Diseases

Affecting
Pregnancy

Prepared by:
MA. CONCEPCION F. COLUMBRES, RN,RM, MN
 DIABETES MELLITUS
DM is a chronic disease in which glucose
metabolism is impaired by lack of insulin
in the body or by ineffective insulin
utilization.
DM, particularly if it is controlled poorly,
can adversely affect pregnancy
outcomes.
 Itis recommended that specialists be involved
in the care of the pregnant woman with DM.
 Sometimes the obstetrician consults with an
Endocrinologist, who then manages the
woman’s DM throughout her pregnancy.
 At other times the OB consults with the
Perinatologist or the Perinatologist manages
the woman with DM during her pregnancy.
A perinatologist, a specialist in maternal-fetal
health, is an obstetrician who has received
further specialized training in high risk
pregnancies.
 Endocrinology is concerned with the study of
the biosynthesis, storage, chemistry, and
physiological function of hormones and with
the cells of the endocrine glands and tissues
that secrete them.
 CLASSIFICATION OF
DIABETES MELLITUS

 TYPE 1: Characterized by a lack of

insulin in the body

 TYPE 2: most often associated with

insulin resistance.
 These 2 diseases are very different in nature.
 They both affect glucose metabolism
 A woman who enters pregnancy with either
TYPE 1 or TYPE 2 DM is said to have
PREGESTATIONAL DIABETES.

 More often, a woman who is at risk for type

2 DM will develop GESTATIONAL DIABETES
(GDM), a type of DM that is unique to
pregnancy but in many respects mimics type
2 DM.
 PREGESTATIONAL D.M.
 Woman with pregestational type 1 DM had a
higher incidence of spontaneous abortions
(miscarriages).
 If the woman was able to carry the pregnancy
to term, the fetus was at risk for Congenital
Anomalies and / or Stillbirth.
 Other pregnancy-related complications
associated with pre-existing DM include:
Pregnancy-induced hypertension

Polyhydramnios (excess levels of

amniotic fluid)
Preterm delivery

Shoulder dystocia (birth trauma)

 The diabetic woman is three times as likely

to experience a CS birth as a woman who
does not have DM (Moore, 2002).
 GESTATIONAL DIABETES
MELLITUS
 The woman who develops GDM is at increased risk
for developing type 2 DM.
 The pancreas of the woman with GDM has sufficient
resources to sustain normal blood sugars when she is
not pregnant; however the stress of pregnancy may be
enough to bring on GDM.
 She then experiences sustained periods of

hyperglycemia and hyperinsulinemia, which puts

her and the unborn child at risk
 PATHOPHYSIOLOGY of GDM is
INSULIN Resistance.

 Normal pregnancy is marked by insulin

resistance.

 Tissues become resistant to insulin to provide

sufficient levels of glucose for the growing
fetus.
 The exact cause of insulin resistance in
pregnancy is unknown, it is thought that the
hormones estrogen, progesterone, and human
placental lactogen (HPL) are at least partially
responsible.
 As these pregnancy hormones rise, insulin
resistance increase. The result in a normal
pregnancy is threefold:
 Blood glucose levels are lower than
normal (mild hypoglycaemia) when fasting.
 Blood glucose levels are higher than

normal (mild hyperglycemia) after meals.

 Insulin
levels are increased (hyperinsulinemia)
after meals.

 Together
these changes are referred to as the
DIABETOGENIC EFFECT OF PREGNANCY.

 GDM develops when the woman cannot

tolerate this normal pregnancy change.
 RISK FACTORS FOR GDM
 History of a large-for gestational age infant
 History of GDM
 Previous unexplained fetal demise
 Advanced maternal age (greater than 35 yrs.)
 Family history of type 2 DM or GDM
 Obesity (greater than 200 pounds)
 Non-Caucasian ethnicity
 Fasting blood glucose of greater than 140mg/dL
 Random blood glucose of greater than 200mg/dL
 Diagnostic Values for the Oral Glucose
Tolerance Test (OGTT)
 NORMAL VALUES ARE:
Fasting - < 95mg/dL

1 hour - < 180mg/dL

2 hours - < 155mg/dL

3 hours - < 140mg/dL

 GDM is diagnosed if two or more values

meet or exceed the levels listed above.
The GREATEST RISK for the fetus – with
woman with GDM is:
Excessive growth, resulting in

MACROSOMIA and
BIRTH TRAUMA (Shoulder Dystocia).

 Insulin does not cross the placenta;

however blood sugar does.
 Aswith any disproportionate intake of sugar,
the excess calories are stored in the fetus’
body in the form of FAT.

 Thefetus is also at risk for delayed lung

maturity and other complications seen in the
newborn of the woman with DM.
 ASSESSMENT

 TYPE1 DM, usually has the disease diagnosed

during childhood or adolescence.

 Shemay be accustomed to monitoring her

blood glucose levels and self-administering
insulin.
ASSESSMENT CONT.
 ONCE GDM as been diagnosed, assess for
understanding of therapeutic regimen
management.
 INSTRUCT the woman to bring her blood sugar
log to every prenatal visit.
 ASSESS her ability to self-manage her
condition.
 INQUIRE regarding S/S of UTI and /or
Candidiasis.
 PREPREGNANCY CARE
 Woman with TYPE 1 DM is advised to consult
with her physician before she becomes
pregnant.
 Persistent maternal hyperglycemia is harmful
to the growing fetus, particularly during the
first 8 weeks of pregnancy, when
organogenesis is occurring.
 It is important for the woman to attain a state
of EUGLYCEMIA (normal blood glucose levels)
in the months before becoming pregnant.
 MONITORING Management of Therapeutic
Regimen
 With the assistance of PRIMARY HEALTH
CARE PROVIDER
Information obtained regularly by self-
monitoring or blood testing at home with a
portable glucose monitor gives immediate
feedback on the effect of diet, activity, and
medications on glucose levels.
 Every office visit carefully review the
woman’s blood sugar log.
 Dietary recall for the past 3 days may be

helpful for identifying patterns of food

intake that interfere with blood sugar
control.
 Refer the woman for a consult with a

registered dietitian.
 Review with the woman her exercise
patterns to determine if improved blood
sugar control might result from
implementation of an exercise regimen.
 Carefully explore the woman’s’

compliance with insulin administration.

 Frequent episodes of
HYPOGLYCEMIA may be
caused by too much insulin or too
little food.
Explore her pattern of food
intake in conjunction with
insulin administration.
SYMPTOMS OF HYPOGLYCEMIA
T – Tremors & Tachycardia
I - Irritability
R - Restless
E - Excessive hunger
D – Diaphoresis & Depression
 Be certain she is eating 3 regular meals and 3
snacks daily.
 Food intake should follow insulin administration.
 A pattern of regular exercise may decrease insulin
needs.
 Notify physician of frequent episodes of
hypoglycaemia, (particularly if the woman began
a regular exercise program 3 to 4 weeks
previously.
 PREVENTING MATERNAL INJURY
 Take particular care to review the S/S of
hypoglycemia with the woman and her family.
 Explain that it is important to pay attention to the
warning signals because she is more prone to
hypoglycaemia during pregnancy.
 Woman with DM is at risk for developing diabetic
ketoacidosis (DKA), the woman with Type 1 DM
during pregnancy is at highest risk.
She should know: Signs of developing
hyperglycemia and avoid triggers for DKA.
DIABETIC KETOACIDOSIS (DKA)
AND PREGNANCY

 The onset of DKA is marked by the classic

symptoms of hyperglycemia, which
include:
Polydipsia (excessive thirst)

Polyuria (increase frequency and

amount of urine)
Polyphagia (excessive hunger)
As DKA develops, the following
symptoms appear:
Glucose > 30mg/dL

Ketonuria

Kussmaul respirations

Acetone (like alcohol) breath

Sleepiness

Language slurring

Decreased consciousness
Triggers for DKA include (but are
not limited to) the following:
Too little insulin or too much
food
Infection

Tocolytic therapy (to prevent

preterm labor)
Corticosteroid use

Insulin pump failure.

o Woman with DM, increased risk for pregnancy-
induced hypertension (PIH)
 Weekly blood pressure and urinary protein
measurements.
 Every office visit carefully screen the woman for
signs of PIH, such as:
Headache

Visual disturbances

Epigastric pain

Generalized edema

Urinary protein

And elevated blood pressure

 MONITORING FOR AND PREVENTNG
INFECTION
 Woman with DM is at increased risk for UTI
because of elevated sugar levels.
 Review the woman with signs of UTI:
Increased frequency

Voiding small amounts,

Burning with urination,

Cloudy urine.
 Teach her to drink 8 to 10
glasses of noncaffeinated
beverages every day to help
prevent UTI.
 Wipe perineal area from front to
back after using the restroom.
 Frequent handwashing
(AC & PC, and using the
restroom) –best way to prevent
infection.
 Remind the woman that if a UTI
occurs, prompt treatment is
essential because UTI can cause
PREMARURE LABOR.
 MONITORING FETAL STATUS
 It is very important for the pregnant woman with
DM to understand the risk of fetal demise,
particularly if blood sugar levels are difficult to
control and / or the woman requires insulin to
manage her diabetes.
The 3rd trimester is generally the time of

greatest danger.
Institute fetal surveillance per the physician’s

orders.
Teach woman to monitor fetal activity and kick

counts, starting at approximately 26 to 28

weeks’ gestation.
FETAL WEIGHT
 DM woman and fetus, At risk for
disproportionate growth resulting in
fetal MACROSOMIA (fetal wt > 4,000
grams).
Measure fundal ht at each prenatal

visit.
Larger-than-expected size may be
related to a large fetus or
polyhydramnios.
 MACROSOMIC infant is much more likely to
experience the delivery complication of
shoulder dystocia (difficulty delivering fetal
shoulder after the delivery of the head),
leading to birth trauma.
 Physicians may induce labor in the woman
as soon as fetal lung maturity can be
established in an attempt to prevent
shoulder dystocia.
 Alternatively, may elect to perform a
cesarean delivery if macrosomia is
suspected.
CARDIAC DISEASE
 What happens during pregnancy?
 Both the blood volume and cardiac
output increase approximately 30%.
 Most of this increase occurs by 8 weeks
of pregnancy.
 Maximize by mild pregnancy
 Functional or transient murmurs can
be heard in many women during
pregnancy.
 Heart palpitations on sudden exertion
 Disappear after pregnancy
Danger!!!
 Occurs primarily due to the increase
in circulatory volume.
 The most dangerous time is in 28-32
weeks, just after the blood volume
peak.
 During pregnancy cardiac output is
increases by more than one third,
reaching a peak by about 20
week’s gestation, the heart rate
accelerates by 10 beats per minute
and the blood volume is expanded by
more than one third, reaching a peak
between 28 to 30 weeks gestation.
Danger!!!
 If heart disease is severe, symptoms can
occur almost immediately.
 The heart may become so over whelmed
by the increase in blood volume that
cardiac output falls.
 Vital organs including the placenta are no longer
perfused adequately.
CARDIAC DISEASE
 This involves a variety of heart
conditions both congenital and
acquired that complicate
pregnancy.

RISK FACTORS:
 Rheumatic fever
 Congenital defects of the heart
 Arteriosclerosis
 MI: pregnancy is general
contraindicated in clients who have
experienced an MI before becoming
pregnant and who have severe left
ventricular damage and heart failure

 Pulmonary disease
 Renal disease
 Heart surgery
 CLASSIFICATION OF HEART
DISEASE BASED ON FUNCTIONAL
CAPACITY OF THE HEART

 CLASS I – no limitation of physical

activity, regular activities do not
produce symptoms
 CLASS II – slight limitation,
asymptomatic at rest but regular
activities produce palpitations ,fatigue,
dyspnea, and anginal pains.
 CLASS III - marked limitation of
activities, less than regular activities
caused symptoms

 CLASS IV – marked limitation of

activities symptomatic at rest
 Diagnosing heart disease in pregnancy is not easy
as there are common signs that mimic heart
disease:
o Palpitations

o Edema

o Tachpnea

o Fatigue

o Syncope

o Dyspnea

o Transient, soft systolic murmur

* The presence of severe dyspnea, syncope with

exertion, hemoptysis, paroxysmal tachycardia
and chest pain on exertion prompt further
evaluation.
 RHEUMATIC HEART
DISEASE

1. Mitral stenosis is the most

common lesion.
2. Severe lesion with pulmonary
hypertension→ pulmonary edema
→ heart failure: terminate the
pregnancy
 Mitral stenosis is a disorder in which the mitral valve
does not fully open. This restricts the flow of blood.
Causes
 Blood that flows between different chambers of your
heart must flow through a valve. The valve between
the two chambers on the left side of your heart is
called the mitral valve. It opens up enough so that
blood can flow from the upper chamber of your heart
(left atria) to the lower chamber (left ventricle). It
then closes, keeping blood from flowing backwards.
 Mitral stenosis means that the valve cannot open
enough. As a result, less blood flows to the body. The
upper heart chamber swells as pressure builds up.
Blood and fluid may then collect in the lung tissue
(pulmonary edema), making it hard to breathe.
  Pulmonary hypertension
begins when tiny arteries in
your lungs, called pulmonary
 Pulmonary arteries, and capillaries
hypertension is a become narrowed, blocked or
type of high blood destroyed. This makes it
pressure that affects harder for blood to flow
through your lungs, and
the arteries in the
raises pressure within your
lungs and the right lungs' arteries. As the
side of your heart. pressure builds, your heart's
lower right chamber (right
ventricle) must work harder
to pump blood through your
lungs, eventually causing
your heart muscle to weaken
and eventually fail.
EFFECTS ON FETUS
 Preterm labor, fetal death, fetal
distress
 Drug used
 Inherited problem
 PERIPARTUM HEART DISEASE
Peripartal Cardiomyopathy
 Extremely rare condition
 Can occur in pregnancy with no
previous history of heart disease
 Cause: unknown
 May be effect of pregnancy on the
circulatory system
 SIGNS OF MYOCARDIAL FAILURE
Shortness of breath
Chest pain
Edema
Cardiomegaly
 If cardiomegaly persist in the
postpartum:
 Advised not to attempt further
pregnancies
 Contraceptives are contraindicated
> Danger of thromboembolism
 Heart transplant
> If disease may progress
EFFECTS OF HEART DISEASE ON FETUS:
 Fetal growth – decrease birth weight
 Fetal distress
 Neurologic – mental involvement –
effects of placental insufficiency
 TREATMENT MANAGEMENT
a) Frequent visits and consultation with
specialist
b) Rest, physical and mental rest. The
amount of rest and activity depends on
the functional ability of the heart. Bed
rest may be needed as mother become
symptomatic or as cardiac function is
impaired.
c.) Digitalis. Check cardiac rate before
administration and withhold if lower
than 60bpm and higher than 100bpm.
d.) Diuretics. If potassium sparing-
excreting - side effect hypokalemia
increases the potential for digitalis
toxicity
- observe and report promptly
danger signs like bradycardia, nausea,
vomiting, diarrhea and colored vision
e.) Antibiotic
f.) Iron supplementation – to prevent
treat/anemia
g.) Oxygen as necessary.
h.) Intrapartum period goals: minimize
hemodynamic changes and optimize
perfusion
• Minimize changes in pulse and blood
pressure.
- lateral position
- adequate pain relief. Analgesia/
anesthesia: To eliminate pain and
spontaneous pushing: regional anesthesia is
commonly used.
 - avoidance of hemorrhage
- avoidance of infection
• Oxygen per mask since parturient tends
to mouth breath
• Forceps/ vacuum extraction to avoid
prolonged valsalva maneuver in pushing
and to shorten the second stage of labor.
• Elective CS, in some specific cardiac
complication.
IMPLEMENTATION
a) Encourage early, regular and frequent
prenatal visit
b) Encourage compliance with therapeutic
regimen
• decrease workload of the heart
- adequate rest and sleep
- avoid/treat early anemia
- prevent exhaustion, fatigue, stress
• Avoid constipation. Take daily fruits and
vegetables, have regular BM, have
regular exercise.
• Avoid activities that decrease oxygen-
smoking, overcrowded places, infection
• Observe proper nutrition that is
compromised of:
- a well balanced diet
- adequate protein, water, fruits, and
vegetables
- low sodium, fats, and carbohydrates
- no junk foods and stimulants
• Early hospitalization
RENAL DISORDERS
URINARY TRACT INFECTIONS

 Assume that a
urinary tract
infection involves all
levels of the tract,
from renal calyces
to urethral meatus
TESTS
 Dipstick, microscopy and urine culture
tests can be used to determine if a urinary
tract infection is present, but will not
differentiate between cystitis and acute
pyelonephritis.
• A dipstick leukocyte esterase test can be
used to detect white blood cells, and a
nitrate reductase test can be used to
detect nitrites.
TESTS
 Microscopy of urine specimen may show
white cells in clumps, bacteria and
sometimes red cells.
 Urine culture and sensitivity tests should
be done, if available, to identify the
organism and its antibiotic sensitivity.
Note: Urine examination requires a clean-
catch mid-stream specimen to minimize
the possibility of contamination.
ASYMPTOMATIC BACTERIURIA

 Causative Organisms:
a. Escherichia coli
b. Klebsiella
c. Procteus
FETAL-NEONATAL EFFECTS
 Fetal effects are due to ascending
bacteria that can result in cystitis or
pyelonephritis in later pregnancy if
condition remains untreated.
CYSTITIS

 Is infection of the
bladder.
 Causative
organisms:
a. Escherichia coli
b. Klebsiella
c. Procteus
SIGNS & SYMPTOMS
 Dysuria
 Increased frequency and urgency of
urination
 Abdominal pain
 Retropubic/suprapubic pain
FETAL- NEONATAL EFFECTS
 Ascending infection may lead to
acute pyelonephritis, which is
associated with preterm labor and
premature birth.
TREATMENT
 Treat with antibiotics :
 Amoxicillin 500 mg by mouth three times
per day for three days;
 OR trimethoprim/sulfamethoxazole one
tablet (160/800 mg) by mouth two times
per day for three days.
 If treatment fails, check urine culture and
sensitivity, if available, and treat with an
antibiotic appropriate for the organism.
 CONT.
 If infection recurs two or more times:
 Check urine culture and sensitivity, if available, and
treat with an antibiotic appropriate for the organism;
 For prophylaxis against further infections, give
antibiotics by mouth once daily at bedtime for the
remainder of pregnancy and two weeks postpartum.
Give:
a. trimethoprim/sulfamethoxazole one tablet
(160/800 mg);
b. OR amoxicillin 250 mg.
Note: Prophylaxis is indicated after recurrent
infections, not after a single episode.
MIDWIFERY CONSIDERATION:
 Emphasize importance of reporting
signs of urinary tract infection to
prevent spread of infection.
 Stress the importance of taking all
the medication prescribed even if
symptoms abate.
 Provide about hygiene measures.
ACUTE PYELONEPHRITIS
 Acute pyelonephritis is an infection
of the upper urinary tract, mainly of
the renal pelvis, which may also
involve the renal parenchyma.
 Causative organisms:
a. Escherichia coli
b. Klebsiella
c. Procteus
SIGNS & SYMPTOMS
 Dysuria
 Spiking fever/chills
 Increased frequency and urgency of
urination
 Abdominal pain
 Retropubic/suprapubic pain
 Loin pain/tenderness
 Tenderness in rib cage
 Anorexia
 Nausea/vomiting
FETAL- NEONATAL EFFECTS
 Increased
risk of preterm labor and
premature delivery
TREATMENT

• If shock is present or suspected, initiate

immediate treatment . Infection (e.g.
unsafe or septic abortion, amnionitis,
metritis, acute pyelonephritis)
• Start an IV infusion and infuse IV fluids
at 150 mL per hour.
• Check urine culture and sensitivity, if
possible, and treat with an antibiotic
appropriate for the organism.
• If urine culture is unavailable, treat with
antibiotics until the woman is fever-free for 48
hours :
 ampicillin 2 g IV every six hours;

 PLUS gentamicin 5 mg/kg body weight IV every

24 hours.
• Once the woman is fever-free for 48 hours, give
amoxicillin 1 g by mouth three times per day to
complete 14 days of treatment.
Note: Clinical response is expected within 48
hours. If there is no clinical response in 72 hours,
re-evaluate results and antibiotic coverage.
• For prophylaxis against further
infections, give antibiotics by mouth
once daily at bedtime for the remainder
of pregnancy and for two weeks
postpartum. Give:
a. trimethoprim/sulfamethoxazole one
tablet (160/800 mg);
b. OR amoxicillin 250 mg.
 Ensure adequate hydration by mouth or
IV.
 Give paracetamol 500 mg by mouth as
needed for pain and to lower
temperature.
 If there are palpable contractions and
blood-stained mucus discharge, suspect
preterm labour .
 COMMON
INFECTIONS
 IMMUNOLOGICAL CHANGES OF
PREGNANCY
 During pregnancy there is decreased immune
surveillance.
 These effects are brought about by maternal
tolerance of the foreign-tissue antigens of the
semi-allogeneric fetal "graft" .
 Although there are subtle changes in circulating
immunoglobulin levels in pregnancy, these
appear to be of no clinical consequence
FETAL AND NEWBORN IMMUNOLOGY
 The active immunological capacity of the
fetus and neonate is compromised
compared with that of older children and
adults
 Fetal cell-mediated and humoral
immunity begin to develop by 9 to 15
weeks.
 The primary fetal response to infection
is immunoglobulin M (IgM).
 Passive immunity is provided by IgG
transferred across the placenta.
 By 16 weeks, this transfer begins to
increase rapidly, and by 26 weeks, fetal
concentrations are equivalent to those of
the mother.
 After birth, breast feeding is protective
against some infections. But this begins
to decline at 2 months of age
 Bacteria, viruses, or parasites may gain
access transplacentally during the viremic,
bacteremic, or parasitemic stage of
maternal infection (Newton, 1999).
 They may also cross intact amnionic
membranes. Fetal infections may develop
early in pregnancy to produce obvious
stigmata at birth.
 Organisms may colonize and infect the
fetus during labor and delivery
 Ascending infection by bacteria (e.g.,
Escherichia coli, group B streptococci,
Ureaplasma urealyticum) is the most
common infectious cause of neonatal
sepsis and stillbirth.
RUBELLA VIRUS (GERMAN MEASLES)

 During pregnancy it has been directly

responsible for abortion and severe
congenital malformations.
 PREVENTION
 To eradicate rubella and prevent
congenital rubella syndrome completely,
a comprehensive approach is
recommended for immunizing the adult
population (Centers for Disease Control
and Prevention, 1998).
 The MMR vaccine should be offered to
women of childbearing age who do not
have evidence of immunity whenever
they make contact with the health care
system.
 Vaccination of susceptible women should:

1. Be part of routine general medical and

gynecological care, including college health
services.

2. Take place in all family planning settings.

3. Be provided routinely to unimmunized

women immediately after hospitalization,
childbirth, or abortion, unless there are
specific contraindications
 Vaccination of all susceptible hospital
personnel who might be exposed to
patients with rubella or who might have
contact with pregnant women is
recommended.
 Rubella vaccination should be avoided 1
month before or during pregnancy
because the vaccine contains attenuated
live virus
 DIAGNOSIS
 Rubella is usually a mild, febrile illness in
adults with a generalized maculopapular
rash. Other symptoms may include
arthralgias or arthritis, lymphadenopathy
(usually suboccipital, postauricular, and
cervical), or conjunctivitis.
 The incubation period is 12 to 23 days,
and 20 to 50 percent of infections may be
asymptomatic. Viremia usually precedes
clinical signs by about a week, and adults
are infectious during viremia through 5 to
7 days of the rash
 Confirmation of rubella infection is
often difficult. Not only are the clinical
features of other illnesses similar, but
about a fourth of rubella infections are
subclinical despite viremia that may
infect the embryo and fetus.
 Specific IgM antibody can be detected
using enzyme-linked immunoassay
from 4 to 5 days after onset of clinical
disease, but it can persist for 6 weeks
after appearance of the rash
 Congenital Rubella Syndrome
 Rubella is one of the most teratogenic
agents known
 With rubella, as with any fetal
infection, the concept of an infected
versus an affected neonate must be
understood.
 Only about half of women with
affected neonates give a history of a
rash during pregnancy.
 Sequelae of fetal infection are worse during
organogenesis.
 Miller and colleagues (1982) have shown
that 80 percent of pregnant women with
rubella infection and a rash during the first
12 weeks have a fetus with congenital
infection.
 At 13 to 14 weeks, this incidence was 54
percent, and by the end of the second
trimester, it was 25 percent.
 As the duration of pregnancy increases,
fetal infections are less likely to cause
congenital malformations
 Congenitalrubella syndrome includes one or
more of the following:

 Eye defects, including cataracts and congenital

glaucoma

 Heart disease, including patent ductus

arteriosus (PDA) and peripheral pulmonary
artery stenosis

 Sensorineural deafness  the most common

single defect
 Central nervous system defects, including
microcephaly, developmental delay, mental
retardation, and meningoencephalitis

 Pigmentary retinopathy

 Purpura

 Hepatosplenomegaly and jaundice

 Radiolucent bone disease. Neonates born

with congenital rubella may shed the virus
for many months and thus be a threat to
other infants, as well as to susceptible
adults who come in contact with them.
 INFLUENZA
 Caused by members of the family
Orthomyxoviridae. Influenza A and B
form one genus of these RNA viruses.

 InfluenzaA viruses are subclassified

further by hemagglutinin (H) and
neuraminidase (N) antigenic makeup.
 Symptoms include fever, dry cough,
and systemic symptoms, and infection
can be confirmed with rapid enzyme
immunoassay or immunofluorescence
assay
 Influenza A is more serious than
influenza B and usually develops
during winter.
 Infection usually is not life-
threatening in otherwise healthy
adults, but pregnant women do not
tolerate serious pulmonary
involvement.
 Prevention

 Vaccination against influenza

 This is most important for women who
have chronic underlying medical
disorders such as diabetes, heart
disease, asthma, or human
immunodeficiency virus (HIV) infection
Treatment
 Amantadine and rimantadine are antiviral
agents with specific activity against influenza
A viruses
 Given as chemoprophylaxis, both antivirals
are 70 to 90 percent effective in preventing
influenza
 They are especially recommended for
prophylaxis for nonimmunized women at high
risk for influenza complications
 If influenza develops, amantadine or
rimantadine, begun within 48 hours of the
onset of symptoms, reduces the duration of
fever and systemic symptoms.
 Neuraminidase inhibitors is highly
effective for the treatment of early
influenza A and B in adults
 FETAL EFFECTS
 There is no firm evidence that influenza
A virus causes congenital
malformations
 Increased neural-tube defects in
neonates born to women with influenza
early in pregnancy
TUBERCULOSIS

 Is a bacterial infection by a germ called

Myobacterium tuberculosis. The
bacteria usually attack the lungs, but
they can also damage other parts of the
body.
 TB spreads through the air (droplet)
when a person with TB of the lungs or
throat coughs, sneezes or talks.
ASSESSMENT
 The diagnosis of TB in pregnancy is made
by:
 Taking health history
 Physical Examination
 Diagnostic Exams:
 Mantoux test (PPD) – and sputum exam
 Chest X-ray is usually not because of the
damaging effects of radiation to the baby
but it can be done carefully as long as the
mother’s abdomen is shielded.
SIGNS AND SYMPTOMS
 Chronic cough
 Weight loss
 Hemoptysis
 Night sweats
 Low grade fever
 Chronic fatigue
EFFECTS OF TUBERCULOSIS
 Although possible, rarely passed from
mother the growing fetus.
 Usually infection is spread after the
baby is born when the mother is still
infected with Tuberculosis.
 The mother should have 3 consecutive
negative sputum culture before she can
hold or care for her infant.
MANTOUX TEST
EFFECTS
 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.
Infant:
Spread thru:
1. Placenta (circulation)
2. After birth (droplet)
a. Should have 3 consecutive negative
sputum for AFB
b. Holding and caring
c. No need to be isolated
d. Newborn with INH prophylaxis
> Skin test with 3 months interval
> If mother is on INH & infant also on INH
– infant should not be breastfed causes
overdose (toxic effects)
TREATMENT
 Anti-tuberculosis therapy
 No increase in congenital malformations
or fetal damage when Rifampicin,
Isoniazid and Ethambutol are used in
combination.
 Isoniazid (INH) - supplement with
Pyridoxine (vit. B6)
 Streptomycin is contraindicated because
it can cross the placenta
HIV/AIDS IN PREGNANCY
 1-2%of every 1000 women giving birth
are HIV positive. (Pillitteri)

RISK FACTORS:
 Multiple sexual partners
 Bisexual partners
 Intravenous drug use by the individual
or sexual partner
 Rarely begins with reproductive tract
irritation
 Symptoms are difficult to differentiate
from other diseases and pregnancy
> Fatigue
> Anemia
> Diarrhea
> Weight loss
 Without therapy, HIV infection may
progress through following stages:
A. Initial invasion of virus
- Mild, flu-like symptoms
B. Seroconversion
C. Asymptomatic period
D. Symptomatic period
A. Initial invasion of virus
> Mild, flu-like symptoms
B. Seroconversion
> HIV serum negative to HIV serum
positive
> 6 weeks to 1 year after exposure
C. Asymptomatic period
> Appears to be disease-free except for
wasting syndrome (weight loss and fatigue)
> Virus can be replicating during this
time
> Length varies – 3 to 11 years
 D.Symptomatic period
> Women develops opportunistic
infections and possibly malignancies
- Toxoplasmosis
- GI illness
- Herpes simplex
- P. carinii pneumonia (PCP)
- Kaposi’s sarcoma
- HIV-associated dimentia
 HIV SCREENING
 Address needs for:
1. Safe sex practices
2. Testing of sexual contacts
3. Continuation or termination of
pregnancy
4. Treatment during pregnancy
 On infants of untreated HIV positive
mothers:
1. Low birth weight
2. Preterm birth
3. 20-50% will contact AIDS in the 1st year
of life
 If
(ZVD) zidovudine is administered
beginning the 14th week of pregnancy and
infant receives antiviral therapy
beginning with birth:
> Risk of developing AIDS falls below
10%
THERAPEUTIC MANAGEMENT
 Usually advised not to get pregnant
P. Carinni pneumonia
 Trimethoprim and

 Sulfamethoxazole (Bactrim)

TRIMETHOPRIM – teratogenic early in

pregnancy
SULFAMETHOXAZOLE – may lead to increase
in bilirubin level if given late in pregnancy
 Pentamidine (PENTAM)

> Drug of choice for non-pregnant women

 Kaposi’s
Sarcoma
 Chemotherapy
> Contraindicated in early pregnancy
> Can be used late pregnancy to halt
malignancy growth
 Thrombocytopenia
 Low platelet count
 May be part of disease pathology or as
response to ZVD
 Woman may need platelet transfusion
close to birth to restore coagulation
ability
 Follow-uptesting of NB being treated
with ZVD for the 1st 6 weeks

 Ifit has 2 negative HIV cultures at 4

moths of age, HIV infection can be
reasonably excluded
POST TEST - GDM
8/16/18
TEST I. IDENTIFICATION
 _______________ 1. A specialists in
physiologic function of hormones that
manages woman with DM throughout
her pregnancy.
 _______________ 2. Type of DM that is
characterized by ineffective insulin
utilization.
 _______________ 3. Referred to as low
or lack of blood glucose level in the
body.
CONT.
 _______________ 4. The most accurate
diagnostic test to detect GDM.
 _______________ 5. Also known as
normal blood sugar level in the body.
 _______________ 6. Hypoglycemia,
hyperglycemia and hyperinsulinemia
all together these changes can lead to
this effect.
CONT.
 ______________ 7. Known as excessive
thirst.
 ______________ 8. Referred to as excessive
amount of amniotic fluid.
 ______________ 9. What is DKA?
 ______________ 10. Known as large or big
babies born in a diabetic mother.
TEST II. ENURMERATION
 Name the 3 symptoms (3Ps) of
hyperglycemia (5 points)
 List the symptoms of hypoglycemia (5
points)
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