Transcript Chronic Hypertension

Dr. Areefa Al Bahri
Chapter 3
Complications
During Pregnancy
Complications that arise during pregnancy are often
challenging and demand the perinatal nurse’s skills,
knowledge, and expertise, combined with the nursing
process, to fi rst identify the pregnant patient at risk and
then formulate, implement, and evaluate an appropriate,
holistic plan of care.
Early Pregnancy Complications
 Hyperemesis gravidarum
 Spontaneous abortion/ miscarriage
 Gestational trophoblastic disease
 Ectopic pregnancy
 Perinatal loss- Fetal death Less than perfect
child
Miscellaneous Complications
Multiple gestation
 Premature rupture of membranes
 Preterm labor
Incompetent cervix
Endocrine Complication
Diabetes Type I & II
Hyper/hypothyroid
Cardiovascular/Hematological
cardiomyopathy
Hematological
• Sickle cell anemia
• Thalassemia
Hypertensive disorders
• Chronic hypertension
• Preeclampsia/eclampsia Proteinuria, edema,
CNS alterations, HELLP
• Chronic hypertension with preeclampsia
• Gestational hypertension
Ectopic Pregnancy
An ectopic pregnancy is one that
implants outside of the uterine
cavity. Implantation may occur in
the fallopian tube (99%), on the
ovary, the cervix, on the outside of
the fallopian tube, the abdominal
wall, or on the bowel. Patients who
present with vaginal bleeding, a
missed period, and abdominal
tenderness or pain should
A number of factors of ectopic pregnancy which include:
• History of STI or pelvic inflammatory disease
• Prior ectopic pregnancy
• Previous tubal, pelvic, or abdominal surgery
• Endometriosis
• In vitro fertilization or other method of assisted reproduction
• Use of an intrauterine device
Diagnosis
ectopic pregnancy should be diagnosed before the onset of
hypotension, bleeding, pain, and overt rupture. The patient’s
history (e.g., unilateral, bilateral or diffuse abdominal pain, missed
period) and physical exam (a palpable mass is present on bimanual
examination in approximately 50% of women) should alert the
health care professional to the possible presence of an ectopic
pregnancy.Diagnostic laboratory tests include a beta-human
chorionic gonadotropin (hCG) . Transvaginal ultrasonography
should be performed to confirm intrauterine or tubal pregnancy
(Farquhar, 2005). Ultrasonographic identification of an
intrauterine pregnancy rules out the presence of an ectopic
pregnancy in most women (Murray, Baakdah, Bardell, & Tulandi,
2005).
Management
Salpingectomy (removal of the ruptured fallopian tube) by
laparotomy (surgical procedure in which the abdomen is
opened to visualize the abdominal organs) has long
offered an almost 100% cure for the treatment of an
ectopic pregnancy. using a laparoscope inserted into the
pelvic cavity through a small incision in the abdomen),
salpingostomy (incision into the fallopian tube to remove
the pregnancy) and partial salpingectomy are replacing
laparotomy as the treatment mode of choice.
GESTATIONAL TROPHOBLASTIC DISEASE
Gestational trophoblastic disease (GTD) is a clinical
diagnosis that includes the histologic diagnoses of
hydatidiform mole (“molar pregnancy”), locally
invasive mole, metastatic mole, and choriocarcinoma.
It is a disease characterized by an abnormal placental
development that results in the production of
fluid-filled grapelike clusters (instead of normal
placental tissue) and a vast proliferation of
trophoblastic tissue. It is associated with loss of the
pregnancy and rarely, the development of cancer. GTD
occurs in 1 in 1200 pregnancies (Berman, DiSaia, &
Tewari, 2004).
Pathophysiology
The cause is unknown, but it is thought that complete
moles result from the fertilization of an empty ovum
(one whose nucleus is missing or nonfunctional) by a
normal sperm. Since the ovum contains no maternal
genetic material. A complete mole is characterized by
trophoblastic proliferation and the absence of fetal parts.
Most fetuses associated with incomplete moles being
spontaneously aborted. Incomplete moles are almost
always benign and have a much lower malignancy
potential than complete moles. Choriocarcinoma is
invasive, malignant trophoblastic disease that is usually
metastatic and can be fatal (Berman et al., 2004).
Signs and Symptoms
vaginal bleeding More than 95% of patients experience
which may be scant or profuse
Uterine enlargement results from the rapidly proliferating
trophoblastic tissue and the large accumulation of clotted
blood.
excessive nausea and vomiting (hyperemesis gravidarum)
and abdominal pain caused by uterine distention.
Preeclampsia may occur, usually between 9 and 12 weeks
of gestation but any symptoms of gestational hypertension
before 24 weeks of gestation may be indicative of
hydatidiform mole. Clinical and laboratory
findings include an absence of fetal heart sounds.
a markedly elevated quantitative serum hCG (may be
100,000 mIU/mL), and very low levels of maternal serum fetoprotein (MSAFP).
Management
removal of the uterine contents
The hCG levels should be assessed
every 1 to 2 weeks until hCG is
undetectable on two consecutive
hCG should be measured every 1 to 2
months for at least a year
Effective contraception is needed.
counsel the patient about different
methods of contraception
avoiding pregnancy for a year
Prognosis
Invasive moles are generally not metastatic and
respond well to single-agent chemotherapy.
Choriocarcinoma spreads to the lungs, vagina,
pelvis, brain, liver, intestines, and kidneys. Since
choriocarcinoma can occur weeks to years after any
type of gestation, patients usually present with signs
and symptoms of active metastases. The long term
prognosis depends on the degree of metastases and
the patient’s response to the chemotherapy.
SPONTANEOUS ABORTION
Not all conceptions result in a live-born infant. Of all
clinically recognized pregnancies, 10% to 20% are
lost, and approximately 22% of pregnancies detected
on the basis of hCG assays are lost before the
appearance of any clinical signs or symptoms (White
& Bouvier, 2005). By definition, an early pregnancy
loss occurs before 12 weeks of gestation; a late
pregnancy loss is one that occurs between 12 and 20
weeks of gestation.
Spontaneous abortions may be classified as the following:
• Abortus: Fetus lost before 20 weeks of gestation, wt. less than
500 g)
• Complete abortion: Complete expulsion before 20 weeks of
gestation
• Incomplete abortion: Partial expulsion of some but not all
before 20 weeks of gestation
• Inevitable abortion: No expulsion of products, but bleeding and
dilation of the cervix such that a pregnancy is unlikely
• Threatened abortion: Any intrauterine bleeding before 20 weeks
of gestation, without dilation of the cervix or expulsion
• Missed abortion: Death of the embryo or fetus before
20 weeks with complete retention these often proceed to a
complete abortion within 1 to 3 weeks but occasionally they are
retained much longer.
Etiology
It is estimated that 60% to 80% of all SABs in the first
trimester are associated with chromosomal abnormalities
Infections (e.g., bacteriuria and Chlamydia trachomatis),
maternal anatomical defects, and immunological and
endocrine factors have also been identified as causes of
early pregnancy loss, although many have no obvious
cause. Second trimester spontaneous abortions (12 to 20
weeks) have been linked to chronic infection,
recreational drug use, maternal uterine or cervical
anatomical defects, maternal systemic disease, exposure
to fetotoxic agents, and trauma (Cunningham et al.,
2005).
Diagnosis
A woman who is experiencing a spontaneous abortion
usually presents with bleeding and may also complain
of cramping, abdominal pain, and decreased symptoms
of pregnancy; cervical changes (dilation) may be
present on vaginal examination. An ultrasound is
performed for placental evaluation and to determine
fetal viability. Laboratory tests include a quantitative
level of -hCG, which should show a lower value than
when associated with a viable pregnancy. hemoglobin
and hematocrit, blood type and Rh status determination,
and indirect Coombs’ screen (Cunningham et al., 2005).
Management
Incomplete, inevitable, and missed abortions are
usually managed via a dilatation and curettage (D &
C: the cervix is dilated and a curette is inserted and
used to scrape the uterine walls and remove the uterine
contents). In the case of an incompetent cervix, an
emergent cerclage (placement of ligature to close the
cervix) may be performed. An unsensitized, Rhnegative woman should be given Rho(D) immune
globulin (RhoGAM) to prevent
INCOMPETENT CERVIX
Patients with cervical incompetence usually present
with painless dilation and effacement of the cervix,
often during the second trimester of pregnancy. They
frequently give a history of repeated second trimester
losses with no apparent etiology. Incompetent cervix is
estimated to cause approximately 15% of all second
trimester losses (Cunningham et al., 2005).
Obstetric Causes of Vaginal Bleeding
PLACENTA PREVIA
Placenta previa is an implantation of the placenta in the lower
uterine segment, near or over the internal cervical os. This
condition accounts for 20% of all antepartal hemorrhages. There
are three recognized variations of placenta previa. With a complete
(total) placenta previa, the placenta covers the entire cervical os. a
complete placenta previa presents the most serious risk. A partial
previa describes a placenta that partially occludes the cervical os.
A marginal previa is characterized by the encroachment of the
placenta to the margin of the cervical os. Placenta accreta,
percreta, and increta are placentas with abnormally fi rm
attachments to the uterine wall. Unusual placental adherence may
accompany a placenta previa.
Placenta previa may be associated with conditions that
cause scarring of the uterus such as a prior cesarean
section, multiparity, or increased maternal age. A previa
may also occur with a large placental mass as seen in
multiple gestations and erythroblastosis. Other risk
factors include smoking, cocaine use, a prior history of
placenta previa, closely spaced pregnancies, African or
Asian ethnicity, and maternal age greater than 35 years
(Clark, 2004).
Signs and Symptoms
The most common symptom is painless vaginal
bleeding. This is believed to occur from small
disruptions in the placental attachment during
normal development and the subsequent stretching
and thinning of the lower uterine segment during the
third trimester. Initially, the bleeding is usually a
small amount that stops as the uterus contracts to
close the open blood vessels. However, bleeding can
reoccur at any time and may be associated with
profuse hemorrhage and shock that leads to signifi
cant maternal and fetal mortality and morbidity. The
blood is bright red (Cunningham et al., 2005).
Diagnosis
The timing of the diagnosis of placenta previa has
undergone significant change in the last decade.
Although thirdtrimester bleeding was often the first
indicator of placenta previa, today, most cases of
placenta previa are detected ante-natally before the
onset of significant bleeding. The common practice of
second-trimester abdominal ultrasound for the
detection of fetal anomalies has led to this change.
However, because most cases of placenta previa
diagnosed in the second trimester tend to resolve as
the uterus enlarges, management of placenta previa
diagnosed in the second trimester differs from that for
the same diagnosis made during the third trimester.
In patients diagnosed before 24 weeks’ gestation, a
repeat ultrasound should be scheduled between 24
and 28 weeks’ gestation to confirm the diagnosis of
placenta previa. However, if patients experience
vaginal bleeding during this interval, they should be
managed as presumed cases of placenta previa.
Placenta previa should be suspected in all patients
who present with bleeding
PLACENTAL ABRUPTION
Placenta abruption (abruptio placenta) is the
premature separation of a normally implanted
placenta from the uterine wall. An abruption results
in hemorrhage between the uterine wall and the
placenta. 15% occur during labor, and 30% are
identified only on inspection of the placenta after
delivery (Cunningham et al., 2005).
Etiology and Classifications
At the initial point of placental separation, non clotted
blood courses from the site of injury. The enlarging
collection of blood may cause further separation of the
placenta. Bleeding can be either concealed or revealed
(apparent). A concealed hemorrhage occurs in 20% of
cases and describes an abruption in which the bleeding is
confined within the uterine cavity. The most common
abruption is associated with a revealed or external
hemorrhage, where the blood dissects downward toward
the cervix (Fig. 11-5). Placental abruption may be
broadly classified into three grades that correlate with
clinical and laboratory findings (Box 11-2).
What causes placental abruption?
The causes of placental abruption are not
completely known. However, women are
more at risk for this condition if they:
 Smoke
 Use cocaine during pregnancy
 Age over 35 y
 Have preeclampsia or hypertension
 Are pregnant with twins or triplets
 Have had a previous placental abruption
 Experience trauma to the abdomen
 Have abnormalities in the uterus
Signs and Symptoms
Vaginal bleeding (although about 20% of cases will have
no bleeding)
Uterine tenderness
Rapid contractions
Abdominal pain
Fetal heart rate abnormalities
Diagnosis
Vaginal bleeding in the third trimester of pregnancy
is the hallmark of placental abruption or placenta
previa and should always prompt an investigation to
determine its etiology. Diagnosis is made by clinical
findings
and,
when
available,
ultrasound
examination. Recent advances in ultrasound imaging
and interpretation have greatly
Classifications of Abruptio Placenta
Grade 1: Slight vaginal bleeding and some uterine
irritability are usually present.
Grade 2: External uterine bleeding is absent to moderate.
The uterus is irritable and tetanic or very frequent
contractions may be present.
Grade 3: Bleeding is moderate to severe but may be
concealed. The uterus is tetanic and painful. Maternal
hypotension is frequently present and fetal death has
occurred.
Management
The potential for rapid deterioration (hemorrhage,
disseminated intravascular coagulation [DIC], fetal
hypoxia) necessitates delivery in some cases of
placental abruption. However, most abruptions are
small and noncatastrophic, and therefore do not
necessitate immediate delivery. Certain actions,
including
hospitalization,
laboratory
studies,
continuous monitoring, and ongoing patient support
should be initiated when placental abruption is
suspected
Care for the Patient Experiencing an Abruptio Placentae
• Hospitalization
• Intravenous placement with a large-bore catheter (16-gauge)
• Labwork: Includes CBC, coagulation studies (fibrinogen, PT,
PTT, platelet count, fibrin degradation products), type and screen
for 4 units of blood Betamethasone may be given to the woman
to promote fetal lung maturity when delivery is not imminent.
• Rh(D)-negative patients should receive RhoGAM to prevent
isoimmunization.
• Continuous evaluation of intake and output
• Continuous electronic fetal monitoring
• Delivery (cesarean or vaginal birth) may be initiated depending
on the status of the mother and the fetus.
• Nursing care is centered on continuous maternal–fetal
assessment, with on-going information and emotional support
for the patient and her family.
Preterm Labor
Preterm labor (PTL) is defined as cervical changes
and regular uterine contractions occurring between 20
and 37 weeks of pregnancy. Many patients present
with preterm contractions, but only those who
demonstrate changes in the cervix are diagnosed with
preterm labor (ACOG, 2001).
Various Risk Factors Associated with Preterm
Labor and Birth
• History of preterm birth
• Uterine or cervical anomalies
• Multiple gestation
• Hypertension
• Diabetes
• Obesity
• Clotting disorders
• Infection, especially urinary tract infections
• Fetal anomalies
• Premature rupture of membranes
• Vaginal bleeding
• Late or no prenatal care
• Smoking
• Alcohol
• Domestic violence
• Age 17 years or 35 years
• Low socioeconomic status
• Stress
• Long working hours with long periods of standing
Contraindications to the Use of Tocolytics in Preterm Labor
•
Significant maternal hypertension (eclampsia, severe
preeclampsia, chronic hypertension)
• Antepartum hemorrhage
• Cardiac disease
• Any medical or obstetric condition
• Hypersensitivity to a specific tocolytic agent
• Advanced cervical dilation
• Fetal demise or lethal anomaly
• Chorioamnionitis
• In utero compromise
• Acute: nonreassuring fetal heart rate pattern
• Chronic: IUGR or substance abuse
Family Teaching Guidelines Preventing Prematurity
Freda and Patterson (2004) suggest that nurses be
proactive by educating women about preterm labor and
teaching them how to recognize the warning signs and
symptoms.
◆ Encourage all pregnant women to obtain prenatal care.
◆ Educate all pregnant women as to the signs and
symptoms of preterm labor.
◆ Eliminate the term “Braxton-Hicks” from teaching
(women may delay seeking treatment if they believe
they are only experiencing Braxton-Hicks contractions).
◆ Ask all pregnant women if they have had any symptoms
of preterm labor.
◆ Screen for vaginal and urogenital infections and treat
appropriately.
◆ Teach women about the dangers of douching.
◆ Assess all pregnant women for intimate partner violence
and intervene.
◆ Discuss stress levels early in pregnancy.
◆ Assess all pregnant women for nutritional status and
weight gain in pregnancy and intervene as necessary.
◆ Assess for illicit drug use, and help the woman get into
treatment.
◆ Encourage women who have preterm labor symptoms
to drink fl uids, lie down for 1 hour, and go to the
hospital for a vaginal exam if symptoms continue.
◆ Remind the woman with symptoms that she should
not hesitate to call her provider repeatedly if her
symptoms recur.
Premature Rupture of the Membranes
To facilitate an understanding of premature rupture of the
membranes (PROM), it is helpful to first define the various
terms used:
• Premature rupture of the membranes (PROM) is
defi ned as rupture of the membranes before the onset
of labor at any gestational age.
• Preterm rupture of membranes is defined as rupture
of the membranes before 37 completed weeks of gestation.
It is a common cause of preterm labor, preterm delivery, and
chorioamnionitis.
• Preterm premature rupture of the membranes (PPROM) is
defined as a combination of both terms—
rupture occurs before the 37th completed week of gestation
and in the absence of labor. PPROM accounts
for 25% of all cases of premature rupture of the amniotic
membranes and is respon sible for 30% to 40% of
all preterm deliveries (Cunningham et al., 2005).
PATHOPHYSIOLOGY
Premature rupture of the membranes is multifactorial.
Choriodecidual infection or inflammation appears to play an
important role in the etiology of PPROM, especially at early
gestational ages. Other factors include decreased amniotic
membrane collagen, lower socioeconomic status, cigarette
smoking, sexually transmitted infections, prior preterm delivery,
prior preterm labor during the current pregnancy, uterine
distention (e.g., multiple gestation, hydramnios), cervical
cerclage, amniocentesis, and vaginal bleeding in pregnancy
(Mercer, 2003). In many cases, the cause is not known.
DIAGNOSIS
The diagnosis is based on the patient’s history of leaking vaginal
fluid and the finding of a pooling of fluid on sterile speculum
examination. Nitrazine and fern tests confirm the diagnosis of
PROM.
The level of amniotic fluid in the uterus may also be checked via
an abdominal ultrasound examination. Leakage of amniotic fl
uid is consistent with findings of oligohydramnios (decreased
amniotic fluid).
MANAGEMENT
• Gestational age should be established based on clinical history
and prior ultrasound assessment when available.
• Ultrasound should be performed to assess fetal growth, position,
and residual amniotic fluid.
The woman should be assessed for evidence of advanced labor,
chorioamnionitis (intrauterine infection), abruptio placentae, and
fetal distress.
• Patients with advanced labor, intrauterine infection, significant
vaginal bleeding, or nonreassuring fetal testing are best delivered
promptly, regardless of gestational age. There is further debate
over the use of tocolytics, corticosteroids, and antibiotics in
patients with PPROM. Tocolysis appears to be of little benefit in
PPROM and may be harmful when chorioamnionitis is present.
However, in many hospitals, tocolytic therapy is instituted for 48
hours, especially with earlier gestational ages, in order to
administer a course of corticosteroids to enhance fetal lung
maturity (Cunningham et al., 2005).
Conservative management includes in patient observation unless
the membranes reseal and the leakage of fluid stops. This
approach initially consists of prolonged continuous fetal and
maternal monitoring combined with modified bed rest to promote
amniotic fluid accumulation and spontaneous membrane sealing.
Delivery of the fetus should be accomplished if signs of infection
are present: maternal temperature of 100.4°F (38°C) or greater,
foul-smelling vaginal discharge, elevated white blood count,
uterine tenderness, and maternal and/or fetal tachycardia.
Without intervention, approximately 50% of patients who have
ROM will go into labor within 24 hours.
maintaining the pregnancy to gain further fetal maturity can be
beneficial, prolonged PPROM has been correlated with an
increased risk of
 Chorioamnionitis
 placental abruption
 cord prolapse
Nursing interventions
explaining to the patient that she will be on:
 full or modified bed rest
 vital signs will be checked at least every 4 hours to detect
early signs of a developing infection
 intermittent fetal monitoring is appropriate
 Frequent ultrasound examinations are performed to assess
amniotic
 providing emotional support to the patient
 encourage the woman and her family members to ask
questions and express fears and concerns.
 The woman should be assessed for evidence of advanced
labor, chorioamnionitis (intrauterine infection), abruptio
placentae, and fetal distress.
Hypertensive Disorders of Pregnancy
Hypertensive disorders are the most common medical complication of
pregnancy. The incidence of hypertensive disorders is between 5% and
10%, and this complication is the second leading cause of maternal death
in the United States (embolic events are the leading cause) (Martin et al.,
2005).
Hypertensive disorders contribute significantly to stillbirth and neonatal
morbidity and mortality and can result in:
 maternal cerebral hemorrhage
 disseminated intravascular coagulation (DIC)
 hepatic failureacute renal failure
 pulmonary edema
 adult respiratory distress syndrome
 aspiration pneumonia
 abruptio placentae (ACOG, 2002a).
CLASSIFICATIONS AND DEFINITIONS
Numerous attempts have been made to accurately describe
pregnancy-related hypertensive disorders. Them NHBPEP,
2000 has recommended the following classifications:
• Chronic hypertension
• Preeclampsia–eclampsia
• Chronic hypertension with superimposed
preeclampsia
• Gestational (or transient) hypertension
Chronic Hypertension
Chronic hypertension is defined as hypertension that is present and
observable before pregnancy or hypertension that is diagnosed before
the 20th week of gestation. Hypertension is defined as a blood pressure
greater than 140/90 mm Hg. Hypertension for which a diagnosis is
confirmed for the first time during pregnancy, and which
persists beyond the 84th day postpartum, is also classified as chronic
hypertension (Roberts, 2004).
Preeclampsia and Eclampsia
Preeclampsia is a pregnancy-specific systemic syndrome clinically
defined as an increase in blood pressure (140/90) after 20 weeks’
gestation accompanied by proteinuria (NHBPEP, 2000; Peters & Flack,
2004). This increase in blood pressure represents a change from the
usual blood pressure findings during pregnancy. Under normal
conditions, the blood pressure increases during the first trimester,
decreases in the second trimester, and
Chronic Hypertension with Superimposed Preeclampsia
According to Roberts (2004), the following criteria are necessary to establish a
diagnosis of superimposed preeclampsia:
1. Hypertension and no proteinuria early in pregnancy (prior to 20 weeks’
gestation) and new-onsetproteinuria, (defined as the urinary excretion of 0.3 g
of protein in a 24-hour specimen)
2.
3.
4.
5.
Hypertension and proteinuria before 20 weeks’ gestation: • A sudden increase
in protein—urinary excretion of 0.3 g protein or more in a 24-hour specimen,
or two dipstick test results of 2 (100 mg/dL), with no evidence of urinary tract
infection
A sudden increase in blood pressure in a woman whose blood pressure has
been well Controlled
Thrombocytopenia (platelet count lower than 100,000/mm3)
An increase in the liver enzymes alanine transaminase (ALT) or aspartate
transaminase (AST) to abnormal levels
Gestational (or Transient) Hypertension
This is a non specific term used to describe the woman who
has a blood pressure elevation detected for the first time during
pregnancy, without proteinuria. This term is used only until a
more specific diagnosis can be assigned postpartum. If
preeclampsia does not develop (e.g., protein does not become
present in the urine), and the woman’s blood pressure falls into
a normal range by 12 weeks postpartum, the diagnosis of
transient hypertension of pregnancy can be made (Roberts,
2004).
Preeclampsia
PATHOPHYSIOLOGY
The normal physiological adaptations to pregnancy are altered in the woman
who develops preeclampsia. Preeclampsia is a multisystem, vasopressive
disease process that targets the cardiovascular, hematologic, hepatic, renal, and
central nervous systems. Preeclampsia is associated with a clinical spectrum of
events that range from mild to severe with a potential endpoint of eclampsia.
Patients do not suddenly “catch” severe preeclampsia or develop eclampsia but
rather progress in a fairly predictable course through the clinical spectrum.
In most cases, the progression is relatively slow, and the disorder may never
proceed beyond mild preeclampsia. in other situations, the disease can progress
more rapidly, and change from a mild to a severe form in a matter of days or
weeks. In the most serious cases, the progression can be rapid: mild
preeclampsia evolves to severe preeclampsia or eclampsia over hours or days
(Roberts, 2004). Hence, the nurse must alert the patient to signs and symptoms
that signal a worsening condition
and continuously assess the patient for any change.
Risk Factors for Preeclampsia
• Primigravida (6–8 times greater risk)
• Age extremes (17 years and 35 years)
• Diabetes
• Preexisting hypertension
• Multiple gestation (5 times greater risk)
• Fetal hydrops (10 times greater risk)
• Hydatidiform mole (10 times greater risk)
• Preeclampsia in a previous pregnancy
• Family history
• Obesity
• Immunological factors
• Chronic renal disease
• Rh incompatibility
• African-American ethnicity
Home Management of the Pregnant
Patient with a Hypertensive Disorder
Before discharge, it is important to ascertain that the home environment is
conducive to rest and the patient will be able to rest frequently throughout the
day. It is essential that the patient can verbalize understanding of the
importance of keeping all prenatal appointments and that she must
immediately notify her physician or midwife at the first appearance of:
◆ higk Blood pressure
◆ Visual changes
◆ Epigastric pain
◆ Nausea and vomiting
◆ Bleeding gums
◆ Headaches
◆ Increasing edema, especially of the hands and face
◆ Decreasing urinary output
◆ Decreased fetal movement
◆ “Just not feeling right”
Nursing Implications: Remember that this is a very potent, high alert
drug!
Explain purpose and side effects of the medication to the patient and
her companion.Explain that she may feel very warm and become fl ushed and
experience nausea and vomiting, visual blurring, and headaches. Magnesium
sulfate must never be abbreviated (i.e., MgSO4 is not
acceptable) and requires a written order by the physician for administration.
Always use an infusion pump for administration and run the medication
piggyback, not as the main line. Monitor pulse, blood pressure, respirations, and
ECG frequently throughout parenteral administration. Respirations should be at
least 16/min before each dose. Monitor neurological status before and throughout
therapy. Institute seizure precautions
Keep the room quiet and darkened to decrease the likelihood of triggering
seizure activity Patellar reflexes should be tested before each parenteral dose of
magnesium sulfate. If absent, no additional dose should be administered until a
positive response returns. Monitor intake and output. Urine output should be
maintained at a level of at least 100 mL/4 hr.
• Correct maternal acidemia. Blood gas analysis allows monitoring
of oxygenation and pH status. Respiratory acidemia is possible after
a seizure.
• Avoid polytherapy. Maternal respiratory depression, respiratory
arrest, or cardiopulmonary arrest is more likely in women who
receive polytherapy to arrest a seizure. Remember that
anticonvulsants are respiratory depressants and may interact.
• Be sure to check the fetus or fetuses (all must be accounted
for). After a seizure there may be loss of FHR variability and
bradycardia on the fetal monitoring tracing.
• Check the patient for ruptured membranes, contractions, and cervical
dilation.
• Prepare for delivery as indicated.
• Support the patient and her family. This is a very frightening
event for them and they will need reassurance and to be kept
aware of the plan of care and the well-being of their baby
critical nursing action Care of the Pregnant
Patient Post-seizure
• Do not attempt to shorten or abolish the initial seizure. Attempts to
administer anticonvulsants intravenously without secure venous
access can lead to phlebitis and venous thrombosis.
• Prevent maternal injury.
• Maintain adequate oxygenation; administer oxygen via face mask
at 10 L/min
• Minimize the risk of aspiration. Position the patient on her side
to facilitate drainage. Suction equipment should be ready and
working.
• Give adequate magnesium sulfate to control seizures. As soon
as possible following the seizure, venous access should be
secured with a 4- to 6-g loading bolus of magnesium sulfate
given over 15–20 minutes. If the patient seizes following the
loading dose, another 2-g bolus may be given intravenously,
over 3–5 minutes.
•
Correct maternal acidemia. Blood gas analysis allows monitoring
of oxygenation and pH status. Respiratory acidemia is possible after
a seizure.
• Avoid polytherapy. Maternal respiratory depression, respiratory
arrest, or cardiopulmonary arrest is more likely in women who
receive polytherapy to arrest a seizure. Remember that
anticonvulsants are respiratory depressants and may interact.
• Be sure to check the fetus or fetuses (all must be accounted
for). After a seizure there may be loss of FHR variability and
bradycardia on the fetal monitoring tracing.
• Check the patient for ruptured membranes, contractions, and cervical
dilation.
• Prepare for delivery as indicated.
• Support the patient and her family. This is a very frightening
event for them and they will need reassurance and to be kept
aware of the plan of care and the well-being of their baby
•
HELLP Syndrome
HELLP is an acronym for:
Hemolysis, Elevated Liver enzymes and Low Platelets Due to the arteriolar
vasospasms in the cardiovascular system that occur in preeclampsia, the circulating
red blood cells (RBCs) are destroyed as they try to navigate through the constricted
vessels (Hemolysis). Vasospasms decrease blood fl ow to the liver, resulting in
tissue ischemia and hemorrhagic necrosis (Elevated Liver enzymes). In response to
the endothelial damage caused by the vasospasms (small openings develop in the
vessels), platelets aggregate at the site and a fi brin network is set up, leading to a
decrease in the circulating platelets (Low Platelets).
HELLP syndrome is a serious complication of preeclampsia that can manifest
itself at any time during pregnancy and the puerperium, but like preeclampsia, it is
rare before 20 weeks’ gestation. However, unlike preeclampsia, HELLP syndrome
occurs more often in Caucasians, multiparas, and in women older than 35 years.
One third of all cases of HELLP syndrome occur during postpartum, and only 80%
of these patients are diagnosed with preeclampsia
before delivery (Sibai et al., 2005).
HELLP syndrome is actually a laboratory diagnosis for a variant of
severe preeclampsia. The primary presentation is consistent with hepatic
dysfunction evidenced by fi ndings from the patient’s liver function tests
(ACOG, 2002a; Poole, 2004b). HELLP syndrome is characterized by
rapidly deteriorating liver function and thrombocytopenia. Liver capsule
distention often produces epigastric pain. Though rare, liver rupture is
one of the most ominous consequences of severe preeclampsia/HELLP
syndrome, with a reported maternal death rate of more than 30%.
The precise cause of liver rupture is unknown, but the prevailing theory
postulates that the increased hepatic pressure leads to rupture. It is
theorized that endothelial dysfunction with intravascular fi brin deposits
and hepatic sinusoidal obstruction leads to intrahepatic vascular
congestion, increased intrahepatic pressure, and distention of Glisson’s
capsule. This pathological process progresses tothe development of a
subcapsular hepatic hematoma and subsequent liver rupture (ACOG,
2002a; Cunningham
et al., 2005).
Therapy for HELLP syndrome centers on improving the
platelet count by transfusion of fresh-frozen plasma or
platelets and delivery as soon as feasible by vaginal or
cesarean birth. Intrapartum nursing care involves
continuous maternal–fetal monitoring. Measurement of
central venous pressure or pulmonary arterial wedge
pressure (Swan–Ganz catheter) may be required to monitor
fl uid status accurately when pulmonary edema or acute
renal failure are present (ACOG, 2002a).