2. DIABETES MELLITUS
A chronic, metabolic disorder
characterized by a deficiency in
insulin production by the islets of
Langerhans resulting in improper
metabolic interaction of
carbohydrates, fats, protein and
insulin
5. DIABETES MELLITUS
Risk Factors
Family history
Rapid hormonal change in
pregnancy
Tumor / Infection of the pancreas
Obesity
Stress
6. DIABETES MELLITUS
Normal Metabolic Changes in Pregnancy
Affect DM
a. Increase INSULIN ANTAGONISTIC
HORMONES – cortisol, estrogen,
progesterone and human chorionic
somatomammotropin (HCS)
otherwise called human placental
lactogen (HPL) – raise maternal
resistance to insulin resulting in
insulin uneffectiveness to use glucose
at the cellular level. Family history
7. DIABETES MELLITUS
b. The increased metabolic rate in
pregnancy causes increased
number of islets of Langerhans
resulting in increased insulin
production but which is rendered
ineffective by the insulin
antagonists primarily HCS/HPL
8. DIABETES MELLITUS
c. If pancreas cannot respond by
producing more insulin, glucose
crosses the placenta to the fetus
where fetal insulin metabolizes it and
by resembling the growth hormone,
causes extra large fetus:
MACROSOMIA
9. DIABETES MELLITUS
d. Increased activity of the APG ->
decreased tolerance for sugar
e. Elevated basal metabolic rate (BMR)
and decreased carbon dioxide
combining power -> tendency to
metabolic acidosis
f. Normal lowered renal threshold for
sugar, increased glomerular filtration
rate -> GLUCOSURIA.
10. DIABETES MELLITUS
g. Vomiting during pregnancy
decreases carbohydrate intake
-> metabolic acidosis.
h. Muscular activity in labor depletes
maternal glucose including glycogen
stores -> requires increased
carbohydrates intake.
11. DIABETES MELLITUS
i. Hypoglycemia is common in
puerperium as involution and
lactation occur.
Effects of DM on the Mother and the
Baby:
When diabetes is well controlled, its
effects on pregnancy may be minimal; if
control is inadequate there may be
maternal and fetal newborn
complications:
12. DIABETES MELLITUS
Mother Baby
Infertility
Spontaneous abortion
PIH
Infections: moniliasis, UTI
Uteroplacental insufficiency
Premature labor
Dystocia
More difficult to control DM ->
hypogycemia / hyperglycemia
Cesarean section often indicated
Uterine atony -> postpartal
hemmorhage
Congenital anomalies
Polyhydramnios
Macrosomia (LGA)
Fetal hypoxia ->nintrauterine fetal
death (IUFD), still births;
increased perinatal mortality
Neonatal hypoglycemia (common
as soon as 1 hr after birth)
Prematurity
RDS (at 6th hr after birth)
Hypocalcemia
13. DIABETES MELLITUS
Effects of Pregnancy on DM
a. DM is more difficult to control:
difficult to maintain blood
sugar.
b. Insulin scock and
ketoacidosis are common.
c. Discomforts nausea and
vomiting predispose to
ketoacidosis.
14. DIABETES MELLITUS
Effects of Pregnancy on DM
d. INSULIN REQUIREMENTS
change in pregnancy.
First trimester: stable insulin;
may not increase need
Second trimester: rapid
increase in insulin need due to
increased secretion of human
placental lactogen (HPL)
15. DIABETES MELLITUS
Third trimester: rapid increase
Labor: IV Regular insulin
Postpartum: rapid decreased
to prepregnant level; may not
need insulin in the first 24
hours after delivery
16. DIABETES MELLITUS
Assesment Findings
a. History
Family history of diabetes;
gestational diabetes in
previous pregnancy
Previous infant with
congenital defects;
polyhydramnios
17. DIABETES MELLITUS
Fetal wastage:
spontaneous
abortion, fetal deaths,
stillbirths
Obesity with very rapid
weight gain
Increased incidence of
viginal moniliasis and UTI
19. DIABETES MELLITUS
b. Signs of hyperglycemia: 3P’s
Polyphagia – excessive
appetite
Polydipsia – excessive thirst
Polyuria – excessive urine
c. Weight loss
d. Increased blood and urine sugar
20. DIABETES MELLITUS
Diagnosing
a. Screening test
Performed at 26 to 28
weeks’ gestational
diabetes (ACOG, 1986).
Uses 50-g oral glucose
challenge
Finding: A plasma glucose of
140 mg/dL needs a follow up
test with 3-hour glucose
tolerance test
21. DIABETES MELLITUS
b. Glucose Tolerance Test
(GCT): 100 g GTT; commonly
done between 28 and 34 weeks of
pregnancy. The presence of two out
of these four venous samples is
considered an abnormal
result:
23. DIABETES MELLITUS
c. 2-hr Postprandial Blood
Sugar (PPBS):
Abnormal result: greater than
120 mg/dL. The goals for
glycemic control include
fasting blood glucose levels
(FBS) less than 105mg/dL and
2-hours postprandial levels of
less than 120 mg/dL
(ACOG, 1994)
24. DIABETES MELLITUS
d. Glycosylated Hemoglobin
(maternal hemoglobin irreversibly
bound to glucose): measures Long-
term (3months) COMPLIANCE to
treatment. Normalvalue: 4% to 8% of
woman’s total hemoglobin, increasing
during hyperglycemia (Saunders et al.,
1980).
25. DIABETES MELLITUS
e. Urine glucose monitoring
INACCURATE as the urine of a
pregnant mother is normally with
sugar.
26. DIABETES MELLITUS
Nursing Implementation
a. Participate in EARLY
DETECTION : history,
symptomatology and prenatal
screening
b. Encourage EARLY PRENATAL
MANAGEMENT and supervision
27. DIABETES MELLITUS
Frequent, regular prenatal visits
Diet: Record dietary intake;
monitor blood glucose levels
several times
28. DIABETES MELLITUS
Insulin: when FBS is not
consistent at lower than
105mg/dL or 2-hour PPBS
is not less than 120 mg/dL
(ACOG, 1994)
29. DIABETES MELLITUS
Serial ultrasonography: for fetal
growth evaluation and fetal
surveillance testing beginning at
about 28 to 34 weeks gestation
(Creasy et al., 2004); earlier
than 26 weeks’ gestation if with
poorly controlled diabetes or
with additional complications
(ACOG, 2004)
31. DIABETES MELLITUS
c. Provide teaching
Nature of DM, effects on
pregnancy on DM, and
effects of DM on pregnancy
Signs and symptoms of
hypoglycemia / hyperglycemia
Need for exercise not only to
regulate glucose levels but
also to enhance feelings of
well-being and to control
weight
32. DIABETES MELLITUS
Insulin regulation /
self-administration of
insulin
Prompt reporting of
danger signs and
signs of infection
33. DIABETES MELLITUS
d. Promote control of DM:
Maintaining maternal
glucose levels within the
normal range during the
prenatal and intranatal
periods is important to
prevent stimulation of the fetal
pancreas resulting in fetal or
neonatal HYPOGLYCEMIA
(Creasy et al, 2004).
34. DIABETES MELLITUS
Diet: cornerstone of DM
management and
control; promote
adherence to
dietary regimen
Calories – 35
calories/kg
EBW or 1800 to
2000
35. DIABETES MELLITUS
Carbohydrates – 30
to 45% (Milk, bread)
or 200 mg/day
Protein – ½ - 2 g/kg
BW or 70 g daily
Fats – unsaturated
Taken regularly
36. DIABETES MELLITUS
Exercise: decreases the
need for insulin excessive
may cause hypoglycemia.
Prevention of
hypoglycemia from
exercise:
Do not exercise
when blood sugar is
low or when
stomach is empty
37. DIABETES MELLITUS
Do not exercise
when blood sugar is
low or when
stomach is empty.
Eat after a prolonged
exercise.
Do not administer
insulin in the extremity
that will be immediately
used in exercise
38. DIABETES MELLITUS
Do not exercise
alone (e.g., have a
partner while
jogging) in case
hypoglycemia
attacks
Always carry
diabetic ID
39. DIABETES MELLITUS
Insulin : oral diabetogenic
agents are contraindicated
Increased need
for insulin in the
second and third
trimesters, needs
may be tripled =
increased
tendency
to ketoacidosis
40. DIABETES MELLITUS
Regular and NPH
insulin are used in
pregnancy; only
regular insulin is
used during labor
are not enough to
prevent
ketoacidosis.
41. DIABETES MELLITUS
o Ketoacidosis is
diagnosed when
glucose levels are
greater than 300
mg/100mL., positive
serum ketones are at
level of 1:4, and
metabolic acidosis
is present ( Creasu
et al,2004)
42. DIABETES MELLITUS
o Causes of ketoacidosis in
pregnancy: poor
compliance,infection,
hyperemes is
gravidarum, or use of
drugs that elevate blood
glucose like
cortocosteroids or beta
sympathomimetic drugs
(Creasy et al., 2004)
43. DIABETES MELLITUS
o Fetal effect of
ketoacidosis: 20%
perinatal mortality rate,
making prompt
recognition and treatment
critical (Cunningham et
al., 2001).
44. DIABETES MELLITUS
Rapid acting REGULAR
INSULIN intravenously aling
with an IV glucose infusion is
used in labor; frequent check
of blood glucose, and
adjustments; and additional
boluses of insulin as needed
(Creasy et al., 2004): The
only insulin that can be given
intravenously is regular
insulin.
46. DIABETES MELLITUS
Encourage hospitalization
for:
Control of Infection
Regulation of insulin
Assesment of fetal
jeopardy and / or
indications for early
termination or
pregnancy
47. DIABETES MELLITUS
• Ultrasound – for fetal growth;
measuring the biparietal diameter
• Urine/blood estriol levels – to
determine fetoplacental functioning
• Amniocentesis – to dtermine lung
maturity. An L/S ration of 2:1 means
mature lungs (above 36 weeks
gestation), if the mother is not diabetic;
but L/S ratio may be falsely elevated in
DM making L/S ratio not an accurate
measure of fetal lung maturity.
48. DIABETES MELLITUS
• Phosphatydyl –Glycerol (PG) – more
accurate way to estimate fetal lung
maturity by determining lung
surfactant if the mother is diabetic.
• Stress and Nonstress Tests
49. DIABETES MELLITUS
Early labor induction or
ceasarian section in the
presence of fetal distress.
• Delivery timing is
INDIVIDUALIZED and
ideally occurs around
TERM. The final time of
terminating pregnancy
depends on the results of
fetal and maternal well-
being surveillance.
50. DIABETES MELLITUS
• When macrosomia
complicates pregnancy
potentially to cause
cephalopelvic disproportion,
then induction of labor may
be done usually around 36
to 37 weeks depending on
ultrasonographic monitoring
of fetal size and evidence of
pulmonary maturity.
51. DIABETES MELLITUS
Continued monitoring,
mother and fetus,
during the intrapartal
period
• Electronic fetal
monitoring
• Left lateral recumbent
to prevent supine
hypotensive syndrome
52. DIABETES MELLITUS
• Fluid and electrolyte balance:
D5W needed to maintain
glucose; Regular insulin added
to IV of 5 to 10% DbW, titrated
to maintain glucose between
100 – 150 mg/dL. In the client
with Type I diabetes (IDDM),
long-acting insulin is avoided (
Creasy et al., 2004) because it
is not enough to prvent
ketacidosis, In addition, only
Regular insulin can be given per
IV.
53. DIABETES MELLITUS
Provide pospartum care
• Monitor maternal need for
POSPARTAL INSULIN:
o The increase insulin
resistance occuring in
pregnancy is usually resolved
in a few hours after delivery,
that IV insulin generally is
discontinued at the time of
delivery (Inzucchi, 1999).
54. DIABETES MELLITUS
o A sharp decrease in insulin
requirement during the first
24 hours necessitates
monitoring of the insulin dose
which is titrated to measured
blood glucose levels in the
immediate postpartun period
(Inzicchi, 1999)
55. DIABETES MELLITUS
o There is a decrease in insulin
need to ½ or 2/3 pregnant
dose on first postpartum day
if on full diet.
56. DIABETES MELLITUS
• Encourage breastfeeding –
has antidiabetogenic effect
o Hypoglycemia raises adrenalin
level resulting in decreased
milk supply and let-down
reflex.
o In acetonuria, stop
breastfeeding while insulin /
diet is / are being adjusted;
may pump breast to maintain
milk production
57. DIABETES MELLITUS
• Be alert for and prevent
COMPLICATIONS IN THE
postpartum:
o Hemorrhage – from uterine atony.
Keep uterine fundus firm.
o Infections – candidiasis, UTI. Avoid
catherization; provide meticulous
perineal hygiene; instruct on the
“front-to-back” technique of perineal
flushing
58. DIABETES MELLITUS
o Insulin shock / hypoglycemic
shock; DANGER SIGNS: sweating
with cold, clammy skin, pallor
tremors, and occurs hunger.
Insulin reactions or hypoglycemic
schock usually at time of PEAK
ACTION of insulin. For Regular
insulin, the peak of action is
usually 2 to 4 hours after
administration.
o Post-partum PIH: monitor BP
59. DIABETES MELLITUS
• Encourage to have 1-hour glucose
tolerance test 6 to 8 weeks postpartally to
ensure return to normoglycemia
(Buchanan &Kjos, 1999).
• Encourage contraception; reinforce
physician’s recommendations
o Barrier (diaphragm/condom) –
recommended
o Oral contraceptive pills – contraindicated;
decrease CHO tolerance
o IUD – contraindicated due to poor response
to infection
61. IRON-DEFICIENCY ANEMIA
Decrease in oxygen –carrying
capacity of the blood due to decrease
hemoglobin in the blood. In
pregnancy, the client has pregnancy-
related factors that predispose her to
iron-deficiency anemia (Littleton and
Engrebetson, 2006):
62. IRON-DEFICIENCY ANEMIA
a. Red blood cell volume increase by
30%, but faster drops
b. Increase blood volume by 30% to
50% higher before labor
The disproportionate increase in
blood volume and blood cells
results to HEMODILUTION thus
physiologic anemia of pregnancy.
63. IRON-DEFICIENCY ANEMIA
c. Increased ability of the intestinal tract
to absorb iron for both maternal and
fetal needs.
d. Increase transport of iron placenta for
fetal liver storage, more rapid in the
third timester (7th to 8th month)
e. Inadequate dietary intake and
maternal stores
64. IRON-DEFICIENCY ANEMIA
Risk Factors
a. Decrease nutritional intake/
malnutrition
b. Heredity, cultural practices, fad
diets
c. Increased demands as in pregnancy
and adolescence
d. Poor absorption as in stomach and
intestinal disease.
65. IRON-DEFICIENCY ANEMIA
Prognosis
a. Associated with fetal problems –
IUGR, increased perinatal mortality
b. Increased incidence of abortion,
infection, premature labor,
postpartal hemorrhage, PIH, heart
failure in existing disease of the
heart.
66. IRON-DEFICIENCY ANEMIA
Assesment Findings
a. Objective: pale skin and mucous lining;
pearl-white sclera; brittle, flattened
nails, altered VS – rise in systolic
pressure; tachycardia and tachypnea
b. Subjective: Fatigue or shortness of
breath on exercise, headache,
anorexia, menorrhagia, heartburn,
flatulence
67. IRON-DEFICIENCY ANEMIA
Diagnosis
a. Physical signs
b. Laboratory findings:
• Low hemoglobin (less than 10g/100mL)
• Low hematocrit (less than 37% in the
first trimester, less than 35% in the
second trimester, and less than 33% in
the third trimester
• Serum iron less than 65 ug/100mL
blood
68. IRON-DEFICIENCY ANEMIA
Nursing Implementation
a. Promote a balance of activity and rest with
avoidance of fatigue. Anemic clients get
fatigued easily.
b. Provide dietary instructions on iron-rich foods-
• Red meats: liver (best source), beef, heart,
and kidneys
• Green leafy vegetables
• Dried fruits: raisin is excellent for snacks
• Egg yolk
• Whole grains, nuts legumes, dried beans
69. IRON-DEFICIENCY ANEMIA
c. Encourage regular intake of ordered
hematinics (ferrous sulfate)
• Take with vitamin C/ASCORBIC
ACID to enhance absorption
• BEST taken between meals to
enhance absorption
• Use a straw, if mixed with fruit juice,
to prevent staining teeth.
• Inform client of the darkening effect
on the stools
70. IRON-DEFICIENCY ANEMIA
d. Administer ordered intramuscular
preparations (Iron dextrans/IMFERON)
• Use second needle for injection
(Rationale: Parenteral iron tattoos
the skin).
• Use sharp, long needle to reach deep
muscles (2-3 inches, 19-20 G)
• Use Z-track method
• Do not rub site.
71. IRON-DEFICIENCY ANEMIA
• Instruct client not to wear
constricting garments around site
• Rotate sites.
e. Keep warm and free from infection
because of increased susceptibility to
infection
f. Avoid hot water bottles/heating pads
because of decreased sensitivity.
74. MULTIPLE PREGNANCY
Risk factors
a. Rise in infertility management and
assisted reproductive technology
(Bowers, 1998). Ovulation induction
and assisted reproductive technology
are identified causes of triplet
pregnancies, 83% and quadruplet
pregnancies, 95% (Eganhouse &
Petersen, 1998).
75. MULTIPLE PREGNANCY
b. Advanced maternal age as a result
of delaying pregnancy by choice
and infertility -> major risk in all
multiple gestations are
pre3maturity and low birth weights
(Bowers, 1998).
76. MULTIPLE PREGNANCY
c. Use of Clomiphene citrate (Clomid,
Serophene) to increase maturation
of follicle as a management of
female infertility has multiple
ovulation as one of the side
effects.
77. MULTIPLE PREGNANCY
d. Parity: as parity increases so does
the chance for multiple births
(Olds, London & Ladewig, 1988;
James, 1981).
78. MULTIPLE PREGNANCY
Types
a. Monozygotic twins – result from a
single ovum that then divides; called
IDENTICAL TWINS
• They share all (one set of traits,
placenta, chorion, usually one
amnion) except the umbilical cord.
They are of the same genotype
(appearance) and of the same sex.
79. MULTIPLE PREGNANCY
• The incidence of monozygotic twins
is about 1 in 250 births
(Cunningham, et al., 2001; Olds,
London & Ladewig, 1988).
• The survival rate of monozygotic
twins is 10% lower than that of
dizygotic twins, and congenital
defects are more prevalent (Oxorn,
1986).
80. MULTIPLE PREGNANCY
• Classification of Monoxygotic
Twins: The number of
amnions and chorions present
depends on the timing of the
division (Pritchard et al.,
1985)
81. MULTIPLE PREGNANCY
o Division occurs within the first 72
hours after fertilization b(efore the
inner cell mass and chorion is
formed), two embryos , two
amnions, two chorions will
develop. Occurs in 20% to 30% of
the time. There may be one
distinct placenta or a single fused
placenta. This is termed
DIAMNIONIC MONOZYGOTIC
TWINS.
82. MULTIPLE PREGNANCY
o If division occurs between four
and eight days after
fertilization (when the inner
cell mass is formed and
chorion cells have
differentiated but those of the
amnion have not), two
embryos develop with
separate amniotic sacs, later
to be covered by a common
chorion.
83. MULTIPLE PREGNANCY
o If the common has already
developed approximately eight
days after fertilization, division
results in two embryos with a
common amnionic sac and a
common chorion, called
MONOCHORIONIC
MONOZYGOTIC TWINS;
occurs in 1% of the tine
(Creasy & Resnik, 1984).
84. MULTIPLE PREGNANCY
b. Dizygotic twins – result from 2 separate
ova; called FRATERNAL TWINS
• The relationship that exists between
the dizygotic twins is similar to the
relationship that exists between
siblings. They may be of the same or
different sex.
• The incidence of fraternal twins
vaires with maternal race, age, parity,
and heredity (ACOG, 1998)
85. MULTIPLE PREGNANCY
c. “Supertwins” – a common term for
rare triplets and other higher-order
multiple births, such as quadruplets
or quintuplets. These babies can be
identical, fraternal, or a combination
of both.
86. MULTIPLE PREGNANCY
Incidence
a. The incidence of twins, tiplets, and
higher-order multiples has
increased because of the wide-
spread use of FERTILITY DRUGS
and advanced reproduction
techniques (ACOG, 1998).
87. MULTIPLE PREGNANCY
b. Fraternal twins: more common –
70%
c. Identical twins: 30%
d. More than 15% weigh less than
2500 g, and most are preterms
e. Most common in blacks least in
Orientals
f. Incidence of fraternal twins
increases with increasing age
88. MULTIPLE PREGNANCY
Assessment Findings
a. Positive history of twinning (family
or past pregnancies)
b. Big uterus
c. Two FHT’s asynchronous
d. Palpation of 3 or more large parts
e. Two fetal outlines on ultrasound
f. Increased maternal weight and
discomforts : edema, varicosities,
shortness of breath; increased
susceptibility to spine hypotensive
syndrome
92. MULTIPLE PREGNANCY
b. FETAL
• Prematurity (most common fetal
complication) and low birth weight babies
(Bowers, 1998)
• Respiratory distress syndrome (leading
cause of deaths in the premature infants)
• Hypoglycemia, hyperbilirubinemia, and
anemia
• Conjoining abnormalities (from
incomplete separation and with common
organ or parts)
93. MULTIPLE PREGNANCY
• Intrauterine asphyxia, stillbirth
and birth injuries -> high morbidity
and mortality
• Cerebral palsy and other
neurologic impairments
94. MULTIPLE PREGNANCY
Medical Management
Goals of medical care: the promotion
of normal fetal development and
preventing the delivery of preterm
fetuses , and dinminishing fetal
trauma labor
95. MULTIPLE PREGNANCY
a. Early diagnosis -> comprehensive prenatal
care.
b. Frequent monitoring: Maternal and fetal
well-being, fetal growth and viability:
• Laboratory
• Serial ultrasonography
• NST and fetal biophysical profile
beginning at 30 to 34 weeks. A reactive
NST is associated with good fetal
outcome; NST done every 3 to 7 days
until delivery, or until rsults are
nonreactive (Polin & Frangipane, 1986)
96. MULTIPLE PREGNANCY
c. Nutritional support
• Calories : Non-pregnant kcal =300
Kcal/day in signleton pregnancy +
another 300 Kcal/day in multifetal
pregnancy
• Iron: 30 to 60 ,
• Mg/day in multifetal pregnancy
• Folic Acid: Adequate protein from a
variety of sources may supply
adequate amount of folate. One
gram of folate a day is beneficial.
d. Cervical assessment for stable labor
staus
97. MULTIPLE PREGNANCY
e. Usually continuos electronic fetal
monitoring in labor to provide
assessment data for both UTERINE
ACTIVITY and FETAL TOLERANCE to
labor ( Littleton & Engbretson, 2006)
f. Delivery vaginal or ceasarian section
98. MULTIPLE PREGNANCY
Nursing Implementation
a. Teaching: More frequent prenatal
care: every 2 weels in the second
trimester, then every week, then
twice a week in the last 4 weeks.
b. Balanced diet with increased
calories, iron and vitamin
supplementation. Folic acid is
extremely important; taken 1 month
prior to and throughout the first 3
months of tube defects such as
spina bifida.
99. MULTIPLE PREGNANCY
c. Frequent test – left lateral position
d. Prompt reporting of danger signals –
bleeding, passage of fluid per
vagina, cramping, and premature
contractions
e. Psychosocial assessment and
support; referral, as needed: social
services, postpartum caregivers and
lactation support person
100. MULTIPLE PREGNANCY
f. Intranatal Management
• Strict asepsis to prevent
infection
• A physician-nurse team for
each newborn is scrubbed
gowned and gloved
• Cord is clamped after
delivery of baby A. (Babies
are labeled as Baby A, B and
so forth)
101. MULTIPLE PREGNANCY
• Assist in the safe delivery of the second
child; optimum time for delivery of the
second baby is 5 to 20 minutes.
• Prevent bleeding
o Administer Pitocin immediately after
delivery of the last baby
o Palpate fundus but do not massage
until after the uterus contracts and
expels the separated placenta, then
give ordered ergot prep (ergotrate),
0.1 mg IV if woman is not
hypertensive. Gently massage and
elevate fundus for 15 to 30 minutes.
102. MULTIPLE PREGNANCY
• Promote bonding and provide
psychological support. The
fetuses are likely to stay longer in
the intensive care unit, may have
complications of prematurity or
may have defects. Encourage
maternal / couple verbalization of
concerns and anxiety.
104. GERMAN MEASLES/RUBELLA
An acute viral infection caused by a
mixovirus. The maternal infection os
mild but effects on the fetus are
severe. Effects of Rubella
105. GERMAN MEASLES/RUBELLA
a. First trimester exposure. The four most
common severe abnormalities resulting
from ceongenital rubella syndrome
(Littleton & Engrebretson, 2006)
• Deafness
• Eye defects (congenital cataract
and blindness)
• Central nervous system defects
(brain defects
106. GERMAN MEASLES/RUBELLA
• Cardiac malformation(patent ductus
arteriosus)
• Other anomalies include:
microcephaly, mental retardation,
susceptibility to pneumonia,
enlarged liver and blood dyscrasia:
hemolytic anemia and
thrombocytopenia.
107. GERMAN MEASLES/RUBELLA
b. Second trimester / Third trimester
exposure may result to the
following complicated: premature
labor, late
• IUFD, subtle abnormalities
present in later life
• DM, thyroid probs, “soft”
neurologic defects
• progressive panencephalitis
108. GERMAN MEASLES/RUBELLA
Incubation Period:
2 to 3 weeks
Period of Communicability:
7 days before to 5 days after rash
appears.
Transmission:
Direct and indirect contact
109. GERMAN MEASLES/RUBELLA
Assesment Findings:
a. Pink maculo-popular rash; starts
on face, caudal spread (d-5d)
b. Slight fever, malaise
c. Nassal catarrh
d. Anorexia
e. Posterior auricular and occipital
adenopathy
f. Arthritis / arthralgia may develop
(especially in adults)
110. GERMAN MEASLES/RUBELLA
Treatment: Symptomatic
a. Supportive treatment
b. Immune serum globulin is given to
exposed women to prevent
aggravation of maternal symptoms
but will not later fetal infections and
will not reverse fetal defects that are
already present.
111. GERMAN MEASLES/RUBELLA
c. IMMUNIZATION: cornerstone
of therapy
• Rubella vaccination All non pregnant
nonimmune women of childbearing
age get 95% immunized after
receiving the vaccine (Bowes,1996).
SAFETY ALERT: Avoid pregnancy for
at least 1 month (4 weeks) after the
immunization (Littleton & Engrebetson,
2006). Not contraindicated in
breastfeeding women
112. GERMAN MEASLES/RUBELLA
• All children to receive MMR at
age 15 months (U.S.A. Standard)
• Pregnant nonimmune women
should be immunized in the
immediate POSTPARTUM
confinement, NEVER during
pregnancy; defects may be delayed
for up to 21 days (Bowes, 1996)
115. SEXUALLY TRANSMITTED
DISEASES (STDS)
1. Vaginal Moniliasis
a. Caused by yeast that thrives best
in acidic medium; alkaline douche
may be used for control
b. Causes thick, cheesy white
patches on vaginal wall
116. SEXUALLY TRANSMITTED
DISEASES (STDS)
c. May be passed to fetus during
delivery and cause ORAL
THRUSH in the newborn.
d. Treatment: topical nystatin
(Mycostatin), gentian violet,
clotrimazole (Gyne-Lotrimin)
117. SEXUALLY TRANSMITTED
DISEASES (STDS)
2. Trichomonas Vaginalis
a. Caused by protozoa which thrives
best in alkaline medium; acidic
douche maybe used for control
b. Causes profuse foamy /frothy
white to greenish vaginal
discharge with pruritus
118. SEXUALLY TRANSMITTED
DISEASES (STDS)
c. Treated for 7 days with
METRODINAZOLE (Flagyl);
teranogenic in the first trimester;
alcohol with Flagyl causes severe
GI upset
d. All sexual partners must seek
treatment; advise use of
condoms during intercourse
119. SEXUALLY TRANSMITTED
DISEASES (STDS)
3. Gonorrhea
a. Caused by gonococcus
Neisseria Gonorrheae
b. Causes profuse purulent and
yellowish vaginal discharge
with pruritus; may be
asymptomatic
120. SEXUALLY TRANSMITTED
DISEASES (STDS)
c. Maybe passed to fetus during
delivery and cause OPHTHALMIA
NEONATARUM and sepsis,
Prophylaxis; Crede’s prophylaxis
d. Treatment: Antibiotic
PENICILLIN; erythromycin if with
allergy to penicillin
121. SEXUALLY TRANSMITTED
DISEASES (STDS)
4. Chlamydia
a. Most common STD
b. Gonorrhea like in symptoms,
treatment and newborn
complication OPTHALMIA
NEONATORIUM
c. If untreated -> pelvic
inflammatory disease (PID).
122. SEXUALLY TRANSMITTED
DISEASES (STDS)
5. Syphilis (SY)
a. Caused by spirochete Treonema
Pallidum
b. With placental barrier to SY in the
first 16 weeks –> crosses placenta
and infect the fetus after 16
weeks -> congenital SY
123. SEXUALLY TRANSMITTED
DISEASES (STDS)
c. Initial synptoms painless, contagious
sore CHANCRE, and
lymphadenopathyl and secondary
symptoms (malaise, rash, alopecia)
may disappear in several weeks
without treatment.
d. Diagnosis: dark-field examination and
serologic test ( VDRL)
e. Treatment: Antibiotic PENICILLIN;
erythromycin if with allergy to penicillin.
124. SEXUALLY TRANSMITTED
DISEASES (STDS)
6. Genital Herpes
a. Caused by herpes simplex virus type 2 (HSV);
may have remission and exacerbation caused
by stress, infection and menses
b. Causes PAINFUL vaginal vesicles -> may be
transmitted to the newborn during vaginal birth -
> may cause neonatal death. PREVENTION:
cesarean delivery during active infection.
c. No cure; Acyclovir (Zovirax) reduces duration
and severity exacerbation.
125. SEXUALLY TRANSMITTED
DISEASES (STDS)
7. Hepatitis B
a. Caused by hepatitis B virus transmitted
through blood and body fluids (semen).
b. Acute infection effects:
• permanent liver damage or
carcinoma
• in pregnancy maternal-infant
transmission
126. SEXUALLY TRANSMITTED
DISEASES (STDS)
o Prenatal: transplacental transmission
which may cause spntaneous abortion
or preterm labor
o Intranatal and postnatal: transmission
through contaminated surfaces and
breast milk or colostrum
c. Treatment given to the newborn infant: hepatitis
B immune globulin and the first of the three
injections of hepatitis B vaccine before
discharged from the hospital (Sweet & Gibbs,
1995).
127. SEXUALLY TRANSMITTED
DISEASES (STDS)
8. Toxoplasmosis
a. Caused by parasite toxoplasma found in animals
(mice, sheep)
b. Transmitted in the feces of cats who have
consumed infected mice, and in meat from
infected animals.
Safety alert: Prenatal teaching – do not
handle cat litter, wash hands after handling
cats, avoid raw and undercooked meats.
c. May be asymptomatic in humans or may cause
influenza-like signs: fatigue sore, throat, rash
fever and eye pain.
128. SEXUALLY TRANSMITTED
DISEASES (STDS)
8. Toxoplasmosis
a. Caused by parasite toxoplasma found in
animals (mice, sheep)
b. Transmitted in the feces of cats who
have consumed infected mice, and
in meat from infected animals.
Safety alert: Prenatal teaching – do
not handle cat litter, wash hands
after handling cats, avoid raw and
undercooked meats.
129. SEXUALLY TRANSMITTED
DISEASES (STDS)
c. May be asymptomatic in humans or may
cause influenza-like signs: fatigue sore,
throat, rash fever and eye pain.
d. May cause spontaneous abortion,
intrauterine growth retardation and
premature delivery.
e. Treatment: Antibiotics if diagnosed early;
however, neonatal disease may still
occur.
130. SEXUALLY TRANSMITTED
DISEASES (STDS)
9. HIV-AIDS
a. Caused by a RETROVIRUS human
immunodeficiency virus (HIV) that
infects helper T-lymphocyted (T4 cells)
-> present in infected person’s blood,
semen and other body fluids.
b. Modes of transmission: sexual contact ,
contaminated blood and blood
products, placental transfer, possibly
through breast milk.
131. SEXUALLY TRANSMITTED
DISEASES (STDS)
Safety alert: The newborn infant born of a mother
infected with HIV mnust ve cared for with strict
attention to STANDARD PRECAUTIONS to
prevent the transmission of HIV from the newborn
infant, if infected, to others, and prevents
transmission of other infectious agents to the
possibly immunicimnpromised newborn infant.
Mothers infected with newborn infant. Mothers
infected with HIV should not breasfeed (Murray et
al,, 2002)
c. Diagnosis: based on clinical criteria and positive HIV
antibody test – ELISA (enzyme-linked
immunosorbent assay)
132. SEXUALLY TRANSMITTED
DISEASES (STDS)
10. Cytomegalovirus (CMV)
a. Can be transmitted transplacentally
and at the time of birth causing flu-
like symptoms in trhe healthy adult
or no symptoms at all. As many as
75% of adult wom,en have
antibodies to CMV (Littleton &
Engebretson, 2006).
b. The pregnant woman can be tested for
immunity or current infection using
TORCH serum screening:
133. SEXUALLY TRANSMITTED
DISEASES (STDS)
T – oxoplasmosis
O – thers (Syphilis)
R – ubella
C – ytomegalovinus
H – erpes
For primary infection, no fully effective
treatments are available; antiviral
treatments are used to limit the extent of
the disease (Littleton & Engebretson),
2006).
134. SEXUALLY TRANSMITTED
DISEASES (STDS)
c. Has been linked to serious neonatal
infection and malformations including
hepatosplenomegaly, jaundice,
deafness and eye problems. Long-
term effects include microcephaly or
hydrocephaly, cerebral calcification,
mental retardation and chorioretinitis .
The likelihood of a healthy outcome is
90% (Sweet and Gibbs, 1995)
