MCN Dysfunction Nursing

High Risk Pregnancy

•When there is an increase chance of
morbidity or mortality to the mother or her
fetus or both.

High Risk Infant

•Is one who is born with less ability or chance
to survive or a greater chance to be left with a
permanent handicap either psychosocial or
physiologic than the average child
Factors:
1.Maternal Age Factor
a.Age > 35 yrs. old
i.Tendency to have:
1.Heavier babies
2.High perinatal mortality
3.High incidence of infants with
down syndrome
b.Adolescent pregnancy <18 yrs. old
i.Lack of perinatal care
1.Low socioeconomic background
 2.Lack of motivation
3.Denial, pride
4.Ignorance, rebellion against
authority
ii.Malnutrition
1.Anemia, vitamin deficiency,
excessive weight gain, toxemias,
prolonged labor, fetopelvic
disproportion, drug abuse,
infections.

2.Social Problems
a.Failure to complete education or
vocational training
b.Dependence on other for support
c.Failure to establish stable family
d.High rate of marital failure
e.High incidence of repeated out-of-
wedlock pregnancies

3.Socioeconomic factors (financial)

a.Low income
 i.Predisposed to low health status – OB
and neonatal complications
ii.2 balanced dietary intake
iii.Low birth weight
iv.Toxemia
v.Malnutrition, mental retardation
b.Use of elicit drugs
i.No prenatal
ii.Malnourished
iii.Drug addicted children
c.Smoke and alcohol drink
i.Low birth weight infants
ii.Higher rate of abortions and stillbirths
4.OB factors
a.Previous difficult pregnancies, fetal loss,
premature
b.Diabetic, hypertension, anemia, cardiac,
renal, or respiratory disease
c.Evidence of vaginal bleeding
d.Rh negative, COPD
e.Exposed to terratogens, chemical,
environmental toxins, or radiation
 f.Multiple pregnancy - close gap
pregnancy – 2 months from last delivery
Conditions:
1. Pre-existing
2. Intra-partum
3. Newly acquired

Conditions: FIRST TRIMESTER

I.Bleeding
•Occurs anytime
•Never normal, no matter how slight
•Frightening experience
•Need to be assessed
•Threatens both mother and fetus
•Client needs reassurance – it is not
because of what she did to free her from
guilt
•DES (diethylstilbestrol)
i.Daughter – born with vaginal cancer
ii.Son – cystic testicular disease
 Table 39 – 1 Signs and Symptoms of Hemorrhagic
Shock
Assessment Significance
Increased pulse rate Heart attempting to
circulate decreased blood
volume
Decreased blood pressure Less peripheral resistance
because of decreased
blood volume
Increased respiratory rate Increased gas exchange to
better oxygenate
decreased red blood cell
volume
Cold, clammy skin Vasoconstriction occurs
to maintain blood volume
in central bloody core
Decreased urine output Inadequate blood is
entering kidney due to
decreased blood volume
Dizziness or decreased Inadequate blood is
level of consciousness reaching cerebrum due to
decreased blood volume
Decreased central venous Decreased blood is
pressure returning to heart due to
 reduced blood volume
Figure 39-1 The process of shock due to blood
loss (hypovolemia)
Blood Loss

Decreased intravascular volume

Decreased venous return, decrease cardiac output,

and lowered blood pressure

Body compensating by increasing heart rate to

circulate the decreased volume faster;
vasoconstriction of peripheral vessels) to save blood
for vital organs). Increased respiratory rate and a
feeling of apprehension at body changes also occur.

Cold, clammy skin decreased uterine perfusion. In

the face of continued blood loss, although the body
shifts fluid from interstitial spaces into intravascular
spaces, blood pressure will continue to fall

Reduced renal, uterine, and brain perfusion

Lethargy, coma, decreased renal output

Renal failure

Maternal and Fetal

death
 Emergency interventions for Bleeding in Pregnancy
Interventions Rationale
Alert health team of emergency Provide maximum coordination of care
situation
Place woman flat in bed on her side on Maintain optimal placental and renal
bed rest function
Begin IV fluid such as lactated Ringers Replace intravascular fluid volume;
with an 18 – 19 gauge needle prepare IV line for blood replacement
Withhold oral fluid Anticipation of emergency surgery
Administer oxygen as necessary at 2 – Provide adequate fetal oxygenation
4L/min despite lowered circulating blood
volume
Monitor uterine and fetal heart rate by Assess whether labor is present and fetal
external monitor status; use external system to avoid
cervical trauma
Omit vaginal or rectal examination If a rectal or vaginal exam is done with
placenta previa, the placenta may be torn
and hemorrhage may occur
Order type and cross-match of 2 units Prepare to restore circulating maternal
whole blood blood volume
Measure intake and output Assess renal function (will decrease with
massive circulating volume loss)
Assess vital signs (pulse, respirations Assess maternal response to blood loss
and blood pressure) every 15 minutes
Assist with placement of central venous Assess pressure of blood returning to
pressure catheter heart
Measure maternal blood loss by Assess extent of continuing blood loss
weighing perineal pads; save any clots
passed
Set aside 5 ml of blood in a clean Assess for possible blood
test tube and observe in 5 minutes coagulation problem (disseminated
for clot formation intravascular coagulation). Suspect
this if no clot forms within time
limit.
Maintain a positive attitude toward Support mother-child bonding
fetal outcome
Support woman’s self-esteem Problem solving is lessened by
 poor self-esteem

Bleeding
•Not directly related to pregnancy e.g. tumor,
polyps, erosions,Originating or as a consequence of
pregnancy
Abortion - loss of fetus before age of viability <24
weeks of AOG
Incidence of abortion increases in:
1.Age
2.Parity – gravida 6
3.History of previous pregnancy
10% of pregnancy end up in abortion – nature’s
way of eliminating undesirable mal-formed fetus
Types:
Induced
•Therapeutic – medically indicated
•Criminal – intentionally done
•Septic – infected abortion; secondary
to infection
Spontaneous
•Threatened
th
oPrior to end of 20 weeks of AOG
oOnly abortion can be save
oVaginal bleeding is slight
oAbdominal cramping is slight to
moderate
oCervix is closed
oComplete bed rest without
bathroom privileges
 oDiet: normal diet high vitamins
and protein
•Imminent (inevitable)
oCervix is opened
oBleeding is moderate to profuse
oAbdominal pain is moderate to
severe
oNPO
oPossibility of neurogenic and
hypovolemic shock
•Incomplete
• One of the products of conception
has not been expelled
• Cervix is opened
• Severe bleeding and pain
• Prepare for complete abortion – D/C
•Complete
•Missed – cervix is closed; foul-
smelling discharge; fetus dies in utero
before 20 weeks AOG and retained
from 2 months or longer and will
undergo changes:
b.Fluffling
1.Thickening body, skull
and thorax
2.12 – 48 hours after the
death of the fetus –
amniotic fluid
c.Maceration – softening
 d.Mummification – leather-like
changes
e.Lithopedion formation – stoney
– material

Therapeutic Abortion: According to US Supreme court

ruling (Jan. 22, 1973) Pregnancy may be terminated as
follows:
st
1.1 trimester abortion – decision is left to the
women and her physician
nd
2.2 trimester – state may not prohibit but may
regulate practice for woman’s health
3.Final trimester – state may choose to protect the
potential life of the fetus by prohibiting abortion
except when there is threat to the life or health of
the mother
4.Religious belief of the mother is always respected.

Habitual Abortion
•Repeated abortion (spontaneous of any type)
•3 or more pregnancies at same age or pre-viable
stage

Causes of Recurrent or Habitual Abortion

1.Defective spermatozoa
2.Hormonal influence
3.Nutritional status
4.Deviation of uterus – mid-septum, decrease BS
bicornate- horns or poles - small areas for
implantation
 5.Psychological factor – personality and stress
6.Blood incompatibility – ABO, Rh factor

Induced Abortion
•Deliberately terminating pregnancy
•Criminal, septic
•Therapeutic, medical, and planned

Purposes:
1.When there is threat to mother’s life (heart disease)
2.Fetal malformation (chromosomal defects)
3.Psychological implication (rape)

Procedures Used to induce Abortion

(Therapeutically)
I.Menstrual Extraction
th th
•Simplest type done on 4 – 6 weeks AOG

•Uterine lining is suction – client bleeds as

normal menses
•Oxytocin given orally
•Follow-up check up and pregnancy test
•Complications:
oHemorrhage
2 pads/ hour
Clots
oInfection
Abdominal pain and tenderness
 Fever over 100 OF
Endometritis

II.Dilatation and Vacuum Extraction

•Paracervical block
•Cervix is dilated with dilators
•LAMINARIA – dried sterilized seaweeds –
cervix swells, after 24 hours becomes dilatable
vacuum extraction is inserted and evacuate
uterus contents in 15 minutes
•Antibiotics, oxytocin, MGH after 4 hours
•Bleeding same as menses
•Complications:
a. Hemorrhage -2 pads/ hour
b. Infection
Abdominal pain and tenderness
O
Fever over 100 F
Endometritis
III.Saline induction
th
•“Salt poisoning Abortion” done on 14 – 16th
weeks of AOG then D and E is used
th
•16 – 24th weeks of AOG Saline and
prostaglandin induction is used
•Mechanisms:
i.Saline interferes with progesterone
functioning causing endometrial sloughing
ii.Done through abdominal wall into uterus –
needle is inserted then 100 – 200 ml amniotic
fluid is aspirated and 20% hypertonic saline
 solution is injected into uterus to replace
aspirated fluid. Then needle is removed 12 –
36

hours ff. injection – labor contractions begin;

supplemented by oxytocin drip
•Complications:
a.Hypernatremia - accidental injection of HSS
to blood vessels in the uterus
i.S/S: increase pulse, flushed face, severe
headache
ii.Mechanism:
1.To equalize osmotic pressure, fluid
from tissue transfer to blood vessel
which then leave the tissue dehydrated
b.Water intoxication
i.To large amount of oxytocin used, ADH
effect
ii.Severe headache, confusion, drowsiness,
edema, decrease urinary output
iii.Rx: D/C oxytocin drip
c.Hemorrhage
d.Infection – D5W – to balance or restore fluid

IV.Prostaglandin Injection
•Hormone which is abortive
•Administration:
1.IV drip
i.½ - 1 hour after administration, labor will
start
ii.No oxytocin needed
 iii.S/E: nausea, vomiting, and diarrhea
iv.Dx: anticholinergic, and antidiarrheal
v.CI: - HPN – vasoconstriction, Respiratory
disorder – bronchial constriction and
bronchospam
2.Vaginal suppository – given every 3-4 hours
as prn until labor starts
3.Oral – not recommended- causes severe
nausea, vomiting, shaky, chills, and increase
temperature
V.Hysterotomy – done in AOG 16 – 18 weeks like CS

II.Ectopic pregnancy
•Extra-uterine
•Does not occupy uterine proper

Types according to sites:

1.Tubal – most common frimbriae (1), ampullar
(2) 60%, Isthmic (3), interstitial (4)
2.Ovarian – tubo-ovarian (5), ovarian (6)
3.Cervical – cervical (7)
4.abdominal/ peritoneal – rare (8)
Causes:
1.Adhesions in tubes – tubo-ovarian, fallopian tubes
2.Infection – chronic salphingitis, PID
3.Congenital malformations – infantile tubes
4.Scars of tubal surgery
5.uterine tumors pressing the tubes
6.endometriosis
7.tube spasms
S/S – ruptured
1.Spotting or bleeding – may or may not be present
2.Abdominal rigidity
3.Cullen’s sign – bluish discoloration around
umbilicus
4.Shoulder pain – blood irritating the diaphragm
5.Mass in Cul-de-Sac of Douglas (pouch) may be
palpated or bloody fluid maybe aspirated by
CULDOCENTESIS
6.Excoriating pain at cervix when IE is done
7.Knifelike pain in either lower quadrant (affected
site)
8.WBC – 15,000/uL>, RBC – decrease, ESR – Slightly
elevated
9.S/S of shock

S/S – early ectopic pregnancy

1.Amenorrhea or abnormal menses – spotting
2.Cul-de-Sac mass

S/S – Acute ruptue

1.Shock
2.Referred shoulder pain
3.Evidence of acute blood loss

S/S – chronic rupture

•Occurs 50 % in tubal ectopic pregnancy
1.Slow-internal bleeding
2.Atypical or inconclusive symptoms as
 a.Slight, dark, vaginal bleeding
b.Renal or pelvic pressure or fullness
c.Lower abdominal tenderness
d.Slight fever
e.Leukocytosis
f.Cullen’s sign
g.Decrease Hct and Hgb

Dx:
1.Utrasound – reveals site of Ectopic pregnancy
2.Culdocentesis – yields free blood that will not clot
or is already clotted
3.Laparoscopy – discloses extrauterine pregnancy

Treatment:
1.Culdotomy – release clotted blood and product of
extra-uterine pregnancy/ conception
2.Laparotomy – reveal correct diagnosis

Nursing Management
1.Monitor V/S, watch for signs of shock
2.Nursing care to bleeding clients
3.Observe nature of bleeding
4.Administration of narcotics or analgesic as
ordered
5.Prepare clients for diagnosis and treatment
6.Provide post-op care
THIRD TRIMESTER BLEEDING
1.Placenta Previa
•Implantation of the plancenta at the lower
uterine segment
•30 % > than average placenta implanted at
the fundus – site and size related (surface
area)
•degree placenta covers the internal os is
estimated by 70 – 100%, 75 % etc.
•2nd trimester – 45% of placenta are
implanted at lower uterine segment
•this elongates and move upward but out of
150 pregnancy remains

Cause of bleeding:
•differentiation of the upper and lower uterus
segment late in pregnancy (30 weeks of AOG) – the
inability of the placenta to stretch to accommodate
this differing shape results to bleeding

Classification
•Based on the degree the internal os is covered by
the placenta

1.Complete or central or total

•Internal or is covered entirely by the placenta
2.incomplete or partial
 i.marginal
•edge of the placenta approaches the internal
os
ii.low-lying (low implantation)
•is when the placenta is situated in the lower
uterine segment but away from the os
Causes:
1.Unknown
2.Can be attributed to the following conditions:
a.Fibroid tumor in the uterus
b.Uterine scars from previous surgery os
c.Abnormal uterine position or shape
d.Multiparity – multiple gestation
e.Age – very young and very old

Ass/ P.E: (7 months AOG)

1.Uterine bleeding – painless

2.Uterine tone
•Normal but relax completely between
contractions
3.Pain
•Painless non-tenderness uterus – may
experience labor contractions
4.Fetal position
•Fundic height is greater – placenta hinders
descent of presenting parts
•Leopolds maneuver reveals malposiition of
fetus – transverse or breech
 5.Diagnostic tests
•Ultrasound
i.Static imaging – diagnostic method of
choice
•Amniocentesis
i.Assess fetal lung maturity LS ratio 1:2
ii.If lung maturity is reached, CS delivery is
done
•No vaginal exam unless patient is place on
double prep procedure (prepared for vaginal or
C/S delivery)
•Laboratory tests – hemoglobin, hematocrit, Rh
factor, urinalysis

Major Problem:
•Preterm delivery

Fetal Outcome:
•Fetal distress or death occurs if placenta previa
becomes detached from deciduas basalis or if
mother suffers shock

Nursing Care/ Management – predelivery –

conservative

1.Keep NPO
O
2.maintain bedrest – head of bed elevated to 20 – 30
(semi-fowlers) – allow fetal body to act as
tamponade
 3.IV – large bore needle is started (LR vol. expander,
blood transfusion 2 units of WHB ready)
4.delivery – if fetus reached maturity
a.if > 30% previa – CS delivery
b.if < 30 % previa – vaginal delivery – if delivery
is not attained within 6 hours – C/S is indicated

2. Abruptio Placenta
•Ablatio placenta
•>20 weks of AOG
•is the premature separation of part or all
of the placenta from its site of implantation
•can be an abnormal separation of a
normally implanted placenta.

Types:
1.Partial separation
a.Concealed
b.Apparent – marginal separation
2.Complete separation
a. Concealed
b. Apparent
Problems:
Mother – shock – placenta separation
Infant – Perinatal death – hypoxia

Predisposing factors:

1.HPN
2.multiple gestation
3.multiparity
 4.adv. Maternal age
5.DM
6.previous premature separation
7.hypotensive syndrome
8.rare – abdominal trauma 5%; short cord 1%
9.history of abortion; stillbirth; pre-natal
hemorrhage; premature labor

Degrees of Separation:

Grade Description
0 No symptoms were apparent from maternal or
fetal side; diagnosis of placental separation is
made during delivery; placenta shows recent
adherent clots on maternal surface
1 Minimal separation enough to cause vaginal
bleeding and changes in the maternal VS; no
fetal distress or hemorrhagic shock occurs
2 Moderate separation with evidence of fetal
distress; uterus is tense, painful on palpation
3 Extreme separation without immediate
intervention; maternal shock and fetal death
will result
Fetal outcome:
•15% perinatal death; also depends on the degree
of separation and fetal hypoxia

PE/Ass: symptoms vary with degrees of placental

separation
 1.Uterine Bleeding
•Painful
•Sharp stabbing pain high in uterus fundus
•Pain is felt on palpation not with contractions
•Heavy bleeding may or may not be apparent
•In severe concealed bleeding, blood may
infiltrate the uterine musculature – COUVELAIRE
uterus or uteroplacental apoplexy – hard,
boardlike uterus – orange or bronze color – uterus
becomes tense and rigid to touch
•S/S of shock follows
•In extensive bleeding, DIC syndrome occurs; the
woman’s reserve blood fibribogen may be used
up in her body’s attempt to accomplish effective
clot formation

2.Laboratory tests
•Hemoglobin level, typing, cross-matching
fibrinogen level (DIC); tests for DIC – 5 ml blood to
stand for 5 minutes; if clots formed – DIC
negative; no clots – DIC positive
Nursing Care/ Management

1.Admit to hospital
2.Give oxygen by mask (fetal anobia)
3.monitor FHT, VS and record
4.baseline fibrinogen determination
5.keep in lateral position – prevent pressure at vena
cava; further compromise fetal circulation
 6.No IE, pelvic exam, enema
7.Depending on degree of separation if labor starts
– rupturing BOW may help speed delivery or
administration of oxytocin
•Purpose of rupturing BOW
a.Prevents development of couvelaire uterus,
prevents pooling of blood in the myometrium of
uterus
b.Prevents DIC
c.Speed up delivery
8. If delivery do not occur, C/S is the method of
choice

9.Cause of maternal death

•Massive hemorrhage which lead to shock;
circulatory collapse or renal failure
•Infection

Post-Partum Bleeding

•Normal delivery average blood loss: 300 – 350 ml

•Post-partal hemorrhage: >500 ml within 24 hours
period
st O
•Immediate: 1 24 bleeding
•Late: occurring during the remaining days of the 6
weeks puerperium

CONDITIONS CAUSING Post Partum bleeding

 1.Uterine Atony
2.lacerations
3.retained placental fragments
4.hematoma
5.D/C

Uterine Atony
•Loss of uterine muscle tone; uterus fails to
contract completely to seal off open uterine
vessel after delivery

Causes:
a.Conditions that distended the uterus beyond
average capacity
i.Multiple gestation
ii.Hydramnios (AF > 2000 cc)
iii.Large baby (>9 lbs.)
iv.Presence of uterus myomas (fibroid tumor)
b.Conditions that leave the uterus too exhausted to
contract readily
i.Deep anesthesia/ analgesics
ii.Labor and oxytocin agent
iii.Maternal age over 30 years
iv.High parity
v.Dystocia
O
vi.2 illness as anemia
vii.endometritis
c.conditions with varied placental site or attachment
i.placenta previa
ii.placenta acreta
iii.placenta ablation
Ass:
1.Uterus suddenly relaxes
2.Occurs gradually – as lethal as sudden gush;
following delivery; post-partum period

Nursing Care/ Management:

A.Prevention
i.Inspect blood loss – blood seeps at back
ii.Palpate fundus
iii.Frequent assessment of lochial discharge/VS
iv.Empty bladder every 4 hours
B.Therapeutic
i.Massage uterus
ii.Apply cold (ice) compress
iii.Refer for administration of Methylergometrin
Maleate

Management:
1.Adminster oxytocin agent – S/E – Hypertension –
BP 140 / 90 mmHg do not administer
2.Blood replacement - >500 ml needs BT; auto-
transfusion
3.Bimanual massage
4.Prostaglandin Administration (IM/ IV)– strong
uterus contractions
5.Hysterectomy – removal of uterus last resort

Lacerations
 •Tearing at birth canal – expected consequence
of childbearing; more common in: primi, large
babies >9 lbs, lithotomy , used of instruments

Structures affected:
1.Cervix
2.Vagina
3.Perinium

Classification of perineal tear

1st degree – vaginal mucosa, skin of perineum,

fourchette
2nd degree - vagina, perineal skin, fascia, levator
anterior muscle and perineal body
3rd degree – entire perineum, external sphincter of
rectum
4th degree – entire perineum, rectal sphincter and
some mucous membranes of rectum

Management:
1.Repair
2.pack
3.no enema/ suppositories/ rectal temperature
4.prevent constipation

Cervical lacerations R/O uterine atony

Retained Placental Fragments

 •placenta failed to be delivered entirely and
fragments or parts are left behind inside the
uterus

Ass:
1.Bleeding depends on size of placental fragments
a.Large – immediate uterus does not contract
th
b.Small – 6 – 10th day post-partum – abrupt
discharge of blood clots
2.On examination, uterus not fully contracted
3.Doctor orders for serum HCG determination, U/S
to determine presence of placenta

Management:
1.Severe bleeding – Blood transfusion
2.D/C
3.placenta acreta – methotrexate – to destroy
placental tissues
4.advise patient to observe lochial discharge (alba,
serosa, rubra)

Abnormalities of Placenta:
Normal weight - 500 gms – 1/6 of fetal weight;
diameter: 15 – 20 cm; thickness: 1.5 – 3 cm

Placenta is expectedly increase size in: ½ of fetal

weight
1.DM
2.Erythroblastosis fetalis
 3.Scars on septum – placenta spread to look for
space to implant (good BS)

TYPES:
A.Placenta Succenturiata
•No fetal abnormality
•Has one or more accessory lobes connected
to placenta by blood vessel
•Small lobes maybe retained – maternal
bleeding
B.Placenta circumvallata
•Fetal side of placenta is covered to some
extent with chorion; no abnormality
C.Placenta marginata
•The fold of chroion reaches just to the edge
of the placenta; no abnrmality
D.Battledore placenta
•Cord is inserted marginally rather than
centrally
•Rare but with no known clinical significance
E.Placenta acreta
•Deep attachment of placenta to uterus
myometrium
•Management:
oManual extraction
oHysterectomy
omethotrexate
 F.Velamentous insertion of the cord
•Cord instead of entering the placenta
centrally, separates into small vessels the
reaches the placenta by spreading across a
fold of amnion
•Found in multiple pregnancies
•Predispose to maternal hemorrhage
G.Vasa previa
•Umbilical vessel of a velamentous cord
insertion cross the cervical os and delivers
before fetus
H.Two vessel cord
•Absence of one artery
•Usually 2 arteries 1 vein
•Fetus congenital kidney and heart anomalies

Hematomas

•Collection of blood with subcutaneous layer of

perineum, skin has no sign of trauma

Causes:
1.Injury to blood vessel – labor/ delivery
2.Rapid spontaneous deliveries – precipitate
delivery
3.Perineal varicosities
4.Episiotomy repair site
5.Anesthesia infiltration

Ass:
 •Feeling of pressure between legs
•Pain, discomfort, tenderness
•Minor bleeding
•Swelling/ bluish discoloration 1 –4 cm

Management:
1.Small - warm/ cold compress – ice pack absorb in
3 – 4 days
2.Large – incision and evacuation
3.Analgesia

Heart Disease in Pregnancy

•Vulvular involvement e.g. Kawasaki disease
30 – 50% increase Expected in
volume/output Pregnancy
Innocent
Heart Physiologic adjustment murmurs,
palpitations
Increase circulatory volume reached its Heart becomes
peak on 28 – 37 weeks AOG overwhelmed

Decrease cardiac output (heart Decrease vital

failure) organ perfusion
(uterus and
placenta

Rheumatic Improve management

heart Skills e.g. Ultra Sound Heart
disease – research and disease
prevented advance technology corrected
and treated early
 Team approach – heart
specialist, obstetrician,
nurses

1. Initial visit to plan

pregnancy of Heart Disease in Pregnancy
Treatment and management
2. Pre-natal check up
1.Promotion of Rest
•LLRP to carry pregnancy to term about 36 weeks
AOG – increase fetal maturity
2.Promotion of healthy diet and Nutrition
•Enough to ensure normal weight gain during
pregnancy toe ensure healthy pregnancy and fetus
•No additional cells to supply with nutrients and
oxygen – burden to the heart – excess weight gain
•Iron supplement – prevent anemia
•Sodium limitations with diuretics – before
pregnancy and to continue during pregnancy
3.Education about medication
1.Digitalis
•Slows and strengthens myocardial
contraction
•Crosses placenta but not teratogenic
2.Penicillin
•Prevent bacterial invasion due to denuded
placenta and subacute bacterial endocarditis
•Non-terratogenic
3.No over the counter drugs but exception to the rule.
NO DRUGS DURING PREGNANCY – client has to
continue heart medication.
4.Education in prevention of infection
1.Spreads more energy – increased cardiac output
 5.Promote reduction of physiologic stress
1.Avoid worries on self and fetus “look at pregnancy
one day at a time”
6.Delivery
a.Position – semi-fowlers + oxygen inhalation }
facilitate effective breathing
Epidural/ caudal anesthesia + forcep delivery
(assisted) } effort free and pain free delivery
C/S not indicated:
•Increase blood loss
•High risk for infection
•Increase throboembolism formation
•High risk of respiratory depression
(due to anesthesia)
b.Start penicillin if not given during pregnancy
c.IV line at KVO – for ER meds
7.Post-partum care
•After delivery – blood supplying placenta goes back
to circulation

•blood volume increase – 20-40% in just 5 minutes –

heart to make major rapid adjustments to increase
blood volume

Intervention:
1.Prevent sudden distention of abdominal vein following
delivery of placenta. Applying pressure to woman’s
abdomen and gradually release it so blood theoretically
enters circulation slowly
2.Ambulate early – to prevent emboli formation
3.Wear elastic stocking (support) – increase venous return
to heart
4.Ergot compound given with caution – increase BP
 5.Estrogen compound with caution - high risk to DVT or
thromboembolism, and decrease lactation
6.Needs for more reassurance on fetal outcome
•Fear for fetus to have cardiac ailments –
acrocyanosis – expectedly normal
7.BF without difficulty but needs assistance – easily get
tired
8.Post partum exercises
i.abdominal exercise – needs doctor’s order
ii.perineal exercise – Kegel’s exercise to
strengthen pelvic floor
9.Stool softener – avoid straining
10.Delay next pregnancy – to stabilize circulatory status
11.Follow – up care of heart disease
•Use of antibiotics, anticoagulants – prone to bleeding,
high risk of congenital anomalies in infant
•Anticoagulant – Heparin, Warfarin (Prothamine antidote)
a.do not cross placenta barrier if given
pre-pregnancy
b.D/C before 2 weeks EDC to prevent
infant to be born with coagulation
defect
c.Regional anesthesia should not be
used – changes of bleeding into spinal
cord (mother)

Effects of heart disease on fetus:

1.Fetal growth – decrease birth weight

2.Fetal distress (acidotic) – immaturity
3.Delivery – lots deceleration (fetal monitor
4.neurologic – mental involvement – effects of placental
insufficiency

Assessment (Maternal)
 1.History of heart disease (class)
2.Dyspnea – type
rd
3.Edema – innocent edema – feet/ankles – 3 trimester
expected
th
•PIH – after 24 weeks AOG – serious/face fingers
•Heart disease – failure + other S/S of heart disease
e.g. chest pain irregular pulse, orthopnea
4.Assess nail bed filling (less than 5 seconds)
a.Jugular venous distention
b.Liver size (right heart failure)
5.ECG – Chest X-ray

Obstetrical Analysis of Heart disease classification

Implication :
Class I and II normal pregnancy and delivery
Class III pregnancy if ok if abide with CBR
Class IV poor candidate, cardiac failure even at rest

Classification of Heart Diseases:

Class Description

I Client have no limitation of physical activity;

ordinary physical activity causes no discomfort,
no symptoms of heart insufficiency and no
anginal pain

II Slight limitations of physical activity; ordinary

physical activity causes excessive fatigue,
palpitations, dyspnea, or anginal pain

III moderate to marked limitations of physical

activity; less than ordinary activity, client
experiences excessive fatigue, palpitations,
dyspnea or anginal pain
 IV unable to carry any physical activity without
experiencing discomfort; even at rest -
experience S/S of cardiac insufficiency and
anginal pain
Pathophysiology of PIH
Peripheral arteriolar
Vasoconstriction Vasospasm

Decrease Blood Supply Hypertension

Decrease Oxygen Supply

TISSUE PERFUSSION TO VITAL ORGANS

Kidney Liver/ Pancreas Eyes Uterus

Tissue Retina
Glomerolar Glomerolar Ischemia Muscle Placenta
degeneration Filtration tissue
Visual
Vascular tissue Changes
Increase Increase
Blurring Ischemia
Glomerolar Tubular
of vision
permeability absorption of Epigastric
Sodium pain
Premature Premature
If with Labor Deterioration
Albumin/
hemorrhage
globulin cross Water Nausea and
Blindness
into urine Retention Vomiting
Fetal Abruptio
Increase nutrients placenta
Proteinuria Edema Oliguria amylase/
crea ratio

Fluid Gen. Water Fetal

diffuse Retention Distress
from
`
circulatory
Lungs Brain Premature Delivery

Pulmonary Edema Cerebral Edema Prematurity

(cyanosis) (Hypoxia)
 Maternal Convulsions
Death

Fetal
CHF Irritability Death

Convulsions
Pregnancy Induced Hypertension
•Main cause is unknown
rd
•3 leading cause of maternal death in the US
•“TOXEMIA” - poison

1.Hemorrhage
2.infection
3.researchers
•pictured a toxin of some kind released by the woman
in response to the foreign protein of the growing fetus
which leads to the Triad Symtptoms of PIH:
oHPN
oEdema
oProteinuria

Predisposing Factors:

1.Primi and less than 18 and older than 35 years

2.Low socioeconomic – poor nutrition and low CHON intake,
low B6 (Pyridoxine)
3.Pregnancy >5x or more
4.Non-white
5.Multiple pregnancy
6.Hydramnios
7.Heart disease, DM renal involvement
8.Essential hypertension
9.Poor calcium intake
10.Parasitic invasion
Types of PIH
1.Gestational Hypertension
•B/P 140/90 mmHg
•30/15 mmHg – increase above pre-pregnancy level
•No proteinuria, no edema
•Woman may develop chronic hypertension later in life
2 3
2.Mild Pre-eclampsia MAP higher 90 mmHg; MAP higher 105
mmHg
•B/P 140/90mmHg
•Protein 1 – 2 + on RS (1 gm/L) – orthostatic proteinuria
– standing excrete CHON but not on bed rest
nd rd
•Weight gain >2lbs/ week (2 trimester); 1 lb./week (3
trimester)
•Mild edema on face
3.Severe Pre-eclampsia
•B/P 160/110 mmHg or higher
•Protein 3-4 + on RS (5 gm/L)
•Oliguria 500 ml or < every 24 hours
•Cerebral or visual disturbances (headache/ blurred
vision)
•Pulmonary edema; extensive peripheral edema –
pitting edema
•Fetal mortality – 10%
•Hepatic dysfunction
•Thrombocytopenia

Description of Edema:
1+ Slightly idented
2+ Moderately idented
3+ Deeply idented
4+ Remain as a pit (pitting edema)
4.Eclampsia
•Mark S/S of severe pre-eclampsia + convulsion
 •15% maternal mortality due to:
oCerebral hemorrhage
oCirculatory collapse
oRenal failure
•Fetal prognosis poor – 25% mortality
oHypoxia with acidosis

Management:

1.Bedrest
2.Monitor m aternal well-being
3.Monitor fetal well being
4.Ensure safety measure
5.Proper diet
6.Promote relaxation
7.Administer medications

Management:

Mild pre-eclampsia – if pregnancy <36 weeks LS ratio decrease

l:2; conservative bring fetus to term

1.Promote Bedrest
a.Sodium is excreted rapidly and recumbent than in
activity
•Evacuation of sodium
•Encouraging/ promoting sodium
b.Labor and delivery needs and spends more energy
(save caloric expenditure)
c.Always on left lateral recumbent position
•Prevent uterus pressure on vena cava – promote
fetal circulation and prevent supine hypotension
syndrome
 d.Patient confinement
•Home; if non-compliant- hospitalization
2.Promote good nutrition
•Increase protein diet with no salt restriction
•Decrease salt or no salt in diet may activate
angiotensin system and increase B/P compounding
the problem
3.Provide emotional support with bed rest
•Do not take instructions seriously
•Medicines not bed rest
•Stop work
•Assess to bring concerns to open work, family,
finances

Severe Pre-eclampsia
1.Bed Rest
a.Admit to hospital
•Private room – undisturbed
•LLRP
•No loud noises – triggers convulsion
•Darkened room (no bright light)
•No visitors – social visitors not support people
2.Monitor maternal well-being
•B/P every 4 hours
•Blood studies – CBC, platelet, Hct, Hgb, Blood
Typing, fibrinogen
•EENT – optic fundus S/S (1) arterial spasm, (2)
edema, (3) hemorrhage
•Urine - >30 ml/hr, insertion FBC for accurate
recording, test for protein, maternal estriol level
•Weight – same time each day
3.Fetal well-being
 •FHT – external monitor (Doppler auscultation
every 4 hours)
•Oxygen administration – face masks
4.Safety
•Side rails
•Padded tongue blade

Diagnostic Tests for Hypertension

1.Roll Over or supine pressure test (SPT)

th th
•28 – 30 weeks of AOG
a. Lateral position – BP check
b.Roll to supine – BP check – repeat after 5 minutes
c.Diastole higher than 20 mmHg or more is significant sign

2.Mean Arterial Pressure (MAP)

•MAP = 1/3(S-D) + 80mmHg
•MAP = 96.6 mmHg
2
•MAP = 90 mmHg
3
•MAP = 105 mmHg
oe.g. BP = 120/70 mmHg = 1/3 (120-70)+80
= 1/3(50)+80
= 16.6+80 = 96.66
3.Infusion angiotensin II
•Results in increase BP (controversial)

Causes of Maternal Death: 15%

a.Aspiration pneumonia
b.Cardiac failure
c.Cerebral hemorrhage
d.Obstetrical bleeding secondary to ablation placenta

Causes of fetal death:

•Intrauterine growth retardation
 •Perinatal death
•Prematurity

Convulsions: (Grand Malconvulsion)

4 phases

1. Aura
•Epigastric pain, sharp smell sight of bright light
•Management:
1.Tongue blade placed in position promote safety
2.Tonic
•All body muscles contract back arch, arms/leg stiffen; jaw
closes abruptly (tongue maybe bitten); respiration halted
(last 20 seconds); cyanotic, cessation of respiratory
•Management:
a.Oxygen administration by mask
b.LLRP; place on side, allow secretion to drain
c.Fetal monitor
d.Insertion of tongue blade NOT RECOMMENDED
•Broken teeth
•Scraped gums
•Bitten fingers (nurse)
•Broken tongue blades
3. Clonic
•Muscle relax, contract, ext. flail
•Respiratory – inhale/ exhales irregularly; as thoracic muscle
relax and contract may aspirate saliva (place on sides) forming
at the mouth (mouth breathing) incontinence of urine and feces
 •Ineffective breathing – remain cyanotic; oxygen therapy for
fetus
•Last up to 1 minute

4. Postictal
•Semi-comatose, cannot be roused except with painful stimuli
•Last 1 –4 hours
•Labor may begin – still unconscious; cannot report labor
contractions painful labor contractions initiate another seizure
•Monitor FHB
•Check for vaginal bleeding every 15 minutes (abruption
placenta)
•Anticipate delivery
•Condition may stabilize in 12 –24 hours; prepare for vaginal
delivery (preferred method); induce labor. Why? Fetus does
not continue to grow after eclampsia (convulsion) occurs. Fetal
lung maturity appears to advance rapidly due to (intrauterine
stress) L/S ratio – mature
•C/S not best
•Disadvantage:
oHazardous to fetus – sufficient strain
oMother not a good candidate for GA and surgery

How to induce labor:

1.Rupture the membrane (ROM)

2.oxytocin drip (OD)

Proper diet and nutrition

1.increase protein – replace protein loss (proteinuria)
2.moderate sodium – sodium restriction (4-6 grams/ 24 hours)
Medications: to prevent eclampsia

IV line – ER medication route; observe insertion site carefully –

infiltration triggers convulsions
Diastole – not lower than 80-90mmHg

I.Hypotensive drugs
a.Hydralazine (Apresoline)
•Lowers BP by peripheral dilatation; DO NOT interfere
with placental perfusion
•S/E – Tachycardia
•Nursing Responsibility – (1) Check BP – pulse before
and after administration
b.Diazonide
•Hyperstat
•Cryptenamine
•Unitensin
•Produce rapid decrease in BP
•Do not use for long term; administration
causes hyperglycemia

II. Cathartics
•Magnesium sulfate
•5 actions:
oHypotensive – dilating effect to blood vessels
oDiuretic – reduce edema by causing shift of fluids from
ECS into intestine
oCNS depressant (blocks peripheral neuromuscular
transmission)
Lower possibility of convulsions
DOSE below – 4 grams in 100 ml D5W
Slow IV – 5 – 20 minutes duration effects 30 – 60
minutes
 IV infusion – 1 – 2 grams/ hour piggy back
IM – 5 grams of a 50% saline every 4 hours
Deep IM – to reduce pain mix with procaine
oAnticonvulsant
oTocolytic
NB. Blood serum level to be monitored
Blood serum Level of Magnesium Sulfate

Blood Serum Level: Response

4 – 7 mg/ 100 ml Therapeutic

level

8 – 10 mg/100 ml Decrease
patellar reflex/disappeared
10 – 12 mg/ 100 ml Respiratory
depression occurs

15 mg/ 100 ml and up

Cardiac conduction defects occur
Patellar Reflex
Scoring

Score: Findings:

0 No response, hypoactive, abnormal

1+ Somewhat diminished response but not

abnormal

2+ Average response

3+ Brisker than average but nor abnormal

4+ +Hyperactive, very brisk - abnormal

III. Diuretics
•Best in pre-eclampsia not in Eclampsia
•Decrease absorption of sodium, thus lowering sodium in
plasma  Fluid shift back from ECS into circulation and
excreted thru urine  edema reduced, plasma already
lowered will be depleted further which result to:
oPoor placental perfusion
oStimulate release of renin; to increases permeability of
glomerular vessels; to increase protein urea angiotensin =
increase BP thus worsening conditions
IV. Sedatives
•Barbiturates (Phenobarbital) PO, IM
•Care should be taken not to depress baby diazepam (Valium)

Nursing Care Management:

1.Assess patellar reflex

2.Assess urine output
3.Assess respiratory rate
4.Keep ready – 10 ml/ 10% of calcium gluconate (antidote
magnesium sulfate) 1 gram
5.Severe oliguria – IV infusion of Salt poor abdomen (colloid
saline will “call” fluid into IVS by osmotic pressure – kidneys
excrete extra fluid with Magnesium Sulfate
 6.Watch for fetal depression – crosses placenta results to:
•Late deceleration
•Sonogram decrease fetal
movements
•Decrease heart beat
7.Administer continued for 12-24 hours to prevent eclampsia,
dose then tapend D/C BF – should be delayed until drug is
discontinued.

Diabetes Mellitus in Pregnancy

1921 – synthetic insulin was discovered

Before 1921 – without insulin

1.Women failed to survive to reach childbearing age
2.Infertile
3.DM causes spontaneous abortion

After 1921 – with insulin

1.Being women thru pregnancy with good control
st
2.care for newborn infant during 1 24 hours after delivery
3.protect infant in utero from adverse effects of DM

S/S:
1.Polydypsia
•Increase fluids to compensate fluids loss
2.polyuria
•Decrease osmotic pressure, increase amount of glucose
in urine; decrease fluid absorption in kidney
3.polyphagia
•Used up nutrients except glucose
4.Glucosuria
 •Kidney attempt to lower glucose level excrete large
quantities into urine

Physiologic Changes:
1.Increase insulin requirement in pregnancy
st
2.Hypoglycemia – 1 half of pregnancy; acidosis; coma – last
trimester
3.Decrease carbohydrate metabolism
4. Stress increase glucose tolerance
5.Increase estrogen level during predisposes DM in pregnancy
(gestational DM)

Assessments:

I.PE – History (large babies, unexplained fetal loss, congenital

anomalies, and family history of DM)
II.Laboratory exams and tests
i.Glucose screening
•Blood
1.FBS – NV 80 –120 mg% (serum)
2.Glucose tolerance test (oral, IV)
One-hour-gtt
a.Fast 8 hours
b.FBS taken more than 90 mg/dL
c.50 grams glucose load
d.After 60 minutes – higher than 140 mg/dL
glucose (NB: if result is positive, patient is
to undergo 3O drop three-hour-gtt)
Three-hour-gtt
b.fast 8 hours
c.FBS taken – 105 mg/dL
d.100 grams glucose load
e.after 1 hour – more than 190 mg/dL
f.after 2 hours – more than 165 mg/dL
g.after3 hours – more than 145mg/dL
 3.HGT (Hemoglucotest)
•Urine
a.Strips that measure only glucose –
preferred method e.g. Clinistik, Testope
i.Breastmilk (lactose) spills into urine
and cause positive reaction
b.Test on strips that measure all sugar e.g.
benedict’s test, clinitest

III.Opthalmic exams
i.DM retinopathy
1.Increase exudates
2.Hemorrhage
3.Edema

Pricilla White’s Classification of DM in Pregnancy (used

to predict pregnancy outcome)

Class Description

A gtt – only slightly abnormal; dietary regulation is minimal; no

insulin
B Dm less than 10 years duration or Dm begins at ages 20 or
older no vascular
involvement
C DM begin between 10 and 19 years or DM lasted from 10-19
years, there is minimal vascular involvement
D DM 30 years or more or DM begun before ages 10 years,
there is greater vascular involvement
 D Subclasses
D1 under 10 years of onset
D2 more than 20 years duration
D3 beginning retinopathy is present
D4 calcified vessels of legs are present
D5 Hypertension is present

E DM with calcification of pelvic arteries seen in X-rays

F DM with nephropathy
H DM with cardiomyopathy
R DM with active retinitis obliterans
T DM have had kidney transplant

Analysis

1.Class A high fetal survival

2.Class D and E – perinatal mortality is 20%
3.Class F and R – perinatal mortality is close to 100% (not to
be pregnant)
4.Class T – can complete pregnancy successfully

Management and Nursing Interventions:

1.Educate on diet during pregnancy

•Good disease control
•Diet regularly should be started as soon as DM is
diagnosed in pregnancy
•Diet control is done to:
oMaintain an adequate glucose intake 80%
oprevent hypoglycemia during pregnancy due to
nausea and vomiting
o1800 – 2200 calories – 3 meals +3 snacks evenly
(less than 1800 calories cause breakdown of fats
=Acidosis)
 ohypoglycemia at night – due to continuous fetal
use of glucose when woman is asleep; final snack
of protein or complex carbohydrate (slow digested)
oDaily nutrient proportion:
20% of protein – 1.3 – 1.7 gm/Kg BW or 125
grams of Protein
50% of carbohydrates – 200 – 500
grams/day
30% of fats – 70 –80 grams/day
oDecrease saturated fats and cholesterol and
increase amount of dietary fibers; high fibers
reduces postprandial hyperglycemia and lowers
insulin requirement
oSuitable weight gain – only 25 lbs.
Limit fetal size to facilitate vaginal delivery

2.Educate on Exercise
a.Goals:
i.Reduce serum glucose
ii.Reduce insulin requirement
1.Exercise program should begin before pregnancy and
not during pregnancy
i.To avoid excessive glucose
fluctuations
ii.Exercise effect last – 12 hours after
exercise
2.Eat protein and carbohydrates complex before exercise
3.Exercise program should be maintained consistently
e.g. best exercise – 30 minutes walking once a day same
time
3.Educate on insulin
a.Hospital admission only for insulin adjustments
b.Change of insulin done – change in metabolism
 i.Early pregnancy – less insulin – fetal developing
cells take more glucose
ii.Late pregnancy – more insulin
c.Oral hypoglycemics not used during pregnancy because
it crosses placental barrier and is potentially teratogenics
d.Humulin Insulin – provokes lesser antibody response
than beef and pork
e.Insulin peaks – makes monitoring meaningful
f.Regular insulin – pre-breakfast 30 minutes to 1 hour or
after breakfast
g.Intermediate – given in the morning – lunch or late in the
afternoon; given in the afternoon peak reaches at rest day
before breakfast
O
h.Injection site – related – 5/8 inch needle – 90 insulin
syringe; arm absorb – than thigh

IDM – will result if DM in pregnancy is poorly controlled

Characteristics:

1.Typically longer and weighs more >9 lbs. (infantile giants)

2.Greater to have congenital anomalies (cardiac defects)
3.Caudal regression syndrome or hypoplasia of L.E
4.cushingoid (fat and puffy)
st
5.Lethargic and limp – 1 few days of life
6.Large size is deceptive
7.polycythemia – to prevent: avoid clamping of cord early to
prevent RBC overload from placenta
8.Will show greater proportion of weight loss from extra fluid
accumulation – prevent accumulation

Complications:
1.Macrosomia – C/S
2.Severe hypoglycemia
3.Hyperbilirubinemia
 •Due to inability of the liver to clear bilirubin from
system at this immature age
•Normal value:
st
o<6 mg/dL Newborn 1 day
o<12 mg/dL 3-5 days
o0-1mg/dL adult
4.hypocalcemia
•lowered blood calcium level due to change in calcium or
phosphorus metabolism (breastmilk)
•Normal Value:
i.9 – 11 mEq/dL Newborn
ii.7-5 mg/dL Adult

•Signs and symptoms: Latent tetany

•(Clinical Manifestations)
a.Chvostek’s Sign
•Ear tapped and facial muscle contract
unilaterally
a.Trousseau’s sign
•Constricts arm 2-3 cm with tourniquet and
blanched and results to carpal spasms
a.Peroneal Sign
•Fibular side of leg is tapped foot abducts and
dorsiflexes
a.Erb’s sign
•Galvanic current is applied over peroneal
nerve, foot abducts and dorsiflexes

Post-partal Adjustments

1.Re-adjustment of insulin to non-pregnant requirement

 a.Gestational DM, glucose normalizes after 24 hours post
delivery; BF- insulin does not pass to breast milk from
bloodstream; hydramnios was present – watch for
hemorrhage
b.Use contraceptives:
i.Pill – high risk for hypertension – estrogen
ii.IUD - high risk for infection
1.plan for next pregnancy – disease must be
stabilized in good control

Tests for Placental function and fetal maturity

I. Amniocentesis
a.L/S ratio – NV 2:1; in DM 3:1 90% reliable lecithin/
spingomyelin – fetal lung maturity synthesis of
phosphatidylglycerol compound that stabilizes surfactant is
delayed in DM
b.Creatinine concentration – excreted in fetal urine; assessfetal
renal function and fetal muscle mass; Normal Value >= 2
mg/dL = 36 weeks of AOG 60% reliable
c.Bilirubin levels – measures liver maturity; Increase level –
abnormal; decrease – normal
d.Cytologic findings – staining of cells with 0.1% nile blue;
nitrate – 20% fetal cells stained

Contraindicated – Amniocentesis
1.Abruptio placenta
2.Placenta previa
3.History of premature of labor
 4.Inc cervix

Kleihaver-Boetke – test to determine whose blood stained of the

amniotic fluid; stains fetal blood/cells Pink

II. OCT – oxytocin challenge test

•Use of temperature stress in a form of utrerud contractions is
applied to the fetus; FHB remain normal
•Normal Value: Negative

III. Estriol excretion studies

O
•Normal Value: >12 mg/ 24
•Continuous rising estriol values indicate normal fetal growth

IV. Non-Stress test (NST) 99% reliable

•Normal Value: Reactive fetus (heart rate acceleration
associated with fetal movement)

V. Ultrasonography (OB echography)

•Harmless, non-invasive, use of sound waves
•Uses:
oDiagnosis of pregnancy
oAssess tumor, molar pregnancy
oDetermine fetal age
oMeasures fetal growth
oIdentify placental abnormality
oDetermine fetal position
•Procedures:
oFluid – water 3-4 glasses one hour before study; ASK
NOT TO VOID – good transmission of waves better
visualization of uterus
 oApply conduction paste cream – enhance transmission
and reception
oContraindicated: recent GI contrast studies – causes
distortion of reflected sound waves

Infant of a Diabetic Mother

Anemia and Pregnancy

Pseudoanemia
•Blood plasma volume expands during pregnancy
•Limits oxygen exchange at the placental site because of the
reduced amount of oxygen present
•Alteration in tissue perfusion (placenta)
o20% of pregnant women
oIncrease puerperal complications esp. infection
o90% - of all anemia – iron deficiency anemia
o10% - other anemias

Circulatory changes in pregnancy (Increase to)

•plasma volume – 30%
•RBC vol. – 20%
•Hgb – 12 – 15%

Blood volume expected to drop (decrease)

th th
•30 – 40 weeks of AOG – due to fetal consumption (circ.)

Anemia in Pregnancy defined:

1.First trimester
•Decrease 11 gm/ dL – Hgb and 37% Hct
2.Second trimester
•Decrease 10.5 gm/dL – Hgb and 35% Hct
3.Third trimester
•Decrease 10 gm/dL – Hgb and 33% Hct
4.High in altitude
•5,000 ft. above sea level
•14 gms/dL – anemia hemoconcentration
Common type of anemia:

I. Iron deficiency Anemia

Causes:
•Poor diet
•Unwise weight reduction program
•Heavy menstrual period

Fetal Outcome:
a.Decrease birth weight
b.Prematurity

Rx: Iron supplement – FeSO4 0.3 gm TID or 1 gram OD

If constipated, take Colace

II. Folic Acid deficiency Anemia (Megaloblastic anemia [enlarged

RBC])
Causes:
•Poor diet
•Cooking in large volume of water
•Malabsorption

Effects:
•Early abortion
•Abuptio placenta
•UTI

RX: Folic acid supplement – 150 ug OD; 5 mg OD maintenance

dose

III. Sickle cell anemia

•Recessively inherited hemolytic anemia
Chances:
•1 out of 12 black American has the sickle cell trait which will
predispose them to: polynephritis, bacteriuria, UTI, hematuria

Occurrence:
•First trimester: Nausea/ vomiting
•Second trimester: pooling of blood in LE
•Third trimester: infection, fever, dehydration

Assessment:
•Diet: decrease water
•Activity: prolong standing (Elevate legs, side lying position)
•Hgb: 6-8 mg/dL – hemolysis can occur if hemoglobin falls to 5-
6 mg/dL
•Hyperbilirubinemia – no conjugation of bilirubin since RBC are
quickly destroyed-jaundiced sclera

Management:
•Oral contraception – C/I
•No iron supplement
oCells cannot incorporate iron-binding to iron-build-up

1.Prevent crisis – exchange transfusion

2.Crisis throughout pregnancy
3.Sickle cell crisis
a.control pain
b.oxygen administration
c.increase fluids
4.delivery – nerve block not GA; avoid tissue anoxia
5.give folic acid – prevent new cells to be megaloblastic
6.prevent infection
Alcohol in Pregnancy and the Newborn

(Ethanol) – substance

Ethanol crosses the placenta (teratogenic) => result to:

I.FAS (fetal Alcohol syndrome)

•Intake of 2 oz. Of alcohol/ day or increase level of alcohol
ingestion during pregnancy
•Prominent nose and bird-like face
•Acetaldehyde
•S/S: post partum manifestation
i.tremors
ii.fidgety
iii.irritable
iv.weak suck reflex
v.always awake or asleep
vi.distinct facial feature as short palpebral fissures,
hypoplastic upper lip (thinned upper lip), thin
vermillion, short upturned noses and flattened nasal
bridges and epicanthic folds
vii.small eyes
viii.flattened maxilla
ix.hirsutism
•long term effects:
a.mental retardation (pre-post natal)
b.growth retardation
c.central nervous system involvement (behavior
problem – hyperactive in school)
d.microcephaly
e.joint and cardiac anomalies
II.Neuroblastoma – a form of cancer
III.Withdrawal symptoms (syndrome)
Management:
•Advice mother to quit alcohol or avoid alcohol when pregnant

Reasons of taking alcohol:

1.Social
2.Therapeutic – ethanol has a tocolytic effect – halt labor (stops
prostaglandin production which is responsible for progress of
labor)

Smoking, Pregnancy and Newborn

Nicotine - >10cigarettes/ day

Harmful to fetus because:

1.Carbon monoxide entrapment by the placenta – decrease
blood flow => uterine hypoxia
2.Vasoconstriction of the uterine vessels – decrease tissue
perfusion
3.Constriction of uterine arteries
Effects:
I. Fetus
1.Premature rupture of the membranes
•Vasoconstriction action of nicotine
•Increase level of CO in blood stream
2.Small for gestation age (SGA)
3.Underweight (IUGR) –Intrauterine growth absorption
•Decrease supply of nutrient and oxygen
•Smokers eat less

Nursing responsibilities:
 1.Advice mother to quit smoking or < smoking less 10 cigarette/
day and none within 48O of delivery
2.Nutritional counseling – avoid junk foods, nutritious food
intake
3.Join non-smoking or stop smoking group.
4.Please No Smoking signs in areas of pregnant mothers
5.Health care provider to serve as model
6.Quit smoking not only for fetus but for self

II. Mothers
1.Halitosis, stained teeth, lips and finger’s
2.Habit forming

Drug Dependence, Pregnancy and the Newborn

Drug abuse -overuse of one or more drugs without

medical prescription
Drug dependence -craving a particular drug for psychological
and physical well-being (influenced)
Drug addiction -using habitually or compulsively
Drug tolerance -capacity to absorb a drug continuously in
large dose without adverse effects

Use of amphetamines, narcotics,barbiturates and alcohol-drug

dependence

CARR – identified factors (3) why a woman becomes involved

deeply in drug
dependence
1.She is from a disrupted family background
•Left home as early as adolescent
•Few meaningful support people
•Few skills or little education
2.She had negative sexual experiences
•Victim of rape and incest
 3.She has low self-esteem
•Ease psychological pain
•A sense of emptiness
•Promote social interactions

Effects:
I. Maternal
•PIH, phlebitis, sub-acute bacterial endocarditis, Hepa B, HIV
(shared infected needle)

II. Fetus
1.FOD – (fetal opiate dependence) with following
characteristics:
•Small for gestational age, fetal distress, meconium
aspiration, SIDS, withdrawal symptoms
2.Physiologic – advantages
•liver forced to mature; decreased
hyperbilirubinemia
•fetal lung to mature; decrease SIDS
3.S/S of withdrawal symptoms
a.Sleep pattern disturbance
b.Abrasions on knees, elbows and nose
c.Others as: vomiting, high pitched cry, sneezing,
diarrhea, poor feeding, excessive sweating, tachycardia
Management:
I. Mother
1.Enroll in a methadone maintenance program during
pregnancy
•Supplied legally, readily available, aseptically
administered, monitored, fetus assured of better
nutrition
2.Reassurance
•“Everything is doing well”; emotional support
 3.Anticipatory guidance throughout pregnancy (no one to
share their problems)

II. Infant
1.preserve heat
2.isolate the infant
3.prepare for NGT insertion if with poor sucking reflex
4.administer IVF for excessive vomiting and diarrhea
5.give sedation – diazepam (valium)
6.high incidence of jaundice if not enrolled in methodone
program – skin care

Thyroid Disease, Pregnancy and the Newborn

Hypothyroidism Hyperthyroidism
- rare condition in young adult - common in pregnancy
than hypo.
- if untreated, woman is unable to - C/M:
conceive- unovulatory *rapid heart rate
-C/M: *Exopthalmos
*history of spontaneous abortion
*easy fatigability *nervousness
* obese, dry skin (myxedema) *palpitations
(tachycardia)
* cold intolerance *weight loss
*if undiagnosed may lead to:
>HPN of pregnancy
>premature labor
Management:
Thyroxine prep. Diagnostic
- To replace what is absent - radioactive uptake of
131
I subtype
during pregnancy, dose is increased
to sustain pregnancy
 after delivery, dose is tapered back this procedure
to pre-pregnant dose; if not then
woman will develop hyperthyroidism
should not be used
during pregnancy
because fetal thyroid
incorporate this drug
and results to fetal
thyroid destruction

effects to fetus: RX:

No known side effects to fetus if dose is - thioamides
Monitored accordingly
(methimazole or
propylthiouracil
* reduce thyroid activity

Management: Effects:
1. Keep dose to the lowest; prevent omission *terratogenic – enlarged
thyroid and
or duplication [goiter]) in the fetus
2. Should not Breastfeed as drug is excreted in * obstruct airway and
make
breast milk resuscitation difficult
in Newborn
Surgical Management: *potential for
bleeding during
- removal but preferably an interpregnancy delivery

procedure
Tuberculosis, Pregnancy and the Newborn
Etiology:
•Mycobacterium Tuberculosis – acid fast bacillus
•Positive PPD-sensitized T lymphocytes

Mode of transmission:
•Droplet

Effects to mother: Risks

I. Mother
Pre-partal:
a.Gravid uterus pushes diaphragm and lungs to
different shape may rupture calcified lesions activating
disease (PTB)
b.Pushing during labor; increase intrapulmonary
pressure
Post-partal:
c.Lungs suddenly returns to pre-pregnant position and
breaks open calcified lesion
II. Drugs – without apparent teratogenic effects
Management:
1.No pregnancy until PTB becomes inactive about 1-2 years
•TB lesions never actually disappear but only
“closed off” and made inactive
2.Maintain adequate level of calcium during pregnancy to
ensure TB pockets “closed”
•Calcium supplements must be given
Effects to infant:
Spread thru:
1.Placenta (circulation)
2.after birth (droplet)
a. Should have 3 concentrated negative sputum for AFB
b. Holding and caring
c. No need to be isolated
d. Newborn with INH prophylaxis
 a.Skin test with 3 months intervals
b.If mother is on INH and infant also on INH – infant
should not be breastfed causes overdose (toxic effects)

Rh – ABO incompatibility
Incidence:
Rh negative mother
•D- antigen
•dd – genotype

Rh positive fetus
•DD – genotype
•Dd – genotype

Rh positive father
•DD – homozygous
•Dd – heterozygous

DD – 100% of children Rh positive

Dd – 50% for trait

100% D D Dd 50% D d Dd

DD Dd DD dd

Pathophysiology:
D antigen (protein factor) an
Rh positive has that Rh-
negative do not have

Rh positive fetus – mother’s

body invaded by a foreign
antigen
 Mother’s body reacts by
forming antibody

Rh factor (fetus) exist as a position of the RBC

in Rh invasion entire RBC must be destroyed
(hemolysis of fetal blood cells occur)

Fetus becomes deficient of RBC (decrease

oxygen transposrt to fetus)

Causes Hemolytic disease of the Newborn or

Erythroblastosis fetalis

No connection between maternal and fetal blood during

pregnancy so mother is not exposed to fetal blood

Occasional villus rupture allowing a drop or two of fetal blood to

enter maternal circulation, which initiates antibody production

As the placenta separates following delivery of the

newborn, there is now an active exchange of fetal and
maternal blood from damage villi

Maternal antibodies are formed against Rh positive blood

by an Rh negative mother in the first 72 hours after

Woman is advised that she should have no more than 3 children

As number of pregnancy increases, amount of

antibodies formed also increases; in many women, a
lethal number of antibodies would be present when 3rd
pregnancy begins
Diagnostic:
1. Anti-D antibody titer test at 1st ANC (32 or 38 weeks of AOG; 0-minimal
l=8)
Titer increases or positive
1st pregnancy – Rh sensitization
oMonitor every 2 weeks throughout pregnancy
oMonitor fetal well-being every 2 weeks or months by
amniocentesis

2. Spectrophotometer
amniotic fluid reveal fluid density - extent of involvement and bile level;
if density remained low (no fetal distress, Rh negative fetus)

Therapeutic management:
I. RhIg (RHO (D) immune globulin) RhoGAM

commercially prepared of passive antibodies against Rh-factor


given to mother 72 hours after delivery of an Rh positive child;
mother forms no maternal antibody
RhIg – passive antibody protection (transient) 2 weeks – 2
months, the passive antibodies are destroyed

Effects:
1.Only those antibodies during pregnancy are left – thus every
pregnancy is like 1st pregnancy  lesser antibodies  assuring
safe intrauterine environment to succeeding pregnancy
2.Newer techniques
RhIg given at 7 – 9 months AOG offers more protection

 RhIg – do not cross placenta in late pregnancy – do not
destroy RBC *antibodies are not the IgG class – the only
type that crosses placenta
RhIg – is ineffective to a woman who is already sensitized to
Rh factor

Reasons why currently Rh sensitization is still a complication of

pregnancy:

1.Childbearing began before RhIg was available -  Rh

antibody titer in blood
2.Woman do not receive RhIg injection following abortions or
ectopic pregnancy so antibody formation begins; when to give
RhIg injection – 32 – 39 weeks AOG no change in woman anti
D fetus
a.Fetus Rh positive

II. Intrauterine Transfusion

Dangers of rising antibody titer in pregnancy:

1.Stillbirth
2.Died of neonatal heart failure (erythroblastosis fetalis)
3.Suffered brain damage
Motor and mental retardation from  bil. level
(Kernicterus)
Injection of red blood cells directly into a vessel in the
fetal cord using amniocentesis techniques using “O”
negative – 75 – 150 ml depending on fetal age
Risk:
1.Cord vessel laceration by needle
2.Uterus irritation by invasive procedure that labor begins
to reduce the possibility of the fetus receiving virus –
contaminated blood – the woman donates blood herself
 woman restore blood volume promptly so no fetal or
maternal injury or hazard will result
Frequency:
once during pregnancy but can be injected every 2 weeks for
5-6 times
Delivery:
once fetal lung maturity is reached
Reassurance:
Day to day approach
III. Exchange transfusion:
To remove hemolyzed cells replace with healthy cells (after
delivery)
Rh – Incompatibility

Pregnancy
(Fetal blood) – Transfer of
Rh antigen into maternal
circulation

M
F

F
 Transfer of Rh
Note: Rh dd mother Antibodies into
Rh DD / Dd fetus fetal circulation
• antibody
F
During normal
Pregnancy → no Hemolysis of RBC in Fetal
connection between Blood Erythroblastosis Fetalis
1st pregnancy
M - maternal and fetal (hemolytic disease of the
Initiate maternal
- - blood newborn)
- antibody production
+
to Rh + blood of fetus
+ +
+
F

M - M +
- - - +
- + -
Occ. Villi rupture
+ + (Desensitization)
allowing a drop or + + + + Rh0D or RHIG
two of fetal blood to + +
F F (Rhogam)
maternal circulation
1.At 7 – 9 months
pregnancy
2.72 hours after
delivery → destroys
After delivery of fetus→ the antibodies
more antibodies formed formed in maternal
against fetal blood in blood in 2 weeks to
maternal circulation 2 months time -
M -
- - transient only those
- antibodies during
+ +
pregnancy are left
+
+ +
(1st pregnancy)
+
F
 2nd pregnancy just like 1st
M - pregnancy, ↑ fetal
- -
+ survival up to 3rd
- pregnancy
+
+ +
+
F

Multiple Gestation

Gestation of 2 or more fetuses with considered as a condition

complicating pregnancy because the mother’s body must
adjust to the effects of more than one fetus

Incidence:
Frequent in non-whites
 in woman’s parity, age, inheritance
dizygote twins has a familial maternal pattern

Types:
I. Twin

Dizygotic Monozygotic
2 ovas 1 ova
2 spermatozoa 1 spermatozoa
2 placentas 1 placenta
2 amnion 2 chorion 2 amnions 1 chorion
2 umbilical cords 2 umbilical cords
Same or different sexes Same sex always
Familial maternal pattern

II. Multiple gestation pregnancy

3-4-5-6 etc
Assessment:
 uterus size; rate faster than usual
ultrasound reveals multiple gestation
Alpha – fetoprotein levels – elevated
Quickening – flurries of action at different portion of the
abdomen rather than one persistent portion (foot area)
2 or more FHB one FHB when other twin’s back at woman’s
back
 appetite
discovered at delivery when uterus not empty backache and
fatigue

Effects to mother – susceptible to: PIH, Hydramios, placenta

previa, anemia
Fetus – prematurity
Management: Bring pregnancy to term

Hyperemesis gravidarum
pernicious vomiting – is nausea and vomiting of pregnancy
that is prolonged past 12 weeks of AOG

S/S:
dehydration, ketonuria, and significant weight loss

Normal Pregnancy:
1.more severe in the morning; woman shuns breakfast
2.noon – nausea disappear – woman eats more
3.dinnertime – prepare lunch = adequate NUT maintained

History of prolonged vomiting past 12 weeks AOG

Assessment:
1. hematocrit or  hemoglobin – hemoconcentration –
dehydration
 2. Na (136 – 145 mEq/L), K (*3.5 – 5 mEq/L), Cl (90 – 110
mEq/L)
3.Polyneuritis – secondary to Vitamin B deficiency
4.weight loss and ketonuria – breakdown of fats and protein –
intrauterine fetal growth retardation

Management:

1.Admission prolonged hospitalization = social isolation

st
2.NPO – 1 12 hours + 3L/LR + B complex
3.sedation – rest Phenobarbital
4.antiemetics (with fetal risk)
5.no visitors – til no more vomiting
6.clear liquids
7.dry toast, crackers, or cereal every 2 – 3 hours
8.soft – astol
9.all above ineffective TPN

Pseudocyesis
false pregnancy

Assessment:
all S/S of pregnancy (Probable)
abdominal enlargement up to 7 – 8 mos. AOG
uterus empty on Ultrasound

Factors:
1.Wish Fulfillment
Woman’s desire to be pregnant = physiologic changes

2.Conflict Theory
Desire or fear of pregnancy = internal conflict leading
to physiologic changes
 3.Depression Theory
Depression attributes the cause to create physiologic
changes

Management:
Psychologic counseling – to learn how to better handle
her needs or conflict

Precipitate labor/ delivery

Occurs when uterine contractions are so strong that the

woman delivers with only a few rapidly occurring contractions
Labor that is completed in less than 3 hours
Likely to occur in multipara, following induction of labor or
amniotomy

Risks:
Fetus – sub-dural hemorrhages (sudden release of pressure
on the head)
Mother – lacerations of the birth canal, premature separation
of the placenta (strong sudden force)

Goal:
To bring the delivery in a controlled surroundings to prevent
risks to fetus and mother

Theories behind precipitate labor:

1.Uterine stretch theory
2.oxytocin theory
3.progesterone/prostaglandin theory
4.placental degeneration
Premature labor/ Delivery
or preterm labor
unknown cause
occurs in approximately 10% of all pregnancies
occurs before the end of 37 weeks AOG or before fetus
weigh 2500 gms.
Results in an immature infant, 2/3 neonatal death is due
to low birth weight

Conditions resulting to premature labor:

1.Cervical surgery as cone biopsy
2.Chorioamnionitis
3.Hydramnios
4.Multiple gestation
5.Maternal age
6.Previous preterm labor
7.Polynephritis, UTI
8.Short inter-pregnancy period
9.Smoking
10.Strenuous or shift work
11.Uterine anomaly as tumor

Assessment:
1.More painless uterine contractions (30seconds duration, or
frequently as every 10 minutes for more than 1 hour)
2.More backaches
3.More vaginal discharges
 4.Associated with UTI or chorioamnionitis

Managements:
1.Halt Labor when [Criteria]
Fetal membranes are intact [BOW]
Fetal heart sounds – good
No evidence of bleeding
Cervical dilatation not more than 3-4 cms
Effacement not more than 50%
(Note: all these criteria must be present)

Measures to halt labor: use of tocolytics:

1.Ethanol
(ethyl alcohol) administer IV
blocks the release of oxytocin by the pituitatry glands
thereby blocking or delaying labor pains
stops production of prostaglandin stopping labor pain
(Note: new knowledge on the effects of alcohol on a growing fetus
nor made halting labor with the use of alcohol questionable thus
use of this method is no longer advised)

2.Beta – sympathomimetic drugs

Most frequently used beta receptor sites
Adipose tissue, heart, liver, pancreatic cells, GIT and
other smooth muscles as uterine muscles, bronchi,
blood vessels

Beta Adrenergic  myometrial cells  release of adremycyclase

 triggers conversion of adenosine triphosphate into  cyclic
adenosine  this substance is responsible for reducing the
intracellular concentration of calcium through protein binding 
with lowered IC calcium concentration, muscle contraction is
ineffective and uterine contractions stop thus labor is halted

e.g. Nifedifine – calcibloc/ adalat [calcium channel blocker]

Check vital signs every 4 hours
Antidote: propanolol [Inderal]

3.Ritodrine Hydrochloride [Yutopar]

Terbutaline (Brethine) – most used
Check pulse – should not be given if pulse exceeds
120 BPM
Also acts entirely on beta 2 receptor sites
Mild tachycardia and hypotensive effects

Beta 2 receptors relax, however bronchial and blood vessels relax

along with the uterine muscles  labor is halted but  hearty rate
increases to move blood effectively  hypocalcemia may occur
from a shift of K into the cells  blood glucose and plasma insulin
increase  pulmonary edema occurs  headache, nausea and
vomiting due to dilation of the blood vessels also manifestes
(note: use with caution in patients with DM – increase BS overly
DM, thyroid dysfunction)
4.MgSO4
Effective to halt labor
Check for signs of toxicity
5.Other Measures
a.Bedrest – to take the pressure of the gravid uterus off
the cervix
b.Hydration – oral, hydration affects the secretion of ADH
and oxytocin by the pituitary gland – oxytocin causes
uterine contraction
c.Avoid psychologic stress
d.Administration of corticosteroid (betamethasone) to
hurry formation of fetal lung surfactant
Premature infant

An infant viable – born before the completion of 37 weeks

AOG (premature in age)
Weighs between 1500 – 2500 grams without regards to
gestational age (premature in weight

Etiology:
1.Unknown
2.Maternal factor
Chronic poor nutrition, DM, multiple births, drug abuse,
IUD in utero, chronic diseases – anemia, heart and
kidney diseases, infection, complication of pregnancy
as PIH and bleeding
3.fetal factor
chromosomal abnormality, anatomic abnormality, feto-
placental unit dysfunction

Characteristics:
I. General appearance
head disproportionately large
hair – lanugo, flaky
fingernails – soft
poor ear cartilage
skin – thin, capillaries visible
lack of subcutaneous fats
sole of feet – smooth (36 weeks AOG, 1/3 of foot is
creased; 38 weeks AOG 2/3 of foot is creased)
breast buds – 5mm (36 weeks AOG none 38 – 3 mm)
testis – undescended, scrotal rugae, very fine
labia minora – undeveloped
abdomen – relatively large
 thorax – relatively small
muscle tone – poor
reflexes – weak
“OLD MAN FACIES”

II. Altered Physiology

immature poorly developed system

A. Respiratory system
respiratory distress – cyanosis
breathing labored irregular, period of apnea
abs. – cough reflex

B. Digestive system
malnutrition
stomach is small – vomiting
 fat absorption
C. Poor thermal stability
 subcutaneous fats – no heat storage and insulation limited
ability to shiver due to poor vasomotor control of blood flow to
skin
 sweat glands – cannot perspire under 32 weeks AOG
large skin area compared to body weight

D. Renal Function
 sodium excretion;  Potassium excretion (hyponatremia
vs. hyperkalemia)
 ability to concentrate urine (prone to dehydrate with
vomiting or diarrhea)
 ability to acidify urine (glomerular tubular imbalance 
accounts for sugar, protein, amino acids, and sodium presence
in urine)
E. Nervous system
center for function control poorly developed
slow response to stimulation
suck, swallow, gag, poor feeding and aspiration are problems

F. Infection
no active immunity, no passive immunity (IgM)
limited chemotaxis (reaction of cells to chemical stimuli)
decreased opsonization (prep. Of cells to phagocytosis)
limited phagocytosis (digestion of bacteria by cells)
decreased anti-inflammatory response (hypofunction of
adrenal glands)

G. Liver function
no ability to handle and conjugate bilirubin (NV: 1 – 12 mg/dl =
NB)
hypoglycemia – does not store or release sugar well
anemia – study  in hemoglobin and production of blood (NV:
hemoglobin NB 12 – 24 gms/dl)
prone to hemorrhagic disease – does not store Vitamin K

H. Eyes
retinal atresia
RFP – retinal detachment
Note: if given oxygen beyond needed

I. Circulatory system
Anemia, polycythemia

Complication:
1. System problem – severity depends on gestational age
2. Major -  birth weight
Note: 1st 24 hours of life, most critical, nursing care depends on
the problem (physiologic)

Postmature pregnancy, delivery, infant

Post-gestational, post-mature
Pregnancy beyond normal AOG – (38 – 42 weeks)
Occurs approximately 10% of all pregnancy

Factors:
1.Faulty due date
E.g. women with long menstrual period or cycle 40 – 45
days – delivery will be late about 12 – 17 days
2.True overdue due to
a.Salicylate ( dose) – for severe sinusitis, headache:
interferes with prostaglandin synthesis which is
responsible for the initiation of labor
b.Myometrial quiescence or uterus do not respond to
normal labor stimulation

Risks:
1.Placenta is unable to adequately function due to  placental
perfusion
2.oligohydramnios <AF – lack of oxygen, fluids and nutrients
3.macrosomia – determine bi parietal diameter
4.meconeum aspiration

Nursing Care:
1.Predict true gestational age – fundic height
2.palpate gross fetal size
3.induce labor – prostaglandin gel, oxytocin drip – CS
Post-Mature Infant

Whose gestation age is 42 weeks or longer

May show signs of weight loss with placental insufficiency

Develop post-mature syndrome

Etiology:
1.Unknown in many instances
2.Maternal Factors
a.Primi and high parity at given age
b.Prolonged gestation in preceding pregnancies

Characteristics: (Seen in 44 weeks or more)

I. Physical Appearance
Reduced subcutaneous tissues
Loose skin turgor at buttocks and thighs
Long curved fingernails and toenails
 Amounts of vernix caseosa
Hypoglycemia-no adequate stores of glycogen
Abundant scalp hair
Poor temperature regulation-Low levels of subcutaneous fat
Wrinkled macerated skin, pale, cracked – parchment- like skin
Alert appearance – 2-3 weeks old infant after delivery
Greenish-yellow stain on skin – fetal distress (meconeum
aspiration)
Intrauterine malnutrition and hypoxia =  placental perfusion
=  oxygen and nutrients
 Low levels of estrogen
One post-term to another post-term
Maternal weight loss and decrease uterine size

III.Complications:
IV.
Meconeum aspiration, hypo or hypercalcemia,
polycythemia(decreased oxygenation), pulmonary
hemorrhage, pneumonia, asphyxia neonatorum,
pneumothorax

Note: severity of problems depends on length of gestation.

Nursing Care is the same with premature

Postpartum Complications

I.Infection
II.Psychosis

I. Endometritis
Inflammation of the lining of the uterus –
endometrium,
often at the site of placental implantation
Incidence is higher after CS
 An ascending infection

Assessment:
rd
3 or 4th day puerperium
Chills
Loss of appetite
WBC: 20,000 – 30,000
General body malaise
Abdominal tenderness
“Boggy” uterus
O
Temperature over 38 C

Strong after pains

Lochia – dark brown, foul

Treatment: Antibiotics, oxytocin, analgesics

Nursing Management
1.Send specimen for lochial culture
2. oral fluids
3.good hand washing
4.fowler’s position – drain secretions
 5.ambulate

Complication tubal scarring – infertility

II. Thrombophlebitis
inflammation of the blood vessels with
formation of clots
Extension of endometrial infection

Precipitating factors
blood clotting abnormality-increased
fibrinogen
dilated veins
pooling
stasis and clotting of blood in LE-
prolonged in stirrups

Types:
a. Femoral
th
femoral, saphenous and popliteal 10 day
postpartum
 “milk leg” or phlegmasia alba dolens”
(white, inflammation)
Homan’s Sign (+)
4-6 weeks

b. Pelvic – ovarian, uterine, hypogastric

veins 14th day puerperium,6 to 8 wks

Management:
1.total bed rest with cradle
2.Early ambulation
3.antibiotics
4.analgesics
5.anticoagulants – do not use heparin with
aspirin
6.moist warm compresses
7.never rub or massage leg
8.assess bleeding sites – if Dicumarol is
used –Check prothrombin or clotting time
before giving
9. Breast Feeding is temp. D/C but breast
is continuously emptied
III. Peritonitis
inflammation of the peritoneal cavity
extension of endometritis
1/3 of all post partal deaths
spread thru lymphatic system
abcess formed in the Cul-de-Sac of
Douglas – the lowest point of the
peritoneal cavity

Assessment:
as a surgical patient – S/S ASA rigid
abdomen, abdominal pain, high fever,
rapid pulse, and vomiting
From Ft to uterus to abdomen

Management
1.NGT – if with paralytic ileus(intestinal
paralysis)
2.IVF – TPN and meds
3.analgesics for pain relief
4.antibiotics
Complications: Adhesions and scarring –
infertility

IV. Mastitis
inflammation of the breast
th
7 post partum or when infant is a week
or month old
pathologic organisms coming from
infant’s nasal-oral
cavity(staphylococcal/streptococcal)
enter cracked nipples (tissues) milk good
culture media
S/S: scanty BM, high fever, mastitis
(unilateral)

Management:
A. To prevent fissures
1.Proper Breast feeding techniques
Not leaving baby too long at breast
Be certain baby sucks the areola
not the nipple only
  Release infants grasp at nipple 1st
before removing infant from breast
2.wash hands between handling perineal
pads and breast
3.expose nipple to are at least a part of the
day
4.use Vit. E or lanolin – based ointment or A
and D cream to soften the nipple daily
B. Broad spectrum antibiotics
C. Breastfeeding can be continued (other breast
and keep other breast empty to prevent bacterial
growth
D. Manual expression of milk 2 – 3 days
E. Warm wet compresses
F. I and D for localized abscess
G. Assure client that this is not breast cancer a
permanent disease; she can still breastfeed after

V. Salphingitis
fallopian tubes are inflamed
portal of entry – uterine cavity, broad
ligament
3 types:
1.Acute
 gonococci; both tubes can lead to local
peritonitis
2.Chronic
Sequel gonococcal infection
Severe scarring of FT
Adhesions
Tubo-ovarian abscess may form
Cause sterility; tubal pregnancy

3.tuberculosis
PTB from TB of lungs
TB endometritis
Attack FT

Assessment:
1.Sudden abdomino-pelvic pain; tenderness,
pressure
2.↑ vaginal discharges

3.fever; malaise
Diagnostic:
I.Gram staining or secretions from
endocervix or cul-de-sac
II.Ultrasound

III.Culdocentesis

Treatment and management:

Antibiotics – penicillin or tetracycline
Bedrest
Analgesics
IV therapy
Culdotomy
TAHBSO in complicated type
AntiTB therapy in Type 3

Postpartum Psychosis

Also called Puerperal psychosis or postnatal

psychosis.
 Brief psychotic disorder
Radical hormonal change with
neurotransmitter overactivity
Mother is unaware she is ill
Response of client to hormone shifts –
estrogen/ progesterone levels and change of
rates
Post-partum Blues-or “baby blues”,emotionally
labile, crying easily for no apparent reason-5th to
10th day.Other symptoms include: depression,
let-down feeling, restlessness, insomnia

Etiology: unknown

Causes: emotional and psychologically

overwhelmed of parental responsibilities,
fatigue after birth, mourn the passage of labor
and birth

Post-partum depression” mild to severe, :good

days” or “bad days”, more on the father

Assessment
 Feeling of sadness; isolation
Short temper and irritability; hurts the baby

1.Postpartum “blues” – 1 – 2 days

Management: Counseling
2.Postpartum depression – good support
system
3.Postpartum psychosis – 1:500 presents C/S
after delivery
2/3 – response to crisis in child bearing

not a response to physical aspect 1st 6

weeks after delivery
1/3 – had history of mental illness prior
to pregnancy
Crisis, which will precipitate postpartum
psychosis

1.Death in the family

2.loss of husband’s job
3.divorce
4.some major crisis

Management:
I. Psychiatric counseling
II. Do not leave woman alone; close watch!
Might harm self or her infant

Dystocia

Difficult labor(placenta, cord, membranes,

and amniotic fluid)
Refers to any labor which does not advance
normally
STAGES OF LABOR:

1) FULL DILATATIONAL(preparatory,
dilatational and deceleration sequence)-12 to
14 hrs primi, 8 hrs multi
 2) Full dilatational until fetus is expelled
from birth canal(pelvic or second stage)
3) Placenta is delivered
Factors:
a.Forces are inadequate
E.g. inertia – sluggishness of uterine
contractions
b.Abnormal position of the passenger (infant)
c.Abnormal passageway (birth canal)

Inadequate forces:
Uterine Contraction- interplay of contractile
hormones( ATP,estrogen and progesterone,
electrolytes such as Na, K and Ca, contractile
proteins such as actin and myosin, epinephrine
and norepinephrine, oxytocin and
prostaglandins
A. Uterine inertia (Dysfunctional labor)
Sluggishness of uterine contractions during
labor
2 types:
 According to time when it occurs
1.Primary uterine inertia
Occurs at onset of labor or prolonged
latent phase of labor
Management: stimulate with not
enemas, administer oxytocin, encourage
to walk
2.Secondary to uterine inertia
Occur later part of labor or prolonged
active phase of labor; fetus does not
descend; cervix not dilated
Management:
• Maintain a serum glucose level e.g

oral -orange juice, IV glucose

• Preventing fluid and electrolyte loss
-fluid administration
• Reduce psychosocial stress
• Reduce pain, promote comfort - back

rubs, change bedsheets

• Maintain a side-lying position
• Keeping the bladder empty
B. Abnormal Uterine Contractions

3 types:
According to strength

1.Hypertonic Uterine Contractions

Greater than normal tension
↑ 15 mmHg resting tone

Very painful – not relieved by exercise

oAnoxic uterine muscles
oLack of relaxation
Management:
oFetal and uterine monitor every 15
min interval
oNo oxytocin
oRest and sedatives
oDarken room; ↓ noise stimulation

oProvide support to client

oAsk client to breath with
contractions
2.Hypotonic uterine contractions
Tension is defective or inadequate to
cause or accomplish dilatation
Resting tone ↓10mmHg

uterine contractions not increasing 2 –

3/ 10 minutes
Causes:
1.Too early administration of
analgesics before 3 – 4 cm
2.Bladder/ bowel distended
3.Overstretch uterus – multiple
gestation
4.Large fetus
5.Hydramnios
Management:
a. Administer oxytocin - ↑strength
tone and effectiveness
Disadvantage
a.Cause maternal
exhaustion and uterine
exhaustion
 ↑ post-partal hemorrhage
b.

secondary to ineffective
contractions
c.Prone to infection –
over-dilation of cervix
b.Administer antibiotics

3.Uncoordinated uterine contractions.

More than one contractions occur at the

same time due to myometrium acts

independently from each other
Management: fetal and uterine external
monitor applied q15
Oxytocin to stimulate labor

Complication:
Mother: exhaustion and dehydration
Fetus: injury and death

II. Abnormal in the Passenger (infant)

A. Congenital anomalies
 1. Hydrocephalus – accumulation of CSF in
brain ventricles
2. anencephalus – absence of the cranium or
top portion of the head,lack of firm cervical
dilation
3. Condition causing abdominal (fetal)
distention; overgrowth of
liver(hepatomegaly), ascetic cysts, cystic
fibrosis(exocrine glands produce excessive
viscous glands secretions causing problems
in respiratory and gastrointestinal functions),
erythroblastosis fetalis (large immature
RBCs compensating for anemia producing
edema in peritoneum,pericardium and
pleural spaces)
Risks:
Rupture of uterus
Difficult delivery
4. Excessive fetal size > 9 lbs or 3, 400 gms.
causes: large parents, DM, prolonged
gestation, overeating, multiparous
 5. Mulitple Gestation-cord prolapsed,uterine
dysfunction,premature separation of
placenta,abnormal fetal
presentation,overdistended uterus-prone to
hemorrhage from uterine atony

B. Abnormal fetal position/ Presentation

1.Persistent occiput posterior

2.Breech
3.Face
4.Brow – fetal head is halfway between
flexion and extension between vertex and
face
5.Transverse – long axis transversely lie
across short axis of uterus
6.Compound – more than one fetal parts
presenting e.g. head and hand; head and foot
7.Umbilical cord – cord lies in front of
presenting part; ‘Vasa Previa” – prolonged
cord
Note: do not allow client to ambulate after
rupture of BOW
Management:
A.Maneuvers
Internal podalic version-Direct
manipulation of the baby inside the uterine
cavity to the breech position is called
internal podalic version

External podalic version-External cephalic

version (ECV) refers to a procedure by
which an obstetrician or midwife turns the
baby from the breech to the cephalic
position by manipulating the baby through
the maternal abdomen.

B.Trendelenburg position
Relieve pressure of presenting part to cord
C.Bed rest after rupture of BOW
C. Cephalopelvic disproportion – CPD-either
Mother (contracted pelvis) fetus abnormally
(large vertex)

III. Abnormal Passageway (Birth Canal)

1.Dysfunction of preparatory phase of labor
2.dysfunction of dilatation phase of the labor
3.dysfunction in the pelvic phase (delivery)
of the labor
a. Preparatory phase
prolonged latent phase due to unequal,
irregular contraction
20 hours – primi
14 hours – multi
Uterus in hypertonic state
Very painful and frightening
Fetal anoxia
Monitor contraction s and FHT
Administer IV to prevent dehydration
Administer morphine to relieve hypertonicity
b. Dilatation Phase
1.Prolonged active labor = 4 – 8 cm
a.Causes- fetal malposition and CPD
b.Multi – 1.5 cm ↑/hour

c.Nulli – 1.2 cm ↑/hour

2.protracted descent
a.multi – descent rate 2cm/hour
b.nulli – descent rate 1cm/hour
starts with good contractions then
diminish gradually and become
infrequent and poor in quality
Assessment : anxiety, fear and apprehension
or discouragement

Management:
amnionotomy (rupture of BOW)
oxytocin drip
keep client and kin informed of situation

Delivery Phase
Causes: CPD
 prolonged deceleration
Characteristics:
oExtend beyond 3 hours (nulli); 1 hour
(multi)
oSecondary arrest of dilatation – no
progress in dilatation of cervix >2 hours
oArrest of descent –no descent occurred in

one hour
oFailure of descent-does not begin

Management:
oNo oxytocin
oPlace in LLRP
oOxygen inhalation
oPrompt assisted delivery large forceps
Management for dystocia:

A. Preventive:
1.Maintain serum glucose level (e.g. juices,
candies, IV – prevent glucose used up)
2.Prevent F/E loss – prevent dehydration;
prevent DVT in Postpartum phase
3.Reduce stress
 4.Give supportive measures; reduce pain, give
praises, back rubs, change soiled sheets
5.LLRP – give oxygen
6.Keep bladder empty

B. Curative Management Care:

1.Antibiotics
2.Sedative – stop abnormal contractions
3.Short acting barbiturates – to promote relax/
rest
4.Monitor FHB
5.NPO – prepare for Surgery – CS
6.Assist in delivery; vaginal or CS
7.Trial labor – in borderline or adequate pelvis

Conditions Complicating Dystocia

A.Precipitate delivery-only few rapidly
occurring uterus
 B.Pathologic Retraction Ring or Bandl’s
ring
Junction of upper and lower uterine
segment
Sign that severe dysfunctional labor
occurs
Forewarning of a uterine rupture
Grip fetus and placenta
Assessment:
1.Horizontal indentation across abdomen
2.Uncoordinated contractions early in labor
3.Dilation phase – caused by obstetrical
manipulation and administration of oxytocin

Pathophysiology:
Fetus is grasped by the ring and can’t
advance or descent
If fetus is delivered, placenta can be held
after delivery

Management:
1.Observe abdominal report immediately
 2.administer IV morphine sulfate and amyl
nitrate
3.C/S – or manual extraction of placenta if not
attended leads to Mother (uterine rupture and
postpartum hemorrhage); fetus (death)
C. Rupture of Uterus
Factors:
Strained uterus
Beyond its capacity
Previous C/S, repair or hysterotomy

Contributory:
Prolonged labor
Faulty presentation
Multiple gestation
Unwise use of oxytocin
Obstruction labor
Traumatic maneuvers using forceps

Assessment
 1.Impending rupture suggested by pathologic
retraction ring, strong uterine contractions
with cervical dilatation
Management:
Immediate CS
2.When uterus rupture
S/S: sudden severe pain during strong
labor, hemorrhage – uterus, vagina,
intra-abdominal, Cullen’s sign

D. Uterine Inversion
Turning of the uterus inside out
Fundus is formed thru the cervix, turned
inside out
Assessment: protrude from vagina,sudden gush
of blood,fundus no longer palpable,sgins of
blood loss,uterus is not contracted
Causes:
1.Attachment of placenta at fundus – sudden
delivery of fetus without support – fundus is
pulled down
2.strong fundal push in an non-contracted state
 3.attempts to deliver placenta before
separation

Management:
Hysterectomy – due to severe
hemorrhage

E. Amniotic Fluid Embolism

Solid particles from amniotic fluid enter

maternal circulation
Amniotic fluid is forced into circulation
thru open maternal sinuses
S/S as any embolism – fatal,woman sits
up and grab chest due to pain and inability
to breathe

Management:
i.Supportive
ii.Oxygen administration
Abnormal Presentation and Delivery

I. Breech presentation/ extraction

Note: Majority of fetuses are in breech

presentation early in pregnancy → by week 38
AOG fetuses normally has turned to cephalic
presentation

Rationale – “retain most comfortable position”

Fetuses
Head is widest in single diameter; buttocks
plus LE = take up more space

Uterus
Fundus – largest part
97% of all pregnancies, fetuses turn so that

the buttocks and LE are in the fundus those

who failed to turn are breech
Prevention:
woman to assume 15 minute knee-chest
position for 3X a day during pregnancy so
breech presentation will be less likely to occur
Classifications:
1.Complete
Feet and legs are flexed on thigh; thighs
flexed on abdomen and buttocks; feet are
presenting parts

2.Frank
Legs are extended and lie against abdomen
and chest; feet at levels of shoulder;
buttocks are the presenting parts
3.Footling
a.Double footling
Legs are unflexed and extended;
presenting part - feet
b.Single footling
One leg is unflexed and extended;

presenting part – one of the foot

Risks:
1.High risk of anoxia
No molding (prolapsed cord, traumatic
injury, intracranial hemorrhage, fracture
spine, arms)

2.Dysfunctional labor
Presenting part does not fit cervix

3.Early rupture of BOW

↑ risk of infection

meconeum aspiration → although meconeum

4.

leakage is not a sign of fetal distress but

expected from buttocks pressure

Assessment:
FHT – heard high in the abdomen
Leopold’s maneuver and vaginal examination
(show breech presentation
Ultrasound – to confirm
What to expect:
Parents
Examine baby more closely; frank breech-

legs extended; footling – one leg extended (1st

2-3 days of life)
Explain this to parents
Delivery by C/S
Etiology/Causes: Unknown
1.Age of Gestation under 40 weeks

2.Abnormal in fetus – anencephaly,

hydrocephalus, meningocele

3.Hydramios – free fetal movement

4.Pendulous abdomen – lax abdominal muscle

5.space-occupying mass in uterus e.g.

midseptum – traps fetus in position

6.multiple gestation – can’t turn to vertex

position
Hazards/Risks:

1.Intracranial hemorrhage
2.cord compression
3.abruption placenta
4.Erb-Duchene paralysis (Erb’s palsy) – injury
to the brachial plexus
S/S:
oLoss of sensation at arm and
paralysis
oAtrophy of deltoid and biceps and
brachial muscles

II. Forceps Delivery

OB forceps – steel or metal instruments (2

blades left and right with lock),used if the fetal
head reaches the perineum
Maybe high forceps(non-engaged head) or mid-
forceps(level of ischial spines)
Maybe used with pudendal block
 5 common types of OB forceps

1.Baxton
With hinge in the right blade used to
rotate fetal head to a more favorable
position such as ROP/ROA
2. Kielland’s - With short handles and a
marked cephalic curve use like Baxton

3. Piper - Used to deliver the head in breech

presentation

4. Simpson’s - Used as outlet forceps

5. Tarnier’s - Axis traction forceps

Indications:
nd
1.To shorten 2 stage of labor
When woman is unable to push with
contractions in pelvic division of labor
i.After regional anesthesia
ii.Cessation of progress of labor
iii.Failure of fetal head to rotate

2.Fetal distress
Prolapsed cord
FHT ↓100 BPM or ↑160 bpm

Meconeum stain in cephalic

presentation

Pre-requisites:
 1.Pelvis should be adequate – no CPD
2.Fetal head must be deeply engaged (+3 - +4
station)
3.Cervix must be completely dilated and
effaced
4.Accurate diagnosis position and station must

be made – vertex presentation

5.Membranes (BOW) must be ruptured
6.Some form of anesthesia must be used e.g.
pudendal block – to achieve pelvic relaxation
and reduce pain
7.Rectum and bladder must be empty

Types of Forceps Application:

I. Low-forceps operation
Easy delivery; forceps are applied after the
head has rendered the perineal floor with
sagittal suture in anterior-posterior of the
outlet – vertex at introitus

II. Mid forceps operation

 Forceps are applied before the criteria for
low forceps are met but after engagement has
taken place – vertex at ischial spine
III. High forceps operation
Forceps are applied before engagement has
taken place (only used in modern OB – rarely
done) – biparietal diameter above ischial spine
Complications:
Maternal:
a.Lacerations – vagina, cervix =
hemorrhage and infection
b.Rupture of uterus
c.Injury to bladder and rectum
Fetus:
a.Cephalhematoma
b.Brain damage
c.Skull fracture
d.Facial paralysis

e.Cord compression
 f. Facial marks – temporary 24 – 48 hours
only

Nursing Management:
1.prepare patient and explain
 2.explain outcome ASAP especially on
outcome of procedure e.g. marks, bruising

III. Vacuum Extraction

 used in place of forceps (duration – 30
minutes)
delivery of a fetus in vertex presentation
with the use of a cap suction device that is
applied to fetal scalp for traction e.g
ventouse vacuum extrication

Complications:
1.Scalp echymoses – expected – posterior
fontanelle

2.cephalhematoma – prolonged used >30

minutes – damage to scalp
3.skull fracture – but occur more in forceps
extractions
Advantages over forceps:
1.Use of little anesthesia (fetus less depressed
at birth)
2.fewer laceration (non-invasive)

Disadvantages:
1.Marked caput - >7 days after birth – assure
mother

2.tentorial tear – from extreme pressure

Contraindicated if:
1.scalp blood sampling was done – bleeds
2.preterm – soft skull
Cesarean Section
History:
st
1879 – Sanger – 1 live C/S and uterus was

saved
1800 – C/S done as post-mortem procedure
“caesus” latin of to cut

Julius Caesar – was believed to be delivered

by cesarean birth and name the procedure after
him
Definition:
 Surgical extraction of the fetus via the
uterine incision through the abdomen – trans-
abdominal incision of the uterus
Indications:
CPD – most common
Uterine inertia
Previous C/S
Severe toxemia
Placental accident (eclampsia)
Fetal distress
DM
OLD primi
Prolapsed cord
Post-term pregnancy
Failed forceps delivery

Types:
I. Low segment or low cervical
Method of choice; incision is made at the
lower uterine segment which is the thinnest
and most passive portion
Advantages:
1.Minimal blood loss
2.easy to repair incision
3.lower incident of post-op infection
4.less activity
5.less possibility of uterine rupture
6.↓ post-op adhesions – complication

7.allow vaginal delivery in the next pregnancy

Incision:”bikini” incision

Skin Uterus or skin and uterus (both)

II. Classical CS
Vertical incision. Recommended in the
following cases:
1.Bladder or lower uterine segment is
involved in extensive adhesions resulting
from previous surgery
2.Transverse lie
3.Anterior placenta previa
4.Active contractile portion of uterus
5.Unable to have subsequent vaginal
delivery
Incision:

Vertical incision of skin and uterus

III. Extra-peritoneal CS
Tissue around bladder is dissected providing
access to lower uterine segment without
entering into peritoneal cavity

Advantages:
1.Prevent peritonitis
2.use of antibiotic and blood is reduced

IV. CS with hysterectomy (PORRO’S

operation)
cesarean followed by the removal of the
uterus
Indications:
1.Hemorrhage due to uterine atony
2.placenta previa and abruption placenta
3.placenta acreta
4.rupture of uterus, non-separable
5.gross multiple fibromyoma
Nursing Care:

A.Pre-op – secure consent

i.Carry out PE (assessment)
ii.Routine lab exams – typing/ cross-
matching
iii.Monitor FHB
iv.Shave abdomen and perineum as directed
v.Insert FUC (retained). Keep away bladder
from operative site
vi.Start IV large bore needle
vii.Administer pre-op meds – Atropine
sulfate – no narcotics are given to prevent
fetal respiratory depression
viii.Prepare oxytocic drug to be added to
infusion following delivery of infant
ix.Notify pedia department – resident – of
surgery to provide initial care and
resuscitation of infant
B.Post-op care: Surgical and OB care
i.Observe hemorrhage in both areas
1.perineum – pads and buttocks
2.abdominal dressing
3.V/S
ii.Ambulation
1.dangle after 12 hours
2.ambulate after 24 hours
3.deep breathing and coughing
exercises, ROM of extremities and
neck
iii.Inspect uterus; massage with proper
splinting; give analgesics as ordered
iv.Administer oxytocin and analgesics
v.I and O
vi.BF – started after 24 hours after delivery
Hysterectomy
Surgical removal of the uterus

Indications:

1.Malignant and non-malignant growth on

uterus, cervix, and adnexa
2.life threatening (severe pelvic infection
3.control of uterine bleeding on hemorrhage
4.correction of problems associate with pelvic
floor – relaxation; rectocele and cystocele
(Wertheim’s operation)
5.Treatment of endometriosis if conservative
treatment failed
Qualifying considerations:

1.Woman’s age
2.woman’s desire to have children
3.possible effectiveness of alt. Treatment
4.degree of dysfunction

Elective indications:

1.voluntary sterilization
2.prophylaxis when there is a strong or
significant history of uterine disease as CA

Types:
A.Abdominal hysterectomy – 70%
 Vaginal hysterectomy
B.

Abdominal Hysterectomy
Types:
1.Subtotal
Corpus (body) of uterus removed;
cervical stump remains
2.Total
 Entire uterus and cervix are removed;
tubes and ovaries remain
3.TAHBSO
Entire uterus, tubes, and ovaries are
removed

Vaginal hysterectomy (Spalding-Richardson’s

operation)
1.Repair of pelvic relaxation; uterine
displacement or prolapsed, urinary stress
incontinence cystocele and rectocele
2.high risk in patients who are very obese or
those who can’t withstand prolonged
anesthesia

Advantages:
1.Less likelihood of paralytic ileus, post-op
pains and intestinal adhesions
2.Less chance of pulmonary complication and
thrombophlebitis
3.Wound dehiscence possibility is less; shorter
hospitalization
 4.No abdominal scar

Disadvantages:
1.More limited surgical field and inability to
examine intra-pelvic and intra-abdominal
organs condition
2.Increased risk of bleeding and postoperative
infection
Psychosocial considerations:
1.Fears that cancer or VD be discovered
2.Conflict between medical diagnosis and
religious beliefs
3.concerns about disturbed reproductive
process
4.disappointments of not having any more
children
5.fear of unable to fulfill role and needs of a
woman
6.heightened depression and emotional
sensitivity

NB – post – op care as abdominal surgery

Discharge Plans/ Health education post-op:
What to expect:
1.Produces surgical menopause (if adnexa
were also removed)
2.hormonal replacement therapy (if TAHBSO
is done)
st
3.“Tired feelings” 1 few days; depressed,
nervousness
4.employment or job resumption on doctor’s
diagnosis
5.follow-up check-up with gynecologist,
report the following: “Peace of mind”
O O
a.temp >38 C(100 F)

b.heavy vaginal bleeding

c.drainage
d.foul odor of discharge

What activities to engage in:

1.not to sit too long at one time as driving long

distance – bleeding and thrombophlebitis –

delay driving after 3rd week post-op
2.Household activity – after 2 months back to
“Normal self”
3.shower baths until post-op wounds healed
4.resume sexual contact after 4-6 weeks; be
cautious danger to cause injuries to incision
site and bleeding
Inflammatory conditions

I. Vulvitis
mucous membranes of the vulva
results from:
odirect irritation of vulvar tissues
e.g. scratching
oextension of irritation from vagina

Etiology:
1.Skin disorders
2.infection
3.vulvar Krauposis (dryness and atrophy of
vulva)
 4.vulvar Leukoplakia (atopic disease of older
woman)
5.vulvovaginitis 6. senile atrophy
7.pediculosis 8.DM
9.Scabies
10.Cancer
11.allergens
12.urinary incontinence
13.poor perineal hygiene
Nursing Care:
1.Apply calamine lotion, hot compresses, sitz
bath
2.Wear light, non-restrictive, well-washed,
cotton underwear
3.avoid feminine hygiene sprays
4.keep vulva dry
5.proper application of perineal pad
For severe type
6.heavy sedation
7.vulvectomy (radical surgical removal of the
vulva)
II. Vaginitis
inflammation of the vagina –
accompanied by vaginal discharge
(leukorrhea) → urethritis – due to
proximity of urethra to vagina
results from:
i.invasion of organsisms e.g. candida
ii.irritation – frequent coitus
iii.poor hygiene
8.apply hydrocortisone ointment or anesthetic
sprays as ordered
S/S:
1.Leukorrheal discharges with itching, redness,

burning, and edema

2.Voiding and defecation aggravate the above
symptoms

Pre-disposing factors/ Organisms:

1.Trichomoniasis vaginalis – protozoa –
bubbly white leukorrheal discharges
2.candida albicans – fungus – cheesy white
discharge s common in DM, prolonged used
of antibiotics, steroids
3.Hemophilus vaginalis-Gardnerella vaginalis-
gram positive,cause of bacterial vaginosis
4.pediculosis pubis
5.contact allergens
6.excessive perspiration
7.poor hygiene
Treatment and care:
1.Enhance natural vaginal flora – lactic acid
2.stimulate growth of Doderleine bacillus-
Doderlein's bacillus: A species of gram-
 positive, rod-shaped bacteria isolated from the
intestinal tract of humans and animals, the
human mouth, and vagina. This organism
produces the fermented product, acidophilus
milk.
3.good wash after voiding and defecation
4.chemotherapy as ordered

III. Cervicitis
inflammation of the cervix

Predisposing factors:
1.Exposure to pathogens
2.douching
3.childbirth
4.trauma – coitus
5.surgical procedures
S/S:
reddened, irritated areas around the
cervical os – bleeds easily

Etiology:
Neisseria gonorrhea
E. coli
Streptococci and staphylococci

Management:
1.Cervical cautery
2.Cryotherapy – freezing with liquid nitrogen
(7-8 weeks healing time)
a.Inform woman on expected outcome
b.Minor vaginal bleeding with pelvic
discomfort at short period
IV. PID
Pelvic inflammatory disease (all structures in
the pelvic cavity)

Etiology:
Non-gonococcal infection e.g Chlamydia
trachomatis
Gonococcal and mixed infection e.g. GC + E.
coli, IUD TB, streptococcus, and
staphylococcus
S/S:
1.Abdominal pain, nausea, vomiting
2.Fever, malaise
3.leukocytosis
4.malodorous, purulent vaginal discharge

Goal of Care:
1.control the spread of infection within the
client
2.control the spread of infection to others
including nurse

Rx and care:
1.Place patient on semi-fowler’s position to
facilitate drainage
2.avoid use of tampoons
3.support with proper nutrition
4.administer drugs – non GC (tetracycline);
GC (penicillin G)
5.Control spread of infection
a.Handle pads with extreme precautions
b.Use of gloves or instrument
c.Proper disposal
 d.Hand washing before and after patient’s
contact
e.Proper disinfection of instruments,
utensils, linens, etc.
f.Instruct patient how to prevent re-
infection
6.use warm douches and heat compresses to
abdomen as Rx
7.give moral support and understanding
Complications: (especially if untreated)
1.↑ risk of spread to others

2.sterility
3.ectopic pregnancy
4.inflammatory masses

Menstrual disorders
Dysmenorrhea

painful menses
2 types:
1.Primary – unknown cause; emotional or
psychologic factor
2.secondary – factors extrinsic to uterus as

endometriosis, pelvic infection

S/S Uterine Spasms:
pain colicky, cyclic and nagging dull
ache at lower abdominal to LE
severe chills, headache, diarrhea, nausea
and vomiting and syncope
Etiology:
I. Endocrine – release of prostaglandin
II. Anatomic – infantile uterus
III. Constitutional – chronic illness as anemia
etc.
IV.Psychogenic – stress, tension, and anxiety

Treatment and care:

1.According to individual needs:
 a.Proper psychological preparatory of girls
for menarche
b.Good posture, exercise
2.psychotherapy and pharmacology
a.prostaglandin inhibitors – mefenamic
acid
b.oral contraception
3.Psychological counseling
4.surgery – pre-sacral and ovarian neurectomy

(cutting nerve fibers)

II. Amenorrhea
absence of menses
2 types:
1.Primary – has not menstruated yet no
menarche
a.Cause: embryonic maldevelopment –
treated as to etiology

2. Secondary – menses has begun but stops

 a.Causes: normal pregnancy and lactation,
menopause, psychogenic (stress),
hypothalamic distress, constitutional (DM,
TB, obesity)
III. Metrorrhagia
Bleeding between regular menstrual periods
Common in pill users
Assess for etiology as disease, tumors, etc
IV. Menorrhagia
Excessive bleeding during regular prior
“Heavy Menses”
Causes: Endometrial distress, inflammatory
disease, and emotional stress
Management:
oAssess underlying cause
ocorrect hemoglobin deficiency with iron
supplement and or hormonal supplement
V. Oligomenorrhea
Markly diminish menstrual flow – nearing
amenorrhea
VI. Polymenorrhea
Frequent menstruation occurring at intervals
of <3 weeks

VII. PMS
Pre-menstrual syndrome
Clusters of symptoms that occur just
before the menses and disappear with
menstrual flow
E.g. feeling of bloating and fullness of
abdomen

4 classes:

1.PMS A
S/S anxiety, irritability, elevated
estrogen, decreased progesterone
RX:

oVit. B6 at 200 – 800 mg/day

oProgesterone therapy
oLimit intake of dairy products
o↑ outdoor exercise
 2.PMS B
S/S: water and salt retention =
bloating, mastalgia, weight gain, ↑
aldosterone, ↓B6, Mg, and ↑
prostaglandin
RX:

i.↓ Na intake

ii.Vit. E (600 u) reduce breast

symptoms
iii.↓ Methyxanthine as coffee, tea,

choco, cola, and nicotine

iv.↓ refined sugar to 5 tbsp/ day

v.prostaglandin inhibitors
3.PMS C
S/S: Premenstrual craving for sweets,

↑ appetite and food binges,

palpitations, fatigue, fainting spells,
headache, shakes, altered GTT, ↓
prostaglandin, ↓Vit. B, Zinc, Vit. C and
Mg
Rx:
 ↓ refined sugar 5 tbsp/ day
↓ alcohol

↓ Na 3 grams/ day

↓ animal fat ↑vegetable oil

4.PMS D
S/S: depression, withdrawn, insomnia,

forgetfulness, confusion, altered

estrogen, and progesterone level ↓B6
and Mg
Rx: Therapy depends on serum
evaluation
VIII. DUB
Dysfunctional uterine bleeding or abnormal
uterine bleeding; a significant deviation from
client’s usual menstrual flow or pattern
Normal menses cycle = 21 days
Lasts for: 7 days
Amount: <80 ml/ day

Causes:
1.Organic
2.Psychological
A. Organic
Anovulation
Assessment – history
Lab exams – coagulation studies, CBC, TSH
Rule out other diseases
Endometrial biopsy
Hysterosalpingography
Hysteroscopy, D and C with biopsy
Rx:

i.Progentin
ii.Clomephine
iii.NSAIDs
iv.D and C
v.Ablation
vi.Hysterectomy if pregnancy is not
anymore desired
Infertility and Sterility

Infertility
 When pregnancy has not occurred
after at least one year of unprotected
coitus

Types:
1.Primary – no previous conception has
occurred
2.Secondary – there has been a previous
viable pregnancy

Sterility
Some definite factors have been
identified to prevent conception

Male infertility
I.Causes:

1.Inadequate sperm count

NV: 20 – 50 mil/cc of seminal fluid
 a.Chornic disease – persistent fever
b.Mumps orchitis
c.Exposure to x-ray

d.Excessive use of alcohol/ drugs

e.Endocrine imbalance
f.↓ Vit. Intake as in Vit. E

g.Surgery on or near the testis

h.Too frequent intercourse

Obstruction of sperm motility secondary

2.

to surgery
a.Adhesions, occlusion, congenital
stricture of spermatic ducts

changes in seminal fluids due to

3.

infection-UTI,STD

4.difficulty with ejaculation

a.anomalies of the penis e.g.
hypospadias, epispadias
b.debilitating diseases may result to
impotence and ejaculation
 c.premature ejaculation – affects
proper deposition of sperms
d.psychological problems
e.use of pre-coital lubricants

II. Male fertility studies:

1.History and PE
2.Semen analysis
After 4 days of sexual abstinences,
seminal fluid is examined for
numbers, appearance and motility
3.Lab Test
Urinalysis, CBC, blood typing
Testicular biopsy
KAHN and WASSERMANN test

Protein-bound iodine

4.Psychological assessment

III. Treatment:
 1.Treat underlying causes as chronic
diseases
2.In ↓ sperm count >abstain 7-10 days at a

time
3.In mumps orchitis > artificial
insemination
Female infertility
A. Causes:
I. Anovulation
Most serious and most difficult to
correct
Causes:
oPituitary or thyroid disturbance
oImmaturity or disease of ovaries
e.g. endometriosis
oChronic or excessive exposure to
x-rays or radioactive substances

II. Tests for ovulation

1.Basal Body temperature (BBT)
Progesterone causes body
temperature to ↑ a day after
ovulation
 2.Spinnbarkheit test
↑ quantity and pH of cervical

mucus during ovulation; thin and

watery, it can be stretched to a
distance of 10 – 13 cm

3.Fern test
↑levels of estrogen just before

ovulation mucus forms fern-like

pattern when smeared and dried
or glass slide (arbonization) when
progesterone ↑ no fern-like
pattern
4.Uterine endometrial biopsy
5.culdoscopy
6.Laparoscopy
7.Hysteroscopy

B. Tubal Factors

I. Causes:
1.Chronic salphingitis – PID, GC
 2. ruptured AP – abdominal surgery
with infection or adhesion
3.congenital webbing or stricture
II. Test for tubal patency:
1.Rubin’s test – procedure
rd
3 day after menses, patient in
lithotomy position is given (100
mmHg) CO2 under pressure
instilled into cervix passes uterus
and fallopian tubes into pelvic
cavity
if tubes are patent if another

200mmHg CO2 administation; no

sound on auscultation; no C/O of
pain in one or both shoulders =
occlusion is present
both diagnositic and therapeutic
test
2.Uterosalpingography

C. Uterine factors
I. Causes:
1.Tumors
 Blocks tubes or limit space for
implantation e.g. leiomyomas
RX:

oMyomectomy
oCongenital deformity
“infantile uterus”
oInadequate endometrium
formation - ↓ estrogen and
progesterone level

D. Cervical factors:
I. Causes:
1.Infection
2.tight cervical os
II. Tests for cervical environment
1. Sims – Huhner test - procedure
ovulation time determination by
BBT
couple do intercourse with
ovulation without pre-coital
lubricant
after intercourse woman lies on
her back for 30 minutes
 no post-coital douches/ washing
within 2-8 hours doctors
examine the cervical mucus for
ferning and spinnbarkheit and for
viable sperms including count

E. Vaginal Factor
I. Cause:
1.Infection
II. Test for vaginal environment
1.History of menstruation and PE
2.Lab tests
3.psycho assessment - R/O
dyspareunia

III. Management:
1.Sodium bicarbonate douche for very
acidic environment
2.treat infection and other underlying
cause
3.surgery for tumors
 4.endocrine therapy e.g. clomid –
HCG

Condition in the Female Reproductive

System
I. Myomas
Circumscribed growth encapsulated

Other name: fibromyomas, fibroma,

fibroids, leiomyomas
Benign tumors
Composed mainly of smooth muscles
with some fibrous connective tissue

Classifications (location):
1.Intramural
Uterine walls; surrounded by
myometrium
Clinical manifestation: ↑ uterus size,

vaginal bleeding between periods,

and dysmenorrhea
2.subserous
Directly beneath (under) the serosa;
penduculated; to wander; to multiply
and enlarge
Clinical manifestation: backache,
constipation, bladder problems
3.parasitic or wandering
  pedunculated tumor attached to
other tissues
4.intraligamentum
subserous tumor into the broad
ligaments; implant on pelvic
ligament; displace uterus
5.submucous
beneath the endometrium; they
grow thin and displace endometrium
over their surface and become the
site of necrosis and infection
6.cervical
rare
7.sarcomatous (malignant)
rapidly enlarging and hemorrhagic
Clinical Manifestation: necrosis,
ulceration, foul smelling vaginal
discharges

Secondary changes (degeneration)

 1.Hyalinization
When tumor outgrows BS
Clinical manifestation: Mature or old
myoma are white containing soft
gelatinous area of hyaline change -
asymptomatic
2.Cystic
Follows hyalinization; tumor
liquefies
3.Calcification
Common in larger tumor
4.Fatty
Follow hyaline and cystic
5.infectious
appears with PID; common in
pedunculated, submucous tumors
6.carneous
red, associated with hemorrhage
into tumor and hemorrhage

Rx/ Management:
 depend on symptoms, age,
location, and size of the tumor; onset
of complication and desire to get
pregnant
fibroid – D and C
small tumor – myomectomy
(removal of tumor without removal of
the uterus)
large tumor – hysterectomy
(removal of entire utero) → tumor/
uterus hysteromyomectomy
radiation and chemotherapy
Nursing Care:
1.Full explanation – removal of uterus –

menses, pregnancy, sexual activity

2.Reassurance
3.surgery – pre and post op care

II. Endometriosis
 chocolate cysts
abnormal growth of extra-uterine
endometrial cells; after in the cul-de-
sac of the peritoneal cavity, uterine
ligaments and ovaries
excessive endometrial cells
production plus reflex of blood during
menses

Incidence:
multi-parous
familial tendency

Clinical manifestation: based on location

e.g lungs – S/S grave and serious

1.uterine displacement – nodules at cul-

de-Sac
2.dyspareunia – lesions at uterosacral
ligaments and posterior fornix of vagina
3.dysmenorrheal – incapacitating pain on
defecation
 4.infertility
5.“Chocolate cyst” in uterine surface
6.abnormal uterine bleeding
Rx:
1.Estrogen/ progesterone – based oral
contraception
2.Danazol – synthetic androgen – shrinks
abnormal tissues
3.laparotomy with excision by laser
surgery
4.salpingo-oophorectomy
5.hysterectomy

III. Polyps
pedunculated tumors from the
mucosa and extending into the
opening of a body cavity
Types:
1.Uterine
a.Hypermenorrhea
b.Metrorrhagia
c.DUB
 2.Cervical
Bleeding following vaginal sexual
activity and may become infected

Rx:
Surgical excision – polypectomy

Nursing Care:
1.Secure Consent
2.Explain every procedure
3.follow up care and check up
4.surgery – pre – op and post – op care

IV. Ovarian Cysts

are non-neoplastic tumors of the
ovaries

Clinical manifestation:
may or may not be present = but is
symptoms occur
i.pelvic pains – often one sided
ii.pressure in the lower abdomen
 iii.backache and menstrual
irregularities
Rx:
surgical excision of the cysts

Nursing care:
1.Explain procedure
2.observe for S/S of tumor growth
3.follow up care

V. Fistulas
Abnormal tube like passages within
body tissues
Abnormal tortuous opening between
two internal hallow organs or between
an internal hallow organ and the
exterior of the body/skin.

Types:
1.Ureterovaginal – between ureter and
vagina
 2.vesicovaginal – between urinary bladder
and vagina
3.rectovaginal – between rectum and
vagina

Causes:
1.Obstetrical injury
2.pelvic surgery (hysterectomy and
vaginal reconstructive surgery – common)
3.extension of carcinoma or complication
of treatment for CA

Clinical manifestation:
1.Trickling of urine into vagina
2.Fecal incontinence and flatus passed
thru vagina and malodorous
3.Irritation and excoriation of vulvar
tissues

Diagnostic:
1.Methylene Blue test
Dye test
 Dye is instilled into bladder
Dye in vagina – vesicovaginal
fistula
None in ureteovaginal fistula
2.Indigo Carmine test
Injected IV
Appears in vagina is ureterovaginal
fistula
3.IVP – for location of fistula
4.Cystoscopy
Determine numbers and locations
of fistulas

Treament:
A. If to heal without surgery (rare)
1.maintain cleanliness - sitz bath;
deodorant douches/ wash
2.use of perineal pads; plastic or rubber
pants
3.prevent excoriations – use of bland
creams dust of cornstarch – sooths
 4.use of feminine morale boosters as:
attractive hairdo, nail polish; perfumes
new beaded jacket; latest fashion, etc
B. Surgery
fistulotomy/ fistulectomy
diagnosed early – time of delivery to
be repaired immediately
post-op heals 2 – 3 months for

inflammation to subside
maintain adequate nutrition, ↑
vitamins, and protein
administer chemotherapeutic
agents
done in healthy tissues
post-menopausal – oral estrogen →

for healthier viable tissues

perineal hygiene
Post-op
Recto-vaginal:
1.limit bowel activity – clear liquids for few

days and diet resolve gradually

 2.warm perineal irrigations, heat lamp
treatments
3.bedrest

Vesicovaginal:
1.proper bladder drainage – FBC – I and
O
2.Gentleness in administration of bladder
and bowel irrigations
Sexually Transmitted Diseases

I. Trichomoniasis

Etiology:
Trichomona Vaginalis – single cell
protozoa (round mobile structure)

S/S:
1.Frothy white to grayish green vaginal
discharge
2.vaginal irritation, redness, and pinpoint
petichiae
3.extreme vaginal itching
4.dyspareunia
5.↑ vaginal pH

6.males – asymptomatic

Diagnositic Test:
scrapping of vaginal discharge with
drops of Ringer’s Solution
Rx:
1.Metronidazole (Flagyl) single 2 gm dose
p.o (given to both woman and sex partner
Note: Should not be administered during
1st trimester of pregnancy and must be
used with caution for the remaining of
pregnancy (teratogenic); should not be
taken with alcohol = causes acute nausea
and vomiting
2.Topical – povidone-iodine or vinegar
douche only to reduce symptoms until
metronidazole can be used

Nursing Interventions:
1.Advise client to abstain from coitus;
male sex partner may use condom
2.Advise woman to use tampons to absorb

discharges and ↑ comfort

3.Emphasize importance of perineal
hygiene
II. Moniliasis
May affect skin, mucous membranes
as in GIT, mouth, vagina, anus,
fingernails, and body folds – groins,
neck, axillae

Common in:
Obese people, perspires profusely,
DM, Pregnancy, using oral
contraceptives pills, pseudopregnancy
state, antibiotic and steroids users.

Etiology: Candida Albicans

S/S:
1.cheesy, white non-odorous vaginal
discharge
2.vaginal and vulvar itching
3.red, beefy appearance of affected areas
dyspareunia
4.causes thrush in newborn
Diagnostic:
scrapping of vaginal discharge with
3:4 gtts of 20% (KOH) potassium
hydroxide

Rx:
1.Rx 4 to 6 months
2.apply Gentium Violet 1% for relief of
pruritus (stains underwear permanently)
3.Nystatin (mycostatin) drug of choice –
DOC –
4.male partner to be treated as well

Nursing Care:
1.Antibiotic by mouth should be stopped
2.rule out DM and treat properly
3.weight reduction for obese people
4.avoid coitus during infection or use
condom during treatment period
III. Herpes Genitalis
spreads by skin to skin contact and
virus enters thru a break in the skin or
mucous membranes
highly contagious
incubation period – 3 – 14 days

Etiology:
Herpes Virus Hominis II
oHVH – 2 – genital virus (not airborn –
not by fomites)
oHVH – 1 – non-genital forms – oral

skin but it is possible for each virus to

cross infects

S/S:
1.Vesicular lesion on cervix, vagina,
vulva, penis
2.systemic symptoms as headache,
malaise, ↓ grade fever
3.dysuria
 4.pain in intense upon contact with
clothing

Diagnostic:

1.History and clinical evaluation

2.isolation of virus in tissue culture (most
accurate)
3.scrapping for pap smear or Tzanck
smear

Rx:
analgesics for pain – aspirin
acyclovir (Zovirax) do not cure only
alleviate symptoms and reduce spread of
virus

Nursing Care:
1.abstinences – condoms and spermicide
less effective
2.keep lesion – clean and dry
 3.culture virus during pregnancy to
safeguard fetus – 50% of newborn will be
infected during delivery
4.when to abstain:
a.presence of fresh lesions
b.last 4 – 6 weeks of pregnancy if
partner has HIV 1

IV. Syphilis

Etiology: Spirochette Treponema Pallidium

Transmission:
Sexual contact/ congenital → moves thru

skin and mucous membrane and into the

bloodstream and destroy tissues in an
organ in the body

Stages:
I. Incubation Period
Characteristics:
1.10 – 90 days – average 21 – days
 2.no S/S or lesion
3.presence of etiology agent – blood is
infective

II. Primary (early) syphilis

Characteristics:
1.Most infectious stage; lasting 1 – 6
weeks
2.S/S:
a.Chancre or primary sore painless
ulcer appears 1st in site of entry of the
organism (genitalia, anorectal, lips,
oral cavity, fingers)
b.Chancre erodes and heals 4 – 6
weeks leaves a scar or none at all
c.Inguinal lymph nodes enlarges
d.Presence of indolent, painless
ulceration in any part of the body
suspect

III. Secondary syphilis

Characteristics:
1.follows onset of chancre – 9 – 90 days
 influenza like symptom and rashes
2.

ulcerations; Condylomata – moist

papules on cell site – highly infectious
3.general patchy hair loss on scalp
4.acute iritis (inflammation of iris)
5.hoarseness, chronic sore throat
IV. Late Syphilis

Characteristics:
10 – 30 days
granulomata – lesions on skin, bones,

liver, CVS (heart, and CNS (brain)

Contact syphilis Chancre

Condylomata + granulomata =
RIP

Diagnostic:
Serologic test – VDRL
 oNon-treponemal or Reagin Test –
detect antibiotic like substance
oTreponemal test – measure specific
antibiotics to TP

Rx: Pen G benzathine – DOC

Nursing Care:
1.Isolation of infected materials
2.case follow-up
3.advise patient to refrain from sexual
contact with untreated previous partner

V. Gonorrhea
Etiology: Gonococcus Neisseria Gonorrea
Transmission: Sexual contact/ direct
contact with discharge

S/S:

Women
 1.Heavy green – purulent discharges,
abnormal uterine bleeding; abnormal
menses
2.urinary frequency, pain and burning
3.ascending infection (PID)

Men
1.purulent discharge following painful
urination, urethritis, prostatitis,
epididymitis (pain-burning)
2.pelvic pain and fever

Pharyngeal gonorrhea
1.Sore throat; maybe asymptomatic

Anorectal gonorrhea
1.anal-rectal burning, itching, and
bleeding mucopurulent discharge, painful
defecation

Adult gonococcal conjunctivitis

 1.Transmitted to eyes by fingers

Diagnostic:
1.gram stains smear, culture
2.direct fluorescent antibody test

Goal of care:
1.eradicate organism
2.educate patient about his condition

Treatment:
Tetracycline, Amoxicillin with
Probenecid and Penicillin with
Probenecid

Nursing Care: Careful Hand washing

Fetal Outcome:
Opthalmia Neonatorum → Crede’s
Prophylaxis – used after delivery
 ( Terramycin Opthalmic Ointment to
both eyes )

Uterine displacements

Normal Uterus:
O
Flexes anteriorly at 45 and movable;
cervix points downward and posterior
More inclined towards the bladder
25% of women – retroversion – still
normal
 to such number of women body lies
back in the posterior cul-de-sac and
rectum; non-pathological

Types:
I. Upward displacement
Lifted forward; becomes on
abdominal organ; internal os is at level
of upper border of symphysis pubis
and can’t be reached by examiner’s
finger

S/S:
Asymptomatic but at times: backache
during menses and/ or prolonged standing
Secondary to amenorrhea, infertility,
feeling of pelvic pressure, dyspareunia
(congestion and adhesion → immobile
uterus)
Treatment:
1. treat underlying cause
 2.Insertion of vaginal pessary
(infrequently used – irritates and erodes
cervical and vaginal mucosa)
Holds the uterus in normal position
Comes in different sizes and style

Nursing care: (Pessary)

1.Be sure it is properly in place
2.douche with weak vinegar solution 2x/
week – remove vaginal debris
3.Pessary to be checked and removed ad
cleansed every 3-4 months. Teach
woman on how to do it by herself
4.make woman understand the needs for
frequent check-ups

Causes:
Vaginal/ paravaginal tumor
low cervical fibroid
 tumor at Cul-de-Sac
collection of pus at pelvis

II. Lateral displacement

lateral deviation; tilting to one side

Causes:
unilateral tumor
fluid collection
pull to one side due to adhesions
Treatment:
treat underlying cause

III. Forward displacement

anterior; towards the front

Anteflexion – fundus bend forward

Anteversion – whole of uterus bend forward

IV. Backward displacement

posterior; towards the back
Retroposition (corrected by knee-chest
position) or retroversion – backward
direction of whole uterus
Retroflexion – fundus bend forward

II.Downward
Or prolapse (protrusion of uterus to
vagina) or descent or procidentia
(protrusion of uterus to or beyond
introitus)
Causes:
Obstetrical trauma
Multiple childbirths
Aging leads to overstretching of
musculofascial support
Prolong standing
Straining
Coughing
Lifting heavy objects

Clinical manifestation:
 1.Awareness of “something is coming
down there”
2.dyspareunia
3.feeling of pressure, heaviness,
backache
4.bladder/ bowel problems cystocele/
rectocele
5.stress incontinence

Management: Hysterectomy

Degrees of Uterus prolapse:

1st degree
Uterus descends at vaginal canal;
cervix reaches but does not go through
the introitus

2nd degree
Body of uterus still in the vagina; cervix
protrudes through the introitus
3rd degree
Entire uterus and cervix protrude through
the introitus; vaginal canal is inverted
(turned inside out)

Cystocele
Protrusion of urinary bladder through
vaginal wall due to weakened pelvic
muscle

S/S:
Stress/ urinary incontinences; UTI
Management:

1.Kegel’s exercise – pubococcygeal

muscle control 50 – 100 times/ day or
BID
2.Anterior Colporrhapy or anterior repair
(Care as in Hysterectomy)
Rectocele
Protrusion of rectum

S/S:
Constipation, heaviness, hemorrhoids

Management:
1.Posterior colporrhapy
Bowel preparation prior to surgery

Hormone Replacement Therapy

Also called: ERT, Estrogen replacement
therapy, HRT, Menopausal hormone therapy
Menopause is the time in a woman's life when
her period stops. It is a normal part of aging. In
the years before and during menopause, the
levels of female hormones can go up and down.
This can cause symptoms such as hot flashes
and vaginal dryness. Some women take
hormone replacement therapy (HRT) to relieve
these symptoms. HRT may also protect against
osteoporosis.However, HRT also has risks. It
can increase your risk of breast cancer, heart
disease and stroke. Certain types of HRT have a
higher risk, and each woman's own risks can
vary depending upon her health history and
lifestyle. You and your health care provider
need to discuss the risks and benefits for you. If
you do decide to take HRT, it should be the
lowest dose that helps and for the shortest time
needed. Taking hormones should be re-
evaluated every six months.