GESTATIONAL CONDITIONS

HYPEREMESIS GRAVIDARUM
– Also known as pernicious vomiting
– Persistent nausea and vomiting of pregnancy that
is prolonged after the first trimester or is so
severe that dehydration, nutritional deficiencies,
acidosis and significant weight loss occur within
the 1st trimester.
 HYPEREMESIS GRAVIDARUM
• Incidence:
– 2% in pregnant women
– peak incidence occurs between 8-12 weeks AOG
usually resolving in the 16th.
• Causes:
– The exact pathology is not clearly understood
– Elevated HCG that disrupts normal activity of GIT by
causing reverse peristalsis
– Thyroid dysfunction\psychological stress –
depression, anxiety and interpersonal problems.
 HYPEREMESIS GRAVIDARUM
• Assessment:
• Excessive vomiting not relieved by ordinary
medications persisting beyond 12 weeks AOG.
• Signs of DHN – thirst, dry skin, increased pulse
rate, weight loss, concentrated urine and
elevated hematocrit in CBC
• fluid and electrolyte imbalance
• ketonuria
 Management:
HYPEREMESIS GRAVIDARUM
• differential diagnosis – rule out other possible
disorders associated with hyperemesis by tests like
liver and thyroid functions, urinalysis and CBC (monitor
blood chemistries).
• monitor I&O
• Diet:
– NPO for the 1st 24 hours – IVF with added B vitamin
– After 24 hours – clear fluid then small quantities of dry
toast, crackers, or cereal every 2 or 3 hours, then gradually
advances to a soft diet, then to DAT
– At home: take dry crackers, frequent feedings and sips of
water to avoid gastric provocation and distention, avoid
hot and very cold food and beverages
 Management:
HYPEREMESIS GRAVIDARUM
• Complementary therapy – i.e. use of ginger to
expel flatus and aroma relieves nausea
• administer anti-emetic drugs as ordered
• avoid noxious stimuli that may precipitate
nausea (tight clothing, iron supplement, spicy
foods, strong odors, loud noises and bright
lights)
• enough relaxation and rest
• enteral or total parenteral nutrition
 Management:
HYPEREMESIS GRAVIDARUM
• hospitalization when severe DHN and F and E
imbalance.
– IV fluids (LRS)
– Vitamin supplements
– NPO for 24-48 hours until nausea subsides
– Oral intake is started after patient is properly
hydrated and nausea subsides
– Give anti-emetics before meals
– Gradual feeding
– Small frequent feedings
– Do not force to eat
 HYPEREMESIS GRAVIDARUM
• Fetal/Neonatal Risks
– Intrauterine Growth Restriction (IUGR)
– Low-birthweight
– Preterm birth
 ECTOPIC PREGNANCY
– Implantation of fertilized ovum in a site other than
the endometrial lining of the uterus (outside the
uterus)
– 7.7% to 20% of cases will suffer a repeat ectopic
pregnancy
– Sites at which ectopic pregnancy may occur
• fallopian tube
• ovary
• cervix
• intestine
• Risk Factors:
• Obstruction
– chronic salphingitis and pelvic inflammatory
disease (PID), STD’s
– congenital malformations
– previous tubal surgery
– uterine tumor pressing on the proximal end of the
tube
• Others:
– use of IUDs for contraception
– smoking
– history of ectopic pregnancy
 Causes:
• mechanical factors – conditions that delay the
passage of ovum in the oviducts and prevent it
from reaching the uterus in time for
implantation. (obstruction)
– Salphingitis
– Peritubal adhesions, kinking and narrowing
– Diverticula formation
– Previous ectopic pregnancy
– Previous tubal operations
– Tubal tumors
– Past induced abortions
 Causes:
• Functional factors
– External migrations of the ovum
– Menstrual reflux
– Altered tubal motility associated with use of IUD,
progestin only contraceptives, morning-after pill
• Assisted reproduction
– Ovulation induction associated with fertility drugs
such as Clomid
– Gamete intrafallopian transfer
– In vitro fertilization
– Ovum transfer
 Causes:
• Failed contraception
– IUD
– Oral contraceptives
– Condom and diaphragm
– Tubal ligation
– Hysterectomy
 Types:
• Tubal: more than 95% occur in the fallopian
tube
– Ampulla is the most common site of implantation.
55%, ruptures at 8-12 weeks
– Isthmic-25%, usually ruptures early at 6 weeks
– Fimbrial- 17%
– Interstitial-2%
– Bilateral- very rare
• Ovarian-0.5%
 Types:
• Abdominal- 1/15,000 pregnancies
– Primary – original implantation outside the tube
– Secondary- implantation is in tube or ovary then
implanted on the abdomen after rupture
– Pregnancy terminates depending on site of
implantation, some carry till term and fetus dies,
it may become mummified and calcified
(lithopedion) or an adipocere (fatty replacement)
• Cervical
 Assessment:
– Normal symptoms of pregnancy
– Vaginal bleeding -painless in cervical implantation
– One-sided lower abdominal pain – sudden knife like
pain
– Referred shoulder pain
– Aries-Stella reaction – uterus will not enlarge as in
normal pregnancy
– Adnexal Mass or tenderness
– Cullen’s sign - bluish discoloration around the
umbilicus due to internal bleeding
– Hard board like abdomen
– Shock signs – cyanosis, pallor, cold clammy skin,
tachycardia, hypotension and oliguria
 Diagnosis:
• Transvaginal UTZ
• Serial HCG determination - in ectopic, HCG is lower
than expected for gestational time and does not
double normally. (HCG doubles every 48-72 hours)
• Culdocentesis aspiration of bloody fluid from cul-de-
sac of douglas
• Serum progesterone levels – a result of greater than
25 nanogram/ml is usually associated with normal
viable pregnancy. A serum level of less than 5 ng/ml
is associated with abortion or ectopic.
 Diagnosis:
• Uterine curettage – to distinguish non viable
pregnancy or ectopic pregnancy
• , if not chorionic villi is obtained from the uterus,
ectopic pregnancy is suspected.
• Colpotomy- direct visualization of oviducts and ovaries
• Laparascopy – visualization of pelvis using a fiber optic
glass
• CBC rate of falling hematocrit can discriminate slow
internal bleeding or sudden hemorrhage of a ruptured
tube
• Elevations in WBC and rule out appendicitis or PID.
 Management
• For unruptured pregnancy – therapeutic
abortion by Methotrexate (chemo drug) IV or
IM
• Salphingectomy – removal of tube
• Oophorectomy
• Hysterectomy
• Products of conception should be completely
removed to prevent new growth of
trophoblastic tissue
GESTATIONAL TROPHOBLASTIC
DISEASE (H-MOLE)
• Abnormal proliferation followed by
the degeneration of the trophoblastic
villi
 Two Distinct types
a. Complete molar pregnancy
– Have only placental parts, forms when a sperm fertilizes
an empty egg
– The chromosome are either 46XX or 46XY but are
contributed by only one parent and the chromosome
material is duplicated.
– It usually leads to carcinoma
 
b. Partial Mole
– It has 69 chromosome in which there are three
chromosomes for every pair instead of two. 23 from the
mother and 2 sets from the father. This could occur when
two cells fertilize one egg.
– It rarely leads to carcinoma
 Assessment:
• Risk factors:
– Higher occurrence in asian
– Women below 18 and above 40 years old
– Women with low socioeconomic status who
have low protein intake
– History of molar pregnancy
 Assessment:

• Signs and Symptoms:

– Uterus larger than expected for the duration of
the pregnancy
– Abdominal cramping from uterine distention
– Vaginal Bleeding
– Vaginal discharge of clear, fluid –filled vesicles
– S/Sx of preeclampsia before 20 weeks’ gestation
 Assessment:
• Signs and Symptoms:
– Severe nausea and vomiting
– HCG serum levels are abnormally high
– Ultrasound reveals characteristic appearance of
molar growth
– Absence of FHR
– s/Sx of anemia
 Management:
• Suction Curettage or dilatation and curettage
to remove mole
• Serum hCG monitoring – HCG should be
monitored for 1 year and should be negative
2-8 weeks after removal of mole. It is
monitored every 2 weeks until normal then
monthly for 6 months then every 2 months for
the next 6 months.
 Management:
• Chest x ray may also be done every 3 months
for 6 months because H- mole cancer cells can
metastasize to lungs.
• Oral Contraceptive use for 1 year- the woman
is advised not to get pregnant yet and pills
should not contain estrogen
• Methotrexate – anti cancer drug for one year
to prevent development of malignancy
• Hysterectomy
 Complications:
• Gestational trophoblastic tumors
– Choriocarcinoma – chorionic villi becomes cancer
cells, can be transferred to different parts of body
by circulation and ymphatic drainage
– Invasive mole – excessive formation of
trophoblastic villin that penetrates myometrium
– Placental site trophoblastic tumor – cancer cells
arising form the placental site
 INCOMPETENT CERVIX
• Characterized by a painless dilation of the
cervical os without contractions of the uterus,
dilation of cervix prematurely (more than 3 cm),
chief cause of habitual abortion due to
mechanical defect that occurs in the 2nd to early
3rd trimester followed by prolapsed of
membranes into the vagina, rupturation of
membranes and expulsion of products of
conception.
• 20-25% of all second trimester losses.
 Etiology:
• Congenital Factors
• Acquired Factors
• Infection
• Inflammation
• Subclinical uterine activity
• Cervical trauma
• Cone biopsy or Late second trimester elective abortion
• Multiple gestation
• Biochemical/Hormonal Factors
• Increased relaxin levels
 Assessment:
• Associated findings:
– History of cervical trauma
– History of repeated, spontaneous, second trimester
terminations.
– Possibly spontaneous rupture of membranes

• A common clinical manifestation is appreciable

cervical dilatation with prolapsed of the
membranes through the cervix without
contractions.
 Diagnosis:
• Manually by pelvic examination/internal
examination to assess dilatation and
effacement degree
• Ultrasonography to view cervical os and canal.
Diagnosis is made if dilatation is greater than
2.5 cm or length of cervix is shortened to 20
mm. sometimes funneling is also seen where
the internal portion of internal os has begun
to efface.
 Signs and symptoms:
• Painless vaginal bleeding/pinkish
show accompanied by cervical
dilatation
• Rupture of membranes and passage
of amniotic fluid
 Management:
• bed rest
• avoidance of heavy lifting
• abstinence to sexual activity
 Management:
• cervical cerclage – suturing of cervix at around
14 weeks AOG to prevent dilatation
(requisites: cervix has not dilated beyond 3
cm, membranes are intact, and no vaginal
bleeding and uterine clamping)
– Mcdonald- temporary and stitches are removed
by 38-39 weeks AOG to allow vaginal delivery, it is
necessary to remove sutures before labor begins
to prevent lacerations
– Shirodkar – permanent, fetus is delivered by CS
 Management:
• After suturing:
– Bedrest for 24 hours to several days
– Observe for bleeding, uterine contractions, and
rupture of BOW
– Report passage of fluid or signs of ruptured BOW,
sutures then are removed to prevent infection
– If contractions occur, Ritodrine is given to stop it
– Restrict activities for 2 weeks after procedure
(sex)
 SPONTANEOUS ABORTION
– Most common bleeding disorder in early
pregnancy
– The expulsion of the fetus and other
products of conception from the uterus
before the fetus is viable (viability) that is
before 20 weeks AOG from LMP or before
the fetus weighs 500 grams.
– Spontaneous abortion occurs in 15-20% of
recognized pregnancy.
• Early abortion - Before 12 weeks AOG
• Late abortion – 12-20 weeks AOG, where bleeding is
more likely since definitive placenta and blood supply
has begun to form
• Abortus - fetus that is aborted weighing less than 500
grams
• Occult pregnancy – zygote aborted before pregnancy is
diagnosed/recognized
• Blighted ovum – small macerated fetus, sometimes
there is no fetus surrounded by fluid inside an open sac
• Lithopedion – calcified fetus/embryo
• Premature infant – infant delivered having birthweight
of 500-1000 grams
 Etiology:
Fetal causes

• Developmental anomalies – 60% of cases

• Chromosomal abnormalities
• Implantation abnormalities
 Etiology:
Maternal factors

• Age – risk increases with increasing age

– Below 35 years old – 15%
– Between 35-39 years old – 20-25%
– Between 40-42 years old – 35%
– Above 42 years old - > 50%
 Etiology:
Maternal factors

• Structural abnormalities of reproductive tract

– Congenital uterine defects
– Cervical incompetencies
• Inadequate progesterone production
• Systemic infection – rubella virus,
cytomegalovirus, toxoplasmosis
 Etiology:
Maternal factors

• Chronic maternal diseases

– Polycystic ovary syndrome
– Uncontrolled DM
– Renal disease
– Systemic Lupus Erythromatosus
– Untreated thyroid disease
– Severe HPN
 Etiology:
Maternal factors

• Ingestion of teratogenic drugs (prohibited or

prescribed)
• Chronic smoking
• Ingestion of alcohol
• Exposure to radiation and high doses of
caffeine
 Complications:

• Hemorrhage
• Infection/septic abortion
• Disseminated intravascular coagulation (DIC) if
missed abortion is retained beyond 1 month,
common in late abortion
 Types:
• Threatened abortion – characterized by cramping
and vaginal bleeding in early pregnancy with no
cervical dilatation. There is a possible loss of the
products of conception. 25-20 of all pregnancies
have some bleeding but only less than a half
proceed to complete miscarriage. It may subside or
an incomplete abortion may follow.
• Signs and symptoms: light vaginal bleeding,
no or mild uterine cramping
 Types:
Threatened abortion
• Management:
– Ask LMP as if it is more than 20 weeks AOG, it may be due
to placenta previa and not abortion, do not do internal
examination
– Instruct mother to save all pads consumed for examination
of passed materials
– Assess pain – usually in the suprapubic area that radiate in
the lower back, buttocks, genitalia and perineum, if
occurring in only one side, consider ectopic pregnancy or
ruptured ovarian cyst. When the pain subsides, it may
suggest completion of the abortion
– Bedrest until 3 days after bleeding has stopped, if bleeding
and pain persist , advise to go to hospital
– No coitus up to 2 weeks after bleeding stopped
 Types:
• Imminent or inevitable abortion – characterized
by bleeding, cramping and cervical dilation and
the termination can not be prevented.
• Signs and symptoms: moderate to profuse
bleeding, moderate to severe uterine cramping,
dilatation of cervix, rupture of membranes, no
tissue has passed yet
• Management: hospitalization, dilatation and
curettage, oxytocin after D and C, emotional
support
 Types:
• Incomplete abortion – Characterized by expulsion of only a
part of the products of conception (usually the fetus) and
bleeding occurs with cervical dilation.
• Signs and symptoms: heavy vaginal bleeding, severe
uterine cramping, open cervix, pasaage of tissue, UTZ
shows that some products of pregnancy are still inside
uterus
• Management: D and C and uterus must remain contracted
after, flat position and massage the uterus, monitor for
shoulder pain and abdominal pain that may suggest
perforation of uterus, monitor vital signs for shock, monitor
blood loss, monitor I and O and blood studies
 Types:
• Complete abortion – characterized by complete
expulsion of all the products of conception.
• Signs and symptoms: light vaginal bleeding, abdominal
pain and passage of tissue then no pain and
tenderness after the passage, no or mild cramping,
closed cervix and in UTZ, empty uterus
• Management: usually needs no further medical or
surgical treatment but monitor still for continuous
bleeding or signs of infection – these are indicators
that not all tissue were expelled, rest and no
intercourse and douching for upto 2 weeks, RhoGAM
administration, advise to seek consultation if with
profuse bleeding, severe pelvic pain, and high grade
fever
 Types:
• Missed abortion – characterized by early fetal
intrauterine death without expulsion of the products
of conception. The cervix is closed and the client may
report dark brown vaginal discharge.
• Signs and symptoms: absence of FHT, cessation of s/s
of pregnancy (uterine enlargement, no HCG level
doubling)
• Management: insertion of 20 mg dinoprostone
(prostaglandin) suppository in the vagina every 3-4
hours as necessary to produce contractions to expel
products of pregnancy, D and C may be needed to
remove fragments of placenta
 Types:
• Recurrent or habitual abortion – is spontaneous
abortion of three or more consecutive pregnancies.
• Management: cervical cerclage, fertility drugs to
improve estrogen and progesterone production for
better uterine nourishment (Clomiphene, Pergonal),
Aspirin or mini-heparin to prevent of fibrinogen clot
formation within small blood vessels, if cause is due to
uterine polyps, tumors and adhesions correction of
these conditions before pregnancy is again attempted,
treatment of medical illness as DM, SLE, thyroid
diseases, STD’s before attempting pregnancy
 Types:
• Septic Abortion – due to dissemination of
bacteria or toxins in maternal circulation often
associated with induced abortion by untrained
persons by non sterile technique.
• Signs and symptoms: foul smelling vaginal
discharge, uterine cramping, fever, chills,
peritonitis, leukocytosis, septic shock
• Management: treat abortion, high dose IV
antibiotic therapy (penicillin, clindamycin and
tobramycin), D and C if incomplete abortion
 PLACENTA PREVIA
• The placenta implants in the lower uterine segment,
near or over the cervical os. The degree to which it
covers the os leads to three different classifications:
• When the placenta implanted low, the size and the
margin are affected by changes in the lower uterine
segment especially in the 3rd trimester when it begins
to stretch and shorten in preparation for labor causing
tear or breakage in placental attachment.
• The lower uterine segment is not as muscular as the
upper portion making it unable to efficiently contract
should a bleeding occurs due to this breakage.
 Types:
• Total placenta previa – occurs when the
placenta completely covers the internal os.
• Partial placenta previa – occurs when the
placenta partially covers the internal os.
• Low lying or low implantation placenta
previa – occurs when the placental border
reaches the border of the internal os
 Predisposing factors:
• Conditions that may make implantation in
upper segment undesirable due to decreased
blood supply/scarring:
• Multiparity
• Previous molar pregnancy
• Endometritis
• Previous CS
• Abortion
• D and C
 Predisposing factors:
• Multiple pregnancy due to adjustment for 2 placentas
• Advanced maternal age, over 35 years of age because
and older uterus is not as vascular as younger uterus
• Decreased blood supply to uterine wall by smoking,
PIH, drug abuse and diabetes
• Short umbilical cord for this will sometimes slide the
placenta to implant in lower segment due to weight of
fetus
• Abnormal placentas – increta and accreta
• Large placenta
 Complications:
– Disseminated Intravascular Coagulation
– Infection
– Abnormal adhesion of placenta
– Renal failure secondary to hemorrhage and DIC
– Anemia
– Postpartum hemorrhage
– More laceration
– Fetal effects: death, prematurity, hemorrhage,
anemia, small for gestational age, brain damage
 Signs and symptoms:
• Sudden/Abrupt, Bright red, painless vaginal
bleeding-begins 24 to 30 weeks AOG, bright
bleeding may be intermittent or in gushes rarely
continuous
• Fetus may assume transverse lie for sometimes
the low implanted placenta prevents fetal head
to enter the true pelvis properly
• Decreased urine output due to hemorrhage
• Confirmed and diagnosed by UTZ
 Management:
• Bed rest with bathroom privileges
• Vaginal exams are contraindicated or may be
done in double set –up (done in the OR)
• Monitoring of blood loss, pain and uterine
contractility
• Evaluation of FHR
• Monitor maternal V/s
 Management:
• Complete laboratory evaluation
• Administration of IV Fluids
• Possible blood transfusion
• Evaluation of fetal maturity by amniocentesis
to enable schedule of delivery
• Administration of betamethasone to speed up
lung maturity
 Management:
• If woman is in active labor, tocolytics like ritodrine or
magnesium sulfate is given to stop contractions, if
inevitable, delivery is done
• CS is more preferred especially in total placenta previa
• If vaginal delivery is possible (marginal and low) –
position is semi fowler so fetal head can serve as
tamponade for bleeding, however trendelenburg in
left lateral recumbent position for (total/partial)
because pressure on the placenta by fetal head
aggravates bleeding
• Postpartum care: monitor for bleeding and keep
uterus contracted, infection and anemia and treat/
manage as appropriately
 ABRUPTIO PLACENTA
• The premature separation of a normally
implanted placenta after the 20th week of
pregnancy, typically with severe hemorrhage.
• Types:
• Central
• Marginal
• Complete
 According to S/S:
• Grade 0 – no symptoms, diagnosed after delivery
when placenta is examined and found to have
retroplacental clot
• Grade 1 – some external bleeding, uterine tetany,
tenderness may or may not be noted, absence of
fetal distress and shock
• Grade 2 – external bleeding,uterine tetany,
uterine tenderness, fetal distress
• Grade 3 – internal and external bleeding (more
than 1000 cc), uterine tetany, maternal shock,
probably fetal death and DIC
According to extent of separation:
• Mild: less than 1/6 of placenta is separated bleeding
may or may not be present (<250 cc), some uterine
irritability with no fetal distress, there may or may not
be vaginal bleeding, vague backache
• Moderate: 1/6-2/3 separation. Dark vaginal bleeding
(<1000 mL), with fetal distress, uterine tenderness
• Severe: more than 2/3 is separated, uterine
tenderness, rigidity, dark vaginal bleeding (>1000 mL)
however it may be absent externally, fetal distress and
fetal death, if separated entirely- maternal shock and
fetal death, severe pain, DIC
 Etiology:
• The cause is unknown
• Behavioral factors:
a. cigarette smoking, methamphetamine,
cocaine abuse
b. maternal alcohol consumption (14 or more
drinks per week)
 Etiology:
• Risk factors may include:
a. Uterine anomalies
b. Multiparity
c. Preeclampsia - Maternal HPN
d. Previous caesarian birth
e. Renal and vascular disease
f. Trauma to the abdomen
g. Previous third trimester bleeding
h. Abnormally large placenta
i. Short umbilical cord
j. Sudden release of AF
 Assessment:
• Sharp, stabbing pain high in the uterine
fundus
• Heavy vaginal bleeding if separation begins at
placental edges
• Concealed bleeding if the center of the
placenta separates first
• Uterus firm to board-like, tense or rigid
• s/sx of anemia
• s/sx of hypovolemic shock
 Management:
• hospitalization
• FHR monitoring
• Maternal V/S monitoring, I and O monitoring,
abdominal circumference and fundic height-
sudden increase may indicate internal bleeding,
uterine contractions secondary to release of
prostaglandins by placental separation
• Proper positioning – bedrest at sidelying position
• IV Fluid administration – LR is usually given at 125
cc per hour
• Blood typing and cross matching
 Management:
• Oxygen administration
• No pelvic, abdominal or vaginal examination
• Administer prescribed medications:
bethametasone, tocolytic therapy (terbutaline
(ritodrine), MgSO4) for mild abruption placenta
but contraindicated in moderate to severe cases
for it may conceal s/s of proper diagnosis and
evaluation.
• Caesarean birth Is preferred
• Vaginal delivery is possible if fetus is already
dead, there is minimal bleeding and mother is
stable
 PREMATURE RUPTURE OF
MEMBRANES
• Spontaneous rupture of the chorion and amnion
before the onset of labor. It is believed that fetal
membranes rupture due to pressure of uterine
contractions and the physiologic weakening
when the cervix dilates
• Occurs between 36-40 weeks AOG just before
true labor begins
• Preterm PROM: Responsible for 30-40% of all
preterm deliveries
• Prolonged ROM: when rupture occurs more than
24 hours before the birth of the baby
 Maternal Risks:
• Chorioamnionitis
• endometritis
• abruption placenta
 Etiology:
• incompetent cervix • Hydramnios
• cervicitis – most /overdistention of
common cause is uterine wall
infection • Trauma
• UTI • Multiple gestation
• Amniocentesis • Maternal genital tract
• Placenta previa anomalies
• Abruption placenta • Cigarette smoking
• Cerclage application
 Fetal/Neonatal Risks:
• Prematurity
• Neonatal infection/sepsis
• Fetal hypoxia due to cord compression
• Fetal pulmonary hypoplasia
• Facial anomalies
• Limb position defects
• Fetal growth restriction
 Assessment:

• Fluid leaking in the vagina

• Nitrazine paper test result of blue-green or blue
• high alpha-fetoprotein (AFP) level in the vagina
• may complain constant wetness in the underwear
• cervical dilatation
• uterine cramping
• pelvic pressure
• ferning pattern in microscopic test of dried AF
 Management:

• hospitalization
• Bed rest to prevent cord prolapsed- if with cord
prolapsed have mother positioned in knee chest
or modified trendelenburg.
• Monitoring of maternal V/S every 2-4 hours
under normal conditions, more frequently if with
s/s of infection, monitor FHT every hour, vaginal
discharge (smell, color, amount) and uterine
contractions (duration, intensity, frequency,
interval)
 Management:

• Regular laboratory evaluation

• “Pelvic Rest”
• Prophylactic antibiotics or if with infection, to
treat it
• Betamethasone administration
• Proper perineal care
 PREGNANCY INDUCED
HYPERTENSION
• Hypertension – a blood pressure reading in two occasions
of at least 140/90 or a rise of 30 mmHg systolic and 15
mmHg diastolic. Blood pressure should be taken in 2
occasions 4-6 hours apart.
• Gestational HPN- BP 140/90 mmHg develops for the first
time during pregnancy, but there is no proteinuria and
within 12 weeks postpartum the BP is normal
• Pregnancy Induced HPN- HPN that develops after the 20th
week of gestation to a previously normotensive woman.
PIH include preeclampsia, eclampsia and gestational HPN.
• Preeclampsia – is a hypertensive disorder of pregnancy
developing after 20 weeks’ gestation and characterized by
edema, hypertension and proteinuria (300mg/24 hours).
 PREGNANCY INDUCED
HYPERTENSION
• is a condition of high blood pressure
(HYPERTENSION) during pregnancy. Your
blood pressure goes up, you retain water
(EDEMA), and protein(PROTEINURIA) is found
in your urine. It is also called toxemia or
preeclampsia. The exact cause of PIH is
unknown.
• 7-10%bof all preg. Major causes of MCn
mortality
Eclampsia – is an extension of preeclampsia and
is characterized by onset of seizure activity.
• Contributory Factors:
– Multiple pregnancy
– Primiparity <20 years old or >40 y/o
– Pre existing diseases- Diabetes mellitus, collagen
vascular disease, chronic HPN, chronic renal dse.
– Low socioeconomic status – inadequate prenatal care
– Poor nutrition
– Pregnancy complications – H-mole, gestational DM,
Rh incompatibility
– Hereditary
– Black race
 Causes:
• No definite cause
• Genetic predisposition
• Autoimmune reaction
• Protein deficiency and poor nutrition
• Endothelin theory- vasoconstrictors
 Assessment (according to type):
Mild pre-eclampsia
• BP of 140/90 mmHg or higher
• Proteinuria (+1 to +2 by dispticks, 300 mg/24 hours
urine collection)
• Weight gain – 2 lb/week
• Mild edema in upper extremities or face – digital,
dependent edema
• Liver enzymes slightly elevated
• No IUGR
• Urine output is not less than 400 mL/24 hours
• Occasional headaches
• DTR – normal to +3
• No epigastric pain
 Assessment (according to type):
Severe pre-eclampsia
• BP of 160/110 mmHg
• Proteinuria (+2 to +4, 5 g/24 hours urine collection)
• Oliguria
• Cerebral disturbances
• Cardiopulmonary involvement due to pulmonary
edema
• Extensive peripheral edema – pitting edema +4,
generalized edema
• Hepatic dysfunction – liver enzymes markedly elevated
 Assessment (according to type):
Severe pre-eclampsia
• More rapid weight gain
• Epigastric pain
• Hyperreflexia (+4)
• Photophobia and visual disturbances
• Severe headache
• Nausea and vomiting
• Oliguria
 Assessment (according to type):
Eclampsia

• S/Sx of pre-eclampsia to include:

– Seizure
– coma
SIGN MILD PREECLAMPSIA SEVERE PREECLAMPSIA
Hypertension 40 /90 or symmHg or more 160/110 or systolic increase at
above the or above the 160 or morethan
Baseline; diastolic rise 15mm 50 mmHg over the baseline;
Hg or more diastolic rise greater than 110
systolic inc. of 30 mmHg or more on 2 readings
taken 6 hours apart after bed
rest

Proteinuria 1+ or 1g/day 3+ to4+ or 5g/day

Edema Generalized, confined to face Generalized, severe facial
(periorbital) and fingers puffiness, severe swelling of
face

Weekly wt. gain-greater than Excessive wt gain- 5 lbs/week

1lb/week or more
Epig. Pain due to edema of
liver capsule
Cerebral disturbances
• severe frontal headache
• inc, irritability
• blurring of vision
• hyper reflexia 87
SIGN MILD PREECLAMPSIA SEVERE PREECLAMPSIA

• severe dizziness
• halo vision, blind spots
• persistent vomiting
•Disorientation

Oliguria Absent output above 500 ml Present; output 400ml or less

in 24 hours in 24 hours

IUGR (intra-uterine growth absent Present

retardation )

Others Hypoproteinemia
Hemoconcentration
Hypernatremia

88
 S&S Eclampsia/HELLP Syndrome
• Eclampsia • HELLP Syndrome
– facial twitching – RUQ pain
– tonic-clonic sz – n/v
– pulmonary edema – edema
– circ/renal failure –  H/H,  plts
–  liver enzymes
TABLE 15–3 Deep Tendon Reflex Rating Scale
 Effects of Preeclampsia and Eclampsia:

• Cardiovascular Changes
– decreased cardiac output due to vasospasm
– failure of blood volume to expand which normally
occurs in pregnancy
– increased levels of clotting factors due to damage
to endothelium of blood vessels secondary to
vasospasm
– abnormal formation of RBC with short lifespan
 Effects of Preeclampsia and Eclampsia:
• endocrine and metabolic changes
• increased levels of renin, angiotensin II (elevates BP),
aldosterone (Na reabsorption and fluid retention), anti-
diuretic hormone, HCG
• edema
• Renal changes
– Reduced renal perfusion and filtration
– Elevated creatinine, uric acid and urea (due to inability
of kidney to efficiently filter waste products)
– Decreased urine output
– Proteinuria (due to damage to renal structures
secondary to poor perfusion)
 Complications:
• Abruptio placenta
• Cerebral hemorrhage and ischemia
• Hepatic failure
• Acute renal failure
• Prematurity
• Perinatal death
• Maternal death
 Management:
• Screening and early diagnosis
– Roll over test
– Tolerance Hyperbaric test – helpful for early
detection before clinical signs could appear. The
pregnant woman wears a portable BP cuff and
monitors and records intermittent BP readings
over a 48 hour period.
 Management:
• Initial hospitalization
– CBC, BUN crea and uric acid levels
– Liver function tests
– 24- hour urine protein and creatinine clearance
determination
– Daily weight
– UTZ
 Management:
• Initial hospitalization
– DTR assessment
• 0 – no response
• 1+ diminished
• 2+ normal
• 3+ brisker than average, possibly developing disease
• 4+ hyperactive, associated with clonus, developing disease
– To assess clonus at the ankle joint, dorsiflex the foot
and observe for movement when it is released.
Rhythmic jerking is present. If absent clonus, foot
returns to plantar position without jerking.
 Management:
• Ambulatory management
– Home management is allowed only if BP is 140/90
or below, there is low proteinurua, no IUGR and
well fetal well being
– Bed rest
– Left lateral position when lying down
– Regular check up – every 2 weeks
 Management:
• Ambulatory management
– Diet high in CHON and CHO – CHON at least 1.5 g/kg
of body weight/day, moderate Na restriction of less
than 2 g/day, calcium 1200 mg/day, avoid salty food,
high eat high fiber, 8-10 glasses of water
– Take weight daily and monitor and record intake and
output, BP monitoring 2x a day, count fetal
movements (3/hr)
– Must report to the hospital if – increasing BP,
epigastric pain, visual disturbances, severe headache,
N/V, weight gain more than 1 lb/week, abnormal fetal
movements
 Management:

• Hospital Management
– The only cure for preeclampsia is delivery
– Determination of fetal maturity (bexamethasone
may be given to speed up lung maturity)
– Fluid therapy of crystalloids (LRS and NSS 100 to
125 mL/ hour)
– Bed rest
– Monitor patient closely – V/S, I and O, fetal well-
being, s/s of convulsions
 Management:
Hospital Management
• Medications:
– MgSO4 (drug of choice) to treat convulsions by
reducing release of acetylcholine at myoneural
junctions, reduce edema, reduce BP
– Loading dose of 4 g infused over 20 minutes followed
by continuous infusion of 2-3 g/ hour
– Check ff before adm.: respiration should be above 14
BPM, UO should be at least 100 mL/4 hour, DTR are
present (loss/absence of DTR is a sign of toxicity to
MgSO4)
– Serum Mg levels are monitored periodically: 7-8
mg/dL is therapeutic. Greater than is toxicity
 Management:
Hospital Management
• Medications:
• If toxicity develops (absent DTR, depressed RR, UO less than
25 mL/hr) – give antidote 1 g (10 mL) 10% calcium gluconate
IV over 2 minutes and notify physician.
• MgSO4 is given upto 24 hours after delivery or from the last
convulsion if it occurs during postpartum.
• If given postpartum, monitor for atony that can lead to
hemorrhage’
• Side effects: mother: CNS depression, hyporeflexia, flushing,
confusion,
• Fetus: tachycardia, hypoglycemia, hypocalcemia,
hypomagnesemia
• Hydralazine (apresoline) – Antihypertensive, initial bolus of 5
mg IV followed by 5-10 mg every 20 minutes if diastolic
pressure is 110 mmHg or more.
 Management:
Hospital Management
• Safety measures:
– Goal – maintain patent airway and prevent injury
– raise padded side rails, put bed at lowest position, have
emergency equipments available – suction apparatus,
MgSO4, Ca gluconate, oxygen, after sizure position
patient in sidelying to drain oral secretions
• Preferred delivery is vaginal but CS for seriously ill
• In postpartum – monitor BP, convulsions, I and O
and uterine atony, liver enzymes and CBC, ergot
products are contraindicated because they are
hypertensive
 Management:
• 2 years should lapse before pregnancy is again
attempted