Vanessa came to the clinic

for check up. She missed

her period about 2 weeks
already and she complains
of excessive vomiting.
 Severe and unremitting nausea and
vomiting that persists after the first
trimester.
 Usually occurs with the first pregnancy
and commonly affects pregnant women
with conditions that produce high levels
of human chorionic gonadotropin
(hCG), such as gestational trophoblastic
disease or multiple gestations.
 Exact cause is unknown, but it’s linked
to trophoblastic activity, gonadotropin
production, and psychological factors
 Various possible causes
-Pancreatitis (elevated serum amylase
levels are common)
-Biliary tract disease
-Decreased secretion of free
hydrochloric acid in the stomach
-Decreased gastric motility
-Drug toxicity
-Inflammatory obstructive bowel
disease
-Vitamin deficiency (especially of B6)
-Psychological factors (in some cases)
-Transient hyperthyroidism
 Unremitting nausea and vomiting
(cardinal sign), with the vomitus usually
containing undigested food, mucus, and
small amounts of bile initially,
progressing to containing only bile and
mucus and finally, blood and material
resembling coffee grounds
 Reports of substantial weight loss and
eventual emaciation
 Thirst
 Hiccups
 Oliguria
 Vertigo
 Headache
 Electrolyte imbalance
 Dehydration
 Metabolic acidosis
 Jaundice
 Decreased serum protein, chloride,
sodium, and potassium levels
 Increased blood urea nitrogen levels
 Elevated hemoglobin levels
 Elevated white blood cell (WBC) count
 Ketonuria and slight proteinuria
 Restoration of fluid and electrolyte
balance with I.V. fluid therapy
 Control of vomiting with an antiemetic
 Maintenance of adequate nutrition and
rest
 Progression of diet to oral feedings as
tolerated (clear liquid diet, then a full
liquid diet and finally, small, frequent
meals of high-protein solid foods); if
necessary, total parenteral nutrition
 Administer I.V. fluids as ordered until
the patient can tolerate oral feedings
 Monitor fluid intake and output, vital
signs, skin turgor, daily weight, serum
electrolyte levels, and urine ketone
levels; anticipate the need for electrolyte
replacement therapy
 Provide frequent mouth care
 Consult a dietitian to provide a diet high
in dry, complex carbohydrates
 Suggest company, diversionary
conversation, and decreased liquid
intake at mealtime
 Instruct the patient to remain upright
for 45 minutes after eating to decrease
reflux
 Suggest that the patient eat two or three
days crackers on awakening in the
morning, before getting out bed, to
alleviate nausea
 Provide reassurance and calm, restful
atmosphere
 Encourage the patient to discuss her
feelings about her pregnancy and the
disorder
 Help the patient develop effective
coping strategies
-Refer her to a mental health
professional for additional counseling,
if necessary
-Refer her to the social service
department for help in caring for other
children at home, if appropriate
 Teach the patient protective measures to
conserve energy and promote rest,
including relaxation techniques; the
importance of fresh air and moderate
exercise, if tolerated; and activities to
prevent fatigue
 Substantial weight loss
 Starvation, with ketosis and acetonuria
 Dehydration, with subsequent fluid and
electrolyte imbalances (hypokalemia)
 Acid-base imbalances (acidosis and
alkalosis)
 Retinal, neurologic, and renal damage
 Tinay, a 19 year old primigravida has
gained a total of 20 pounds since her last
clinic visit. Upon examination, the nurse
has obtained the following findings: BP
130/90 mmHg, proteinuria +2, puffiness
of the face and lower extremity edema.
 A potentially life threatening disorder
that usually develops after the 20th
week of pregnancy
 Most common in nulliparous patients
 Most common cause of maternal death
in developed countries
 Can occur pospartally: seizures develop
within 6-24 hours after birth
 Preeclampsia
 Nonconvulsive form of the disorder
 Develops in about 7% of pregnancies and
may be mild or severe
 Marked by the onset of hypertension after
20 weeks’ gestation
 Higher in low socio-economic groups
 Eclampsia
 Convulsive form of the disorder
 Occurs between the 24th week of
gestation and at the end of first
postpartum week
 Incidence increases among women who
are pregnant for the first time, multiple
fetuses and have a history of vascular
diseases.
 Exact cause is unknown
 Systemic peripheral vasospasm occurs, affecting
every organ system
 Geographic, ethnic, racial, nutritional,
immunologic and familial factors may contribute
to preexisting vascular disease, which, in turn, may
contribute to its occurrence
 Age is also a factor; adolescents younger than age
19 and primiparas older than age 35 are at higher
risk
 History of systemic vasospasm

Effects on the vascular Effects on the renal

Effects on the
system system
interstitial tissue

Vasoconstriction Reduced GFR

Increased glomerular Fluid diffusion from
membrane vascular space into
Permeability interstitial space
Impaired organ
perfusion
Increased serum BUN and Crea
Edema

Hypertension Oliguria and proteinuria

 Blood pressure over 140/90 mm Hg
 Increase in generalized edema
 sudden weight gain of more than 5 lb (2.3kg)
per week
 Usually appears between the 20th to 24th
weeks of gestation and disappears within 42
days after delivery
 A final diagnosis usually deferred
 increased blood urea nitrogen, creatinine, and
uric acid levels
 frontal headaches
 blurred vision
 Hyperreflexia
 Nausea and vomiting, epigastric pain
 Irritability
 cerebral disturbances
 Triad of symptoms: “HEP”
 Hypertension
 Edema
 Proteinuria (specifically
albuminuria)
 Mild Preeclampsia
 Sudden, excessive weight gain of 1-5
lbs per week
 Systolic BP of 140, or increase of 30
mmHg or more and a diastolic of
90, rise of 15 mmHg or more
 Proteinuria of 0.5 gms/liter or more
 Severe pre-eclampsia
 BP of 160/110 mmHg
 Proteinuria of 5 gm/liter or more in
24 hours
 Oliguria of 400 ml or less in 24
hours (normal urine output/day =
1500 ml)
 Cerebral or visual disturbances
 Pulmonary edema and cyanosis
 Epigastic pain
 Eclampsia
 presence of “convulsions”
 Signs & symptoms as in
preeclampsia plus
 Increased BUN
 Increased Uric Acid
 Decreased Co2 combining power
 Mild Preeclampsia Severe Preeclampsia Eclampsia
•Sudden, excessive •BP of 160/110 mmHg. •(The main difference
weight gain of 1-5 lbs •Proteinuria of 5 between preeclampsia
per week (earliest sign gm/liter or more in 24 and eclampsia is the
of preeclampsia) due to hours. presence of
edema which is •Oliguria of 400 ml or “convulsions” in
persistent and found in less in 24 hours (normal eclampsia).
the upper half of the urine output/day = 1500 •Sgns & symptoms as in
body (e.g. inability to ml) preeclampsia plus:
wear the wedding ring). •Cerebral or visual Increased BUN
•Systolic BP of 140, or disturbances. Increased Uric Acid
increase of 30 mmHg or •Pulmonary edema and Decreased Co2
more and a diastolic of cyanosis. combining power
90, rise of 15 mmHg or •Epigastic pain
more, taken twice 6 (considered ab “aura” to
hours apart. the development of
•Proteinuria of 0.5 convulsions.
gms/liter or more
 Proteinuria
 In preeclampsia, more than 300
mg/24 hours [1+]
 In eclampsia, 5 g/24 hours [5+] or
more
 High-protein diet with adequate fluid intake
with restriction of excessively salty foods
 Diet:
 For mild preeclampsia – high protein, high
carbohydrate, moderate salt restriction
 For severe eclampsia – high protein, high
calorie and salt-poor (3 gms of salt per day)
 Bed rest in a lateral position
 Close observance of blood pressure, fetal heart
rate, edema, proteinuria, and signs of pending
eclampsia
 Administration of antihypertensive, such as
methyldopa and hydralazine (Apreszide)
 Administration of magnesium sulfate
 Signs and symptoms of magnesium sulfate
toxicity must be promptly identified and
management initiated
 Calcium gluconate kept at the bedside
 Nonstress tests every one to two times per week
 Biophysical profile every 3 weeks
 Monitor the patient regularly for changes vital
signs, fetal heart rate
 Monitor level of consciousness, and deep
tendon reflexes and for headache unrelieved by
medication
 Do the following before administering
medication
 Observe the patient for signs of fetal
distress by closely monitoring the
results of stress and nonstress tests
 Keep emergency resuscitative
equipment and an anticonvulsant
readily available
-Maintain a patent airway and have oxygen readily
available
-Prepare for emergency cesarean delivery if
indicated
-Maintain seizure precautions to protect the
patient from injury; never leave unattended any
patient whose condition is unstable
 If the patient is receiving magnesium sulfate I.V.,
administer the loading dose over 15 to 30 minutes
and then maintain the infusion at a rate of 1 to 2
g/hour
 Carefully monitor the I.V. infusion of magnesium
sulfate, watching for signs and symptoms of
toxicity
 Keep calcium gluconate readily available at the
bedside
 Monitor the extent and location of edema, and
take the necessary precautions
 Elevate affected extremities to
promote venous return
 Avoid constricting hose, slippers, or
bed linens
 Assess fluid balance
 Provide a quiet, darkened room until the
patient’s condition stabilizes
 Enforce absolute bed rest
 Provide emotional support for the patient and
family
 Encourage them to verbalize their feelings
 Help the patient and her family to develop
effective coping strategies
 seizures (eclampsia)
 maternal mortality in eclampsia is 10%
to 15%
 Severe complications includes:
 cerebral edema
 Stroke
 abruption placentae with or without
disseminated intravascular coagulation
 fetal death.
 Refers to category of gestational
hypertension that primarily involves
changes in blood components and
liver functions
 HELLP stands for hemolysis, elevated
liver enzymes and low platelets
 As many as 12 % of patients with
gestational hypertension develop
HELLP syndrome
 occurring in both primigravidas
and multigravidas
 Patients with severe preeclampsia
are at high risk for developing this
syndrome.
 When it occurs, maternal and
infant mortality is high (about one-
fourth of the mothers and one-
third of the infants)
 After birth, laboratory results
returns to normal
 Exact cause is unknown
 Proposed caused:
 Hemolysis is believed to result
from damage to erythrocytes as
they pass through small
damaged blood vessels
 Elevated liver enzyme levels are
believed to result from obstruction
in liver flow by fibrin deposits
 Low platelet count is believed to be
the result of vascular damage
secondary to vasospasm.
 Pain
 Nausea and vomiting
 General malaise
 Severe edema
 Right upper quadrant possibly
tender on palpation
 Signs and symptoms of
preeclampsia
 Hemolysis of RBCs on a peripheral blood
smear)
 Thrombocytopenia
 Elevated liver enzyme levels alanine
aminotransferase and serum aspartate
aminotransferase
 Intensive care management for the patient and
her fetus
 Drug therapy, such as magnesium sulfate
 Transfusions and fresh frozen plasma or platelets
 Delivery of the fetus, either vaginally or by the
cesarean delivery, as soon as possible
 Assess maternal vital signs and FHR frequently
 Be alert for signs and symptoms of complications
 Maintain a quiet, calm, dimly lit environment
 Avoid palpating the abdomen
 Institute bleeding precautions
 If the patient develops hypoglycemia, expect to
administer I.V. dextrose solutions
 Patient may not be a candidate for epidural
anesthesia
 Assess the patient carefully throughout labor
and delivery for possible hemorrhage
 Fetal or maternal death
 Hemorrhage
 Hypoglycemia
 Subcapsular liver hematoma
 Renal failure
 Xan, 20 years old, 34 weeks
gestation is rushed to the
emergency room because of
passage of fluid per vagina.
 Also termed hydramnios
 Refers to an abnormally large amount of
amniotic fluid in the uterus
 amniotic fluid is greater than 2,000 ml
 Fluid may have increased gradually (chronic
type) by the third trimester or rapidly (acute
type) between 20 and 24 weeks’ gestation
 Exact cause unknown in about 35% of all cases
 It may be associated with:
 diabetes mellitus (about 25%)
 erythroblastosis (about 10%)
 multiple gestations (about 10%)
 anomalies of the central nervous
system, such as neural tube defects
 GI anomalies that prevent ingestion of
the amniotic fluid (about 20%)
 Normally, amniotic fluid is produced by
the membrane cells and from fetal urine
-This fluid is swallowed by the fetus and
then absorbed through the intestinal
membranes, eventually being
transferred across the placenta
-With polyhydramnios, fluid accumulates
due to a problem with the fetus’s ability
to swallow or absorb the fluid or due to
overproduction of urine
 Signs and symptoms depends:
 length of gestation
 the amount of amniotic fluid
 whether the disorder is chronic or
acute
 Mild signs and symptoms include:
 abdominal discomfort
 slight dyspnea
 edema of feet and ankles
 Severe signs and symptoms include:
 severe dyspnea
 Orthopnea
 edema of the vulva, legs, and
abdomen
 Symptoms common to mild and severe cases
include:
 uterine enlargement greater than
expected for the length of gestation
 difficulty in outlining the fetal parts
and in detecting fetal heart sounds
 Ultrasonography reveals evidence
of excess amniotic fluid
 It also reveals underlying
conditions
 High-protein, low-sodium diet
 Mild sedation
 Indomethacin (Indocin), which crosses
the placenta to decrease fetal urine
production leading to a decrease in
amniotic fluid
 Amniocentesis to remove excess fluid
 Induction labor if the fetus is mature
and symptoms are severe
 Maintain bed rest to aid in increasing
uteroplacental perfusion and
decreasing pressure on the cervix
 Monitor the patient for signs and
symptoms of premature labor
 Encourage the patient to avid
straining on defecation
 Immediately report any
complaints of increasing dyspnea
 Monitor vital signs frequently,
including fetal heart rate for
changes
 Prepare the patient for
amniocentesis and possible labor
induction as appropriate
 Prolapsed umbilical cord when
membranes rupture
 Increased incidence of
malpresentations and increased
perinatal mortality from fetal
malformations and preterm deliveries
 Increased incidence of postpartum
maternal hemorrhage
 Amniotic fluid volume is severely
reduced (typically, the amount is less
than 500 ml at term) and the fluid is
highly concentrated
 May result in prolonged, dysfunctional
labor usually beginning before term
 Places the fetus at risk for various conditions
 Renal anomalies
 Pulmonary hypoplasia
 Wrinkled, leathery skin
 Increased skeletal deformities
 Fetal hypoxia
 Exact cause is unknown
 The condition is associated with
obstruction of the fetal urinary tract
 in some cases, fetal kidneys fail to
develop
 Placental blood flow is inadequate;
premature rupture of the membranes
may occur
 Patients are typically asymptomatic

Diagnostic test findings

 Ultrasonography reveals no pocket
larger than 1 cm
 Close medical supervision of the
mother and fetus
 Fetal monitoring
 Amnionifusion
 Monitor maternal and fetal status closely
 Monitor vital signs and fetal heart rate
patterns
 Monitor maternal weight gain pattern,
notifying health care provider if weight
loss occurs
 Provide emotional support before,
during, and after ultrasonography
 Assist parents with coping measures if
fetal anomalies are suspected
 Instruct the mother in signs and
symptoms of labor, including possible
danger signs
 Reinforce the need for close supervision
and follow-up
 Assist with amnioinfusion as indicated
 Encourage the patient to lie on her left
side to prevent pressure on the vena cava
 Ensure that solution is warmed to
patient’s body temperature to prevent
chilling of the mother and fetus
 Continuously monitor vital signs and
fetal heart rate during procedure
 Note development of any uterine
contractions, notify the health care
provider, and continue to monitor
closely
 Maintain strict sterile technique
during the procedure
 Watch for continuous fluid drainage
via the vagina; report any sudden
cessation of fluid flow
 Dystocia
 Umbilical cord compression
 Abnormalities in FHR patterns, such as
variable decelerations and reduced
variability