By: Variations in blood pressure/hemodynamic readings,
edema, shortness of breath, change in mental status
DESIRED OUTCOMES/EVALUATION Remain normotensive throughout remainder of
CRITERIA—CLIENT WILL: pregnancy.
Report absence and/or decreased episodes of
dyspnea.
Alter activity level as condition warrants.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Monitor and graph BP and pulse. The client with PIH does not manifest the
normal cardiovascular response to pregnancy
(left ventricular hypertrophy, increase in plasma
volume, vascular relaxation with decreased
peripheral resistance). Hypertension (the second
manifestation of PIH after edema) occurs owing
to increased sensitization to angiotensin II,
which increases BP, promotes aldosterone release
to increase sodium/water reabsorption from
the renal tubules, and constricts blood vessels.
Assess MAP at 22 weeks’ gestation. A pressure Pulmonary edema may occur, with changes in
of 90 mm Hg is considered predictive of PIH. peripheral vascular resistance and decline in
Assess for crackles, wheezes, and dyspnea; plasma colloid osmotic pressure.
note respiratory rate/effort.
Institute bedrest with client in lateral position. Increases venous return, cardiac output, and
renal/placental perfusion.
Collaborative
Monitor invasive hemodynamic parameters. Provides accurate picture of vascular changes and
fluid volume. Prolonged vascular constriction,
increased hemoconcentration, and fluid shifts
decrease cardiac output.
Administer antihypertensive drug such as If BP does not respond to conservative measures,
hydralazine (Apresoline) PO/IV, so that diastolic short-term medication may be necessary in
readings are between 90 and 105 mm Hg. Begin conjunction with other therapies, e.g., fluid
maintenance therapy as needed, e.g., methyldopa replacement and MgSO4. Antihypertensive
drugs
(Aldomet) or nifedipine (Procardia). act directly on arterioles to promote relaxation of
cardiovascular smooth muscle and help increase
blood supply to cerebrum, kidneys, uterus, and
placenta. Hydralazine is the drug of choice because it
does not produce effects on the fetus. Sodium
nitroprusside is being used with some success to
lower BP (especially in HELLP syndrome).
Monitor BP and side effects of antihypertensive Side effects such as tachycardia, headache,
nausea,
drugs. Administer propranolol (Inderal), as and vomiting, and palpitations may be treated with
appropriate. propranolol.
Prepare for birth of fetus by cesarean delivery, If conservative treatment is ineffective and
labor
when severe PIH/eclamptic condition is induction is ruled out, then surgical procedure is
stabilized, but vaginal delivery is not feasible. the only means of halting the hypertensive
problems.
NURSING DIAGNOSIS: Tissue Perfusion, altered: uteroplacental
May Be Related To: Maternal hypovolemia, interruption of blood flow
(progressive vasospasm of spiral arteries)
Possibly Evidenced By: Intrauterine growth retardation, changes in fetal
activity/heart rate, premature delivery, fetal demise
DESIRED OUTCOMES/EVALUATION Demonstrate normal CNS reactivity on nonstress
CRITERIA—FETUS WILL: test (NST); be free of late decelerations; have no
decrease in FHR on contraction stresstest (NST); be free of late decelerations; have no
decrease in FHR on contraction stress test/oxytocin
challenge test (CST/OCT).
Be full-term, AGA.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Provide information to client/couple regarding Reduced placental blood flow results in reduced
home assessment/recording of daily fetal gas exchange and impaired nutritional functioning
movements and when to seek immediate of the placenta. Potential outcomes of poor placental
medical attention. perfusion include a malnourished, LBW infant, and
prematurity associated with early delivery, abruptio
placentae, and fetal death. Reduced fetal activity
indicates fetal compromise (occurs before detectable
alteration in FHR and indicates need for immediate
evaluation/intervention.
Identify factors affecting fetal activity. Cigarette smoking, medication/drug use, serum
glucose levels, environmental sounds, time of day,
and sleep-wake cycle of the fetus can increase or
decrease fetal movement.
Review signs of abruptio placentae (i.e., vaginal Prompt recognition and intervention increases
the
bleeding, uterine tenderness, abdominal pain, likelihood of a positive outcome.
and decreased fetal activity).
Provide contact number for client to ask questions, Provides opportunity to address concerns/
report changes in daily fetal movements, and so forth. misconceptions and intervene in a
timely manner, as
indicated.
Evaluate fetal growth; measure progressive fundal Decreased placental functioning may
accompany
growth at each office visit or periodically during PIH, resulting in IUGR. Chronic intrauterine
stress
home visits, as appropriate. and uteroplacental insufficiency decrease amount of
fetal contribution to amniotic fluid pool.
Note fetal response to medications such as MgSO4, Depressant effects of medication reduce
fetal respiraphenobarbital,
and diazepam. tory and cardiac function and fetal activity level, even
though placental circulation may be adequate.
Monitor FHR manually or electronically, as indicated. Helps evaluate fetal well-being. An
elevated FHR
may indicate a compensatory response to hypoxia,
prematurity, or abruptio placentae.
Collaborative
Assess fetal response to BPP criteria or CST, as BPP helps evaluate fetus and fetal environment
on
maternal status indicates. (Refer to ND: Injury, five specific parameters to assess CNS function
risk for maternal.) and fetal contribution to amniotic fluid volume.
CST assesses placental functioning and reserves.
Assist with assessment of fetal maturity and In the event of deteriorating maternal/fetal
well-being using L/S ratio, presence of PG, condition, risks of delivering a preterm infant are
estriol levels, FBM, and sequential sonography weighed against the risks of continuing the
beginning at 20–26 weeks’ gestation. (Refer to pregnancy, using results from evaluative
studies
CP: The High-Risk Frequency; ND: Injury, risk of lung and kidney maturity, fetal growth, and
for fetal.) placental functioning. IUGR is associated with
reduced maternal volume and vascular changes.
Assist with assessment of maternal plasma volume Identifies fetus at risk for IUGR or
intrauterine
at 24–26 weeks’ gestation using Evans’ blue dye fetal demise associated with reduced plasma
when indicated. volume and reduced placental perfusion.
Using ultrasonography, assist with assessment of Decreased placental function and size are
placental size. associated with PIH.
Administer corticosteroid (dexamethasone, Corticosteroids are thought to induce fetal
pulmonary
betamethasone) IM for at least 24–48 hr, but not maturity (surfactant production) and prevent
respiramore
than 7 days before delivery, when severe tory distress syndrome, at least in a fetus delivered
PIH necessitates premature delivery between prematurely because of condition or inadequate
28 and 34 weeks’ gestation. placental functioning. Best results are obtained when
fetus is less than 34 weeks’ gestation and delivery
occurs within a week of corticosteroid administration.
NURSING DIAGNOSIS: Injury, risk for maternal
May Be Related To: Tissue edema/hypoxia, tonic-clonic convulsions,
abnormal blood profile and/or clotting factors
Possibly Evidenced By: [Not applicable: Presence of signs/symptoms
establishes an actual diagnosis]
DESIRED OUTCOMES/EVALUATION Participate in treatment and/or environmental
CRITERIA—CLIENT WILL: modifications to protect self and enhance safety.
DESIRED OUTCOMES/EVALUATION Be free of signs of cerebral ischemia (visual
CRITERIA—CLIENT WILL (cont.): disturbances, headache, changes in mentation).
Display normal levels of clotting factors and liver
enzymes.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Assess for CNS involvement (i.e., headache, Cerebral edema and vasoconstriction can be
irritability, visual disturbances or changes on evaluated in terms of symptoms, behaviors, or
funduscopic examination). retinal changes.
Stress importance of client promptly reporting Delayed treatment or progressive onset of
symptoms
signs/symptoms of CNS involvement. may result in tonic-clonic convulsions or eclampsia.
Note changes in level of consciousness. In progressive PIH, vasoconstriction and vasospasms
of cerebral blood vessels reduce oxygen consumption
by 20% and result in cerebral ischemia.
Assess for signs of impending eclampsia: Generalized edema/vasoconstriction, manifested
hyperactivity of deep tendon reflexes (3+ to 4+), by severe CNS, kidney, liver, cardiovascular,
and
ankle clonus, decreased pulse and respirations, respiratory involvement, precede convulsive
state.
epigastric pain, and oliguria (less than 50 ml/hr).
Institute measures to reduce likelihood of seizures; Reduces environmental factors that may
stimulate
i.e., keep room quiet and dimly lit, limit visitors, irritable cerebrum and cause a convulsive
state.
plan and coordinate care, and promote rest.
Implement seizure precautions per protocol. If seizure does occur, reduces risk of injury.
In the event of a seizure: Maintains airway by reducing risk of aspiration and
Turn client on side; insert airway/bite block only preventing tongue from occluding airway.
if mouth is relaxed; suction nasopharynx, as Maximizes oxygenation. Note: Be cautious with
indicated; administer oxygen; remove restrictive use of airway/bite block, because attempts to
insert
clothing; do not restrict movement. Document when jaws are set may result in injury.
motor involvement, duration of seizure,
and postseizure behavior.
Palpate for uterine tenderness or rigidity; These signs may indicate abruptio placentae,
check for vaginal bleeding. Note history especially if there is a preexisting medical problem,
of other medical problems. such as diabetes mellitus, or a renal or cardiac
disorder causing vascular involvement.
Monitor for signs and symptoms of labor Convulsions increase uterine irritability; labor may
or uterine contractions. ensue.
Assess fetal well-being, noting FHR. During seizure activity, fetal bradycardia may occur.
Monitor for signs of DIC easy/spontaneous bruising, Abruptio placentae with release of
thromboplastin
prolonged bleeding, epistaxis, GI bleeding. predisposes client to DIC.
(Refer to CP: Prenatal Hemorrhage.)
Collaborative
Hospitalize if CNS involvement is present. Prompt initiation of therapy helps to ensure safety
and limit complications.
Administer MgSO4 IM or IV using infusion pump. MgSO4 a CNS depressant, decreases
acetylcholine
release, blocks neuromuscular transmission, and
prevents seizures. It has a transient effect of lowering
BP and increasing urine output by altering vascular
response to pressor substances. Although IV
administration of MgSO4 is easier to regulate and
reduces the risk of a toxic reaction, some facilities
may still use the IM route if continuous surveillance
is not possible and/or if appropriate infusion
apparatus is not available. Note: Adding 1 ml of 2%
lidocaine to the IM injection may reduce associated
discomfort. (Current research suggests the use of
phenytoin infusion may be effective in the treatment
of PIH without the adverse side effects, such as
respiratory depression, and tocolytic effect on uterine
smooth muscle, which can impede labor during
intrapartal therapy.)
Monitor BP before, during, and after MgSO4 A therapeutic level of MgSO4 is achieved with
administration. Note serum magnesium levels in serum levels of 4.0–7.5 mEq/L or 6–8 mg/dL.
conjunction with respiratory rate, patellar/deep Adverse/toxic reactions develop above 10–12
tendon reflex (DTRs), and urine output. mg/dL, with loss of DTRs occurring first, respiratory
paralysis between 15–17 mg/dL, or heart block
occurring at 30–35 mg/dL.
Have calcium gluconate available. Administer Serves as antidote to counteract adverse/toxic
10 ml (1 g/10 ml) over 3 min as indicated. effects of MgSO4.
Administer amobarbital (Amytal) or diazepem Depresses cerebral activity; has sedative effect
(Valium), as indicated. when convulsions are not controlled by MgSO4. Not
recommended as first-line therapy because sedative
effect also extends to the fetus.
Perform funduscopic examination daily. Helps to evaluate changes or severity of retinal
involvement.
Monitor test results of clotting time, PT, PTT, Such tests can indicate depletion of coagulation
fibrinogen levels, and FPS/FDP. factors and fibrinolysis, which suggests DIC.
Monitor sequential platelet count. Avoid Thrombocytopenia may occur because of platelet
amniocentesis if platelet count is less than adherence to disrupted endothelium or reduced
50,000/mm3. If thrombocytopenia is present during prostacyclin levels (a potent inhibitor of
platelet
operative procedure, use general anesthesia. aggregation). Invasive procedures or anesthesia
Transfuse with platelets, packed red blood cells, requiring needle puncture (such as spinal/
fresh frozen plasma, or whole blood, as indicated. epidural) could result in excessive bleeding.
Rule out HELLP syndrome.
Monitor liver enzymes and bilirubin; note hemolysis Elevated liver enzyme (AST, ALT) and
bilirubin
and presence of Burr cells on peripheral smear. levels, microangiopathic hemolytic anemia,
and
thrombocytopenia may indicate presence of HELLP
syndrome, signifying a need for immediate cesarean
delivery if condition of cervix is unfavorable for
induction of labor.
Prepare for cesarean birth if PIH is severe, When fetal oxygenation is severely reduced owing
placental functioning is compromised, and cervix is to vasoconstriction within malfunctioning
not ripe or is not responsive to induction. placenta, immediate delivery may be necessary to
save the fetus.
NURSING DIAGNOSIS: Nutrition: altered, risk for less than body
requirements
May Be Related To: Intake insufficient to meet metabolic demands and
replace losses
Possibly Evidenced By: [Not applicable; presence of signs/symptoms
establishes an actual diagnosis]
DESIRED OUTCOMES/EVALUATION Verbalize understanding of individual dietary
CRITERIA—CLIENT WILL: needs.
DESIRED OUTCOMES/EVALUATION Demonstrate knowledge of proper diet as evidenced
CRITERIA—CLIENT WILL (cont.): by developing a dietary plan within own financial
resources.
Display appropriate weight gain.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Assess client’s nutritional status, condition of Establishes guidelines for determining dietary
hair and nails, and height and pregravid weight. needs and educating client. Malnutrition may
be a
contributing factor to the onset of PIH, specifically
when client follows a low-protein diet, has
insufficient caloric intake, and is overweight or
underweight by 20% or more before conception.
Provide information about normal weight gain in The underweight client may need a diet
higher in
pregnancy, modifying it to meet client’s needs. calories; the obese client should avoid dieting
because it places the fetus at risk for ketosis.
Provide oral/written information about action and Daily intake of 80–100 g/day (1.5 g/kg) is
uses of protein and its role in development of PIH. sufficient to replace proteins lost in urine
and allow
for normal serum oncotic pressure. Provide information about effect of bedrest and Reducing
metabolic rate through bedrest and
reduced activity on protein requirements. limited activity decreases protein needs.
Collaborative
Refer to dietitian, as indicated. Helpful in creating individual dietary plan
incorporating specific needs/restrictions.
NURSING DIAGNOSIS: Knowledge deficit [Learning Need] regarding
condition, prognosis, self care and treatment
needs
May Be Related To: Lack of exposure/unfamiliarity with information
resources, misinterpretation
Possibly Evidenced By: Request for information, statement of misconceptions,
inaccurate follow-through of instructions, development
of preventable complications
DESIRED OUTCOMES/EVALUATION Verbalize understanding of disease process and
CRITERIA—CLIENT/COUPLE WILL: appropriate treatment plan.
Identify signs/symptoms requiring medical evaluation.
Perform necessary procedures correctly.
Initiate lifestyle/behavior changes as indicated.
ACTIONS/INTERVENTIONS RATIONALE
Independent
Assess client’s/couple’s knowledge of the Establishes data base and provides information
disease process. Provide information about about areas in which learning is needed. Receiving
pathophysiology of PIH, implications for information can promote understanding and
mother and fetus; and the rationale for reduce fear, helping to facilitate the treatment plan
interventions, procedures, and tests, as needed. for the client. Note: Current research in
progress may
provide additional treatment options, such as using
low-dose (60 mg/day) aspirin to reduce
thromboxane generation by platelets, limiting the
severity/incidence of PIH.
Provide information about signs/symptoms Helps ensure that client seeks timely treatment
indicating worsening of condition, and instruct and may prevent worsening of preeclamptic
state
client when to notify healthcare provider. or additional complications.
Keep client informed of health status, results of Fears and anxieties can be compounded when
tests, and fetal well-being. client/couple does not have adequate information
about the state of the disease process or its impact on
client and fetus.
Instruct client in how to monitor her own weight Gain of 3.3 lb or greater per month in second
at home, and to notify healthcare provider if gain trimester or 1 lb or greater per week in third
is in excess of 2 lb/wk, or 0.5 lb/day. trimester is suggestive of PIH.
Assist family members in learning the procedure Encourages participation in treatment
regimen,
for home monitoring of BP, as indicated. allows prompt intervention as needed, and may
provide reassurance that efforts are beneficial.
Review techniques for stress management and Reinforces importance of client’s responsibility
in
diet restriction. treatment.
Provide information about ensuring adequate Protein is necessary for intravascular and
protein in diet for client with possible or extravascular fluid regulation.
mild preeclampsia.
Review self-testing of urine for protein. Reinforce A test result of 2+ or greater is significant
and
rationale for and implications of testing. needs to be reported to healthcare provider. Urine
specimen contaminated by vaginal discharge or RBCs
may produce positive test result for protein.

III. DIAGNOSIS

Ectopic Pregnancy. With ectopic pregnancy, fertilization occurs as usual in


the distal third of the fallopian tube. Immediately after the union of ovum
and spermatozoon, the zygote begins to divide and grow normally.
Unfortunately, because an obstruction is present, such as an adhesion of the
fallopian tube from a previews infection, congenital malformations, scars
from tubal surgery, or a uterine tumor pressing on the proximal end of the
tube, the zygote cannot travel the length of the tube. It lodges at the
strictured site along the tube and implants there instead of in the uterus.
There are seven sites where implantation occurs: ampullary, isthmic (most
common is in the fallopian tube), fimbrial, cornual, abdominal, ovarian, and
cervical.

Approximately 2% of pregnancies are ectopic; ectopic pregnancy is the


second most frequent cause of bleeding early in pregnancy. The incidence is
increasing because of the increasing rate of pelvic inflammatory disease,
which lead to tubal scarring. Ectopic pregnancy occurs more frequently in
women who smoke compared to those who do not. There is some evidence
that intrauterine devices ( IUD ) used for constipation may slow the transport
of the zygote and lead to an increased incidence of tubal or ovarian
implantation. The incidence also increases following in vitro fertilization.
Women who have one ectopic pregnancy have a 10% to 20% chance that a
subsequent pregnancy will also be ectopic. This is because salpingitis that
leaves scarring is usually bilateral. Congenital anomalies such as webbing
may also be bilateral. Surprisingly, oral contraceptive may reduce the
possibility of ectopic pregnancy.

Causes of ectopic pregnancy include PID, tubal abnormalities, endometriosis,


scarring, caused by previous tubal surgery, prior ectopic pregnancies. Tubal
sterilization administration of hormones and the “morning after pill”.

An ectopic pregnancy results from a fertilized egg's inability to work its way
quickly enough down the fallopian tube into the uterus. An infection or
inflammation of the tube may have partially or entirely blocked it. Pelvic
inflammatory disease (PID) is the most common of these infections.

Endometriosis (when cells from the lining of the uterus detach and grow
elsewhere in the body) or scar tissue from previous abdominal or fallopian
surgeries can also cause blockages. More rarely, birth defects or abnormal
growths can alter the shape of the tube and disrupt the egg's progress.
Some birth control methods can also increase your risk of ectopic pregnancy.
If you get pregnant while using progesterone-only oral contraceptives,
progesterone intrauterine devices (IUDs), or the morning-after pill, you're
more likely to have an ectopic pregnancy.

Manifestations. Signs and symptoms would include lower abdominal/pelvic


pain, mild cramping on one side of the pelvis, amenorrhea, abnormal vaginal,
bleeding (spotting), breast tenderness, nausea, low back pain. If rupture,
and hemorrhaging occurs before treating the pregnancy, symptoms may
worsen and include severe, sharp, and sudden pain in the lower abdominal
area, feeling faint, or actually fainting and referred pain to the shoulder area.

Diagnostic tests. Usually, a positive pregnancy test, hematocrit test may be


normal or decreased, white blood count may be normal or increased, a
culdocentesis may be performed to determine if free blood is present in the
abdomen, an ultrasound illustrates an empty uterus, a D&C may be indicated
to rule out a non-viable intra-uterine pregnancy.

ASSESSMENT

Subjective Data. The client describes amenorrhea, nausea, breast


tenderness, and a dull ache on one side that has increasingly become more
severe. When the tube ruptures, the client will describe a single excruciating
pain in the abdomen and may also have referred shoulder pain. With the
case of our patient, Rosenda, she verbalizes that she has had abdominal pain
that has become very intense on the third day.

Objective Data. Some vaginal bleeding may be apparent. Laboratory


reports may show a low hemoglobin and hematocrit, a rising leukocyte level,
and a slowly rising hCG level. The RBC count is low and sedimentation rate
level elevated. The abdomen may be rigid and tender. Vital signs may
indicate hypovolemic shock. The lowering trend of Rosenda’s blood pressure
of 90/60 from the initial 100/70 reflects a significant amount of blood loss.

IV. MANAGEMENT

Shock is the first symptom of nearly 20% of ectopic pregnancies if it has


ruptured. Initial treatment is needed by keeping the womb warm, elevating
her legs and administrating oxygen. Surgical laparotomy is performed to stop
the immediate loss of blood and repair surrounding tissue damage as much
as possible. In some cases, removal of the involved fallopian tube
(Salpingectomy) may be necessary. In the event that rupture has not
occurred, methotrexate is administered. Ectopic pregnancies cannot continue
to term, so the removal of the developing cells is necessary to save the life of
the mother.

The Therapeutic Management of Ectopic Pregnancy

Although some ectopic pregnancies spontaneously resolve, requiring no


treatment, it is difficult to predict when this will happen. Once an ectopic
pregnancy ruptures, it is an emergency situation and the woman’s condition
must be evaluated quickly. Keep in mind that the amount of blood evident is
a poor estimate of the actual blood loss. Blood needs to be drawn
immediately for hemoglobin level, typing and cross matching, and possibly
HCG level for immediate pregnancy testing, if pregnancy has not been
confirmed. Intravenous fluid using a large-gauge catheter to restore
intravascular volume is begun. Blood also can be administered though this
same line if necessary.

The therapy for a ruptured ectopic pregnancy is laparoscopy to ligate the


bleeding vessels and to remove or repair the damaged fallopian tube. A
rough suture line on a fallopian may lead to another tubal pregnancy, so
either the tube will be removed or suturing on the tube is done with
microscopical technique.

If a tube is removed, the woman is theoretically only 50% fertile, because


every other months, when she ovulates from the ovary next to the removed
tube, sperm cannot reach the ovum on that side. However, this is not a
reliable contraceptive measures. Research in rabbits has shown that
translocation of ova can occur-that is an ovum released from the right ovary
can pass through the pelvic cavity to the opposite (left) fallopian tube and
became fertilized and vice versa (Cunningham et al 2001)

As with miscarriage, women with Rh-negative blood should receive Rh (D)


immune globulin (RhIG) after an ectopic can be diagnosed by a routine
sonogram before the tube has been ruptured, it can be treated medically by
the oral administration of methotrexate followed by leucovorin. Methotrexate,
folic acid antagonists chemotherapy agent, attacks and destroys fast-growing
cells. Because trophoblast and zygote growth is rapid, the drug is drawn to
the site of the ectopic pregnancy. Women are treated until a negative hcg
titer is achieved. A hysterosalpingogram or sonogram is usually performed

Therapeutic management of an unruptured ectopic pregnancy with


intramuscular methotrexate is common and cost-effective. Two treatment
protocols, the "single dose" and the "multidose," have been advocated and
independently reported in the medical literature. This analysis systematically
compares the success and prevalence of side effects of these two regimens.
Diagnosis in the unruptured state allows for a more conservative approach to
patient management. Different conservative surgical and medical lines of
management have been associated with increased chance of subsequent
intrauterine pregnancy and decline in the incidence of repeat ectopic
pregnancy.

Laparoscopic salpingostomy has been the main definitive conservative


surgical procedure of choice for unruptured ectopic pregnancy, although
salpingectomy, salpingotomy and direct injection of cytotoxic agents are also
modes of treatment.

Laparoscopy was performed under general anesthesia. The abdominal cavity


was examined thoroughly; separation of adhesions if present, removal blood
clot and ectopic mass was detected. Unilateral salpingostomy, salpingectomy,
salpingo-ophrectomy, partial ovarian resection, removal of the sac was done
by mono and bipolar coagulation. Peritoneal cavity was irrigated thoroughly
with Ringer’s lactate solution and proper hemostasis was established.

Medical treatment includes use of methotrexate alone, or a combination of


methotrexate and mifepristone. Medical treatment has been reported to be
successful in 83% of cases when the mean duration of amenorrhoea was not
more than 54 days, the mean serum beta human chorionic gonadotrophin
level was not higher than 15, 127 miU/ml and the mean size of the ectopic
mass was not larger than 23mm. In cases of persistent fetal cardiac activity
after methotrexate treatment, complimentary potassium iodide injection into
the pregnancy proved to be effective.

Prevention. Forms of ectopic pregnancy other than tubal, are probably not
preventable. However, tubal pregnancies may be prevented by avoiding those
conditions that might cause scarring of the fallopian tubes. Such prevention
may include avoiding risk factors for PID (e.g. multiple partners, intercourse
without a condom, and contracting STD’s), early diagnosis and adequate
treatment of STD’s, early diagnosis and adequate treatment of PID and
salpingitis.

Complications. Rupture, with resulting hemorrhage leading to shock and


the risk of requiring a blood transfusion, or rarely death, is the most common
complication. Also infertility occurs in 10-15% of women who experience an
ectopic pregnancy.
V. NURSING CARE PLAN

Assessment Diagnosis Planning Intervention Rationale Evaluation


Subjective Acute pain At the end of Assess the To know what After 2 hours
cues: related to 2-hours location, is the cause of of nursing
tubal nursing etiology and pain and intervention
“tatlong rupture intervention, severity of determine what the client
araw ng and blood the patient pain. action will be verbalize
sumasakit in the will be done. that there is
ang tiyan ko, abdomen. relieved from no more pain
ngayon severe pain. To alleviate the or has at
masakit na Administer pain. least become
talaga.” analgesic as tolerable.
ordered and
evaluate its Pain scale: 4
effectiveness.
The patient be
Provide knowledgeable
Objective information about the pain
cues: about the she feels.
cause of pain.
BP: 90/60 So the patient
mmHg Provide will increase
Temp: 36.7 comfort self-esteem.
C measures.
PR: 88 bpm To determine if
RR: 23 cpm The patient the patient is in
can verbalize Observe pain. The patient
>pain scale: that the pain nonverbal can now
8 severe is subsided. cues. To determine verbalize
>pale skin patient’s ability that the pain
>eye lack Assess to control pain. is subsided.
luster patient’s
>guarding attitude
behavior toward pain To check any
and focus of changes in the
control. patients
condition.
Monitor vital
signs usually
altered in
acute pain.
Assessment Diagnosis Planning Intervention Rationale Evaluation

Subjective Anticipatory Assist Use therapeutic To promote a The patient


Cues: grieving client to communication free is able to
“Expression related to deal with skills of active discussion of express her
sorrow on the lost of the listening, silence, feelings and feelings
clients face.” pregnancy. situation. acknowledgement concerns. with ease.
Respect client’s
desire/request not
Objective Cues: to talk.
Patient can
>patient Ascertain response interact
withdraws from of family/SO(s) to To know what positively
interaction with client’s is the family’s with other
other people or situation/concerns. understanding people.
shows sign of of patient’s
social isolation. Observe client’s situation.
body language and
Patient is check out meaning
changing with the client.
mood.
Note emotional
Patient doesn’t responses such as To know how
want withdrawal, angry to deal with
companionship. behavior, crying. patient’s
behavior.
Instruct in use of
visualization and
relaxation To lessen
techniques. patient’s
grieving.

Assessme Diagnosi Planning Interventio Rationale Evaluation


nt s n

Subjective Impaired Client will Identify client To ensure the Procedure


Cues: tissue regain for surgery as procedure is successfully
integrity tissue ordered. appropriate to done.
related to integrity of the problem.
rupture of the fallopian
Objective the fallopian tube or it
Cues: tube. will be
removed.
BP: 90/60
Temp: 36.7 c
PR: 88 bpm
RR: 23 cpm

>pain scale: 8
severe
>guarding
behavior
>crying

Pregnancy
test (+)
LMP: 4/19/07
AOG: 8 weeks

Ultrasound
Result
Revealed: (+)
Ampullary
Pregnancy

Assessment Diagnosis Planning Intervention Rationale Evaluation

Subjective Fear related Assist Provide Gives the client Client


Cues: to potential client to information as a sense of verbalizes
“Natakot po subsequent deal with to what ectopic control over that she has
ako baka ectopic the fear. pregnancy is, the situation. less, or no
maulit ang pregnancy. what puts one more, fear
ganitong at risk, and of her next
sitwasyon.” how to prevent pregnancy
it. being
ectopic.
Sense of
Objective abandonment
Cues: Stay with the can exacerbate
client or make fear. Client
>the patient arrangements verbalizes
continuously to have confidence
asks someone else in having
questions be there. pregnancy in
about ectopic the future.
pregnancy.

>the patient’s
facial grimace
expresses
fear.

Reason for rising incidence


Adequate treatment for P.I.D. which in the past rendered women sterile
IUCD use Increase in surgical procedures for tubal disease Improved
diagnostic technique.

2 types of ectopic pregnancy


Ruptured Unruptured

Location (sites) of implantation


Fallopian tube (96%).
– – – – Ampullary region more common in (distal ⅔) Isthmus, Fimbriae,
Interstitial(2%)

Cervical, abdominal and ovarian 2% Heterotopic: combination of


intrauterine and extrauterine gestation 1:30,000 (1:4000-15,000).
Common in assisted reproduction (pregnancies) techniques 1:100.
Bilateral ectopic( Incidence unknown). Broad ligament. (Which sides of
the tube is very common= RT)

Aetiology
Unknown.

Risk factors ( impair the migration of the fertilized ovum to the


uterus or those that affect the tubal motility). P.I.D, contribute to
50% of all cases. Tubal endometriosis (rare). Tubal surgery (previous),
tubo-tubal fistula . Intrauterine devices( IUCD). Transmigration
(migration of the ovum). Previous Hx of ectopic pregnancy. Hx of
Infertility. Intrauterine diethylstilbestrol exposure. Conception
following IVF-ET. G.I.F.T. Z.I.F.T. Previous abdominal surgery
Induction of ovulation following menopause gonadotrophins. Progestogen
contraception. Induction of ovulation with menopausal gonadotrophin

Natural course of ectopic gestation.


Tubal abortion with the formation of haematocele. Rupture into the
peritoneal cavity. Resorption. Rupture into the broad ligament.
Abdominal pregnancy.

Diagnosis.
Symptoms
Amenorrhoea (89%). May occur before the patient misses her period
especially if it is in the isthmus). Pain (94%).Irritation of the
peritoneum, distension of the gravid tube. Shoulder tip pain if blood
tracks to the diaphragm and stimulates the phrenic nerve. Lower
abdominal pain. Irregular vaginal bleeding (80%). (Effect of E2
withdrawal occurs after death of the ovum. Spotting. Decidua grows
abundantly, it can be expelled as decidual cast).

Signs.
Evidence of blood loss
– – – – Anaemia shock (Hypovolaemia) collapse (Hypotension) distension
of the abdomen (shifting dullness)

-Abdominal tenderness, guarding, rebound tenderness. Fluid thrill +ve


Shifting dullness. VE: - Cx-al excitation tenderness.
– Bleeding = brownish. – Fornices will be tender and bulging
occasionally
Other methods for making diagnosis. Culdocentensis / cul-de-sac-
puncture USS imaging especially transvaginal using vaginal probe. B
Submit of hCG (RIA) (abnormal progression of BhCG level) = In normal
pregnancy levels double every 2.4 days with a predictable slope of
increase. Absence of this slope is abnormal (ectopic pregnancy).
Laparoscopy

Differential Diagnosis
Chronic PID Acute PID Acute appendicitis Chronic appendicitis
Spontaneous or induced abortion Threatening abortion Incomplete
abortion Torsion of an ovarian cyst Rupture of an ovarian cyst.

TREATMENT
Surgical Medical

SURGICAL

I.V.Line. D/S. Use a wide-bore cannula Aspirate blood for grouping and
cross-matching-1hr crossmatch.Uncrossmatched O negative blood Get to
theatre as quickly as possible Inform anaesthetist Open and arrest the
bleeding.TECHNIQUE. The scrub nurse can double as an assistant.

Incision to make: Preferably midline vertical LAWSON TAIT of Birminghan


who performed the first successful surgery for ectopic in 1880; MAKE AT
ONCE AT THE SOURCE OF HAEMORRAGE,TIE IT ,THEN OTHER THINGS CAN BE DONE
AT LEISURE. At surgery inspect both ovaries and Fallopian tubes
– Partial salpingectomy – TotaL Salpingectomy – Salpigostomy

AUTOTRANSFUSION.STEPS:duration of haemoperitoneum < 24hrs.


Laparoscopy.RU486(MIFIPRISTONE) Iinjected to abortit from the fimbrial
end.

Steps in autotransfusion Place 8 layers of sterile gauze over a sterile


measuring jar to filter clots,fat globules. Use kidney dish or gallipot
to remove free unclotted blood from the peritoneal cavity. Tge filtered
blood is transferred into citratd bottle(s). Transfuse back through
blood giving set.
14

MEDICAL:
Systemic methotrexate, Actinomycin D Local administration of KCL,
methotrexate, mifipristone, prostanglandin E2 into the gestation.

Closure of the abdomen -there is no need closing both visceral and


parietal peritoneum. -use continuous O or no. 1 polyglycolic or nylon
suture for the rectus sheet. -if not more than 2cm,the subcutaneous
layer may be left. If it becomes necessary,interrupted O plain or 2/0
chromic catgut may be used. Drainage is not necessary unless in chronic
ectopic pregnancy.
18 16

Postoperative Care -blood transfusion if necessary -i.v. fluid until


bowel sound is present -analgesia (analgin or pentazocine) -broad
spectrum antibiotics(ampicillin or ampiclox i.v.) -Commence orally as
soon as the i.v. line is discontinued -Sit the patient out as soon the
condition permits ,usually on the second day of the operation.
-discharge home on the 5th or 6th day -give 2 weeks appointment to the
outpatient clinic, there after 4 weeks.

Discharge
Counselling Prognosis Family planning method Correct anaemia with
ferrous sulphate Follow up visit.

Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in


which women without previously diagnosed diabetes exhibit high blood glucose
levels during pregnancy.

Gestational diabetes generally has few symptoms and it is most commonly


diagnosed by screening during pregnancy. Diagnostic tests detect inappropriately
high levels of glucose in blood samples. Gestational diabetes affects 3-10% of
pregnancies, depending on the population studied.[1] No specific cause has been
identified, but it is believed that the hormones produced during pregnancy
increase a woman's resistance to insulin, resulting in impaired glucose tolerance.

Babies born to mothers with gestational diabetes are at increased risk of


problems typically such as being large for gestastional age (which may lead to
delivery complications), low blood sugar, and jaundice. Gestational diabetes is a
treatable condition and women who have adequate control of glucose levels can
effectively decrease these risks.

Women with gestational diabetes are at increased risk of developing type 2


diabetes mellitus after pregnancy, while their offspring are prone to developing
childhood obesity, with type 2 diabetes later in life. Most patients are treated only
with diet modification and moderate exercise but some take anti-diabetic drugs,
including insulin.
Diabetes mellitus
Types of Diabetes
Diabetes mellitus type 1
Diabetes mellitus type 2
Gestational diabetes

Pre-diabetes:
Impaired fasting glycaemia
Impaired glucose tolerance
Disease Management
Diabetes management:
•Diabetic diet
•Anti-diabetic drugs
•Conventional insulinotherapy
•Intensive insulinotherapy
Other Concerns
Cardiovascular disease

Diabetic comas:
•Diabetic hypoglycemia
•Diabetic ketoacidosis
•Nonketotic hyperosmolar

Diabetic myonecrosis
Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy

Diabetes and pregnancy


Blood tests
Blood sugar
Fructosamine
Glucose tolerance test
Glycosylated hemoglobin

Contents
[hide]

• 1 Definition
• 2 Epidemiology
• 3 Pathophysiology
• 4 Risk factors and symptoms
• 5 Screening and diagnosis
o 5.1 Screening pathways
o 5.2 Non-challenge blood glucose tests
o 5.3 Screening glucose challenge test
o 5.4 Oral glucose tolerance test (OGTT)
o 5.5 Urinary glucose testing
• 6 Complications
• 7 Prognosis
• 8 Classification
• 9 Treatment
• 10 Controversy
• 11 See also
• 12 Footnotes

• 13 External links

[edit] Definition
Gestational diabetes is formally defined as "any degree of glucose intolerance
with onset or first recognition during pregnancy".[2] This definition acknowledges
the possibility that patients may have previously undiagnosed diabetes mellitus,
or may have developed diabetes coincidentally with pregnancy. Whether
symptoms subside after pregnancy is also irrelevant to the diagnosis .[3]

[edit] Epidemiology
The frequency of gestational diabetes varies widely by study depending on the
population studied and the study design. It occurs in between 5 and 10% of all
pregnancies (between 1-14% in various studies).[3]

[edit] Pathophysiology

Effect of insulin on glucose uptake and metabolism. Insulin binds to its receptor (1) on
the cell membrane which in turn starts many protein activation cascades (2). These
include: translocation of Glut-4 transporter to the plasma membrane and influx of glucose
(3), glycogen synthesis (4), glycolysis (5) and fatty acid synthesis (6).

The precise mechanisms underlying gestational diabetes remain unknown. The


hallmark of GDM is increased insulin resistance. Pregnancy hormones and other
factors are thought to interfere with the action of insulin as it binds to the insulin
receptor. The interference probably occurs at the level of the cell signaling
pathway behind the insulin receptor.[4]. Since insulin promotes the entry of
glucose into most cells, insulin resistance prevents glucose from entering the
cells properly. As a result, glucose remains in the bloodstream, where glucose
levels rise. More insulin is needed to overcome this resistance; about 1.5-2.5
times more insulin is produced in a normal pregnancy.[4]

Insulin resistance is a normal phenomenon emerging in the second trimester of


pregnancy, which progresses thereafter to levels seen in non-pregnant patients
with type 2 diabetes. It is thought to secure glucose supply to the growing fetus.
Women with GDM have an insulin resistance they cannot compensate with
increased production in the β-cells of the pancreas. Placental hormones, and to a
lesser extent increased fat deposits during pregnancy, seem to mediate insulin
resistance during pregnancy. Cortisol and progesterone are the main culprits, but
human placental lactogen, prolactin and estradiol contribute too.[4]

It is unclear why some patients are unable to balance insulin needs and develop
GDM, however a number of explanations have been given, similar to those in
type 2 diabetes: autoimmunity, single gene mutations, obesity, and other
mechanisms.[5]

Because glucose travels across the placenta (through diffusion facilitated by


GLUT3 carriers), the fetus is exposed to higher glucose levels. This leads to
increased fetal levels of insulin (insulin itself cannot cross the placenta). The
growth-stimulating effects of insulin can lead to excessive growth and a large
body (macrosomia). After birth, the high glucose environment disappears, leaving
these newborns with ongoing high insulin production and susceptibility to low
blood glucose levels (hypoglycemia).[6]

[edit] Risk factors and symptoms


Classical risk factors for developing gestational diabetes are the following:[7]

• a previous diagnosis of gestational diabetes or prediabetes, impaired glucose


tolerance, or impaired fasting glycaemia
• a family history revealing a first degree relative with type 2 diabetes
• maternal age - a woman's risk factor increases as she gets older (especially for
women over 35 years of age)
• ethnic background (those with higher risk factors include African-Americans,
Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people
originating from the Indian subcontinent)
• being overweight, obese or severely obese increases the risk by a factor 2.1, 3.6
and 8.6, respectively.[8]
• a previous pregnancy which resulted in a child with a high birth weight (>90th
centile, or >4000 g (8 lbs 12.8 oz))
• previous poor obstetric history

In addition to this, statistics show a double risk of GDM in smokers.[9] Polycystic


ovarian syndrome is also a risk factor.[7] Some studies have looked at more
controversial potential risk factors, such as short stature.[10]

About 40-60% of women with GDM have no demonstrable risk factor; for this
reason many advocate to screen all women.[11] Typically women with gestational
diabetes exhibit no symptoms (another reason for universal screening), but some
women may demonstrate increased thirst, increased urination, fatigue, nausea
and vomiting, bladder infection, yeast infections and blurred vision.

[edit] Screening and diagnosis


A number of screening and diagnostic tests have been used to look for high
levels of glucose in plasma or serum in defined circumstances. One method is a
stepwise approach where a suspicious result on a screening test is followed by
diagnostic test. Alternatively, a more involved diagnostic test can be used directly
at the first antenatal visit in high-risk patients (for example in those with polycystic
ovarian syndrome or acanthosis nigricans).[6]

Tests for gestational diabetes

Non-challenge blood glucose tests

• Fasting glucose test


• 2-hour postprandial (after a meal) glucose test

• Random glucose test


Screening glucose challenge test
Oral glucose tolerance test (OGTT)

Non-challenge blood glucose tests involve measuring glucose levels in blood


samples without challenging the subject with glucose solutions. A blood glucose
levels is determined when fasting, 2 hours after a meal, or simply at any random
time. In contrast challenge tests involve drinking a glucose solution and
measuring glucose concentration therafter in the blood; in diabetes they tend to
remain high. The glucose solution have a very sweet taste that some women find
unpleasant; sometimes therefore artificial flavours are added. Some women may
experience nausea during the test, and more so with higher glucose levels.[12][13]

[edit] Screening pathways

There are different opinions about optimal screening and diagnostic measures, in
part due to differences in population risks, cost-effectiveness considerations, and
lack of an evidence base to support large national screening programs.[14] The
most elaborate regime entails a random blood glucose test during a booking visit,
a screening glucose challenge test around 24-28 weeks' gestation, followed by
an OGTT if the tests are outside normal limits. If there is a high suspicion,
women may be tested earlier.[3]

In the United States, most obstetricians prefer universal screening with a


screening glucose tolerance test.[15] In the United Kingdom, obstetric units often
rely on risk factors and a random blood glucose test.[16][6] The American Diabetes
Association and the Society of Obstetricians and Gynecologists of Canada
recommend routine screening unless the patient is low risk (this means the
woman must be younger than 25 years and have a body mass index less than
27, with no personal, ethnic or family risk factors)[3][14] The Canadian Diabetes
Association and the American College of Obstetricians and Gynecologists
recommend universal screening.[17][18] The U.S. Preventive Services Task Force
found that there is insufficient evidence to recommend for or against routine
screening.[19]

[edit] Non-challenge blood glucose tests

When a plasma glucose level is found to be higher than 126 mg/dl (7.0 mmol/l)
after fasting, or over 200 mg/dl (11.1 mmol/l) on any occasion, and if this is
confirmed on a subsequent day, the diagnosis of GDM is made, and no further
testing is required.[3] These tests are typically performed at the first antenatal visit.
They are patient-friendly and inexpensive, but have a lower test performance
compared to the other tests, with moderate sensitivity, low specificity and high
false positive rates.[20][21][22]

[edit] Screening glucose challenge test

The screening glucose challenge test is performed between 24-28 weeks, and
can be seen as a simplified version of the oral glucose tolerance test (OGTT). It
involves drinking a solution containing 50 grams of glucose, and measuring blood
levels 1 hour later.[23]

If the cut-off point is set at 140 mg/dl (7.8 mmol/l), 80% of women with GDM will
be detected.[3] If this threshold for further testing is lowered to 130 mg/dl, 90% of
GDM cases will be detected, but there will also be more women who will be
subjected to a consequent OGTT unnecessarily.

[edit] Oral glucose tolerance test (OGTT)

Main article: oral glucose tolerance test

The OGTT[24] should be done in the morning after an overnight fast of between 8
and 14 hours. During the three previous days the subject must have an
unrestricted diet (containing at least 150 g carbohydrate per day) and unlimited
physical activity. The subject should remain seated during the test and should not
smoke throughout the test.

The test involves drinking a solution containing a certain amount of glucose, and
drawing blood to measure glucose levels at the start and on set time intervals
thereafter.

The diagnostic criteria from the National Diabetes Data Group (NDDG) have
been used most often, but some centers rely on the Carpenter and Coustan
criteria, which set the cutoff for normal at lower values. Compared with the
NDDG criteria, the Carpenter and Coustan criteria lead to a diagnosis of
gestational diabetes in 54 percent more pregnant women, with an increased cost
and no compelling evidence of improved perinatal outcomes.[25]

The following are the values which the American Diabetes Association considers
to be abnormal during the 100 g of glucose OGTT:

• Fasting blood glucose level ≥95 mg/dl (5.33 mmol/L)


• 1 hour blood glucose level ≥180 mg/dl (10 mmol/L)
• 2 hour blood glucose level ≥155 mg/dl (8.6 mmol/L)
• 3 hour blood glucose level ≥140 mg/dl (7.8 mmol/L)

An alternative test uses a 75 g glucose load and measures the blood glucose
levels before and after 1 and 2 hours, using the same reference values. This test
will identify less women who are at risk, and there is only a weak concordance
(agreement rate) between this test and a 3 hour 100 g test.[26]

The glucose values used to detect gestational diabetes were first determined by
O'Sullivan and Mahan (1964) in a retrospective cohort study (using a 100 grams
of glucose OGTT) designed to detect risk of developing type 2 diabetes in the
future. The values were set using whole blood and required two values reaching
or exceeding the value to be positive. [27] Subsequent information led to
alterations in O'Sullivan's criteria. When methods for blood glucose determination
changed from the use of whole blood to venous plasma samples, the criteria for
GDM were also changed.
[edit] Urinary glucose testing

Women with GDM may have high glucose levels in their urine (glucosuria).
Although dipstick testing is widely practiced, it performs poorly, and discontinuing
routine dipstick testing has not been shown to cause underdiagnosis where
universal screening is performed.[28] Increased glomerular filtration rates during
pregnancy contribute to some 50% of women having glucose in their urine on
dipstick tests at some point during their pregnancy. The sensitivity of glucosuria
for GDM in the first 2 trimesters is only around 10% and the positive predictive
value is around 20%.[29][30]

[edit] Complications
GDM poses a risk to mother and child. This risk is largely related to high blood
glucose levels and its consequences. The risk increases with higher blood
glucose levels.[31] Treatment resulting in better control of these levels can reduce
some of the risks of GDM considerably.[32]

The two main risks GDM imposes on the baby are growth abnormalities and
chemical imbalances after birth, which may require admission to a neonatal
intensive care unit. Infants born to mothers with GDM are at risk of being both
large for gestational age (macrosomic)[31] and small for gestational age.
Macrosomia in turn increases the risk of instrumental deliveries (e.g. forceps,
ventouse and caesarean section) or problems during vaginal delivery (such as
shoulder dystocia). Macrosomia may affect 12% of normal women compared to
20% of patients with GDM.[6] However, the evidence for each of these
complications is not equally strong; in the Hyperglycemia and Adverse
Pregnancy Outcome (HAPO) study for example, there was an increased risk for
babies to be large but not small for gestational age.[31] Research into
complications for GDM is difficult because of the many confounding factors (such
as obesity). Labelling a woman as having GDM may in itself increase the risk of
having a caesarean section.[33][34]

Neonates are also at an increased risk of low blood glucose (hypoglycemia),


jaundice, high red blood cell mass (polycythemia) and low blood calcium
(hypocalcemia) and magnesium (hypomagnesemia).[35] GDM also interferes with
maturation, causing dysmature babies prone to respiratory distress syndrome
due to incomplete lung maturation and impaired surfactant synthesis.[35]

Unlike pre-gestational diabetes, gestational diabetes has not been clearly shown
to be an independent risk factor for birth defects. Birth defects usually originate
sometime during the first trimester (before the 13th week) of pregnancy, whereas
GDM gradually develops and is least pronounced during the first trimester.
Studies have shown that the offspring of women with GDM are at a higher risk for
congenital malformations.[36][37][38] A large case-control study found that gestational
diabetes was linked with a limited group of birth defects, and that this association
was generally limited to women with a higher body mass index (≥ 25 kg/m²).[39] It
is difficult to make sure that this is not partially due to the inclusion of women with
pre-existent type 2 diabetes who were not diagnosed before pregnancy.

Because of conflicting studies, it is unclear at the moment whether women with


GDM have a higher risk of preeclampsia.[40] In the HAPO study, the risk of
preeclampsia was between 13% and 37% higher, although not all possible
confounding factors were corrected.[31]

[edit] Prognosis
Gestational diabetes generally resolves once the baby is born. Based on different
studies, the chances of developing GDM in a second pregnancy are between 30
and 84%, depending on ethnic background. A second pregnancy within 1 year of
the previous pregnancy has a high rate of recurrence.[41]

Women diagnosed with gestational diabetes have an increased risk of


developing diabetes mellitus in the future. The risk is highest in women who
needed insulin treatment, had antibodies associated with diabetes (such as
antibodies against glutamate decarboxylase, islet cell antibodies and/or
insulinoma antigen-2), women with more than two previous pregnancies, and
women who were obese (in order of importance).[42][43] Women requiring insulin to
manage gestational diabetes have a 50% risk of developing diabetes within the
next five years.[27] Depending on the population studied, the diagnostic criteria
and the length of follow-up, the risk can vary enormously.[44] The risk appears to
be highest in the first 5 years, reaching a plateau thereafter.[44] One of the longest
studies followed a group of women from Boston, Massachusetts; half of them
developed diabetes after 6 years, and more than 70% had diabetes after 28
years.[44] In a retrospective study in Navajo women, the risk of diabetes after
GDM was estimated to be 50 to 70% after 11 years.[45] Another study found a risk
of diabetes after GDM of more than 25% after 15 years.[46] In populations with a
low risk for type 2 diabetes, in lean subjects and in patients with auto-antibodies,
there is a higher rate of women developing type 1 diabetes.[43]

Children of women with GDM have an increased risk for childhood and adult
obesity and an increased risk of glucose intolerance and type 2 diabetes later in
life.[47] This risk relates to increased maternal glucose values.[48] It is currently
unclear how much genetic susceptibility and environmental factors each
contribute to this risk, and if treatment of GDM can influence this outcome.[49]

There are scarce statistical data on the risk of other conditions in women with
GDM; in the Jerusalem Perinatal study, 410 out of 37962 patients were reported
to have GDM, and there was a tendency towards more breast and pancreatic
cancer, but more research is needed to confirm this finding.[50][51]
[edit] Classification
The White classification, named after Priscilla White[52] who pioneered in research
on the effect of diabetes types on perinatal outcome, is widely used to assess
maternal and fetal risk. It distinguishes between gestational diabetes (type A) and
diabetes that existed prior to pregnancy (pregestational diabetes). These two
groups are further subdivided according to their associated risks and
management.[53]

There are 2 subtypes of gestational diabetes (diabetes which began during


pregnancy):

• Type A1: abnormal oral glucose tolerance test (OGTT) but normal blood glucose
levels during fasting and 2 hours after meals; diet modification is sufficient to
control glucose levels
• Type A2: abnormal OGTT compounded by abnormal glucose levels during
fasting and/or after meals; additional therapy with insulin or other medications is
required

The second group of diabetes which existed prior to pregnancy is also split up
into several subtypes.

[edit] Treatment
The goal of treatment is to reduce the risks of GDM for mother and child.
Scientific evidence is beginning to show that controlling glucose levels can result
in less serious fetal complications (such as macrosomia) and increased maternal
quality of life. Unfortunately, treatment of GDM is also accompanied by more
infants admitted to neonatal wards and more inductions of labour, with no proven
decrease in cesarean section rates or perinatal mortality.[54][55] These findings are
still recent and controversial.[56]

Counselling before pregnancy (for example, about preventive folic acid


supplements) and multidisciplinary management are important for good
pregnancy outcomes.[57] Most women can manage their GDM with dietary
changes and exercise. Self monitoring of blood glucose levels can guide therapy.
Some women will need antidiabetic drugs, most commonly insulin therapy.

Any diet needs to provide sufficient calories for pregnancy, typically 2,000 - 2,500
kcal with the exclusion of simple carbohydrates.[11] The main goal of dietary
modifications is to avoid peaks in blood sugar levels. This can be done by
spreading carbohydrate intake over meals and snacks throughout the day, and
using slow-release carbohydrate sources. Since insulin resistance is highest in
mornings, breakfast carbohydrates need to be restricted more.[7]
Regular moderately intense physical exercise is advised, although there is no
consensus on the specific structure of exercise programs for GDM.[7][58]

A kit with a glucose meter and diary used by a woman with gestational diabetes.

Self monitoring can be accomplished using a handheld capillary glucose dosage


system. Compliance with these glucometer systems can be low.[32] Target ranges
advised by the Australasian Diabetes in Pregnancy Society are as follows:[7]

• fasting capillary blood glucose levels <5.5 mmol/L


• 1 hour postprandial capillary blood glucose levels <8.0 mmol/L
• 2 hour postprandial blood glucose levels <6.7 mmol/L

Regular blood samples can be used to determine HbA1c levels, which give an
idea of glucose control over a longer time period.[7]

If monitoring reveals failing control of glucose levels with these measures, or if


there is evidence of complications like excessive fetal growth, treatment with
insulin might become necessary. The most common therapeutic regime involves
premeal fast-acting insulin to blunt sharp glucose rises after meals.[7] Care needs
to be taken to avoid low blood sugar levels (hypoglycemia) due to excessive
insulin injections. Insulin therapy can be normal or very thight; more injections
can result in better control but requires more effort, and there is no consensus
that it has large benefits.[6][59][60]

There is some evidence that certain oral glycemic agents might be safe in
pregnancy, or at least, are significantly less dangerous to the developing fetus
than poorly controlled diabetes. However, few studies have been performed as of
this time and this is not a generally accepted treatment. These agents may be
used in research settings, or if the patient needs intervention but refuses insulin
therapy, and is aware of the risks.[7] Glyburide, a second generation sulfonylurea,
has been shown to be an effective alternative to insulin therapy.[61][62] In one study,
4% of women needed supplemental insulin to reach blood sugar targets.[62]

Metformin has shown promising results. Treatment of polycystic ovarian


syndrome with metformin during pregnancy has been noted to decrease GDM
levels.[63] A recent randomized controlled trial of metformin versus insulin showed
that women preferred metformin tablets to insulin injections, and that metformin
is safe and equally effective as insulin.[64] Severe neonatal hypoglycemia was
less common in insulin-treated women, but preterm delivery was more common.
Almost half of patients did not reach sufficient control with metformin alone and
needed supplemental therapy with insulin; compared to those treated with insulin
alone, they required less insulin, and they gained less weight.[64] There remains a
possibility of long-term complications from metformin therapy, although follow-up
at the age of 18 months of children born to women with polycystic ovarian
syndrome and treated with metformin revealed no developmental
abnormalities.[65]

If diet, exercise, and oral medication are inadequate to control glucose levels,
insulin therapy may become necessary.

The development of macrosomia can be evaluated during pregnancy by using


sonography. Women who use insulin, with a history of stillbirth, or with
hypertension are managed like women with ouvert diabetes.[11]

Research suggests a possible benefit of breastfeeding to reduce the risk of


diabetes and related risks for both mother and child.[66]

A repeat OGTT should be carried out 2-4 months after delivery, to confirm the
diabetes has disappeared. Afterwards, regular screening for type 2 diabetes is
advised.[7]

1.1 Reasons for the Development of Gestational Diabetes:


The causes for the onset of gestational diabetes is still uncertain.
Normally, 2 to 5 percent
of women are affected by gestational diabetes. Pregnant women are
more likely to develop
gestational diabetes if they meet the following criteria:
Have a family history of type-2 (adult-onset) diabetes.
With an age of 25 and above.
Have obesity.
2
Have previously given birth to a large baby or, with an
abnormality.
Previously had a stillbirth, late in pregnancy.
Have a history of gestational diabetes in the past pregnancy.
Though gestational diabetes usually does not cause any symptoms,
increase in blood sugar
levels, increased thirst and hunger, and frequent urination, are some of
the symptoms,
which are also common late in the pregnancy. Thus, it is difficult to
easily figure out the
patient having gestational diabetes without going for a glucose
tolerance test.
Also, women are susceptible to gestational diabetes if they had the
same in their past
pregnancy. However, it should be noted that every pregnancy is
different. Previous history
of gestational diabetes does not necessarily result in its manifestation
in subsequent
pregnancy. Similarly, gestational diabetes may appear in subsequent
pregnancies, but
could not have shown up in the earlier pregnancy. Thus, during every
pregnancy, mother
should be tested for gestational diabetes, irrespective of their past
medical history.
1.2 Effects of Gestational Diabetes:
Since the changes in mother’s body that cause gestational diabetes
normally occur only
during pregnancy, most of the time, gestational diabetes disappears
after the birth of the
baby. After the baby is born, mother’s body goes back to normal
function, and the
condition of gestational diabetes goes away. Moreover, gestational
diabetes is treatable,
especially if it is found in early stages of pregnancy. If gestational
diabetes is found in the
early stage, necessary and adequate treatment can be given to
safeguard both the mother
and the child from its detrimental effects. If it is not detected in the
early stages, then it can
3
cause several problems to the mother during delivery of the child, and
to the child both
during pregnancy and after the birth.
In general, the effect of gestational diabetes can be classified into
three groups based on
whether it affects baby or mother, and at what stage, viz.,
1. Effect of gestational diabetes on the foetus during pregnancy.
2. Effect of gestational diabetes on the baby after birth.
3. Effect of gestational diabetes on the mother.
Detailed discussion is presented below.
1.2.1 Effect of Gestational Diabetes on the Foetus During
Pregnancy:
Due to increased blood glucose levels in mother’s blood, the baby
grows larger. This
makes delivery of the baby injurious and difficult. In some cases, this
condition leads to
caesarean. If untreated, gestational diabetes can result in still birth
babies.
1.2.2 Effect of Gestational Diabetes on the Baby after Birth:
The offspring of gestational diabetes mother can face any one or,
combination of the
following problems:
1. In order to tolerate the increased blood glucose levels of mother, the
pancreas of
the baby secretes more amount of insulin while the foetus is growing.
This
condition continues even after birth, while higher blood glucose levels
no longer
4
exists. Thus, after birth, the baby develops hypoglycaemia (low blood
glucose
level). This condition can be overcome by administering glucose
through drip.
2. It is highly probable that the newborn baby will develop jaundice
(yellowing of
the skin and whites of the eyes). This condition fades away over a few
weeks
without the need for a medical treatment.
3. There is an increased risk for the baby to be born with congenital
problems, such
as a heart defect. At times, infants can be born with respiratory
distress syndrome
(RDS), in which the baby has breathing problems since the lungs have
not
matured as normal. But, this condition usually clears up with time.
4. The babies are more likely to be obese (overweight) as children or
adults, which
can lead to other health problems later in their life.
5. There is an increased risk for the child to develop type-2 diabetes
(development
of diabetes during adult stage).
6. There is also a slightly higher chance of stillbirth or death as a
newborn. This can
be avoided if the problem is detected earlier, and the glucose levels
were well
managed so as to avoid infant death.
1.2.3 Effect of Gestational Diabetes on Mother:
Normally, gestational diabetes does not affect the mother. However,
the mother who
developed gestational diabetes during first pregnancy is highly likely to
develop the same
5
at the second pregnancy. They are also likely to develop type-2
diabetes. In some mothers,
gestational diabetes leads to high blood pressure. It is also found to be
associated with
poly cystic ovary syndrome (PCOS; Bloomgarden, 2003), which leads to
infertility.
If mothers control their condition after detection of gestational
diabetes, most of them
have healthy pregnancies and healthy babies. If treatment is not taken,
mothers with this
condition could have very large babies. Since very large babies are
difficult to deliver
through natural delivery (delivery through the vagina), some mothers
may need surgery to
deliver their bigger babies. Surgery done towards this end can increase
the mother's
chances of getting an infection. Moreover, mothers who have their
babies by surgery also
take a longer time to recover.
1.3 Diagnosis for Gestational Diabetes:
Normally it is difficult to detect gestational diabetes unless the doctor
has a medical
history of the patient, and ascertain that the patient is likely to develop
it. Under this
circumstance, the blood glucose level of pregnant mother is monitored
regularly during the
entire pregnancy period through urine test. If pregnant mother
develops high blood
glucose levels between 24 – 28 weeks of pregnancy, then she is said to
have gestational
diabetes. In order to confirm that the mother has gestational diabetes,
glucose tolerance
test is conducted. During this test, the pregnant mother is given a 100
g of glucose
solution to drink after fasting for 8 hours. Then, blood samples are
taken at regular
intervals and glucose level is estimated. This is the only way to
ascertain the condition of
gestational diabetes in the pregnant mother.
6
1.4 Treatment for Gestational Diabetes
The most important part of treatment is to control blood sugar levels.
This can be
achieved by:
1. A carefully planned diet.
2. Regular exercise.
3. Taking proper medicines.
4. Monitoring the blood sugar at regular intervals.
5. Checking blood sugar after the birth.
1.4.1 Keeping Diet Under Control
Keeping the diet under control is another important factor for the
patients affected by
gestational diabetes. Taking a balanced diet is important in order to
keep the blood sugar
at the optimum level. Normally the diet should consist of a variety of
foods including
plenty of starchy fillers such as bread, pasta, rice and potatoes, and at
least five portions of
fruit and vegetables each day. Moreover, it is important to limit
consumption of sugary
foods like cakes, biscuits and soft drinks. A diet that is low in fat, is also
desirable. This
can be achieved by avoiding full-fat dairy products such as butter and
cream, and limiting
fatty meat, pies, sausages and burgers. Grilling, steaming or,
microwaving food, rather
than frying or roasting means, less fat is added during cooking.
7
1.4.2 Regular Physical Exercise
Apart from diet control and proper medication, gentle and regular
exercise, such as
walking, can help reduce blood sugar levels and promote the body
condition of the
mother. However, the doctor should be consulted before choosing
proper body exercises.
1.4.3 Taking Proper Medicines
Despite making the above lifestyle changes, a few women's blood
sugar levels remain too
high, and they may need daily injections of insulin. The extra insulin
will not cross the
placenta and will not affect the baby. Any woman who needs to take
insulin will be taught
how to take it by her doctor or nurse. Sometimes, it is possible to have
too much insulin
and this can cause low blood sugar (hypoglycaemia). Common
symptoms of this are
weakness, shaking, hunger and sweating. Thus, for people taking
insulin, it is a good idea
to keep a snack handy at all times in case low blood sugar develops.
1.4.4 Regular Monitoring of Blood Glucose Levels
Normally, the blood glucose level should be tested once a week. For
some women,
frequent testing may be needed, and a good doctor should be
consulted to keep the
gestational diabetes under control. For those who need frequent
testing, blood glucose
level needs to be measured in the morning, before breakfast, and
again two hours after
breakfast. Sometimes, it may be necessary to test blood glucose levels
in the midafternoon.
8
1.4.5 Checking Blood Sugar After the Birth of baby
In almost every case, gestational diabetes disappears after the
delivery of the baby.
However, to be sure that the blood glucose levels have become
normal, it is necessary to
check the mother's blood sugar levels a few times after the birth.
the onset of gestational diabetes in diverse groups of the people.
causes for gestational diabetes are still not clearly known, the following
factors are said to
be important in inducing women with gestational diabetes:
1. Have a family history of type-2 (adult-onset) diabetes.
2. Age over 25 years.
3. Obesity.
4. Previously given birth to a large baby (macrosomia).
5. Previously given birth to a baby with congenital abnormality.
6. Previously had a stillbirth, late in pregnancy.
10
Thus, in this study all the patients were screened for the following
critical parameters viz.,
Age.
_

GRA/PARA.
_

Responds positively to medication in reducing its detrimental


effect both on the child
and on the mother?
Have drugs administered for gestational diabetes inflict any
effect on the health of
foetus and mother?
11
To what extend the foetus is affected by gestational diabetes?
Whether women are more likely to develop gestational diabetes
in the first
pregnancy or, in the subsequent pregnancies?
taken into
account.
2.3.1 Glucose Tolerance Test for Gestational Diabetes:
The patients’ urine was routinely tested for sugar throughout
pregnancy. If high blood
sugar was detected between 24 and 28 weeks of pregnancy, then they
were supposed to
have gestational diabetes.
12
However, a confirmation for gestational diabetes was ascertained only
after a test for
glucose tolerance was undertaken. This glucose tolerance test was
carried out after eight
hours without food – i.e., the patients were advised to come to the
hospital in the morning
without taking any food – including tea/coffee/milk or, other drinks. At
the hospital the
patient was given a solution of 100 g of glucose to drink, and then
blood samples were
taken at every half-an hour intervals and analysed to see how their
body deals with the
glucose, over time (O'Sullivan and Mahan, 1964). If higher glucose
levels were detected
during glucose tolerance test, then the patient was classified as having
gestational diabetes.

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