GESTATIONAL CONDITIONS

HYPEREMESIS GRAVIDARUM
-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.
Incidence:
-2% in pregnant women-peak incidence occurs between 8-12 weeks AOG usually resolving in
the16th.
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.
Assessment:
1.Excessive vomiting not relieved by ordinary medications persisting beyond 12 weeks AOG.
2.
Signs of DHN thirst, dry skin, increased pulse rate, weight loss, concentrated urine and
elevated hematocrit in CBC
3. fluid and electrolyte imbalance
4. ketonuria
Management:
1.differential diagnosis rule out other possible disorders associated with hyperemesis by
tests like liver and thyroid functions, urinalysis and CBC (monitor blood chemistries).
2.monitor I&O
3.Diet:
a.NPO for the 1st 24 hours IVF with added B vitamin b.
After24 hours clear fluid then small quantities of dry toast, crackers, o rcereal every 2
or3hours, then gradually advances to a soft diet, then to DAT c.
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
4.Complementary therapy i.e. use of ginger to expel flatus and aroma relieves nausea
5.administeranti-emetic drugs as ordered
6. avoid noxious stimuli that may precipitate nausea (tight clothing, iron supplement, spicy
foods ,strong odors, loud noises and bright lights)
7. enough relaxation and rest
8.enteral or total parenteral nutrition
9. hospitalization when severe DHN and F and E imbalance. Y
IV fluids (LRS)y
Vitamin supplements y
NPO for24-48 hours until nausea subsides y
Oral intake is started after patient is properly hydrated and nausea subsides y
Give anti-emetics before meals y
Gradual feeding y
Small frequent feedings y
Do not force to eat

Fetal/Neonatal Risks
1.
IntrauterineGrowth Restriction (IUGR)
2. Low-birthweight
3.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
a. fallopian tube
b .ovary
c. cervix
d. intestine
RiskFactors:
1. Obstruction
a. chronic salphingitis and pelvic inflammatory disease(PID),STDs
b. congenital malformations
c. previous tubal surgery
d .uterine tumor pressing on the proximal end of the tube
2.Others:
a. useof IUDs for contraception
b. smoking
c. history of ectopic pregnancy
Causes:
1. mechanical factors conditions that delay the passageof ovum in the oviducts and
prevent it from reaching the uterus in time for implantation.(obstruction)
Salphingitis
- Peritubal adhesions, kinking and narrowing
- Diverticular formation
- Previous ectopic pregnancy
- Previous tubal operations
-Tubal tumors
- Past induced abortions
2.Functional factors
-External migrations of the ovum
- Menstrual reflux
-Altered tubal motility associated with use of IUD, progestin only contraceptives
,morning-after pill
3.Assisted reproduction
- Ovulation induction associated with fertility drugs such as Clomid
- Gamete intrafallopian transf er
- In vitro fertilization
-Ovum transfer
4.Failed contraception
-IUD
-Oral contraceptives
-Condom and diaphragm

- Tubal ligation
-Hysterectomy
Types:
a.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
b.Ovarian-0.5%
c. 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 be come mummified and calcified (litho pedion) oran adipocere (fatty replacement)
d.Cervical
Assessment:
1.Normal symptoms of pregnancy
2. Vaginal bleeding -painless in cervical implantation
3.One-sided lower abdominal pain sudden knife like pain
4.Ref erred shoulder pain
5.Aries-Stellareaction uterus will not enlarge as in normal pregnancy
6.AdnexalMass or tenderness
7.Cullens sign - bluish discoloration around the umbilicus due to internal bleeding
8.Hard board like abdomen
9.Shock signs cyanosis, pallor, cold clammy skin, tachycardia, hypotension and oliguria
Diagnosis:
1.Transvaginal UTZ
2.Serial HCG determination in ectopic, HCG is lower than expected for gestational time and
does not double normally.(HCG double severy 48-72 hours)
3. Culdocentesis aspiration of bloody fluid from cul-de-sac of douglas
4. 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.
5.Uterine curettage to distinguish non viable pregnancy of ectopic pregnancy , if not
chorionic villi is obtained from the uterus ,ectopic pregnancy is suspected.
6. Colpotomy- direct visualization of oviducts and ovaries
7.Laparascopy visualization of pelvis using a fiberoptic glass
8.CBC rateof falling hematocrit can discriminate slow internal bleeding or sudden hemorrhage
of a ruptured tube
9.Elevations in WBC and rule out appendicitis or PID.
Management
1.Forunruptured pregnancy therapeutic abortion by Methotrexate(chemo drug) IV or IM
2.Saphingectomy removal of tube
3.Oopherectomy
4.Hysterectom
5.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
-Haveonly placental parts, forms when a sperm fertilizes an empty egg
-Thechromosomeareeither46XX or 46XY but are contributed by only one parent and the
chromosome materialis duplicated.
-It usually leads to carcinoma
b.Partial Mole
-It has 69 chromosome in which there are three chromosomes fore very pair instead of two.23
f rom themotherand2sets f rom the father. This could occur when two cells fertilize one egg.
-It rarely leads to carcinoma
Assessment:
Risk factors:
1.Higher occurrence in Asian
2.Women below 18 and above40 years old
3.Women with low socioeconomic status who have low protein intake
4.History of molar pregnancy
Signs and Symptoms:
1.Uterus larger than expected for the duration of the pregnancy
2.Abdominal cramping from uterine distention
3.Vaginal Bleeding
4. Vaginal discharge of clear, fluid filled vesicles
5.S/Sx of preeclampsia before20 weeks gestation
6.Severe nausea and vomiting
7.HCG serum levels are abnormally high
8.Ultrasound reveals characteristic appearance of molar growth
9.Absence of FHR10.s/Sx of anemia
Management:
1.Suction Curettage or dilatation and curettage to remove mole
2.Serum hCG monitoring HCG should be monitored for1 year and should benegative28weeks after removal of mole.It is monitored every 2 weeks until normal then monthly
for6months the every 2 months for the next 6 months. 3. Chest xray may also be done every 3
months for6 months because H- mole cancer cells can metastasize to lungs.
4.Oral Contraceptiveusefor1 year- the woman is advised not to get pregnant yet and pills
should not contain estrogene. Methotrexate anti cancer drug for one yarto prevent
development of malignancy . Hysterectomy
Complications:
Gestational trophoblastic tumors-Chorio carcinoma
chorionic villi becomes cancer cells, can be transferred to different parts of body by
circulation and lymphatic drainage
-Invasive mole
excessive formation of trophoblastic villin that penetrates myometrium
-Placental site trophoblastic tumor
cancer cells arising form the placental site