Ectopic Pregnancy Definition of Disorder

1.
Hyperemesis Gravidarum
2. Bleeding disorders
3. Abortion
a. Spontaneous Abortion
b. Threatened
c. Imminent
d. Complete
e. Incomplete
f. Missed
g. Recurrent/Habitual
Ectopic pregnancy
Definition of Disorder
Ectopic pregnancy is
a complication of pregnancy in
which the embryo attaches
outside the uterus. Signs and
symptoms classically
include abdominal
pain and vaginal
bleeding. Fewer than 50
percent of affected women
have both of these symptoms.
The pain may be described as
sharp, dull, or crampy. Pain may also spread to the shoulder if bleeding into the abdomen has
occurred. Severe bleeding may result in a fast heart rate, fainting, or shock. With very rare
exceptions the fetus is unable to survive.
Etiology
The risk factors for ectopic pregnancy include the following:
Previous ectopic pregnancy
Prior fallopian tube surgery
Previous pelvic or abdominal surgery
Certain sexually transmitted infections (STIs)
Pelvic inflammatory disease
Endometriosis
Other factors that may increase a woman’s risk of ectopic pregnancy include
cigarette smoking
age older than 35 years
history of infertility
use of assisted reproductive technology, such as in vitro fertilization (IVF)
About one half of all women who have an ectopic pregnancy do not have known risk factors.
Sexually active women should be alert to changes in their bodies, especially if they experience
symptoms of an ectopic pregnancy.
Pathophysiology
The most common site of ectopic implantation is a fallopian tube, followed by the uterine
cornua. Pregnancies in the cervix, a cesarean delivery scar, an ovary, the abdomen, or fallopian
tube interstitial are rare. Heterotopic pregnancy(simultaneous ectopic and intrauterine
pregnancies) occurs in only 1/10,000 to 30,000 pregnancies but may be more common among
women who have had ovulation induction or used assisted reproductive techniques such as in
vitro fertilization and gamete intrafallopian tube transfer (GIFT); in these women, the overall
reported ectopic pregnancy rate is ≤1%.The structure containing the fetus usually ruptures after
about 6 to 16 wk. Rupture results in bleeding that can be gradual or rapid enough to cause
hemorrhagic shock. Intraperitoneal blood irritates the peritoneum. The later the rupture, the
more rapidly blood is lost and the higher the risk of death.
Nursing Diagnosis
Fear related to abdominal pain and pregnancy status.
Grief related to loss of pregnancy.
Anxiety related to unfamiliarity of the health/pregnancy condition.
Risk for fluid volume deficit related to blood loss secondary to ruptured tube.
Acute pain related to growing products of conception against the site of implantation.
Nursing Intervention
Since the termination of pregnancy is inevitable, the overall goal of nursing management is the
provision of supportive care and health teachings towards the loss of pregnancy. For cases
indicative of surgery, providing preoperative and postoperative care are the major concerns.
A. Assessment
Monitor the following for it indicates the severity of the case, leading to the precise diagnosis
and plan of care:
Vital signs
Vaginal bleeding
Characteristics and location of pain
Abdominal tenderness
Last menstrual period (LMP)
Pregnancy test results
B. Interventions
1. Fluid volume
Ensure a patent IVF and blood transfusion line
Obtain blood samples for laboratory workouts as ordered (CBC and typing)
Monitor vital signs
Monitor I&O
2. Grief
Encourage verbalization of feelings
Be available to provide emotional support at all times
Include family and significant others in the therapy
Suggest referrals if necessary (clergy, psychiatrists, work groups)
3. Pain
Administer analgesics as ordered
Use of relaxation techniques and diversional activities
C. Educative
Teach on facts and chances of having another ectopic pregnancy. Try incorporating the signs
such as abnormal vaginal bleeding, abdominal pain and irregularity of menstruation.
Teach on signs of postoperative infections such as fever and malodorous vaginal discharges,
and report them promptly.
Discuss on other forms of contraception available.
Nursing Evaluation
Stable vital signs
No signs of postoperative infections
Client and significant others have gone through a successful grieving process and now shows
acceptance and willingness to move-on.
https://www.rnspeak.com/ectopic-pregnancy-case-study/
Gestational Trophoblastic disease

(hydatidiform mole)
Definition of disorder
Gestational trophoblastic disease
(GTD) is a group of rare tumors that
involve abnormal growth of cells inside
a woman's uterus. GTD does not
develop from cells of the uterus like
cervical cancer or endometrial (uterine
lining) cancer do. Instead, these tumors
start in the cells that would normally develop into the placenta during pregnancy. (The term
gestational refers to pregnancy.)
GTD begins in the layer of cells called the trophoblast that normally surrounds an embryo.
(Tropho- means nutrition, and -blast means bud or early developmental cell.) Early in normal
development, the cells of the trophoblast form tiny, finger-like projections known as villi. The villi
grow into the lining of the uterus. In time, the trophoblast layer develops into the placenta, the
organ that protects and nourishes the growing fetus.
Etiology
This incidence happens in 1 of every 1, 500 pregnancies. There are risk factors that could
precipitate the formation of hydatidiform mole, and they are as follows:
Low protein intake. Women with low protein intake have a possibility of developing a
hydatidiform mole because protein is needed for the development of the trophoblastic villi.
Women older than 35 years old. Being pregnant beyond 35 years old presents a lot of risky
conditions like H-mole.
Asian women. Asians have a higher chance of acquiring this disease because of their genetic
formation.
Women with a blood group of A who marry men with blood group O. these blood groups, when
combined together, results in unfavorable conditions like H-mole.
Pathophysiology
Fertilization occurs as the sperm enters the ovum. In instances of a partial mole, two sperms
might fertilize a single ovum.
Reduction division or meiosis was not able to occur in a partial mole. In a complete mole, the
chromosome undergoes duplication.
The embryo fails to develop completely. There are 69 chromosomes that develop for the partial
mole, and 46 chromosomes for the complete mole.
The trophoblastic villi start to proliferate rapidly and become fluid-filled grape-like vesicles.
Nursing Diagnosis
Grieving related to loss of pregnancy as evidenced by anger and social detachment.
Nursing intervention
Measure abdominal girth and fundal height to establish baseline data regarding the growth of
the uterus.
Assist patient in obtaining a urine specimen for urine test of hCg.
Save all pads used by the woman during bleeding to check for clots and tissues she may have
discharged.
Provide your patient with an open environment and a trusting relationship so she would be
encouraged to express her feelings.
Honestly answer the patient’s questions to foster a trusting relationship between nurse and
client.
Provide an assurance that it is not her own fault that this happened to her to lessen her sense of
guilt and self-blame.
Nursing evaluation
Patient must be able to express her feelings effectively.
Patient must acknowledge the situation and seek for appropriate help.
Patient must learn to look forward for the future step by step.
https://nurseslabs.com/gestational-trophoblastic-disease/
Incompetent cervix
Cervical insufficiency is the inability
of the cervix to retain fetus, in the
absence of uterine contractions or
labor (painless cervical dilatation),
owing to a functional or structural
defect. It is cervical ripening that
occurs far from the term. Cervical
insufficiency is rarely a distinct and
well defined clinical entity but only
part of a large and more complex
spontaneous preterm birth syndrome.
Etiology
Cervical insufficiency usually occurs during the middle of the second or early third trimester,
depending upon the severity of insufficiency. Cervical incompetence may be congenital or
acquired. The most common congenital cause is a defect in the embryological development of
Mullerian ducts. In Ehlers-Danlos syndrome or Marfan syndrome, due to the deficiency in
collagen, the cervix is not able to perform adequately, leading to insufficiency.
The most common acquired cause is cervical trauma such as cervical lacerations during
childbirth, cervical conization, LEEP (loop electrosurgical excision procedure), or forced cervical
dilatation during the uterine evacuation in the first or second trimester of pregnancy. However, in
most patients, cervical changes are the result of infection/inflammation, which causes early
activation of the final pathway of parturition.
Pathophysiology
The competent human cervix is a complex organ that undergoes extensive changes throughout
gestation and parturition. A complex remodeling process of the cervix occurs during gestation,
involving timed biochemical cascades, interactions between the extracellular and cellular
compartments, and cervical stromal infiltration by inflammatory cells. Any disarray in this timed
interaction could result in early cervical ripening, cervical insufficiency, and preterm birth or
miscarriage. Current evidence suggests that cervical incompetence functions along with a
continuum that is influenced by both endogenous and exogenous factors, such as uterine
contraction and decidual/membrane activation.
Nursing Diagnostic
Anxiety related to impending loss of pregnancy as evidenced by premature dilation of the cervix.
Determine any factors that further contribute to the anxiety of the woman so it could be avoided.
Monitor vital signs to determine any physical responses of the patient that could affect her
condition.
Convey empathy and establish a therapeutic relationship to encourage client to express her
feelings.
Provide accurate information about the situation to help client back into reality.
Nursing Evaluation
Patient would appear relaxed and report that anxiety has been reduced.
Verbalize awareness of feelings of anxiety.
Enumerate ways to deal with anxiety.
Use resources or support system effectively.
https://www.ncbi.nlm.nih.gov/books/NBK525954/
https://nurseslabs.com/incompetent-cervix/#Nursing-Management
Placenta previa
Placenta Previa is a
condition where the
placenta lies low in the
uterus and partially or
completely covers the
cervix. The placenta may
separate from the uterine
wall as the cervix begins to
dilate (open) during labor.
Case Scenario
A 29-year-old woman, gravida 1, para 1, was referred to our hospital because of vaginal
bleeding after cervical cerclage. She had previously delivered vaginally her first female infant
(3,536 g) after cervical cerclage under the diagnosis of cervical incompetency. In the pregnancy
discussed here, cervical cerclage was performed at 15 weeksí gestation for the prevention of
preterm delivery. Ultrasonography at that time demonstrated no abnormal findings. Twelve days
after surgery sudden vaginal bleeding occurred. On admission in the 17th week of gestation,
slight bleeding from the external cervical os was noted, and ultrasonography in our hospital
demonstrated placenta previa (Fig. 1). The placenta overlapped the internal cervical os and the
distance from the lower placental edge to the internal os was 28 mm.
Despite the administration of oral ritodrine hydrochloride, a β-adrenergic stimulant, bleeding
continued in the amount
of approximately 800 ml
per day. The position of
the placenta did not
change. After appropriate
counseling, the patient
chose to terminate the
T. YAMADA, et al.
FIG. 1. Ultrasonography
(case 1). Placental edge
(long arrows) is located
over the internal os (thick
arrow) at 17 weeksí
gestation.
pregnancy because she
did not want to undergo
the risk of life-threatening
bleeding. Cervical os was
still closed, and
emergency cesarean
section was performed at 18 weeksí gestation, 6 days after admission. We opened the
abdomen with a vertical midline incision. A transverse incision of the lower uterine segment was
made, and an infant weighing 175 g was delivered. The placenta covered the internal cervical
os and was ablated easily. A double-layer closure was performed as usual. The operative
bleeding, including amniotic fluid, was 900 ml, but bleeding continued after surgery. The
hemoglobin value was decreased from 8.3 g/dl to 5.6 g/dl, and 5 units of banked concentrated
red blood cells were transfused with prophylactic administration of gabexate mesilate for
disseminated intravascular coagulation. After blood transfusion, bleeding decreased gradually.
The patient was discharged in good condition 12 days after surgery. Two years later, she had a
normal pregnancy, with the placental position being normal, and delivered by cesarean section
a male infant weighing 3,010 g. No uterine abnormalities were evident during the surgery.
Etiology
Predisposing factors include:
Multiparity (80% of affected clients are multiparous)
Advanced maternal age (older than 35 years in 33% of cases)
Multiple gestation
Previous cesarean birth
Uterine incision
Prior placenta previa (incidence is 12 times greater in women with previous placenta previa)
Pathophysiology
Pathologic process seems to be related to the conditions that alter the normal function of the
uterine deciduas and its vascularization.
Bleeding, which results from tearing of the placental villi from the uterine wall as the lower
uterine segment contracts and dilates, can be slight or profuse.
Nursing Diagnosis
Deficient Fluid Volume
Fluid volume deficit is a state in which an individual is experiencing decreased intravascular,
interstitial and/or intracellular fluid. Active blood loss or hemorrhage due to disrupted placental
implantation during pregnancy may manifest signs and symptoms of fluid vol. deficient that may
later lead to hypovolemic shock and cause maternal and fetal death.
Assessment
Patient may manifest:
Bleeding episodes (amount, duration)
Abdomen soft/hard when palpated
Manifests body weakness
Low blood pressure
Increased heart rate
Decreased respiratory rate
Fetal heart rate less than normal (120-160 bpm)
Decreased urine output
Increased urine concentration
Pale, cold, clammy skin
Nursing Diagnosis
Deficient Fluid Volume r/t Active Blood Loss Secondary to Disrupted Placental Implantation
Decreased Cardiac Output
Placenta Previa is the development of placenta in the lower uterine segment partially or
completely covering the internal cervical os. Placenta Previa causes bleeding. Due to large
amounts of blood lost, the heart tries to pump faster in order to compensate for blood loss. As a
result, the heart pumps faster with lesser blood pumped.
Assessment
dysrhythmias
prolonged capillary refill
cold clammy skin
Dyspnea
restlessness
variations in BP reading
Nursing Diagnosis
Decreased cardiac output r/t altered contractility
Ineffective Tissue Perfusion

Placenta Previa causes painless and continuous bleeding. With bleeding, there is decreased
Hemoglobin. Hemoglobin carries oxygen to different parts of the body. If there is decreased
hemoglobin there is a failure to nourish the tissues at the capillary level.
Assessment
Patient may manifest
Restlessness
Confusion
Irritability
Manifest Body Weakness
Capillary refill more than 3 sec
Oliguria
Nursing Diagnosis
Ineffective tissue perfusion r/t decreased HgB concentration in blood & hypovolemia
Nursing Interventions Rationale

Establish Rapport To gain patient’s trust
Monitor Vital Signs To obtain baseline data
Provides information about active bleeding
Assess color, odor, consistency and amount of
versus old blood, tissue loss and degree of blood
vaginal bleeding; weigh pads
loss
Provides information about maternal and fetal
Assess hourly intake and output.
physiologic compensation to blood loss
Assessment provides information about
Assess baseline data and note changes. Monitor possible infection, placenta previa or abruption.
FHR. Warm, moist, bloody environment is ideal for
growth of microorganisms.
Assess abdomen for tenderness or rigidity- if
Detecting increased in measurement of
present, measure abdomen at umbilicus (specify
abdominal girth suggests active abruption
time interval)
Assess SaO2, skin color, temp, moisture, turgor, Assessment provides information about blood
capillary refill (specify frequency) vol., O2 saturation and peripheral perfusion
Assess for changes in LOC: note for complaints
To detect signs of cerebral perfusion
of thirst or apprehension
Provide supplemental O2 as ordered via face Intervention increases available O2 to saturate
mask or nasal cannula @ 10-12 L/min. decreased hemoglobin
Initiate IV fluids as ordered (specify fluid type and
For replacement of fluid vol. loss
rate).
Position decreases pressure on placenta and
Position Pt. in supine with hips elevated if
cervical os. Left lateral position improves
ordered or left lateral position.
placental perfusion
Monitor lab. Work as obtained: Hgb & Hct, Rh Lab Work provides information about degree of
and type, cross match for 2 units RBCs, blood loss; prepares for possible transfusion.
urinalysis, etc. Scheduled for ultrasound as Ultrasound provides info about the cause of
ordered. bleeding

History taking To determine contributing factors
Assess patient condition To assess contributing factors
Review lab data For comparison with current normal values
Monitor BP & Pulse frequently To note response to activity
Provide information on test procedures To gin pt’s participation
Provide adequate rest & Reposition client To promote venous return
Encourage relaxation techniques To alleviate stress & anxiety
Elevate HOB To promote circulation
Encourage use of relaxation techniques To decrease tension level
Ineffective Tissue Perfusion

Assess patient condition To assess contributing factors
Note customary baseline data (usual BP, weight,
For comparison with current findings
lab values)
Determine presence of dysrhythmias To identify alterations from normal
Perform blanch test To identify and determine adequate perfusion
Check for Homan’s Sign To determine presence of thrombusformation
Encourage quiet & restful environment To lessen O2 demand
Elevate HOB To promote circulation
Encourage use of relaxation techniques To decrease tension level
http://www.med.kobe-u.ac.jp/journal/contents/49/51.pdf
https://www.ncbi.nlm.nih.gov/books/NBK539818/
https://www.rnpedia.com/nursing-notes/maternal-and-child-nursing-notes/placenta-previa/
https://nurseslabs.com/3-placenta-previa-nursing-care-plans/
Abruptio placenta
Abruptio placentae is defined
as the premature separation
of the placenta from the
uterus. Patients with abruptio
placentae, also called
placental abruption, typically
present with bleeding, uterine
contractions, and fetal
distress. A significant cause
of third-trimester bleeding
associated with fetal and maternal morbidity and mortality, placental abruption must be
considered whenever bleeding is encountered in the second half of pregnancy.
Case scenario
SCENARIO: A 22-year old gravida 4 para 3303 Caucasian woman carrying a singleton
pregnancy at 35 weeks estimated gestational age presents to the emergency room with vaginal
bleeding. She has had limited prenatal care and she reports that she is approximately 36 weeks
estimated gestational age by dates. Her records indicate she is carrying a singleton pregnancy
in the vertex presentation. Her past medical history is uncomplicated, she has no allergies, and
she takes no medications other than prenatal vitamins. She admits to smoking one-half pack of
cigarettes per day. Her prenatal labs are not available. She states that her pregnancy has been
uncomplicated except for occasional spotting in the last trimester. She is uncertain if she has
experienced rupture of membranes. An external fetal monitor is in place.
Physical examination reveals:
Vital signs heart rate = 132 beats per minute, blood pressure 135/80 mm Hg
Uterus: longitudinal fetal lie, vertex presentation
Cervix: dilatation 2 cm, effacement 40%, station -2, small amounts of bright
red blood per vagina are noted Fetal Monitor Output:
Fetal Heart Rate
Baseline: 140 beats per minute
Deviations from baseline: accelerations seen initially, then vanishing; variable decelerations
evolving into persistent late decelerations
Fetal Heart Rate Variability
Short-term: normal becoming decreased
Long-term: normal becoming decreased
Maternal Uterine Activity
Frequency of contractions: normal progression with increased
frequency progressing to hypertonus near time of delivery
Duration of contractions: gradually increasing to 80 seconds
intensity of contractions: gradually increasing to 120mm Hg
CASE SUMMARY: Abruptio placentae or placental abruption is the premature detachment of a
normally implanted placenta from the uterus. The incidence is approximately 0.5-1%. 1The
majority of cases actually occur prior to the initiation of labor. The combination of uterine
bleeding, increased frequency of uterine contractions or hypertonus, and a non-reassuring fetal
heart rate tracing is highly suspicious for placental abruption. As functional placental surface
area decreases with evolving abruption, placental gas exchange becomes increasingly impaired
resulting in fetal hypoxemia and acidosis. A retroplacental clot is often found upon inspection of
the placenta after delivery.
Etiology
Risk factors in abruptio placentae include the following:
Maternal hypertension - Most common cause of abruption, occurring in approximately 44% of all
cases
Maternal trauma (eg, motor vehicle collision [MVC], assaults, falls) - Causes 1.5-9.4% of all
cases
Cigarette smoking
Alcohol consumption
Cocaine use
Short umbilical cord
Sudden decompression of the uterus (eg, premature rupture of membranes, delivery of first
twin)
Retroplacental fibromyoma
Retroplacental bleeding from needle puncture (ie, post-amniocentesis)
Idiopathic (probable abnormalities of uterine blood vessels and decidua) [4]
Previous placental abruption
Chorioamnionitis
Prolonged rupture of membranes (24 h or longer)
Maternal age 35 years or older
Maternal age younger than 20 years
Male fetal sex
Low socioeconomic status
Elevated second trimester maternal serum alpha-fetoprotein (associated with up to a 10-fold
increased risk of abruption)
Sub chorionic hematoma [6]
Pathophysiology
Nursing Diagnosis
Deficient fluid volume related to bleeding during
premature placental separation.
Place the woman in a lateral, not supine position to
avoid pressure in the vena cava.
Monitor fetal heart sounds.
Monitor maternal vital signs to establish baseline
data.
Avoid performing any vaginal or abdominal examinations to prevent further injury to the
placenta.
Nursing evaluation
Maternal vital signs are all within the normal range, especially the blood pressure.
Urine output should be more than 30mL/hr.
No bleeding or minimal amount of bleeding observed.
Uterus is not tense and rigid.
Fetal heart sounds are within the normal range.
https://emedicine.medscape.com/article/252810-differential#1
https://www.cmqcc.org
https://nurseslabs.com/abruptio-placentae/
https://www.slideshare.net/homeworkping3/82580276-casestudyofabruptioplacenta
Preterm labor
Preterm labor is defined as the
presence of uterine contractions
of enough frequency and
intensity to effect progressive
effacement and dilation of the
cervix prior to term gestation.
Occurring at 20-37 weeks’
gestation, preterm labor
precedes almost half of preterm
births and is the leading cause of
neonatal mortality in the United
States.
Case scenario
A 29-year old woman presents to the hospital with contractions at 30 weeks gestation. This is
her first pregnancy and it was previously uncomplicated. She did not experience loss of fluid or
vaginal bleeding and did not have a history of recent illness or fever. A swab for group
B Streptococcus (GBS) was collected and the patient was started on prophylactic penicillin.
Clinical evaluation revealed evidence of acute infection with an elevated C-reactive protein and
an increased white blood cell count with 97% neutrophils. Amniocentesis was performed and
the amniotic fluid was sent to the laboratory for Gram Stain and culture.
Labor could progress, and the infant was delivered vaginally. Cultures of cerebrospinal fluid and
blood from the neonate were negative. The placenta was sent for histologic evaluation.
The laboratory workup revealed a gram-negative bacillus with rounded ends that grew small
grey to pale yellow colonies on blood and chocolate agars. The colonies had three regions; a
raised central region, a refractile flat region, and an outer rougher spreading region. The
colonies had a distinct bleach-like smell. There was no growth on MacConkey agar. The
organisms were oxidase positive, catalase and indole negative. Mass spectrometry was utilized
to identify the organism as Eikenella corrodens.
Discussion:
Eikenella corrodens is a component of normal mouth and upper respiratory tract flora. It is most
notable for causing head and neck infections, periodontal disease, and as a significant player in
“fight bite” infections. “Fight bite” results when a clenched fist hits another person’s mouth and
the teeth cause lacerations to the hitter’s hand, which can subsequently lead to
infection. Eikenella is implicated approximately 25% of the time in these types of infections. Only
on very rare occasion is Eikenella known to cause gynecologic infections. Endometritis or
cervicitis may infrequently be caused by colonization of an intrauterine contraceptive device
(IUD) by Eikenella. And rarely, Eikenellais implicated as the isolated bacteria in cases of acute
chorioamnionitis.
In the medical literature there are currently only 8 reported cases of chorioamnionitis caused by
a pure Eikenellainfection. As in our case, each of the women in the case reports had clinically
silent infections and only presented with preterm labor. Most of the women were found to have
elevated white blood cell counts in the absence of fever or alterations in other vital signs. In
each case, the fetal membranes were intact. Two of the cases resulted in fatal infection of the
neonates. Of note, three of the women were mentioned to be the recipients of oral intercourse
throughout their pregnancies.
One of the reported cases involved a woman whose partner had a tongue piercing and it was
noted that they engaged in daily oral sex during the pregnancy. The authors speculated that the
tongue piercing played a role in the development of chorioamnionitis by either ascending
vaginal infection or hematogenous spread caused by trauma from the tongue ring.
It is not known if a similar history was present in this case. The patient was treated with
ampicillin and gentamycin and discharged following delivery. She is currently doing well. The
infant has had no signs of infection, but at the time of this writing he is being treated in the
neonatal intensive care unit for sequelae of prematurity.
Etiology
The following are etiologies that may contribute to preterm labor: stress, infection, placental
abruption, placenta previa, substance use, history of preterm birth or abortion, inadequate
prenatal care, smoking, maternal age <18 or >40, poor nutrition, low body mass index, fetal
anomaly, fetal growth restriction, oligohydramnios, polyhydramnios, vaginal bleeding, premature
preterm rupture of membranes (PPROM), and environmental factors. This list is not
comprehensive, and various other factors contribute to preterm labor. However, it encompasses
the most common reasons patients present in clinical settings.
It is important to familiarize oneself with PPROM as it affects about 3% of all pregnancies in the
United States. Membrane rupture can be physiologic or pathologic. The intra-amniotic infection
has been most commonly associated with PPROM, especially at earlier gestational ages. Other
causes contributing to PPROM include short cervical length, second and third trimester
bleeding, low BMI, low socioeconomic status, cigarettes, and illicit drug use. Typically, about
half of mothers with PPROM deliver within a week of ROM.
The main concern with PPROM is prematurity. The most common complication of preterm birth
is respiratory distress. However, one must consider sepsis, intraventricular hemorrhage, and
necrotizing enterocolitis. PPROM with intrauterine inflammation can lead to neurodevelopmental
impairment, and early gestational age at membrane rupture has an association with an
increased risk of neonatal white matter damage. Infection and umbilical cord accidents
contribute to 1-2% risk of antenatal fetal demise after preterm PROM.
Pathophysiology
Nursing diagnosis
Anxiety
Anxiety: Vague uneasy feeling of discomfort or dread accompanied by an autonomic response.
May be related to
Situational crisis
Perceived or actual threats to self and fetus
Possibly evidenced by
Increasing tension
Apprehension
Sympathetic stimulation
Desired Outcomes
Patient will verbalize understanding of individual situation and possible outcomes
Patient will report anxiety is reduced and/or manageable
Patient will appear relaxed; with maternal vital signs within normal limits.
Activity Intolerance
Activity Intolerance: Insufficient physiologic or physiological energy to endure or complete
required or desired activity.
May be related to
Prolonged physical activity and stress
Muscle hypersensitivity
Continued uterine contractions and/or irritability
Reduced activity level
Desired Outcomes
Identify and/or engage in activities appropriate to situation.
Demonstrate reduction and/or cessation of uterine contractions.
Risk for [Fetal] Injury

Risk for Injury: Vulnerable for injury as a result of environmental conditions interacting with the
individual’s adaptive and defensive resources, which may compromise health.
Risk factors
Delivery of preterm infant
[Not applicable]
Desired Outcomes
Patient will maintain pregnancy at least to the point of fetal maturity.
Obtain gynecological and obstetrical history from patient
Previous preterm labor or pregnancies too close together can increase risk of preterm labor.
Determine what symptoms began and when.
Assess patient’s vital signs
Get a baseline set of vitals prior to any interventions
Place external fetal monitoring device to monitor fetal activity/ heart rate and contractions
This allows you to observe and monitor frequency and quality of contractions as well as notice
any signs of fetal distress
Place patient in position of comfort on left side
Positioning patient in left side-lying position may help with comfort, reduce contractions and
maintain maternal-fetal blood flow
Initiate IV access and administer medications
Magnesium sulfate
Antiemetics
Tocolytics
Corticosteroids
Antibiotics
Analgesics
IV fluids should be given to prevent or treat dehydration, which can cause premature labor.
Medications are given to try to stop labor from progressing, or to prepare for delivery.
Magnesium sulfate- to relax uterus and stop contractions
Antiemetics – to control nausea
Tocolytics – to stop labor from progressing
Corticosteroids – to speed up fetal lung maturity
Antibiotics – prophylactic if membranes have ruptured
Analgesics – to manage pain
Perform vaginal exam to assess for dilation and effacement
Avoid multiple digital exams if membranes have ruptured.
Determine progression, if any, of labor. If cervix is dilated >4 cm, it may not be possible to stop
labor from progressing.
Provide patient education
Symptoms of early labor
When to notify the doctor
How to time contractions
Avoid smoking
Avoid alcohol and substance abuse
Nutrition
Chronic condition management
Educate patient and caregivers regarding warning signs and symptoms, healthy diet and
lifestyle choices to help prevent repeat preterm labor.
Encourage patient to properly manage chronic medical conditions to prevent further labor
symptoms.
If labor cannot be stopped, prepare patient for delivery
In cases where labor cannot be stopped, prepare patient for delivery by providing education and
information, resources for family members and emotional support.
https://labmedicineblog.com/2015/12/15/microbiology-case-study-29-year-old-in-preterm-labor-
at-30-weeks-gestation/
https://nurseslabs.com/preterm-labor-nursing-care-plans/
Premature rupture of membranes
Premature rupture of membranes
(PROM) is a rupture (breaking open) of
the membranes (amniotic sac) before
labor begins. If PROM occurs before 37
weeks of pregnancy, it is called preterm
premature rupture of membranes
(PPROM).
PROM occurs in about 8 to 10 percent of all pregnancies. PPROM (before 37 weeks) accounts
for one fourth to one third of all preterm births.
Case scenario
We report the case of a 26-year-old pregnant woman of Arab ethnicity in her 32nd gestational
week with a history of two previous full-term eutocic deliveries and no medical-surgical history of
interest except for body mass index >30 kg m−2 and non-operated umbilical hernia. She did not
smoke, drink alcohol, or use illicit drugs. She reported no drug allergies. She arrived at the
emergency obstetrics and gynecology department due to the vaginal discharge of clear fluid
(hydrorrhea), with no uterine contractions or bleeding. According to her clinical records, she had
not previously undergone an ultrasonography examination during the pregnancy. The
gestational age was estimated as 32 weeks+5 days by ultrasonic fetal biometry. The patient had
normal blood pressure (126/79 mmHg) and a good general health status, with no fever (36.5
°C). Examination with a sterile speculum in the emergency department revealed the release of
clear amniotic fluid, while transvaginal ultrasound showed a closed multiparous cervix with a
length of 22 mm. Because of the clinical manifestation of amniorrhea, there was no need to
apply techniques to confirm PPROM. Abdominal ultrasound showed the fetus in cephalic
position with cardiac activity and active fetal movements, a normally inserted placenta on the
upper anterior side, and a normal amount of amniotic fluid. The fetus weight estimated by the
Hadlock formula was 2045 g, and the biometrics indicated 32+0 weeks of gestation. Urine,
endocervical, and vaginal-rectal cultures were taken, and complete blood and urine analyses
were performed. The cardiotocographic record at admission showed good fetal reactivity and
the absence of uterine contractions.
Post-admission, the hospital protocol for PPROM was followed, administering antibiotherapy
with intravenous ampicillin (2 g ampicillin then 1 g/6 h for 48 h) and oral azithromycin (1 g
azithromycin in monodosis), withdrawing ampicillin after the first 48 h and then administering
500 g/8 h for 5 days completing the lung maturation regimen with betamethasone. The urine
culture was negative, while the vaginal-rectal culture was positive for group
B Streptococcus (GBS) (susceptible to ampicillin). Endocervical culture evidenced the growth
of Staphylococcus aureus (susceptible to azithromycin), serogroup B Neisseria meningitides
(susceptible to azithromycin), and Haemophilus influenza (susceptible to ampicillin). The N.
meningitidis isolate was sent to the Neisseria Reference Laboratory of the Spanish National
Microbiology Center for characterisation, confirming the isolation of N. meningitidis serogroup B
by agglutination with specific monoclonal antibodies. Molecular characterisation of the strain
included determination of the genosubtype by sequencing VR1 and VR2 variable regions of the
external membrane protein PorA [9], and evaluation of the sequence type (ST) and clonal
complex by Multilocus Sequence Typing (MLST) [10]. Molecular study of the isolate revealed a
7–2, 30 genosubtype strain belonging to the ST-53 clonal complex, which is frequently
associated with nasopharyngeal carriage [11]. Screening for Chlamydia trachomatis,
Neisseria gonorrhoeae, Mycoplasma spp., and Ureaplasma spp. yielded negative results.
Although the patient remained clinically stable and afebrile, the labor was induced with
intravenous oxytocin followed by eutocic delivery in gestation week 33+4 after the patient
signed her informed consent. The motive for the induction was suspicion of subclinical
chorioamnionitis, based on her increasing leukocytosis, neutrophilia, and C-reactive protein
(CRP) levels since admission (leukocytosis of 11 030 at admission vs 14 650 at induction,
neutrophilia of 83 % at admission: vs 81 % at induction, and CRP of 11.27 mg l−1 at admission
vs 37 mg l−1 at induction). The CTG remained normal, with no uterine tenderness. The newborn
was female and weighed 1970 g, with Apgar scores at 1 and 5 min of 9 and 10, respectively,
umbilical artery pH of 7.32, and umbilical vein pH of 7.37, and she was admitted to the Neonatal
Intensive Care Unit (NICU). During her NICU stay, the newborn remained clinically stable, with
no need for vasoactive drugs or other advanced support measures, and she received
prophylactic antibiotherapy in accordance with the hospital protocol. Cultures taken at
admission and throughout the NICU stay were negative for infections. Transfontanelar
ultrasound at admission ruled out intraventricular hemorrhage. The newborn was discharged at
13 days of life with a weight of 2180 g, cephalic perimeter of 32 cm and length of 47 cm, and no
abnormal clinical findings.
Etiology
The fetal (amniochorionic) membrane results from fusion of the amnion and chorion
concomitant with obliteration of the chorionic cavity in the first trimester. This complex is fused
to the decidua capsularis, which is juxtaposed to the decidua parietalis through the remainder of
pregnancy. Membrane rupture usually occurs near the internal cervical os, but it may occur
remote from that site.9, 10
A number of mechanisms have been proposed for PROM.11, 12, 13 These include intrinsic
membrane weakness, mechanical stress, and ascending infection among others. Factors that
could cause weakening of the fetal membranes and have been associated with PROM include
local inflammation and infection, poor maternal nutrition, maternal smoking, and collagen
deficiency syndromes. Choriodecidual inflammation plays an important role in pPROM,
particularly when membrane rupture occurs remote from term.14 The lower genital tract is a
potential reservoir for bacteria that may ascend through the cervical canal and cause localized
inflammation. Bacteria and maternal neutrophils are able to produce a number of proteolytic
enzymes (e.g. collagenase, elastase, gelatinase) that can cause local weakening of the
membranes. Subsequent prostaglandin production resulting from localized inflammation can
lead to occult contractions and increased shearing stress at the internal cervical os. Factors
associated with mechanical distention of the membrane near the internal os include
polyhydramnios, twin gestation, and incompetent cervix. Trauma may be associated with
pPROM through an acute increase in intra-amniotic pressure or through the production of occult
contractions. In many cases, the cause of premature membrane rupture remains unknown.
Pathophysiology
Nursing diagnosis
. Risk for Infection: maternal
related to:
invasive procedures,
recurrent vaginal examination,
amniotic membrane rupture.
2. Impaired gas exchange: fetus

related to: the presence of disease.
3. Acute pain
related to: the rhythmic contraction of uterine smooth muscle.
4. Anxiety
related to:
crisis situation,
threat to the mother / fetus.
Assess for signs of infection

Maternal and fetal infection may prompt PROM and must be treated quickly to avoid fetal
compromise.
Perform single digital or sterile speculum vaginal exam
Vaginal exam may be required to confirm diagnosis but avoid multiple digital vaginal exams to
reduce the risk of infection. Reserve these exams for when delivery is imminent.
Obtain history from patient regarding complications and status of pregnancy.
Treatment depends on gestational age and existing complications
Patient may need to remain on bed rest to continue pregnancy if preterm, or labor may be
induced.
Initiate fetal monitoring
PROM may be an indicator of fetal distress. Monitor for signs of fetal compromise to include
changes in fetal heart rate.
Administer medications and IV fluids as appropriate
Prophylactic antibiotics
Corticosteroids
Tocolytics
Magnesium sulfate
PPROM may indicate a need for corticosteroids to speed up the fetal lung maturity
Antibiotics are given prophylactically to prevent infection
Tocolytics may be given to stop preterm labor
Magnesium sulfate may be given if prior to 32 weeks gestation to prevent fetal neurological
dysfunction
Prepare patient for induction of labor and delivery
If indicated, labor will likely be induced if it does not spontaneously begin within 12-24 hours.
Explain process to patient to reduce fears.
Provide patient education if preterm
Pelvic rest
Avoid tampons and intercourse
Avoid tub baths (showers ok)
If delivery is not indicated(<34 weeks gestation), patient will likely remain in the hospital until
delivery is an option.
Regardless of location, patient will be required to remain on bed rest and antibiotics will
continue prophylactically until delivery.
Nursing evaluation
Patient will be free from infection (maternal and fetal); viable birth
https://www.glowm.com/section_view/heading/Preterm%20Premature%20Rupture%20of
%20the%20Membranes/item/120
https://nursekomar.blogspot.com/2013/09/nursing-diagnosis-for-premature-rupture.html
Pregnancy Induce hypertension

Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of

new hypertension in a pregnant woman after 20 weeks' gestation without the presence of
protein in the urine or other signs of pre-eclampsia.[1]Gestational hypertension is defined as
having a blood pressure greater than 140/90 on two separate occasions at least 6 hours apart.
[1]
Case scenario
A 21-year-old pregnant woman, gravida 2 para 1, presented with hypertension and proteinuria
at 20 weeks of gestation. She had a history of pre-eclampsia in her first pregnancy one year
ago. During that pregnancy, at 39 weeks of gestation, she developed high blood pressure,
proteinuria, and deranged liver function. She eventually delivered by emergency caesarean
section following failed induction of labor. Blood pressure returned to normal post-partum and
she received no further medical follow-up. Family history was remarkable for her mother's
diagnosis of hypertension in her fourth decade. Her father and five siblings, including a twin
sister, were healthy. She did not smoke nor drink any alcohol. She was not taking any regular
medications, health products, or herbs.
At 20 weeks of gestation, blood pressure was found to be elevated at 145/100 mmHg during a
routine antenatal clinic visit. Aside from a mild headache, she reported no other symptoms. On
physical examination, she was tachycardic with heart rate 100 beats per minute. Body mass
index was 16.9 kg/m2 and she had no cushingoid features. Heart sounds were normal, and
there were no signs suggestive of congestive heart failure. Radial-femoral pulses were
congruent, and there were no audible renal bruits.
Baseline laboratory investigations showed normal renal and liver function with normal serum
urate concentration. Random glucose was 3.8 mmol/l. Complete blood count revealed
microcytic anemia with hemoglobin level 8.3 g/dl (normal range 11.5–14.3 g/dl) and a slightly
raised platelet count of 446 × 109/l (normal range 140–380 × 109/l). Iron-deficient state was
subsequently confirmed. Quantitation of urine protein indicated mild proteinuria with protein:
creatinine ratio of 40.6 mg/mmol (normal range <30 mg/mmol in pregnancy).
Catecholamine levels in 24-hour urine collections were found to be markedly raised. Urinary
noradrenaline excretion was markedly elevated at 5,659 nmol, 8,225 nmol, and 9,601 nmol/day
in repeated collections at 21 weeks of gestation (normal range 63–416 nmol/day). Urinary
adrenaline excretion was normal. Pregnancy may induce mild elevation of catecholamine levels,
but the marked elevation of urinary catecholamine observed was diagnostic of
pheochromocytoma. Conditions that are associated with false positive results, such as acute
myocardial infarction, congestive heart failure, acute cerebrovascular event, withdrawal from
alcohol, withdrawal from clonidine, and cocaine abuse, were not present in our patient.
The working diagnosis was therefore pheochromocytoma complicating pregnancy. Magnetic
resonance imaging (MRI) of neck to pelvis, without gadolinium enhancement, was performed at
24 weeks of gestation. It showed a 4.2 cm solid lesion in the mid-abdominal aorto-caval region,
while both adrenals were unremarkable. There were no ectopic lesions seen in the rest of the
examined areas. Based on existing investigation findings, it was concluded that she had extra-
adrenal paraganglioma resulting in hypertension.
Etiology
pre-existing hypertension (high blood pressure)

kidney disease
diabetes
PIH with a previous pregnancy
mother's age younger than 20 or older than 40
multiple fetuses (twins, triplets)
Pathophysiology
Nursing diagnosis

Deficient Fluid Volume: It is defined as decreased intravascular, interstitial, and intracellular
fluid.
May be related to
Osmotic pressure
Plasma protein loss
Decreasing plasma colloid
Allowing fluid shifts out of the vascular compartment
Edema formation
Sudden weight gain
Decreased urine output
Hemoconcentration
Nausea/vomiting
Epigastric pain
Headaches
Visual changes

Decreased Cardiac Output: Inadequate blood pumped by the heart to meet metabolic demands
of the body.
May be related to
Hypovolemia/decreased venous return
Increased systemic vascular resistance
Change in blood pressure/hemodynamic readings
Edema
Shortness of breath
Alteration in mental status
Altered Tissue Perfusion (Uteroplacental)
Impaired Tissue Perfusion: Decreased in the oxygen resulting in the failure to nourish the
tissues at the capillary level.
May be related to
Maternal hypovolemia
Interruption of blood flow (progressive vasospasm of spiral arteries)
Intrauterine growth retardation
Changes in fetal activity/heart rate
Premature delivery
Fetal demise
Risk for Maternal Injury
Risk for Injury: Vulnerable for injury as a result of environmental conditions interacting with the
individual’s adaptive and defensive resources, which may compromise health.
May be related to
Tissue edema/hypoxia
Tonic-clonic convulsions
Abnormal blood profile and/or clotting factors
[Not applicable: Presence of signs/symptoms establishes an actual diagnosis]
Abrupt, notable weight gain (e.g., more than 3.3 lb (1.5
Weigh patient regularly. Tell patient
kg)/month in the second trimester or more than 1 lb (0.5 kg)/wk
to record weight at home in
in the third trimester) reflects fluid retention. Fluid moves from
between visits.
the vascular to interstitial space, resulting in edema.
The presence of pitting edema (mild, 1+ to 2+; severe, 3+ to
Differentiate physiological and 4+) of face, hands, legs, sacral area, or abdominal wall, or
pathological edema of pregnancy. edema that does not disappear after 12hr of bedrest is vital.
Locate and determine degree of Note: Significant edema may actually be present in nonpre-
pitting. eclamptic patient sand absent in patients with mild or
moderated PIH.
Note signs of progressive or Edema and intravascular fibrin deposition (in HELLP syndrome)
excessive edema i.e., within the encapsulated liver are manifested by RUQ pain;
epigastric/RUQ pain, cerebral dyspnea, indicating pulmonary involvement; cerebral edema,
symptoms, nausea, vomiting). possibly leading to seizures; and nausea and vomiting,
Assess for possible eclampsia. indicating GI edema.
Identifies degree of hemoconcentration caused by fluid shift. If
Note alteration in Hct/Hb levels.
Hct is less than 3 times Hb level, hemoconcentration exists.
Proper nutrition decreases incidence of prenatal hypovolemia
Check on dietary intake of proteins
and hypoperfusion; insufficient protein/calories increases the
and calories. Give information as
risk of edema formation and PIH. Intake of 80–100 g of protein
needed.
may be required daily to replace losses.
Urine output is a sensitive indicator of circulatory blood volume.
Monitor intake and output. Note Oliguria and specific gravity of 1.040 indicate severe
urine color, and measure specific hypovolemia and kidney involvement. Note: Administration of
gravity as indicated. magnesium sulfate (MgSO4)may cause transient increase in
output.
Aids in identifying degree of severity/progression of condition. A
2+ reading implies glomerular edema or
Examine clean, voided urine for
spasm. Proteinuria affects fluid shifts from the vascular tree.
protein each visit, or daily/hourly as
Note: Urine contaminated by vaginal secretions may test
appropriate if hospitalized. Report
positive for protein, or dilution may result in a false-negative
readings of 2+, or greater.
result. In addition, PIH may be present without significant
proteinuria.
Assess lung sounds and respiratory Dyspnea and crackles may mean pulmonary edema, which
rate/effort. needs immediate treatment.
Rise in BP may happen in response to catecholamines,
Check BP and pulse. vasopressin, prostaglandins, and, as recent findings suggest,
decreased levels of prostacyclin.
Diuretics further increase chances of dehydration by
Respond to questions and review decreasing intravascular volume and placental perfusion, and
rationale for avoiding use they may cause thrombocytopenia, hyperbilirubinemia, or
of diuretics to treat edema. alteration in carbohydrate metabolism in fetus/newborn. Note:
May be useful in treating pulmonary edema.
Schedule prenatal visit every 1–2 Important to monitor changes more closely for the well-being of
wk if PIH is mild; weekly if severe. the patient and fetus.
Review moderate sodium intake of
up to 6 g/day. Tell patient to read
Some sodium intake is necessary because levels below 2–4
food labels and avoid foods high in
g/day result in greater dehydration in some patients. However,
sodium (e.g., bacon, luncheon
excess sodium may increase edema formation.
meats, hot dogs, canned soups,
and potato chips).
Collaborate with dietitian as Nutritional consult may be beneficial in determining individual
indicated. needs/dietary plan.
Lateral recumbent position decreases pressure on the vena
cava, increasing venous return and circulatory volume. This
Place patient on strict regimen of
enhances placental and renal perfusion, reduces adrenal
bedrest; encourage lateral position.
activity, and may lower BP as well as account for weight loss
through diuresis of up to 4 lb in 24-hr period.
Educate patient and family Some mildly hypertensive patients without proteinuria may be
members or significant others on managed on an outpatient basis if adequate surveillance and
home monitoring/day-care program, support is provided and the patient/family actively participates
as appropriate. in the treatment regimen.
Fluid replacement treats hypovolemia, yet must be given
cautiously to prevent overload, especially if interstitial fluid is
Substitute fluids either orally or drawn back into circulation when activity is reduced. With renal
parenterally via infusion pump, as involvement, fluid intake is restricted; i.e., if output is reduced
indicated. (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 patient is hospitalized:
Insert indwelling catheter if kidney
output is reduced or is less than 50 Allows more accurate monitoring of output/renal perfusion.
ml/hr.
Help with insertion of lines and/or
monitoring of invasive Gives a more precise measurement of fluid volume. In normal
hemodynamic parameters, such as pregnancy, plasma volume increases by 30%–50%, yet this
CVP and pulmonary artery wedge increase does not occur in the patient with PIH.
pressure (PAWP).
Elevated levels, especially of uric acid, indicate impaired kidney
Monitor serum uric acid
function, worsening of maternal condition, and poor fetal
and creatinine levels, and BUN.
outcome.
Patients with HELLP syndrome awaiting delivery of the fetus
Administer platelets as indicated. may benefit from transfusion of platelets when count is below
20,000.

Record and graph vital signs especially BP and The patient with PIH does not display the normal
pulse. 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 transpire, with
of 90 mm Hg is considered predictive of PIH.
modification in peripheral vascular resistance and
Assess for crackles, wheezes, and dyspnea;
drop in plasma colloid osmotic pressure.
note respiratory rate/effort.
Improves venous return, cardiac output, and
Institute bedrest with patient in lateral position.
renal/placental perfusion.
Provides precise picture of vascular changes and
fluid volume. Prolonged vascular constriction,
Check for invasive hemodynamic parameters.
increased hemoconcentration, and fluid shifts
decrease cardiac output.
If BP does not respond to conservative measures,
short-term medication may be needed in
conjunction with other therapies, e.g., fluid
replacement and MgSO4. Antihypertensive drugs
Give antihypertensive drug such as hydralazine
work directly on arterioles to promote relaxation of
(Apresoline) PO/IV, so that diastolic readings are
cardiovascular smooth muscle and help increase
between 90 and 105 mm Hg. Begin maintenance
blood supply to cerebrum, kidneys, uterus,
therapy as needed, e.g., methyldopa (Aldomet)
and placenta. Hydralazine is the drug of choice
or nifedipine (Procardia).
because it does not produce effects on the fetus.
Sodium nitroprusside is being used with some
success to lower BP (especially in HELLP
syndrome).
Check on BP and side effects of Side effects such as tachycardia, headache,
antihypertensive drugs. nausea, and vomiting, and palpitations may be
Administer propranolol (Inderal), as appropriate. treated with propranolol.
Prepare for birth of fetus by cesarean If conservative treatment is ineffective
delivery, labor when severe PIH/eclamptic and labor induction is ruled out, then surgical
condition is stabilised, but vaginal delivery is not procedure is the only means of halting the
feasible. hypertensive problems.

Decrease in placental blood flow results in reduced gas
exchange and impaired nutritional functioning of the placenta.
Present information to patient/couple
Potential outcomes of poor placental perfusion include a
concerning home assessment or
malnourished, LBW infant, and prematurity associated with
noting daily fetal movements and
early delivery, abruptio placentae, and fetal death. Reduced
when to seek immediate medical
fetal activity means fetal compromise (occurs before
attention.
detectable alteration in FHR and indicates demand for
immediate evaluation/intervention.
Name 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.
Report signs of abruptio placentae
(i.e., vaginal the bleeding, uterine Immediate attention and intervention increases the likelihood
tenderness, abdominal pain, and of a positive outcome.
decreased fetal activity).
Present contact number for patient to
Provides chance to address concerns/misconceptions and
direct questions, address changes in
intervene in a timely manner, as indicated.
daily fetal movements, and so forth.
Evaluate fetal growth; measure
Reduced placental functioning may accompany PIH, resulting
progressive fundal accompany growth
in IUGR. Chronic intrauterine stress and uteroplacental
at each office visit or periodically
insufficiency decrease amount of fetal contribution to
during stress home visits, as
amniotic fluid pool.
appropriate.
Note fetal response to medications Depressant effects of medication reduce fetal respiratory and
such as MgSO4, phenobarbital, and cardiac function and fetal activity level, even though placental
diazepam. circulation may be adequate.
Helps evaluate fetal well-being. An elevated FHR may show
Check FHR manually or
a compensatory response to hypoxia, prematurity, or abruptio
electronically, as indicated.
placentae.
BPP helps evaluate fetus and fetal environment on five
Assess fetal response to BPP criteria specific parameters to assess CNS function and fetal
or CST, as maternal status indicates. contribution to amniotic fluid volume. CST assesses placental
functioning and reserves.
In the event of declining maternal/fetal condition, risks of
Assist with assessment of fetal
delivering a preterm infant are weighed against the risks of
maturity and well-being using L/S
continuing the pregnancy, using results from evaluative
ratio, presence of PG, estriol levels,
studies of lung and kidney maturity, fetal growth, and
FBM, and sequential sonography
placental functioning. IUGR is associated with reduced
beginning at 20–26 weeks’ gestation.
maternal volume and vascular changes.
Assist with assessment of maternal
Identifies fetus at risk for IUGR or intrauterine fetal demise
plasma volume at 24–26 weeks’
associated with reduced plasma volume and reduced
gestation using Evans’ blue dye when
placental perfusion.
indicated.
Utilizing an ultrasonography, assist
Reduced placental function and size are associated with PIH.
with assessment of placental size.
Corticosteroids are thought to induce fetal pulmonary
Give corticosteroid (dexamethasone,
maturity (surfactant production) and prevent respiratory
betamethasone) IM for at least 24–48
distress syndrome, at least in a fetus delivered prematurely
hr, but not more than 7 days before
because of condition or inadequate placental functioning.
delivery, when severe PIH
Best results are obtained when fetus is less than 34 weeks’
necessitates premature delivery
gestation and delivery occurs within a week of corticosteroid
between 28 and 34 weeks’ gestation.
administration

Check 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.
Delayed treatment or progressive onset of
Emphasize importance of patient promptly
symptoms may result in tonic-clonic convulsions
reporting signs/symptoms of CNS involvement.
or eclampsia.
In progressive PIH, vasoconstriction and
vasospasms of cerebral blood vessels reduce
Check for alterations in level of consciousness.
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,
ankle clonus, decreased pulse and respirations, and respiratory involvement, precede convulsive
epigastric pain, and oliguria (less than 50 ml/hr). state.
Establish measures to lessen likelihood of
Lessens environmental factors that may
seizures; i.e., keep room quiet and dimly lit, limit
stimulate irritable cerebrum and cause a
visitors, plan and coordinate care, and promote
convulsive state.
rest.
Enforce seizure precautions per protocol. If seizure does occur, reduces risk of injury.
In the event of a seizure:
Maintains airway by reducing risk
Position patient on side; insert airway/bite block
of aspiration and preventing tongue from
only if mouth is relaxed; suction nasopharynx,
occluding airway. Maximizes oxygenation. Note:
as indicated; administer oxygen; avoid restrictive
Be cautious with use of airway/bite block,
clothing; do not restrict movement. Document
because attempts to insert when jaws are set
motor involvement, duration of seizure, and
may result in injury.
postseizure behavior.
These signs may indicate abruptio placentae,
Palpate for uterine tenderness or rigidity; check for
especially if there is a preexisting medical
vaginal bleeding. Review history of other medical
problem, such as diabetes mellitus, or a renal or
problems.
cardiac disorder causing vascular involvement.
Observe for signs and symptoms of labor or Convulsions increase uterine irritability; labor
uterine contractions. may ensue.
During seizure activity, fetal bradycardia may
Assess fetal well-being, noting FHR.
occur.
Monitor for signs of DIC easy/spontaneous
Abruptio placentae with release of
bruising, prolonged bleeding, epistaxis, GI
thromboplastin predisposes patient to DIC.
bleeding.
Immediate introduction of therapy helps to
Hospitalize if CNS involvement is present.
ensure safety and limit complications.
Give 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 phenytoininfusion 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 intrapartum therapy.)
A therapeutic level of MgSO4is achieved with
Monitor BP before, during, and after MgSO4 serum levels of 4.0–7.5 mEq/L or 6–8 mg/dL.
administration. Note serum magnesium levels in Adverse/toxic reactions develop above 10–12
conjunction with respiratory rate, patellar/deep mg/dL, with loss of DTRs occurring first,
tendon reflex (DTRs), and urine output. respiratory paralysis between 15–17 mg/dL, or
heart block occurring at 30–35 mg/dL.
Ready calcium gluconate. Give 10 ml (1 g/10 ml) Serves as antidote to counteract adverse/toxic
over 3 min as indicated. effects of MgSO4.
Depresses cerebral activity; has sedative effect
Administer amobarbital (Amytal) or diazepem when convulsions are not controlled by MgSO4.
(Valium), as indicated. Not recommended as first-line therapy because
sedative effect also extends to the fetus.
Helps to evaluate changes or severity of retinal
Perform funduscopic examination regulary.
involvement.
Review 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.
Scan sequential platelet count. Avoid
Thrombocytopenia may arise because of platelet
amniocentesis if platelet count is less than
adherence to disrupted endothelium or reduced
50,000/mm3. If thrombocytopenia is present
prostacyclin levels (a potent inhibitor of platelet
during operative procedure, use
aggregation). Invasive procedures or anesthesia
general anesthesia. Transfuse with platelets,
requiring needle puncture (such as
packed red blood cells, fresh frozen plasma, or
spinal/epidural) could result in excessive
whole blood, as indicated. Rule out HELLP
bleeding.
syndrome.
Elevated liver enzyme (AST, ALT) and bilirubin
levels, microangiopathic hemolytic anemia, and
Monitor liver enzymes and bilirubin; note
thrombocytopenia may indicate presence of
hemolysis and presence of Burr cells on peripheral
HELLP syndrome, signifying a need for
smear.
immediate cesarean delivery if condition of
cervix is unfavorable for induction of labor.
When fetal oxygenation is severely reduced
Prepare for cesarean birth if PIH is severe,
owing to vasoconstriction within malfunctioning
placental functioning is compromised, and cervix
placenta, immediate delivery may be necessary
is not ripe or is not responsive to induction.
to save the fetus.
Nursing evaluation
Desired Outcomes
Patient engages in therapeutic regimen and monitoring, as indicated.
Patient verbalizes understanding of need for close monitoring of weight, BP, urine protein, and
edema.
Patient is free of signs of generalized edema (i.e., epigastric pain, cerebral symptoms, dyspnea,
nausea/vomiting)
Patient exhibits Hct WNL and physiological edema with no signs of pitting.
Desired Outcomes
Patient remains normotensive throughout remainder of pregnancy.
Patient reports absence and/or decreased episodes of dyspnea.
Patient alters activity level as condition warrants.
Desired Outcomes
Patient demonstrates normal CNS reactivity on nonstress test (NST)
Patient is free of late decelerations;
Patient has no decrease in FHR on contraction stress test/oxytocin challenge test (CST/OCT).
Patient is full-term, AGA.
Desired Outcomes
Patient participates in treatment and/or environmental modifications to protect self and enhance
safety.
Patient is free of signs of cerebral ischemia (visual disturbances, headache, changes in
mentation).
Patient displays normal levels of clotting factors and liver enzymes
https://en.wikipedia.org/wiki/Gestational_hypertension
https://nurseslabs.com/pregnancy-induced-hypertension-nursing-care-plans/
Postmature Pregnancy
Postterm pregnancy is when a woman has not yet delivered her baby after 42 weeks
of gestation, two weeks beyond the typical 40 week duration of pregnancy.[1] Post-mature births
carry risks for both the mother and the baby, including fetal malnutrition, meconium aspiration
syndrome, and stillbirths.[2] After the 42nd week of gestation, the placenta, which supplies the
baby with nutrients and oxygen from the mother, starts aging and will eventually fail. Postterm
pregnancy are a reason to induce labor.[3]
Case Sceneario
Etiology
Pathophysiology
Nursing diagnosis
Nursing evaluation
Oligohydramnios
Definition Of Disorder
Oligohydramnios refers to amniotic fluid volume that is less than expected for gestational age. It
is typically diagnosed by ultrasound examination and may be described qualitatively (eg,
normal, reduced) or quantitatively (eg, amniotic fluid index [AFI] ≤5). An adequate volume of
amniotic fluid is critical to allow normal fetal movement and growth, and to cushion the fetus and
umbilical cord. Oligohydramnios may inhibit these processes and can lead to fetal deformation,
umbilical cord compression, and death.
Case Scenario
J. L. is a healthy, 20-year-old gravida 2 para 0010 at 41 and 0/7 weeks' gestation, based on the
first day of her last menstrual period and first trimester ultrasound. She was admitted to the
labor and delivery unit at 10:00 AM for induction of labor. Earlier in the day, J. L. had a
biophysical profile (BPP) performed per hospital protocol for all women whose pregnancies
continued beyond 40 weeks' gestation. The BPP revealed an amniotic fluid index of 4.97 cm. All
other components of the BPP were normal (fetal breathing, fetal tone, fetal movement, and
reactive nonstress test). The estimated weight of the fetus was 3178 grams. J. L.'s prenatal
course was uncomplicated. She had adequate fetal growth and no signs of maternal or fetal
morbidity. Her initial cervical exam was 2 cm dilated, soft, posterior, 50% effaced, -2 station, and
vertex. She was not having any uterine contractions. The amniotic membranes were intact. The
baseline fetal heart rate (FHR) was 140 to 150 beats per minute (bpm) with moderate variability,
accelerations, and no decelerations. The collaborating obstetrician recommended inducing labor
with oxytocin infusion if labor did not begin spontaneously within 12 hours after admission. After
12 hours of observation, her vaginal exam was unchanged. The FHR pattern was reassuring
throughout the day.
At this time, after obtaining the patient's informed consent, the midwife began induction of labor
per protocol, starting at 1 milliunits (mU) per minute of oxytocin, increasing 1 mU/minute every
20 minutes until a contraction pattern of every 2 minutes with moderate intensity was
established. Three hours later, at an infusion rate of 6 mU/min, uterine contractions were every
3 to 4 minutes. At that time, an episode of prolonged fetal bradycardia occurred (to 70 bpm,
lasting 90 seconds before returning to a baseline of 140-150 bpm). The oxytocin infusion was
stopped, and an amniotomy was done. This revealed a small amount of clear, odorless fluid. A
fetal scalp electrode was inserted.
Nineteen hours after admission, 7 hours after beginning the labor induction, J. L. requested pain
medication. One milligram of butorphanol tartrate augmented with 25 mg of promethazine was
administered via intravenous (IV) push for pain relief. The oxytocin infusion was restarted at 1
mU/min, increasing by 1 mU every 20 minutes. Twenty-four hours after admission, an epidural
was placed at J. L.'s request. At this time, her cervix was 5 cm, 80%, and -1 station. The FHR
was reassuring and contractions were every 2 to 4 minutes. At 3:00 PM, 29 hours after
admission, the consulting physician and midwife decided to do an amnioinfusion and place an
intrauterine pressure catheter (IUPC) secondary to the presence of repetitive variable
decelerations that had a quick recovery to baseline. At the time of the amnioinfusion and IUPC
placement, J. L.'s vaginal exam was 8 cm, 100% effaced, and -1 station. The patient reported
exhaustion and felt that she could not continue with the labor. Seven hours later, J. L. was
contracting irregularly and reported that she had the urge to push but felt too exhausted; her
cervix was anterior lip (9 cm), 100%, +1 fetal station. Thirty-five hours after being admitted to
the labor unit, maternal pushing efforts began, the anterior lip was reduced, and the fetus's
station was +2 with a well-flexed head. The FHR pattern was reassuring. After 1 hour and 50
minutes of maternal pushing effort, a decision was made by the patient, midwife, and physician
to proceed with a cesarean section because of the arrest of fetal descent and maternal reports
of exhaustion and inability to continue pushing. A vigorous baby boy was born at 11:45 PM,
weighing 3265 grams, with Apagar scores of 9 and 9, at 1 and 5 minutes. Both mother and baby
did well postpartum.
Etiology
Causes of oligohydramnios include the following:

Fetal urinary tract anomalies, such as renal agenesis, polycystic kidneys, or any urinary
obstructive lesion (eg, posterior urethral valves [5] )
Premature rupture of membranes and chronic leakage of the amniotic fluid; chorioamnionitis is
an additional important maternal complication from oligohydramnios due to rupture of the
membranes, which has an incidence of 21-74%. The earlier chorioamnionitis occurs in
pregnancy, the greater the fetal risk of bronchopulmonary dysplasia, neurologic complications,
pulmonary hypoplasia, and, in severe cases, respiratory failure in the neonate.
Placental insufficiency, as seen in pregnancy-induced hypertension, maternal diabetes, or
postmaturity syndrome when the pregnancy extends beyond 42 weeks' gestation
Maternal use of prostaglandin synthase inhibitors or angiotensin-converting enzyme
Pathophysiology
Rupture of the membranes is the most common cause of oligohydramnios. However, because
the amniotic fluid is primarily fetal urine in the latter half of the pregnancy, the absence of fetal
urine production or a blockage in the fetus's urinary tract can also result in oligohydramnios.
Fetal swallowing, which occurs physiologically, reduces the amount of fluid, and an absence of
swallowing or a blockage of the fetus's gastrointestinal tract can lead to polyhydramnios.
A near term fetus produces 500-1200 mL of urine and swallows between 210 and 790 mL of
amniotic fluid per day. [3]
Nursing Diagnosis
Acute pain r / t movements of the baby
Impaired sleep pattern r / t pain
Risk of injury: the fetus r / t reduction in amniotic fluid
Anxiety
Knowledge deficit r / t do not know information
Nursing Interventions
Monitor maternal and fetal status closely, including vital signs and fetal heart rate patterns.
Monitor maternal weight gain pattern, notifying the health care provider if weight loss occurs.
Provide emotional support before, during, and after ultrasonography.
Inform the patient about coping measures if fetal anomalies are suspected.
Instruct her about signs and symptoms of labor, including those she’ll need to report
immediately.
Reinforce the need for close supervision and follow up.
Assist with amnioinfusion as indicated.
Encourage the patient to lie on her left side.
Ensure that amnioinfusion solution is warmed to body temperature.
Continuously monitor maternal vital signs and fetal heart rate during the amnioinfusion
procedure.
Note the development of any uterine contractions, notify the health care provider, and continue
to monitor closely.
Maintain strict sterile technique during amnioinfusion.
Nursing evaluation
https://www.uptodate.com/contents/oligohydramnios#H1
https://www.medscape.com/viewarticle/551032
https://reference.medscape.com/article/975821-overview#a4
https://www.uaz.edu.mx/histo/pathology/ed/ch_6/c6_1.htm
https://nursingcrib.com/nursing-notes-reviewer/maternal-child-health/oligohydramnios/
https://ncp-nursingcareplan.blogspot.com/2017/01/oligohydramnios-nursing-care-plan.html
Polyhydramnios
Polyhydramnios is the presence
of excess amniotic fluid in the
uterus. By
definition, polyhydramnios is
diagnosed if the deepest vertical
pool is more than 8 cm or
amniotic fluid index (AFI) is
more than 95th percentile for
the corresponding gestational
age. With a deep pocket of 8 cm
or more as the criterion of
polyhydramnios, the incidence is 1-3% of all pregnancies. Most cases of mild polyhydramnios
are idiopathic, but the 2 most common causes are maternal diabetes mellitus and fetal
anomalies. The amniotic fluid index (AFI) defines polyhydramnios defined as 24 cm or more.
The increase in amniotic fluid, in many of cases, can be attributed to impaired fetal swallowing
or the overproduction of fetal urine due to a high-output cardiac state, renal abnormality, or
osmotic fetal diuresis.
The degree of polyhydramnios is frequently categorized as mild, moderate, or severe, based on
an AFI of 24.0–29.9 cm, 30.0–34.9 cm, and ≥35 cm, respectively, or a deep vertical pocket of
8–11 cm, 12–15 cm, or ≥16 cm, respectively.
Polyhydramnios has a variety of causes affecting the mother or the fetus. The presence of
polyhydramnios should prompt a search for other fetal anomalies. Some of the anomalies can
be diagnosed with ultrasonography, while others require karyotyping.
Case Scenario
Debbie is a 27-year-old woman in her first pregnancy. She attends her 20-week anomaly
ultrasound, which shows a normal fetus, normal liquor volume and normally sited placenta.
As she has no health problems, Debbie is 'low risk' and attends her midwife and GP for shared
antenatal care.
At 30 weeks' gestation, Debbie presents to her GP feeling bloated and uncomfortable. On
examination she is normotensive, apyrexial and not unwell. Her urine shows no abnormality. On
palpation, Debbie's uterus measures 33cm from pubic symphysis to fundus. As this is within the
allowed discrepancy from gestation (in weeks) this is noted, and the fetal heart is heard.
A fortnight later, Debbie attends feeling breathless on minimal exertion. On examination her
urine shows a trace of protein. Her BP and other observations are normal. Her ankles show mild
edema bilaterally.
Debbie's symphysio fundal height measures 40cm. This is significantly greater than expected
(32 weeks = 32cm +/3cm). It is also noted that the fetus is difficult to palpate and seems very
mobile inside the uterus. The fetal heart is heard but sounds slightly muffled.
Debbie's GP arranges a next-day appointment for her in the hospital day assessment unit.
Transverse lie
The ultrasound scan shows a live fetus in transverse lie, with an AFI exceeding the 95th centile
for 32 weeks. The deepest vertical pool of liquor measures 11cm. The fetus appears to be
structurally normal. A glucose tolerance test and bloods taken for viral serology are normal.
Debbie is discharged with a follow-up ultrasound arranged.
The day before her follow-up scan, at 33 + 5 gestation, Debbie starts having painful
contractions. She attends the delivery suite where she is found to have a soft, effacing cervix.
The fetus is still in transverse lie.
Debbie is now contracting two to three times in a 10-minute period. As the pregnancy is less
than 34 weeks' gestation, her obstetrician prescribes steroids (to enhance fetal lung maturity)
and a tocolytic to relax the uterus for long enough that the steroids can take effect. Debbie is
admitted to the ward.
Two days later, Debbie's waters break. The attending midwife immediately places her in the
knee-chest position. This is adopted when membranes rupture with a transverse or unstable lie.
There is a risk of cord prolapse in this situation and knee-chest aims to take any pressure of
gravity off the possibly prolapsed cord.
Debbie is transferred for caesarean section.
A live male infant is born in good condition and examination confirms him to be normal.
Tracheo-esophageal fistula is excluded by passing a nasogastric tube.
No cause is found for the polyhydramnios, so Debbie is advised that the risk of recurrence is
extremely low.
Etiology
The underlying cause of the excessive amniotic fluid volume is obvious in some clinical
conditions and is not completely understood in others. Causes include the following:
Twin gestation with twin-to-twin transfusion syndrome (increased amniotic fluid in the recipient
twin and decreased amniotic fluid in the donor) or multiple gestations
Fetal anomalies, including esophageal atresia (usually associated with a tracheoesophageal
fistula), tracheal agenesis, duodenal atresia, and other intestinal atresias
Central nervous system abnormalities and neuromuscular diseases that cause swallowing
dysfunction
Congenital cardiac-rhythm anomalies associated with hydrops, fetal-to-maternal hemorrhage,
and parvovirus infection
Poorly controlled maternal diabetes mellitus (Oligohydramnios may also be seen if severe
vascular disease is present.)
Chromosomal abnormalities, most commonly trisomy 21, followed by trisomy 18 and trisomy 13.
Fetal akinesia syndrome with absence of swallowing
In a study by Kollmann et al of 860 singleton pregnancies complicated by polyhydramnios,
68.8% of the polyhydramnios cases were idiopathic, whereas maternal diabetes was found in
19.8% of cases; congenital anomalies, in 8.5%; and a positive TORCH (toxoplasmosis, other
[such as syphilis, varicella-zoster, parvovirus B19], rubella, cytomegalovirus, herpes infection)
serology, in 2.9%. [4]
Pathophysiology
The volume of amniotic fluid increases steadily until 33 weeks of gestation. It plateaus from 33-
38 weeks, and then declines – with the volume of amniotic fluid at term approximately 500ml.
It is predominantly comprised of the fetal urine output, with small contributions from the placenta
and some fetal secretions (e.g. respiratory, oral).
The fetus breathes and swallows the amniotic fluid. It gets processed, fills the bladder and is
voided, and the cycle repeats. Problems with any of the structures in this pathway can lead to
either too much or too little fluid.
Mild to moderate degrees usually does not require treatment.
Hospitalization if symptoms are severe dyspnea, abdominal pain and difficult ambulation.
Maintain bed rest with sedation to make the situation endurable.
Monitor the patient for signs and symptoms of premature labor.
Monitor maternal vital signs and fetal heart rate frequently; report changes immediately.
Prepare the patient for amniocentesis and possible labor induction, as appropriate; keep in mind
that amniocentesis for fluid removals is only temporary and may need to be done repeatedly.
https://emedicine.medscape.com/article/404856-overview#a1
https://reference.medscape.com/article/975821-overview#a5
https://teachmeobgyn.com/pregnancy/fetal-abnormality/polyhydramnios/
Multiple Pregnancy
A multiple pregnancy is a pregnancy in
which more than one fetus develops in
the uterus at the same time. Multiple
pregnancies occur in 1-2% of
pregnancies. The rate of twinning (the
bearing of twins) is believed to be
underestimated, as twin pregnancies with
a singleton (an offspring born singly) birth
are usually not recorded as twins.
A multiple pregnancy may be the result of

the natural process of twinning, or it may
be the result of the woman having taken
fertility drugs. Because of the increase in
artificial reproductive technology (ART),
the incidence of multiple pregnancies has
increased. An April 1999 National Vital
Statistics report from the Centers for Disease Control and Prevention (CDC) states that since
1980 the number of twins has risen by 52% and the number of triplets and high order multiples
(more than three) has increased by 404%. An older maternal age and the use of fertility
techniques are the two major factors in these increases. While singletons have a 10% risk of
being born preterm, multiple births have a 57% chance of being born prematurely. Premature
birth places a neonate at higher risk for morbidity and mortality.
Etiology
The etiology of monozygotic twinning is unknown. Dizygotic twins are thought to result from the
ovulation of multiple follicles caused by elevations in serum gonadotropin levels. Hence,
advanced maternal age is associated with an increased prevalence of twin birth.
The availability of assisted reproductive technology has contributed to the increase in multiple
gestations seen over the past 20 years. During ovulation induction treatment, the ovaries are
stimulated to produce several follicles, thus increasing the risk of multiple eggs being released
and subsequently fertilized. The risk of multiple gestations during in-vitro fertilization is directly
related to maternal age and number of embryos transferred. With two embryos transferred, the
risk of a multiple gestation was found to be 22.7% and 19.7% for women aged 20-29 years and
30-34 years, respectively. This risk increased to 45.7% in women aged 20-29 years and 39.8%
for women aged 30-34 years if 3 embryos were transferred. [2]
Dizygotic twinning can occur more frequently in some families. This is thought to be secondary
to genetic factors leading to ovulation of several eggs during the menstrual cycle. In contrast,
monozygotic twinning has not been shown to have a familial inheritance.
Predisposing factors
Advanced maternal age (> 35 years)
Previous multiple pregnancy
Use of fertility enhancing treatments
Maternal family history of dizygotic twins
Twins can be classified as monozygotic, originating from the fertilization and subsequent
division of one egg, or dizygotic, originating from the fertilization and development of two eggs.
Approximately one third of twins are thought to be monozygotic in the United States.[1]
Twins can be further classified by their chorionicity. Dizygotic twins are almost always
dichorionic, diamniotic. The chronicity of monozygotic twins depends on the timing of division of
the fertilized egg. Dichorionic, diamniotic twins result if the fertilized egg splits 0-3 days after
fertilization. This is thought to occur in approximately 20-30% of monozygotic twins.
Monochorionic, diamniotic twins occur at days 4-8 after fertilization and account for
approximately 70% of monozygotic twins. Monochorionic, monoamniotic twins are rare (1-5% of
monozygotic twins) and result secondary to division 8-12 days postfertilization. Conjoined twins
occur with division 13 days or later; this is extremely rare.
Nursing Diagnosis
Physical examination
Fundal height and abdominal girth are unusually large for the gestational age.
The presence of more than one fetus may, in some cases, be confirmed by palpation.
Two or more fetal heart rates can be heard on auscultation.
Ultrasound
Evidence of more than one fetus
Differentiation between monochorionic and dichorionic twins during early pregnancy
Dichorionic twins: lambda sign
Monochorionic twins: T-sign
Multifetal pregnancies are high-risk pregnancies and require more frequent prenatal care visits.
Frequent early evaluations for monochorionic twins to assess for twin-twin transfusion syndrome
From the 32nd week of pregnancy: weekly prenatal care visits, including ultrasound, to monitor
fetal growth
Management of multiple pregnancy may include the following:
Increased nutrition
Mothers carrying two or more fetuses need more calories, protein, and other nutrients, including
iron. Higher weight gain is also recommended for multiple pregnancy. The Institute of Medicine
recommends that women carrying twins who have a normal body mass index should gain
between 37 and 54 pounds. Those who are overweight should gain 31-50 pounds; and obese
women should gain 25-42 pounds.
More frequent prenatal visits
Multiple pregnancy increases the risk for complications. More frequent visits may help detect
complications early enough for effective treatment or management. The mother's nutritional
status and weight should also be monitored more closely.
Referrals
Referral to a maternal-fetal medicine specialist, called a perinatologist, for special testing or
ultrasound evaluations, and to coordinate care of complications, may be necessary.
Increased rest
Some women may also need bedrest--either at home or in the hospital depending on pregnancy
complications or the number of fetuses. Higher-order multiple pregnancies often require bedrest
starting in the middle of the second trimester. Preventive bed rest has not been shown to
prevent preterm birth in multiple pregnancy.
Maternal and fetal testing
Testing may be needed to monitor the health of the fetuses, especially if there are pregnancy
complications.
Tocolytic medications
Tocolytic medications may be given, if preterm labor occurs, to help slow or stop contractions of
the uterus. These may be given orally, in an injection, or intravenously. Tocolytic medications
often used include magnesium sulfate.
Corticosteroid medications
Corticosteroid medications may be given to help mature the lungs of the fetuses. Lung
immaturity is a major problem of premature babies.
Cervical cerclage
Cerclage (a procedure used to suture shut the cervical opening) is used for women with an
incompetent cervix. This is a condition in which the cervix is physically weak and unable to stay
closed during pregnancy. Some women with higher-order multiples may require cerclage in
early pregnancy.
https://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-
maps/multiple-pregnancy
Isoimmunization (Rh
Incompatibility)
The Rh factor (ie, Rhesus
factor) is a red blood cell surface
antigen that was named after
the monkeys in which it was first
discovered. Rh incompatibility,
also known as Rh disease, is a
condition that occurs when a
woman with Rh-negative blood
type is exposed to Rh-positive
blood cells, leading to the
development of Rh antibodies.
Rh incompatibility can occur by
2 main mechanisms. The most
common type occurs when a Rh-negative pregnant mother is exposed to Rh-positive fetal red
blood cells secondary to feto-maternal hemorrhage during the course of pregnancy from
spontaneous or induced abortion, trauma, [1] invasive obstetric procedures, or normal delivery.
Rh incompatibility can also occur when a Rh-negative female receives an Rh-positive blood
transfusion. In part, this is the reason that blood banks prefer using blood type "O negative" or
"type O, Rh negative," as the universal donor type in emergency situations when there is no
time to type and crossmatch blood.
The most common cause of Rh incompatibility is exposure from a Rh-negative mother by Rh-
positive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal
circulation may leak into the maternal circulation, and, after a significant exposure, sensitization
occurs leading to maternal antibody production against the foreign Rh antigen.
Once produced, maternal Rh immunoglobulin G (IgG) antibodies persist for life and may cross
freely from the placenta to the fetal circulation, where they form antigen-antibody complexes
with Rh-positive fetal erythrocytes and eventually are destroyed, resulting in a fetal alloimmune-
induced hemolytic anemia. [2] Although the Rh blood group systems consist of many antigen
subtypes (eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most
commonly is involved in Rh incompatibility.
Case Scenario
The first case involving Rh incompatibility was reported in 1939, although the Rh factor, a
protein found on the surface of red blood cells, had not yet been discovered. This first case was
reported by immunohematologist, Philip Levine and physician, Rufus Stetson, who published
their case in The Journal of the American Medical Association. The authors presented an
anonymous, twenty-five year old woman who checked into a local hospital during her thirty-third
week of pregnancy complaining of labor pains and vaginal bleeding. The next day, she
delivered an emaciated, stillborn fetus weighing only one pound and five ounces. The
physicians had to expel the woman’s placenta to stop her from bleeding to death. The patient
received a blood transfusion from her husband, as the two of them were of blood-type O. Ten
minutes after completing the transfusion, the patient developed a chill and began feeling pain in
her head and legs. When her vaginal bleeding resumed she was given a hysterectomy, followed
by another blood transfusion from a different donor. Throughout her entire visit, the patient
received transfusions from 104 Type O blood donors. Remarkably, the mother showed no blood
transfusion reaction to twenty-one of those donors. Further tests indicated that the patient’s
serum, or the plasma in the blood minus the clotting factors, specifically agglutinated her
donors’ cells—or rather, 80 percent of all her blood transfusions.
The two physicians tried to discover what was causing the patient’s reaction. Initially, they
believed that temperature was affecting agglutination in the patient’s blood, but they soon
realized that temperature did not affect agglutination. The physicians reported that it was difficult
to recreate these agglutinations for further testing since they still had not yet solved what was
causing these isoimmunizations, or the development of antibodies in response to an antigenic
stimulation.
It was not until a year later, Karl Landsteiner and Alexander S. Wiener coined the term “Rh
factor” as the cause of the isoimmunization. They originally believed that Macacus rhesus, or
Rhesus monkey, contained the same red blood cell surface antigen (Rh) as the one found in
human red blood cells. This was soon proven wrong, as the composition of human sera and
rhesus sera are different. Nonetheless, the term “Rh factor” has continued to be used to
describe these human antigens, and the term “anti-Rh” is used to describe human antibodies
formed against the Rh factor.
Etiology
A Rh-negative woman who conceives a child with a Rh-positive man is at risk for
Rh incompatibility.
Rh factor is inherited (passed from parents to children through the genes). If you're Rh-negative
and the father of your baby is Rh-positive, the baby has a 50 percent or more chance of having
Rh-positive blood.
Simple blood tests can show whether you and the father of your baby are Rh-positive or Rh-
negative.
If you're Rh-negative, your risk of problems from Rh incompatibility is higher if you were
exposed to Rh-positive blood before the pregnancy. This may have happened during:
An earlier pregnancy (usually during delivery). You also may have been exposed to Rh-positive
blood if you had bleeding or abdominal trauma (for example, from a car accident) during the
pregnancy.
An ectopic pregnancy, a miscarriage, or an induced abortion. (An ectopic pregnancy is a
pregnancy that starts outside of the uterus, or womb.)
A mismatched blood transfusion or blood and marrow stem cell transplant.
An injection or puncture with a needle or other object containing Rh-positive blood.
Certain tests also can expose you to Rh-positive blood. Examples include amniocentesis (AM-
ne-o-sen-TE-sis) and chorionic villus (ko-re-ON-ik VIL-us) sampling (CVS).
Amniocentesis is a test that you may have during pregnancy. Your doctor uses a needle to
remove a small amount of fluid from the sac around your baby. The fluid is then tested for
various reasons.
CVS also may be done during pregnancy. For this test, your doctor threads a thin tube through
the vagina and cervix to the placenta. He or she removes a tissue sample from the placenta
using gentle suction. The tissue sample is tested for various reasons.
Unless you were treated with the medicine that prevents Rh antibodies (Rh immune globulin)
after each of these events, you're at risk for Rh incompatibility during current and future
pregnancies.
Pathophysiology
Nursing Diagnosis
Rh incompatibility is diagnosed with blood tests. To find out whether a baby is developing

hemolytic anemia and how serious it is, doctors may use more advanced tests, such as
ultrasound.
Specialists Involved
An obstetrician will screen for Rh incompatibility. This is a doctor who specializes in treating
pregnant women. The obstetrician also will monitor the pregnancy and the baby for problems
related to hemolytic anemia. He or she also will oversee treatment to prevent problems with
future pregnancies.
A pediatrician or hematologist treats newborns who have hemolytic anemia and related
problems. A pediatrician is a doctor who specializes in treating children. A hematologist is a
doctor who specializes in treating people who have blood diseases and disorders.
Diagnostic Tests
If you're pregnant, your doctor will order a simple blood test at your first prenatal visit to learn
whether you're Rh-positive or Rh-negative.
If you're Rh-negative, you also may have another blood test called an antibody screen. This test
shows whether you have Rh antibodies in your blood. If you do, it means that you were exposed
to Rh-positive blood before and you're at risk for Rh incompatibility.
If you're Rh-negative and you don't have Rh antibodies, your baby's father also will be tested to
find out his Rh type. If he's Rh-negative too, the baby has no chance of having Rh-positive
blood. Thus, there's no risk of Rh incompatibility.
However, if the baby's father is Rh-positive, the baby has a 50 percent or more chance of
having Rh-positive blood. As a result, you're at high risk of developing Rh incompatibility.
If your baby's father is Rh-positive, or if it's not possible to find out his Rh status, your doctor
may do a test called amniocentesis.
For this test, your doctor inserts a hollow needle through your abdominal wall into your uterus.
He or she removes a small amount of fluid from the sac around the baby. The fluid is tested to
learn whether the baby is Rh-positive. (Rarely, an amniocentesis can expose you to Rh-positive
blood).
Your doctor also may use this test to measure bilirubin levels in your baby. Bilirubin builds up as
a result of red blood cells dying too quickly. The higher the level of bilirubin is, the greater the
chance that the baby has hemolytic anemia.
If Rh incompatibility is known or suspected, you'll be tested for Rh antibodies one or more times
during your pregnancy. This test often is done at least once at your sixth or seventh month of
pregnancy.
The results from this test also can suggest how severe the baby's hemolytic anemia has
become. Higher levels of antibodies suggest more severe hemolytic anemia.
To check your baby for hemolytic anemia, your doctor also may use a test called Doppler
ultrasound. He or she will use this test to measure how fast blood is flowing through an artery in
the baby's head.
Doppler ultrasound uses sound waves to measure how fast blood is moving. The faster the
blood flow is, the greater the risk of hemolytic anemia. This is because the anemia will cause
the baby's heart to pump more blood.
Antenatal
Once a woman has been found to have made anti-D (or any clinically significant antibody
against fetal red cells), she is followed as a high-risk pregnancy with serial blood draws to
determine the next steps
Once the titer of anti-D reaches a certain threshold (normally 8 to 16), serial Ultrasound and
Doppler examinations are performed to detect signs of fetal anemia
Detection of increased blood flow velocities in the fetus are a surrogate marker for fetal anemia
that may require more invasive intervention
If the flow velocity is found to be elevated a determination of the severity of anemia needs to
ensue to determine if an intrauterine transfusion is necessary
This is normally done with a procedure called percutaneous umbilical cord blood sampling
(PUBS or cordocentesis) [23]
Intrauterine blood transfusion
Intraperitoneal transfusion—blood transfused into fetal abdomen
Intravascular transfusion—blood transfused into fetal umbilical vein—This is the method of
choice since the late 1980s, and more effective than intraperitoneal transfusion. A sample of
fetal blood can be taken from the umbilical vein prior to the transfusion.
Often, this is all done at the same PUBS procedure to avoid the needs for multiple invasive
procedures with each transfusion
Postnatal
Phototherapy for neonatal jaundice in mild disease
Exchange transfusion if the neonate has moderate or severe disease
Intravenous Immunoglobulin (IVIG) can be used to reduce the need for exchange transfusion
and to shorten the length of phototherapy.

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1.

Gestational Trophoblastic disease

Ineffective Tissue Perfusion

Nursing Interventions Rationale

Nursing Interventions Rationale

Nursing Interventions Rationale

Risk for [Fetal] Injury

Premature rupture of membranes

2. Impaired gas exchange: fetus

Assess for signs of infection

Pregnancy Induce hypertension

Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of

pre-existing hypertension (high blood pressure)

Deficient Fluid Volume

Decreased Cardiac Output

Nursing Interventions Rationale

Nursing Interventions Rationale

Nursing Interventions Rationale

Causes of oligohydramnios include the following:

A multiple pregnancy may be the result of

Rh incompatibility is diagnosed with blood tests. To find out whether a baby is developing

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