2. Gestational Complications
When women experience pregnancy complications,
astute assessment, rapid intervention, and a
collaborative team approach are essential to optimize
maternal and neonatal outcomes.
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3. Preterm Labor and Birth
Preterm labor (PTL) is the onset of labor before 37 weeks’ gestation.
Preterm birth (PTB) refers to gestational age at birth of less than 37 weeks.
- Preterm births are a result of spontaneous preterm labor; however, between
20% and 25% of preterm births are intentional, necessary, and indicated for
problems such as hypertension, preeclampsia, hemorrhage, and intrauterine
growth restriction (IUGR) where early delivery would improve either
maternal or fetal status.
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4. A preterm/premature infant is born after 20 weeks
and before 37 completed weeks of gestation.
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5. Pathophysiological Pathways of Preterm
Labor
Spontaneous preterm birth may be characterized by a syndrome composed of
several components including uterine (preterm labor), chorioamnionic-decidual
(premature rupture of membranes), and cervical (cervical insufficiency) (Owens &
Harger, 2007).
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7. Risk Factors for Preterm Labor and Birth
■ Prior preterm birth (single most important
factor reoccurrence rates of up to 40%)
■ History of second trimester loss
■ History of incompetent cervix
■ Cerclage
■ IVF pregnancy
■ Multiple gestation (50% of twins
delivered preterm,
≥90% higher multiples delivered preterm)
■ Uterine/cervical abnormalities
■ Hydramnios or oligohydramnios
■ Infection, especially genitourinary
infections and periodontal disease
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8. ■ Premature rupture of membranes
■ Pregnancy associated problems such as hypertension,
diabetes, and vaginal bleeding
■ Chronic health problems such as hypertension, diabetes,
or clotting disorders
■ Inadequate nutrition, low BMI, low pre-pregnancy
weight, or poor weight gain. Obesity, high BMI, or
excessive weight gain.
■ Age younger than 17 or older than 35 years old
■ Working long hours, long periods of standing
■ Lack of social support
■ Smoking, alcohol, and illicit drug use
■ Lower education and socioeconomic status, poverty
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9. Diagnosis of Preterm Labor
The diagnosis of preterm labor is made when the following criteria are met:
■ Gestational age of >20 weeks and <37 weeks
■ Documented regular uterine contractions (UCs) >6 / hour and at least one of the
following:
■ Rupture of membranes (ROM)
■ Cervical change: Cervix >1 cm dilated or 80% effaced (criteria for cervical
dilation varies)
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10. Medical Management
Typically management is focused on delaying delivery for
several days (optimal is 72 hours) to give glucocorticoids
(corticosteroids) time to facilitate fetal lung maturity..
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11. ■ Tocolytic drugs are medications that are
used to suppress uterine contractions in
preterm labor.
■ Tocolytic drugs may prolong pregnancy
for 2 to 7 days, which may allow for
administration of steroids to
improve fetal lung maturity.
- Magnesium Sulfate (MgSO4)
- Prostaglandin Synthesis Inhibitors
Indomethacin Naproxen
- Calcium Channel Blockers
Nifedapine
- Beta-adrenergic Agonists
Terbutaline
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12. ■ Intravenous hydration is a common strategy to reduce
preterm uterine contractions because it increases vascular
volume and may help to decrease contractions.
■ Antibiotics are commonly used to treat genital urinary
Infections.
■ Progesterone supplementation may be useful to prevent
preterm birth for women with a history of spontaneous preterm
birth..
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13. Corticosteroids
Betamethasone
■ Indication: Given to women at 24 and 34 weeks’ gestation with signs of preterm
labor or at risk to deliver preterm
■ Action: Stimulate the production of more mature surfactant in the fetal lungs to
prevent respiratory distress syndrome in premature infants
■ Route and dose: Betamethasone 12 mg IM every 24 hours × 2 doses
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14. ■ Contraindications to treating preterm labor include:
• Active hemorrhage
• Severe maternal disease
• Chorioamnionitis
• Fetal death
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15. Nursing Actions
■ Assess fetal heart rate (FHR) and uterine contractions.
■ Position the patient on her side to increase
uteroplacental perfusion and decrease pressure on the
maternal inferior vena cava.
■ Assess cervical status
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16. Amniotic Fluid Imbalances
Polyhydramnios ( hydramnios)
Is a condition in which there is too much amniotic fluid (more than 2,000 mL)
surrounding the fetus between 32 and 36 weeks.
• It occurs in approximately 3% of all pregnancies
and is associated with fetal anomalies of development.
• It is associated with poor fetal outcomes because of the increased incidence of
preterm births, fetal malpresentation, and cord prolapse..
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18. There are several causes of polyhydramnios.
Generally, too much fluid is being produced, there is a problem
with the fluid being taken up, or both. It can be associated with
maternal disease and fetal anomalies, but it can also be
idiopathic in nature
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19. Therapeutic Management
• Close monitoring and frequent follow-up visits with the health care provider if the
hydramnios is mild to moderate.
• In severe cases in which the woman is in pain and experiencing shortness of breath,
an amniocentesis or artificial rupture of the membranes is done to reduce the fluid
and the pressure.
• A noninvasive treatment may involve the use of a prostaglandin synthesis inhibitor
(indomethacin) to decrease amniotic fluid volume by decreasing fetal urinary
output, but this may cause premature closure of the fetal ductus arteriosus..
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21. Nursing Assessment
• Begin the assessment with a thorough history, being alert to risk factors
such as maternal diabetes or multiple gestation.
• Determine the gestational age of the fetus and measure the woman’s fundal
height. With hydramnios, there is a discrepancy between fundal height
and gestational age, or a rapid growth of the uterus is noted.
• Assess for shortness of breath resulting from pressure on her diaphragm
and inspect her lower extremities for edema, which results from increased
pressure on the vena cava.
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22. • Often the fetal parts and heart rate are difficult to obtain
because of the excess fluid present.
• Prepare the woman for possible diagnostic testing to
evaluate for the presence of possible fetal anomalies.
• An ultrasound usually is done to measure the pockets of
amniotic fluid to estimate the total volume.
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23. Oligohydraminos
• is a decreased amount of amniotic fluid (less than 500 mL) between 32 weeks and 36
weeks’ gestation.
• It occurs in 5% to 8% of all pregnancies.
• Oligohydramnios may result from any condition that prevents the fetus from making
urine or blocks it from going into the amniotic sac.
• Reduction in amniotic fluid reduces the ability of the fetus to move freely without risk of
cord compression, which increases the risk for fetal death and intrapartal hypoxia..
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25. Therapeutic Management
As long as fetal well-being is demonstrated with frequent testing, no
intervention is necessary.
If fetal well-being is compromised, however, birth is planned along with
amnioinfusion (the transvaginal infusion of crystalloid fluid to compensate
for the lost amniotic fluid). The fluid is introduced into the uterus through
an intrauterine pressure catheter. Amnioinfusion is thought to improve
abnormal fetal heart rate patterns, decrease cesarean births, and possibly
minimize the risk of neonatal meconium aspiration syndrome..
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26. Nursing Assessment
Review the maternal history for factors associated with
oligohydramnios, including:
• Uteroplacental insufficiency
• Premature rupture of membranes prior to labor onset
• Hypertension of pregnancy
• Maternal diabetes
• Intrauterine growth restriction
• Postterm pregnancy
• Fetal renal agenesis
• Polycystic kidneys
• Urinary tract obstructions
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27. • Assess the client for complaints of fluid leaking from
the vagina.
• Typically, the reduced volume of amniotic fluid is identified on ultrasound.
• Continuous monitoring of fetal well-being during nonstress testing or during labor and birth
by identifying nonreassuring patterns on the fetal monitor.
• Variable decelerations indicating cord compression are
common. Changing the woman’s position might be
therapeutic in altering this fetal heart rate pattern..
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28. • Provide comfort measures such as changing the bed
linens and the woman’s bed clothes frequently because
of the constant leakage of fluid from the vagina..
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30. Premature rupture of membranes
is defined as rupture of the chorioamniotic membranes
before the onset of labor but at term.
Preterm premature rupture of membranes (PPROM) is rupture of membranes with
a premature gestation (<37 weeks).
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31. Risk Factors for Preterm PROM
■ Previous preterm PROM or preterm delivery
■ Bleeding during pregnancy
■ Hydramnios
■ Multiple gestation (up to 15% in twins, up to 20% in triplets)
■ Sexually transmitted infections (STIs)
■ Cigarette smoking
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32. Risks for the Woman
■ Maternal infection (i.e., chorioamnionitis)
■ Preterm labor and birth
■ Increased rates of cesarean birth
Risks for the Fetus and Newborn
■ Fetal or neonatal sepsis
- The earlier the fetal gestation at ROM, the greater the risk for infection
■ Preterm delivery and complications of prematurity
■ Hypoxia or asphyxia because of umbilical cord compression due to decreased
fluid
■ Fetal deformities if preterm PROM before 26 weeks’ gestation
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33. Management
- Hospitalized in an attempt to prolong the
pregnancy unless intrauterine infection, significant
vaginal bleeding, placental abruption, preterm
labor, or fetal compromise.
■ Assess for signs of infection including:
- Maternal and/or fetal tachycardia
- Maternal fever 100.4°F (38°C) or greater
- Uterine tenderness
- Malodorous fluid or vaginal discharge
- Daily fetal assessment
- Antenatal corticosteroids for less than 32 weeks of
gestation
- 7 – day course of broad – spectrum antibiotics
- Keep genital area clean and nothing should be
introduced into the vagina
- If Chorioamnionitis develops, labor will induced.
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34. Nursing Actions
■ Assess FHR and uterine contractions.
■ Monitor for labor and for fetal compromise.
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35. Hyperemesis gravidarum
When vomiting during pregnancy becomes excessive enough to cause weight loss, electrolyte
imbalance, nutritional deficiencies, and ketonuria, the disorder is termed hyperemesis
gravidarum.
Hyperemesis gravidarum usually begins during the first trimester, but approx. 10% of women with the
disorder continue to have symptoms throughout the pregnancy.
Hyperemesis appears to be related to rapidly rising serum levels of pregnancy related hormones such
as chorionic gonadotropin (hCG), progesterone, and estrogen levels.
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36. It has been associated with women who are nulliparous, have increased body
weight, have a history of migraines, multiple gestation, gestational
trophoblastic disease, carrying a fetus with chromosomal abnormality e.g.,
trisomy 21.
- Women carrying a female fetus are more likely than those carrying a male
fetus to develop hyperemesis.
- a family history of hyperemesis may also be present.
- Interrelated psychologic component has been associated with hyperemesis
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37. Complications accompanying severe hyperemesis gravidarum include:
• Esophageal rupture and deficiencies of vit. K , and thiamine.
Fetal and neonatal complications include SGA, LBW, prematurity, and 5 minute
Apgar scores less than 7.
Clinical Manifestations
Dry mucous membranes, decreased BP, increased pulse rate, and poor skin turgor. Lab
tests reveal electrolyte imbalances..
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38. Management divided into:
Assessment
• Include frequency, severity, and duration of episodes of N/V .
• Assess the approx. amount and the color of the vomitus.
• Ask the woman to report any preciptating factors
• Any use of pharmacologic or nonpharmacologic treatment.
• Prepregnancy wt. and wt. gain or loss should be recorded
• V/S, signs of fluid and electrolyte imbalance.
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39. • Monitor lab test : ketonuria, UA, CBC, S.
electrolytes, liver enzyme, bilirubin levels.
• Ask the woman about anxiety, fears.
• Observe the woman for any signs of complications
such as metabolic acidosis, jaundice, or hemorrhage.
- Initial care
• Admission to hospital
• Start IV therapy for correction of fluid and
electrolyte imbalance.
• Medications ( for N/V may use pyridoxine (Vit. B6,
metoclopramid) ( antiemetic medication e.g.,
compazine, zofran)
• Enteral or parenteral nutrition
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40. • Oral hygiene
• Provide quite environment free from odors
• When vomiting stopped, feeding are started in small amounts at frequent
intervals.
• Promote adequate rest
• Diet ( low fat, high protein foods, dairy products, ginger tea)
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41. Diabetes in Pregnancy
■ Women with diabetes in pregnancy can be divided into two groups:
pregestational and gestational diabeties.
■ Pregestational diabetes (either type 1 or type 2 diabetes)
■ Gestational diabetes mellitus (GDM) is glucose intolerance that had
not previously been present prior to pregnancy..
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42. Gestational Diabetes Mellitus
- Gestational diabetes mellitus (GDM) is glucose intolerance that had not
previously been present prior to pregnancy.
- GDM is likely to recur in future pregnancies, and the risk for
development of overt diabetes in later life is also increased. This
tendency is especially true of women whose GDM is diagnosed early in
pregnancy or who are obese.
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43. Classic risk factors for GDM include:
- Maternal age over 25years
- Previous macrosomic infant
- Previous unexplained IUFD
- Previous pregnancy with GDM
- Strong immediate family history of type 2 diabetes
or GDM
- Obesity (weight >90kg), and fasting blood glucose
above 140mg/dl or random blood glucose above
200mg/dl.
*Women at high risk for developing GDM should have
glucola screening at the first prenatal visit and
again at 24 to 28 weeks of gestation if the initial
screen is negative.
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44. GDM is usually diagnosed during the second half of pregnancy.
Pathophysiology
• As fetal nutrient demands rise during the late second and the third trimester,
maternal nutrient ingestion induces greater and more sustained levels of blood
glucose. At the same time , maternal insulin resistance is also increasing
because of the insulin – antagonistic effects of the placental hormones.
Consequently , maternal insulin demands rise as much as three fold. Most
pregnant women maintain a normal glucose level in pregnancy despite
increasing insulin resistance by producing increased insulin.
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45. Because maternal insulin does not cross the placenta, the
fetus is exposed to maternal hyperglycemia and in
response the fetus produces more insulin, which promotes
growth and subsequent macrosomia.
When the pancreas is unable to produce sufficient insulin or
the insulin is not used effectively, however, gestational
diabetes can result..
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46. ACOG recommends routine screening for all pregnant women at 24–28 weeks
of gestation, with a nonfasting 1-hour 50-g oral glucose tolerance test.
A glucose value of 130 or 140mg/dl is considered a positive screen and should
be followed by a 3 –hour (100-g) oral glucose tolerance test (OGTT), plasma
glucose levels are drawn at 1, 2, and 3 hours post glucose load.
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47. OGTT is administered after an overnight fast and at least 3 days of unrestricted
diet and physical activity.
- Woman is instructed to avoid caffeine because it will increase glucose levels.
- Abstain from smoking for 12 hours before the test.
- FBG is drawn before giving 100-gram glucose load.
- BG levels are then drawn, 1,2, and 3 hours later.
- The woman is diagnosed with GDM if two or more values are met or exceeded.
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48. If two or more glucose levels are above these thresholds, a
diagnosis of GDM is made:
fasting ≥95 mg/dL, 1-hour ≥180 mg/dL, 2-hour ≥155
mg/dL, and 3-hour ≥140 mg/dL.
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49. 1 –hr(50g) oral glucose
tolerance test (OGTT)
Positive (≥130 – 140 mg/dl)
3 – hr
(100g)O
GTT
Negative (&lt;130
– 140 mg/dl)
Routine prenatal
care
Positive for GDM
2 or more levels are met or exceeded:
Fasting < 95m/dl
1 – hr < 180 mg/dl
2 – hr < 155 mg/dl
3 – hr < 140
m9/dl
Negative
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50. Medical Management:
■ For most women with GDM, the condition is controlled with diet and exercise.
■ Up to 40% of women with GDM may need to be managed with insulin.
■ Oral hypoglycemic agents may be used, but there is not agreement on their recommended use
during pregnancy.
■ Cesarean birth is recommended for estimated fetal
weight >4,500 g.
■ Women with GDM need to be monitored for type 2 diabetes after the birth. About one third of
women will have recurrent GDM in subsequent pregnancies
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51. Care management
Antepartum
- Strict blood glucose control. FBG levels should less than 95mg/dl and between 120–135 mg/dL
after meals.
Diet. Carbohydrate intake is restricted to approx. 50% of caloric intake
Exercise. helps lower blood glucose levels and decreasing the need for insulin.
Monitoring blood glucose levels.
Medications for controlling blood glucose levels..
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52. - If fasting plasma glucose levels are greater than 95 mg/dl or 2 – hour postprandial levels
are greater than 120 mg/dl then insulin therapy is begun.
Glyburide (oral hypoglycemic agent is used with women with GDM instead of insulin).
1. Minimal amounts cross the placenta … for that, good drug use during pregnancy.
2. Recent studies have shown that should be taken at least 30minutes before the meal so
its peak effect covers the 2 – hour postprandial blood glucose level.
3. Episodes of hypoglycemia can occur between meals, women taking Glyburide always
carry with them sources of fast sugar..
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53. - Women with GDM can continue pregnancy until 40 weeks of gestation and the spontaneous onset of
labor.
- Fetal growth should be monitored
Intrapartum
- During the labor and birth process, blood glucose levels are monitored hourly to maintain levels at 80 to
120 mg/dl ( this decrease the incidence of neonatal hypoglycemia).
- Infusing regular insulin IV during labor to maintain blood glucose levels within this range.
- IV fluids containing glucose are not commonly given during labor.
- C/S not necessary unless in the presence of preeclampsia or macrosomia.
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54. Postpartum
- Most women with GDM will return to normal glucose levels after
childbirth.
- Women should encouraged to make lifestyle changes that include
weight loss and exercise.
- 75-g OGTT should performed at 6 to 12 weeks post partum.
- Children born to women with GDM are also at risk for becoming obese
in childhood or adolescence. .
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55. Gestational hypertension
• Is the onset of hypertension without proteinuria after week 20 of pregnancy.
• Hypertension is defined as a systolic BP greater than 140 mmHg or a diastolic BP
greater than 90 mmHg.
• The hypertension should be recorded on at least two separate occasions at least 4 to 6
hour apart but within a maximum of a 1 –week period.
• Incidence of gestational hypertension in primigravidas 6% to 17% and 2% to 4% in
multiparous women.
• Occurs much more frequently in women with multifetal pregnancies than in other
women.
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56. Pregnancy Hypertension
Significance and incidence
- Hypertensive disorders are the most common medical complication of
pregnancy, occurring in 5% to 10% of all pregnancies.
- Hypertensive disorders are a major cause of maternal and perinatal morbidity
and mortality worldwide..
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57. The four most common types of hypertensive disorders
occurring in pregnancy are :
1. Gestational hypertension
2. Preeclampsia
3. Chronic hypertension
4. Preeclampsia superimposed on chronic hypertension
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58. Classification
1. Gestational hypertension
- Systolic BP ≥ 140/90 for the first time after 20 weeks, without proteinuria.
- Almost 50% of women with gestational hypertension develop preeclampsia
syndrome.
2. Preeclampsia and eclampsia syndrome
Preeclampsia is a systemic disease with hypertension accompanied by proteinuria
after the 20th week of gestation. Eclampsia is the development of convulsions
or coma in preeclampsia woman.
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59. 3. Chronic hypertension
Hypertension (BP ≥ 140/90) or proteinuria (or both) in pregnant woman present before pregnancy or diagnosed
before 20 weeks of gestation and persistent after 12 weeks postpartum.
4. Superimposed preeclampsia or eclampsia
Hypertensive women who develop new-onset proteinuria;
proteinuria before the 20th week of gestation; or sudden
increase in proteinuria or BP or platelet count <100,00/μL
in women with hypertension and proteinuria before
20 weeks’ gestation.
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60. • Gestational hypertension usually develops at or after 37
weeks of gestation.
• Women with gestational hypertension have no evidence
of preexisting hypertension, and their BPs return to
normal levels within 6 weeks after giving birth.
• Women with mild gestational hypertension usually have
good pregnancy outcomes.
.
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61. Preeclampsia
Is a hypertensive, multisystem disorder of pregnancy
whose etiology remains unknown. Preeclampsia is best
described as a pregnancy-specific syndrome of reduced organ
perfusion secondary to vasospasm and endothelial activation.
Preeclampsia is a disease of pregnancy that ranges from mild to
severe and is hypertension accompanied by underlying systemic
pathology that can have severe maternal and fetal impact.
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62. • Preeclampsia complicates approx. 3% to 7% of all pregnancies.
Proteinuria is defined as a concentration at or above 30mg/dl (≥ 1+ on
dipstick ) or more in at least two random urine specimen collected at
least 6 hours apart with no evidence of UTI.
In a 24 – hour specimen, proteinuria is defined as a concentration at or
above 300mg/24hours.
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64. Preeclampsia is a condition unique to human pregnancy; signs and symptoms
usually develop only during pregnancy and disappear quickly after birth of
the fetus and passage of the placenta.
Etiology
• Cause of preeclampsia is not known
• Preeclampsia is generally a disease of primigravidas, its cause may not be the
same for all women.
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65. Pathophysiology
Normal pregnancy is a vasodilated state in which peripheral vascular resistance
decreases 25%. Within the first weeks, the woman’s blood pressure falls,
largely due to a general relaxation of muscles within the blood vessels.
Diastolic blood pressure drops 10 mm Hg at midpregnancy and gradually
returns to pre-pregnant levels at term. There is a 50% rise in total blood
volume by the end of the second trimester, and cardiac output increases 30%–
50%. Increased renal blood flow leads to an increased glomerular filtration
rate.
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66. Changes that occur in the woman with preeclampsia are
caused by disruptions in placental perfusion and
endothelial cell dysfunction, leads to placental
ischemia. Placental ischemia is thought to cause
endothelial cell dysfunction by stimulating the release
of a substance that is toxic to endothelial cells.
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67. This causes generalized vasospasm, which results in
poor tissue perfusion in all organ systems, increased
peripheral resistance and BP, and increased endothelial
cell permeability, leading to intravascular protein and
fluid loss and ultimatley to less plasma volume.
The main pathogenic factor is not increase an BP but poor
perfusion as a result of vasospasm and reduced plasma
volume.
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69. Consequences of endothelial dysfunction
Vasospasm and decreased organ perfusion
- Liver ischemia ….. can lead to periportal hemorrhagic necrosis in
the liver that can cause a subcapsular hematoma, which can result in
right upper quadrant pain or epigastric pain and may signal
worsening preeclampsia. Liver damage may be mild or may
progress to HELLP syndrome (Hemolysis, Elevated Liver enzymes,
and Low Platelets). N/V.
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70. - Glomerular damage ….. fibrin deposition, and resulting ischemia
reduce renal plasma flow and glomerular filtration rate. Protein is
excreted in the urine. Uric acid, creatinine, and calcium clearance are
decreased and oliguria develops as the condition worsens.
- Coagulation system is activated in preeclampsia and thrombocytopenia
occurs, possibly due to increased platelet aggregation and deposition at
sites of endothelial damage, activating the clotting cascade. A platelet
count below 100,000 cells/mm3 is an indication of severe
preeclampsia.
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71. - Endothelial damage to the brain results in fibrin deposition, edema, and cerebral
hemorrhage, which may lead to hyperreflexia and severe headaches and can progress to
eclampsia.
- Retinal arterial spasms may cause blurring or double
vision, photophobia, or scotoma عتمة.
- The leakage of serum protein into extracellular spaces
and into urine, by way of damaged capillary walls, results in decreased serum albumin and
tissue edema..
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72. - Pulmonary edema is most commonly caused by volume
overload related to left ventricular failure as the result of
extremely high vascular resistance.
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73. Risks factors
- Nulliparity
- Age younger than 19
or older than 35 years
- Obesity
- Multifetal gestation
- Preexisting
hypertension or renal
disease
- Previous preeclampsia
or eclampsia
- Diabetes mellitus
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75. Risks for the Fetus and Newborn
■ Prematurity delivery may be indicated preterm related to deterioration of maternal
status.
■ Intrauterine growth restriction (IUGR) related to
decrease uteroplacental perfusion
■ Low birth weight
■ Fetal intolerance to labor because of decrease placental perfusion
■ Stillbirth
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76. Care Management
1- Physical examination
- Consistent in taking and recording BP measurements in a standardized
manner .
- Assessment of edema (distribution, degree, and pitting) if pregnant women
is ambulatory, the edema may be first evident in the ankles and feet, if she
confined to bed the edema more likely to occur in the sacral area.
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78. - Deep tendon reflexes (DTRs)
Biceps and patellar reflexes, and ankle clonus are assessed and recorded.
Mild gestational hypertension and mild preeclampsia
Goals of therapy are to ensure maternal safety and to deliver a healthy newborn as close
to term as possible.
Maternal Assessment includes:
- Measurement of Hct, Plt count, liver function test, 24 hour urine collection / week.
- Assess BP twice / week
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80. Severe gestational hypertension or
severe preeclampsia
- Hospitalized immediately for a 24 hour observation
period.
- Start magnesium sulfate
- Antihypertensive medications ( to keep systolic BP
between 140 and 155 mmHg and her diastolic BP
between 90 and 105mmHg).
- Women less than 34wk given corticosteroids.
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81. - Maternal Assessment includes:
Monitoring BP, urine output, cerebral status, presence of epigastric pain,
labor, vaginal bleeding, lab test (platelet count, liver enzymes, and serum
Creatinine) .
- Bed rest , noise and external stimuli should be reduced, precaution for
seizures should be prepared, emergency trolley readily available. .
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82. Fetal assessment includes:
Continuous FHR monitor, U/S
if the pregnancy is 34wk or greater, the woman give birth by C/S or
labor induction.
If she less than 34wk, close observation until reach 34wk.
BUT women with uncontrolled BP, thrombocytopenia, elevated liver
enzymes with epigastric pain and tenderness will need to give birth
right away.
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82 HANADI MALAYSHEH
83. Magnesium sulfate
- Drug of choice in the prevention and treatment of convulsions caused by
preeclampsia or eclampsia.
- The routine use of magnesium sulfate is indicated for severe preeclampsia, HELLP
syndrome, or eclampsia.
- Given IV by infusion pump (RL solution)
Initial loading dose 4 to 6 g is infused over 15 to 30 minutes then maintenance dose 40g
in 1000 ml RL by infusion pump at 2g /hour to maintain serum magnesium level of
4 to 7mEq/L.
- Rarely given IM
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83 HANADI MALAYSHEH
84. Magnesium sulfate interferes with the release of a acetylcholine at the
synapses, decreasing neuromuscular irritability, depressing cardiac
conduction, and decreasing CNS irritability.
•
Expected side effects of magnesium sulfate are a feeling of warmth,
flushing, and nausea. Symptoms of mild toxicity include lethargy,
muscle weakness, decreased DTRs, and slurred speech.
Increasing toxicity may be indicated by maternal hypotension,
bradycardia, bradypnea, and cardiac arrest
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84 HANADI MALAYSHEH
85. Observe magnesium toxicity
- Respiratory depression, decreased or absent DTRs, oliguria, decreased level of
consciousness.
Measure serum magnesium level at 4–6 hours, after onset of treatment. Dosage should be
adjusted to maintain a therapeutic level of 4–7 mEq/L.
If magnesium toxicity is suspected
- D/C infusion immediately
The antidote for magnesium toxicity is calcium gluconate or calcium chloride 5–10 mEq
given IV slowly over 5–10 minutes..
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85 HANADI MALAYSHEH
86. Control of BP
Because a degree of maternal hypertension is necessary to
maintain uteroplacental perfusion, antihypertensive
therapy must not decrease the arterial pressure too
much or too rapidly.
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86 HANADI MALAYSHEH
87. First-Line Drugs of Choice
Hydralazine (Apresoline, Neopreol) vasodilator: IV administration is used in severe
preeclampsia; however, caution should be used to prevent rapid decreases in blood
pressure. Rapid reduction in maternal blood pressure can decrease uteroplacental
perfusion and decrease oxygen to fetus.
Methyldopa (Aldomet): Exact mechanism is unknown; may work on CNS. May take a
few days for onset, so this drug is not a first choice in an acute situation.
Labetalol (beta blocker): Slows the heart rate and decreases systemic vascular
resistance.
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87 HANADI MALAYSHEH
89. Postpartum care
- Magnesium sulfate infusion is continue for 12 to 24 hours after birth for
seizure prophylaxis.
- Assess V/S, I&O, DTRs, level of consciousness, uterine tone, and lochial
flow.
- Assess for any preeclampsia symptoms.
- Oxytocin or prostaglandin products to control bleeding postpartum.
- Methergine contraindicated because they increase BP.
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89 HANADI MALAYSHEH
90. Eclampsia
Is the onset of seizure activity or coma in a woman with preeclampsia
but with no history of a preexisting abnormality that can result in
seizure activity.
The initial presentation of eclampsia varies; one third of the women
develop eclampsia during the pregnancy, one third during labor, and
one third within 72 hours postpartum.
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91. Warning signs of potential eclampsia include:
■ Severe persistent headaches
■ Epigastric pain
■ Nausea and vomiting
■ Hyperreflexia with clonus
■ Restlessness■
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91 HANADI MALAYSHEH
92. Eclampsia Management
- Keep air way patent
- Patient safety
After convulsion
- O2 via nonrebreather mask
- IV fluid
- Give magnesium sulfate, anticonvulsant drug
- Observe BP, monitor FHR, uterine contraction
- Lab test request
- Provide hygiene, quite environment
- Be prepare for birth
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92 HANADI MALAYSHEH
93. HELLP Syndrome
• Is a laboratory diagnosis for a variant of severe preeclampsia that involves
hepatic dysfunction, characterized by hemolysis (H), elevated liver enzymes
(EL), and low platelets (LP), not a separate illness.
• A unique form of coagulopathy occurs with HELLP syndrome. The platelet
count is low, but coagulation factor assays, PT, PTT, and bleeding time remain
normal.
• In some instances, hemolysis does not occur, and the condition is termed
ELLP or partial HELLP syndrome..
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94. ■ Hemolysis is a result of red blood cell destruction as the cells travel
through constricted vessels.
■ Elevated liver enzymes result from decreased blood flow and damage to
the liver.
■ Low platelets result from platelets aggregating at the
site of damaged vascular endothelium causing platelet
consumption and thrombocytopenia
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96. - HELLP syndrome is often non specific in clinical
presentation.
- Majority of women report a history of malaise for several days
and some have nonspecific viral – like syndrome.
- Many women (30% to 90%) experience epigastric pain, RUQ
abdominal pain, N/V, headaches.
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96 HANADI MALAYSHEH
97. Risks for the Woman
■ Abruptio placenta
■ Renal failure
■ Liver hematoma and possible rupture
■ Death
Risks for the Fetus and Newborn
■ Preterm birth
■ Death
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97 HANADI MALAYSHEH
98. Medical Management
The only definitive cure for HELLP syndrome is immediate
delivery of the fetus and placenta. Resolution of disease is
generally in 48 hours postpartum.
Nursing Actions
■ Perform a thorough assessment of the woman related to the
diagnosis of preeclampsia.
■ Evaluate laboratory tests.
■ Administer platelets as per orders.
■ Assessment and management are the same for the
women with severe preeclampsia..
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99. Hemorrhagic complication
A. Early pregnancy bleeding
1. Abortion
is the spontaneous or elective termination of pregnancy before 20
weeks’ gestation. Abortions are referred to as induced, elective,
therapeutic, and spontaneous.
Induced abortion is the medical or surgical termination of
pregnancy before fetal viability. Elective abortion is termination
of pregnancy before fetal viability at the request of the woman
but not for reasons of impaired health of the mother or fetal
disease.
.
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100. Therapeutic abortion is termination of pregnancy for serious
maternal medical indications or serious fetal anomalies.
Spontaneous abortion (SAB) is abortion occurring without
medical or mechanical means, also called miscarriage.
- Greater than 80% of miscarriages are early pregnancy losses,
occurring before 12 wk. of gestation.
- At least 50% of pregnancy losses result from chromosomal
abnormalities.
- Late spontaneous abortions are between 12 and 20 weeks’
gestation.
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100 HANADI MALAYSHEH
101. Other types of miscarriage
Threatened, inevitable, incomplete, complete, and missed. All
types of miscarriage can recur in subsequent pregnancies. All
types except the threatened miscarriage can lead to infection.
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102. Risk Factors for Spontaneous Abortion
■ Increased parity
■ Increased maternal age
■ Endocrine abnormalities such as diabetes or luteal
phase defects
■ Drug use or environmental toxins
■ Immunological factors such as autoimmune
diseases
■ Infections
■ Systemic disorders
■ Genetic factors
■ Uterine or cervical abnormalities
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105. Clinical manifestations
- If miscarriage occurs before the sixth week of pregnancy, the woman may report
only a heavy menstrual flow.
- Miscarriage occurs between weeks 6 and 12 of pregnancy causes moderate
discomfort and blood loss.
- After 12 weeks, miscarriage is typified by severe pain, similar to that of labor,
because the fetus must be expelled.
- Symptoms of a threatened miscarriage include spotting of blood but with cervical
os closed. Mild uterine cramping may be present.
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106. Inevitable and incomplete miscarriage involve a moderate to heavy
amount of bleeding with an open cervical os. Mild to severe uterine
cramping may be present. An inevitable miscarriage is often
accompanied by SROM and cervical dilation, passage of the
products of conception will occur.
An incomplete miscarriage involves the expulsion of the fetus with
retention of the placenta.
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107. In a complete miscarriage, the cervix has already closed after all fetal tissue
was expelled and slight bleeding may occur. Mild uterine cramping may be
present.
Missed miscarriage, refers to a pregnancy in which the fetus has died but the
products of conception are retained in utero for up to several weeks.(uterus
stops increasing in size or even decreases in size) there may be no bleeding
or cramping, and the cervical os remains closed.
Recurrent early (habitual) miscarriage is three or more spontaneous
pregnancy losses before 20 weeks of gestation..
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107 HANADI MALAYSHEH
108. Miscarriage can become septic, symptoms of a septic miscarriage include fever and
abdominal tenderness. Vaginal bleeding which may be slight to heavy, is usually
malodorous.
Management
Management depends on the classification of the miscarriage and on signs and symptoms.
- Repetitive measurement of hCG levels to evaluate the viability of the pregnancy.
- Dilation and curettage (D&C) is a surgical procedure in which the cervix is dilated and
a curette is inserted to scrap the uterine walls and remove uterine contents. ( commonly
performed to treat inevitable and incomplete miscarriage).
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110. - Dilation and evacuation, performed after 16 weeks of
gestation, consists of wide cervical dilation followed by
instrumental removal of the uterine contents.
- Outpatient management of first- trimester pregnancy given
misoprostol (Cytotec) intravaginally for up to 2 days.
- For late incomplete, inevitable, missed miscarriages (16 to 20
weeks), prostaglandins may be administered into the amniotic
sac or by vaginally supp. to induce or augment labor and cause
the products of conception to be expelled.
- IV oxytocin may also be used. (also after evacuation given
oxytocin 10 to 20 units in 1000ml of IV fluids may be given to
prevent bleeding)
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110 HANADI MALAYSHEH
112. - Rh negative woman is given an IM injections of Rh(D) immune
globulin within 72 hours of the miscarriage.
- Monitor vital signs.
- Monitor bleeding.
- Review labs..
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112 HANADI MALAYSHEH
113. 2. Recurrent premature Dilation of the Cervix (Incompetent Cervix)
- Cause late miscarriage
- Passive and painless dilation of the cervix during the second trimester.
Etiology
Hx. Of previous cervical trauma such as lacerations during childbirth, excessive
cervical dilation for curettage or biopsy, or ingestion of diethylstilbestrol(DES) by
the woman’s mother while pregnant.
- Short cervix
- Cervical or uterine anomalies
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115. Risks to the Woman
■ Repeated second trimester or early third trimester births
■ Recurrent pregnancy losses (e.g., spontaneous abortions)
■ Preterm delivery
■ Rupture of membranes/infection
Risk to the Fetus and Newborn
■ Preterm birth and consequences of prematurity
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115 HANADI MALAYSHEH
116. Management
■ Obtain transcervical ultrasound to
evaluate cervix for cervical length.
■ Cervical cultures for chlamydia,
gonorrhea, and other
cervical infections.
.
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116 HANADI MALAYSHEH
117. Surgical management, with placement of a cervical cerclage. A cerclage is
usually placed between 12 and
16 weeks of gestation and removed when the woman reaches 37 weeks of
gestation or it may be left in place until spontaneous labor begins.
Post op care
- Monitor for contractions
- PROM
- Signs of infection
- A void sexual intercourse
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122. 3. Ectopic pregnancy
develops as a result of the blastocyst
implanting somewhere other than the endometrial lining
of the uterus.
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124. - The incidence of ectopic pregnancy in the general population is
2%.
- Ectopic pregnancies are often called tubal pregnancies because
approx. 95% are located in the fallopian tube.
- Of all tubal ectopic pregnancies, more than half (approx. 55%)
are located in the ampulla, or largest portion of the tube.
- Ectopic pregnancies is responsible for 10% to 15% of all
pregnancy- related maternal deaths. It is the most common cause
of maternal mortality in the first trimester.
- Ectopic pregnancy is a leading cause of infertility.
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124 HANADI MALAYSHEH
125. Risk Factors for Ectopic Pregnancy
(in order of risk)
■ Prior tubal damage
- Tubal corrective surgery
- Tubal sterilization
- Previous ectopic pregnancies
■ Assisted reproduction
■ Pelvic inflammatory disease
■ Smoking
■ Abdominal adhesions
■ Popularity of contraceptive methods (
e.g., IUD)
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125 HANADI MALAYSHEH
126. Risks for the Woman
■ Hemorrhage related to rupture of fallopian tube
■ Decreased fertility related to removal of fallopian tube
Risk for fetal deformity in an abdominal pregnancy is also high as a result of pressure
deformities caused by oligohydramnios. The most common problems include facial or
cranial asymmetry, various joint deformities, limb deficiency, CNS anomalies.
.
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126 HANADI MALAYSHEH
128. Assessment Findings before Tubal Rupture
Common findings are:
■ Pelvic or abdominal pain (95%)
■ Abnormal bleeding (60%–80%)
Mild to moderate dark red or brown intermittent vaginal
bleeding occurs in up to 80% of women.
■ Abdominal and pelvic tenderness is uncommon.
■ Uterine changes are minimal.
■ Vital signs are stable prior to rupture. ■
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128 HANADI MALAYSHEH
129. Assessment Findings After Tubal Rupture
■ Severe lower abdominal pain
■ Pelvic pain described as sharp, stabbing, or tearing
■ Vertigo or syncope
■ Vital signs become unstable, indicating hypovolemia if hemorrhage is
significant.
■ Pain in neck or shoulder with peritoneal hemorrhage because of
diaphragmatic irritation.
An ecchymotic blueness around the umbilicus (Cullen sign ), indicating
hematoperitoneum, may also develop in an undiagnosed, ruptured
intraabdominal ectopic pregnancy.
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129 HANADI MALAYSHEH
130. Tubal pregnancy management
Every woman with abdominal pain, vaginal spotting or bleeding, and a positive pregnancy
test should undergo screening for ectopic pregnancy.
- Most screening tools for ectopic pregnancy are serial quantitative B-hCG levels and
transvaginal U/S.
Immediate care
Surgical management. If the tube has not ruptured, salpingostomy.
Another option is removal of the entire tube
( salpingectomy).
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130 HANADI MALAYSHEH
131. Medical management. Giving methotrexate (type of
chemotherapy agent) to dissolve the tubal pregnancy.
Methotrexate is an antimetabolite and folic acid antagonist that
destroys rapidly dividing cells.
Which women who are eligible to methotrexate therapy:
- Hemodynamically stable women
- If mass is unreuptured and measures less than 3.5cm in diameter
by U/S
- No fetal cardiac activity
- Serum B-hCG level is less than 5000 international units/L .
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132. 4. Gestational trophoblastic disease (GTD)
Is a spectrum of placental related tumors. GTD includes gestational
trophoblastic neoplasia (GTN).
GTN refers to persistent trophoblastic tissue that is presumed to be
malignant.
Hydatidiform mole (Molar pregnancy), is benign proliferative
growth of the placental trophoblast in which chorionic villi
develop into edematous, cystic, a vascular transparent vesicles
that hang in a grapelike cluster.
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134. With a hydatiform mole pregnancy, there is a proliferation of the
placenta and trophoblastic cells, which absorbs fluid from the maternal
blood.
Fluid accumulates into the chorionic villi and vesicles form out of the
chorionic villi. The erythroblastic tissue of the complete hydatiform
mole never develops into a fetus. The erythroblastic tissue of a partial
hydatiform mole may include some fetal tissue, but this is always
abnormal and never matures.
.
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135. Incidence and etiology
■ Occurs in 1 to 2 of 1000 pregnancies in the USA.
Risk Factors
■ Maternal age younger than 15 or older than 45 years.
■ Previous molar pregnancy
■ Women who have had ovulation stimulation with clomiphene (Clomid).
Risks for the Woman
■ Increased risk of choriocarcinoma.
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136. Assessment Findings
■ Amenorrhea
■ Excessive N/V (hyperemesis gravidarum)
■ Vaginal discharge may be dark brown ( resembling prune juice البرقوق )عصير or
bright red and either scant or profuse.
■ Uterus is significantly larger than expected from menstrual dates.
■ Abdominal cramping and expulsion of vesicles
■ Anemia from blood loss
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136 HANADI MALAYSHEH
138. Diagnosis
- Transvaginal U/S and serum hCG levels are used for diagnosis.
Trophoblastic tissue secretes the hCG hormone (hCG levels are
persistently high or rising beyond 10 to 12 weeks of gestation, the time
they would begin to decline in a normal pregnancy).
- A characteristic pattern snowstorm pattern
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138 HANADI MALAYSHEH
139. Management
- Most moles abort spontaneously, suction curettage offers a safe, rapid, and effective method of evacuating
a hydatidiform mole.
- Anti D immunoglobulin to women who are Rh negative.
- Biweekly measurements of B- hCG level until the level decreases to normal and remains normal for 3
weeks. Monthly measurements are taken for 6 months and then every 2 months for a total of 1 year.
- A rising titer and an enlarging uterus may indicate choriocarcinoma (malignant GTD).
- Pregnancy should be avoided for 6 months to 1 year.
- Any contraceptive method except an IUD is acceptable.
- .
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140. B. Late pregnancy Bleeding
1. Placenta Previa
The placenta is implanted in the lower uterine segment. It may
completely or partially covers the cervix or is close enough to the
cervix to cause bleeding, when the cervix dilates or the lower
uterine segment effaces..
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140 HANADI MALAYSHEH
141. There are four classifications of placenta previa (
Cunningham et al., 2010):
■ Total placenta previa: The placenta completely covers the internal cervical os.
■ Partial placenta previa: The placenta partially covers the internal cervical os.
■ Marginal placenta previa: The edge of the placenta is at the margin of the internal
cervical os.
■ Low-lying placenta: The placenta is implanted in the lower uterine segment in close
proximity to the internal cervical os.
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141 HANADI MALAYSHEH
147. Incidence and etiology
- Placenta previa affects approx. 1 in 200 pregnancies at term.
Risk factors
- Hx. Of previous cesarean birth
- Advanced maternal age (> 35 – 40 years of age)
- Multiparity, multiple gestations
- Hx. Of prior suction curettage
- Smoking
- Hx. Of placenta previa in a previous pregnancy.
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147 HANADI MALAYSHEH
148. Clinical manifestations
Placenta previa is typically characterized by painless, bright- red
vaginal bleeding during the second or third trimester.
The bleeding associated with the disruption of placental blood
vessels that occurs with stretching and thinning of the lower
uterine segment.
- V/S may be normal, even with heavy blood loss, because a
pregnant woman can loss up to 40% of her blood volume
without showing signs of shock. Clinical presentation and
decreasing urinary output may be better indicators of acute
blood loss than vital signs alone.
.
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148 HANADI MALAYSHEH
149. - Abdominal examination usually reveals a soft, relaxed, nontender
uterus with normal tone.
- Presenting parts of the fetus usually remains high because the placenta
occupies the lower uterine segment .
- Fundal height is greater than expected for gestational age.
- Fetal malpresentation (breech and transverse or oblique lie)
Complications associated with placenta previa Include PROM, preterm
labor and birth, abnormal placental attachments, PPH, anemia,
thrombophlebitis, and infection
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149 HANADI MALAYSHEH
150. Fetal complication includes fetal death, fetal anemia, SGA, IUGR
Diagnosis
- All women with painless vaginal bleeding after 20 weeks of gestation
should be assumed to have a placenta previa until proven otherwise.
- Abdominal U/S then transvaginal U/S
- Speculum examination to rule out local causes of bleeding (e.g., polyps,
carcinoma)
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150 HANADI MALAYSHEH
151. Management
Expectant management. (observation and bed rest)
If the fetus is at less than 36 weeks of gestation and has a reassuring
FHR, the bleeding is mild (<250 ml) and stops, and the patient is not
in labor.
- Give corticosteroids to accelerate fetal lung maturity, if indicated.
- Hospitalized, continuous FHR and contraction monitoring.
- Large – bore IV access
- Lab test (CBC, Platelet count, pt, ptt)
- Bed rest , limited activity
- No vaginal or rectal examinations are performed, and the woman is
placed on “pelvic rest” (nothing in the vagina)
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152. - U/S may performed every 2 to 3 weeks
- Checking the amount of blood on perineal pads, bed pads, and linens
- Magnesium sulfate can be given for tocolysis if uterine contractions are
identified.
Active management.
- Immediate C/S if bleeding is excessive or persistent
- Assess maternal V/S
- Continuous EFM
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153. 2. Abruptio placenta (premature separation of placenta / Placental
Abruption)
Is the premature detachment of part or all of a normally implanted placenta
from the uterus. Separation occurs in the area of the decidua basalis after 20
weeks of gestation and before the birth of the infant.
Incidence and etiology
- Approx. 1 in 75 to 1 in 226 of pregnancies is complicated by abruptio
placentae.
- Approx. one third of all antepartum bleeding is caused by placental
abruption.
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153 HANADI MALAYSHEH
154. The separation may be partial or total and can
be classified as grade 1 (mild), 2 (moderate), or 3 (severe).
قد
يكون
الفصل
اًيجزئ
أو
اًيكل
ويمكن
يتم
تصنيفها
على
أنها
درجة 1 ()خفيفة أو2 ()متوسطة أو3 ()شديدة.
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154 HANADI MALAYSHEH
156. Risk factor
- Maternal hypertension ( chronic , gestational) is the most common cause for
abruption.
- Cocaine use is causes vascular disruption in the placental bed.
- Blunt external abdominal trauma ( MVAs)
- Cigarette smoking
- Hx. Of abruption in previous pregnancy and PROM
- More likely to occur in twin gestation
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156 HANADI MALAYSHEH
157. Clinical manifestations
The separation may be partial or complete, or only the margin of the placental may
be involved.
- 70% 80% bleeding from the placental site may flow out through the vagina.
- 10% - 20 % bleeding remain concealed (retroplacental hemorrhage)
- Or both
- Clinical symptoms of abruptio placentae include vaginal bleeding, abdominal
pain, and uterine tenderness and contractions.
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161. - Pain is mild to severe and localized over one region of the uterus or
diffuse over the uterus with a boardlike abdomen.
- If blood accumulates between the separated placenta and the uterine
wall, it may produce a Couvelaire uterus.
- Uterus appears purple or blue, and contractility is lost.
- Decrease in hemoglobuin and hematocrit levels, decrease
coagulation factors level later.
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163. - Kleihauer–Betke test in maternal blood may be positive and indicate the
presence of fetal red blood cells.
Maternal complications includes hemorrhage, hypovolemic shock,
hypofibrinogenemia, and thrombocytopenia are associated with severe abruption.
Renal failure and pituitary necrosis may result from ischemia.
Fetal complications includes IUGR, preterm birth. Risks for neurologic defects
and death from SIDS are increased in newborns following placental abruption.
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164. Diagnosis
- Abdominal U/S (at least 50% of abruption cannot be identified on U/S)
- Diagnosis of abruption is confirmed after birth by visual inspection of the
placenta.
- Abruptio placenta should be highly suspected in the woman with a sudden
onset of intense, usually localized, uterine pain, with or without vaginal
bleeding.
- Physical examination usually reveals abdominal pain, uterine tenderness, and
contractions. The fundal height should be measured over time, because an
increasing fundal height indicates concealed bleeding..
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164 HANADI MALAYSHEH
166. Management
Expectant management.
If the abruption is mild and the fetus is less than 36 weeks of gestation and not
in distress the following done for women:
- Hospitalized under closely observation for signs of bleeding and labor.
- FHR monitoring
- Corticosteroids should be given
- Rh negative may be given (anti D)
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167. Active management
- Immediate birth if bleeding is moderate to severe
- Large bore IV line should be started
- Maternal V/S are monitored
- Lab test result
- Continuous FHR monitoring
- Foley catheter is inserted to monitor U.O
- Vaginal birth in case of fetal death
- Labor induction or augmentation may be initiated for any evidence of compromise.
- C/S should not be attempted when the women has severe uncorrected coagulopathy.
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169. Cord insertion and placental variations
Velamentous insertion of the cord (vasa previs) is a rare placental
anomaly associated with placenta previa and multiple gestation.
The cord vessels begin to branch at the membranes and then course
onto the placenta. ROM or traction on the cord may tear one or more
of the fetal vessels.
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170. Battledore (marginal) insertion of the cord increase the risk of fetal
hemorrhage.
In the rare case the placenta may be divided into two or more separate
lobes, resulting in Succenturiate placenta.
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172. Clotting disorders in pregnancy
- Disseminated intravascular coagulation (DIC) or consumptive
coagulopathy.
Is a pathologic form of clotting that is diffuse and consumes large amounts of
clotting factors, causing widespread external bleeding, internal bleeding, or
both, and clotting.
DIC is never a primary diagnosis. Instead, it is results from some problem that
triggered the clotting cascade, either extrinsically, by the release of large
amounts of tissue thromboplastin, or intrinsically, by widespread damage to
vascular integrity
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173. In the obstetric population, DIC is most often triggered by
the release of large amounts of tissue thromboplastin,
which occurs in abruptio placenta and in retained dead
fetus and amniotic fluid embolus. Severe preeclampsia,
HELLP syndrome, and gram – negative sepsis are
examples of conditions that can trigger DIC because of
widespread damage to vascular integrity.
DIC is an overactivation of the clotting cascade and the
fibrinolytic system, resulting in depletion of platelets and
clotting factors, which results in the formation of multiple
fibrin clots throughout the body’s vasculature, even in
microcirculation. DIC results in a clinical picture of
clotting, bleeding, and ischemia.
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175. Management
Medical management in all cases of DIC involves correction of
underlying cause (e.g., removal of the dead fetus, treatment of
existing infection or of preeclampsia or eclampsia, or removal of
a placental abruption).
- Volume replacement
- Blood component therapy
- Optimization of oxygenation and perfusion status
- Vitamin K administration, activated factor V11a
- Blood replacement, V/S monitoring
- Closely monitor of U.O (U.O must be maintained at more than
30ml/hr.
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176. - Because renal failure is one consequence of DIC, urinary output
is carefully monitored (minimum
of 30 ml/h) using an indwelling Foley catheter. Vital
signs are assessed frequently.
- If DIC develops before birth, the woman should be maintained
in a side – lying tilt to maximize blood flow to the uterus.
- Oxygen may be administered through a tight-fitting rebreathing
mask at 8 to 10 L/min, or per hospital protocol or physician
order.
- DIC usually is cured with the birth and as coagulation
abnormalities resolve.
- .
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177. Surgical Emergencies
During Pregnancy
An enlarged uterus and displaced internal organs may
make abdominal palpation more difficult, alter the
position of an affected organ, or change the usual signs
and symptoms associated with a particular disorder..
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178. Appendicitis
- Appendicitis is the most common nongynecological cause of an acute
surgical abdomen during pregnancy, occurring in as many as 1 in 1500
pregnancies.
- The diagnosis of appendicitis is often delayed because the usual signs and
symptoms mimic some normal changes of pregnancy such as nausea and
vomiting and increased WBC count.
- As pregnancy progresses, the appendix is pushed upward and to the right of
its usual anatomic location.
Because of these changes, rupture of the appendix and the subsequent
development of peritonitis occur two to three times more often in pregnant
women than in nonpregnant women..
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179. The most common symptom of appendicitis in pregnant women
is;
- Right lower quadrant abdominal pain, regardless of gestational
age.
- N+V , loss of appetite is not reliable indicator of appendicitis.
- Fever, tachycardia, a dry tongue, and localized abdominal
tenderness less likely indicators for the pregnant women.
- U/A , chest x-ray examination to rule out UTI and right lower
lobe pneumonia.
- U/S (during first and second trimesters), less accurate during
third trimester
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180. - CT third trimester of pregnancy
- MRI may be used if appendicitis has not been confirmed by other
imaging techniques.
Appendectomy before rupture usually does not require
either antibiotic or tocolytic therapy. If surgery is delayed until after
rupture, multiple antibiotics are ordered. Rupture is likely to result
in preterm labor and perhaps fetal loss..
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181. Sexually Transmitted Infections
The Centers for Disease Control and Prevention (CDC,
2010) estimates that 19 million new infections occur
every year, almost half of them among young people aged
15–24 years. STIs affect women of every
socioeconomic and educational level, age, race, and
ethnicity.
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182. Risks for the Woman
■ STIs can cause pelvic inflammatory disease.
■ Pelvic inflammatory disease (PID) can lead to infertility,
chronic hepatitis, and cervical and other cancers.
■ STIs during pregnancy can lead to PTL, PROM, and
uterine infection.
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183. Risks for the Fetus
■ STIs can pass to the fetus by crossing the placenta; some can be
transmitted to the baby during delivery as the baby passes through the birth
canal .
■ Harmful effects to babies include preterm birth, low birth weight,
neonatal sepsis, and neurological damage..
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184. Assessment Findings
■ Many STIs in women are “silent” without signs and symptoms, making
routine screening for STIs during the first prenatal visit an important part of
routine prenatal care.
■ Physical findings include low-grade temperature, poor personal hygiene,
genital warts, purulent urethral or cervical discharge, friable cervix, genital
lesions, tender uterus, pain on motion of cervix, inguinal adenopathy, and rash
on palms and soles of feet.
■ Positive STI cultures and test results
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185. Medical Management
■ Provide routine screening of STIs and HIV at first
prenatal visit.
■ Treat bacterial STIs with antibiotics.
■ Prescribe antiviral medications for viral STIs to reduce symptoms..
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186. Nursing Actions
■ Provide information on STIs.
■ Provide emotional support.
■ Instruct the woman on correct
administration of medications and other
treatments and importance of completing
treatment.
■ Instruct the patient on the warning signs of
complication (fever, increased pain,
bleeding).
■ Provide information on the importance of
abstaining
from intercourse until the patient and her
partner are free of infection.
■ Provide the partner with treatment as
indicated.
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187. TORCH Infections
TORCH is an acronym that stands for Toxoplasmosis,
Other (hepatitis B), Rubella, and Cytomegalovirus and
Herpes simplex virus..
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188. Risk for the Woman
■ Depends on the infectious agent .
Risks for the Fetus
■ The usual route of transmission to the fetus is transplacentally.
■ Infections acquired in utero can result in intrauterine growth
restriction, prematurity, chronic postnatal infection, and even
death.
Assessment Findings
■ Maternal assessment findings vary with the organism.
.
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189. Medical Management
■ Nursing Actions
■ Nursing considerations vary with the organism.
■ Provide emotional support.
■ Instruct woman on treatment plan
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