Transcript High Risk Maternal # 2

Gestational Diabetes Melitus
RISKS:
Previous GDM
Familial Hx of GDM, type 2 or type 1 diabetes
previous macrosomial infant
unexplained stillbirth
congenital anomalies
advanced maternal age
Insulin needs of Type 1 diabetes
May need decrease in beginning of 2nd trimester, but needs increase after
Complications for hyperglycemia
To decrease complications, key is euglycemia – normal blood sugar
Peoria is lower than book, frequent blood glucose checking & injections of
Insullin
Oral hypoglycemic agents are teratogenic & contraindicated during pregnancy
If HbA1C is above 8 she probably is type 2 diabetic before PG – monitor
closely after PG
Peak insullin resistance usually at 24 – 28 wks. (remember 1st unit)
placental lactogen hormone
Many more type 2 diabetics and on increase. Many are not diagnosed
If develop GDM have a great % of developing diabetes (usually type 2)
some time in your life. New research states the female child has in
increase chance of developing GDM, both sexes have increased
likelihood for type 2 diabetes
Most screen at 24-28 weeks. Newer research says we should be screening
earlier.
Diabetes types
1 = insulin dependent
2 = diet & exercise or hypoglycemic agents
3 = GDM
PRECONCEPTION COUNSELLING KEY – uglycemia for 3-6 mos before
conception and throughout will decrease complications
Hyperemsis gravidarum (HEG): persistent uncontrollable vomining that
begins before 20th wk
can lead to loss of weight, dehydration, ketosis, acid-base & electrolyte
(Na+ and K+ are lost) imbalance, Metabolic alkalosis may develop due to loss
of hydrochloric acid.
Increase risk: young age, first PG, problems with N&V in previous PG,
a Hx of intolerance to oral contraceptives, Hx of gallbladder disease
One theory is high levels of HCG – why many times N&V decrease after 12 wks
but some with even low HCG levels develop HEC
theory psychosomatic – no longer acceptable
allergic theory – to fetus and placenta challenges mom immune system
metabolic theory – Vit B6 deficiency but research is conflicting
Tx: prevent complications, hydrate IV’s, vitamins
meds – Phenergan, Benadryl, histamine-receptor antagonists such as Pepcid
or Zantac, Zofran, Prilosec.
reduce N&V find triggers – smells, try low-fat foods and easily digested
carbohydrates, need salt to replace loss fluids
K+ source fruits, vegetables, meat; magnesium=seeds, nuts, legumes & green veg
Thyroid problems:
Hyperthyroid: many antithyroids such as Tapazole and PTU (preferred)
are category D which may result in neonatal goiter or hypothyroidism
Increased PIH, PP hemorrhage if not well controlled
Hypothyroid: Thyroid replacement hormone Synthroid is category A crosses
placenta only to a limited extent
increased preeclampsia, abruptio placentae, low birth weight or stillborn
infants, increase neonatal goiter and congenital hypothyroidism
Cardiovascular problems: PG increase work load by heart
are a high risk PG and need to be monitored carefully and often
Rheumatic heart disease: stenosis of openings between chambers of heart due
to scarring of the valves. Mitral valve is most common affected.
Congenital heart disease: basically fall into left to right shunt category or
right to left shunt. Study in cardiac
Mitral Valve Prolapse: most common cardiac condition. Most of time a benign
condition, some MD’s administer prophylactic antibiotics before &during labor
(bacterial endocarditis)
Peripartum & postpartum cardiomyopathy = rare, no underlying
cardiac conditions, but symptoms of cardiac decompensation appear
during the last weeks of PG or from 2-20 wks PP. S&S = congestive heart
failure (dyspnea, edema, weakness, chest pain, heart palpitations )
TX: digitalis, diuretics, sodium restrictions and prolonged bedrest
Tendency to reoccur in later PG – PG are generally not advised
Drug therapies:
anticoagulants ; Heparin not Warfarin
antiarrhythemics: digoxin & quinidine are generally thought of as safe
B-blocker therapy only in late PG – fetal growth restriction
anti-infectives: ampicillin and gentamicin
diurtics: usually avoided
Some with cardiac disease will need to have CS to avoid increase cardiac
work during labor & vag delivery
Pulmonary disorders:
asthma: inhaled corticosteriods are OK, encourage to breastfeed may
decrease allergies & asthma in infant
Anemia:
iron-deficiency anemia: hemoglobin content
mom: pica, inflammations of lips and tongue. Lab show RBC that are
microcytic & hypochromic (pale)
fetus: usually OK, but if mom severely anemic can reduce fetal RBC &
hemoglobin
Tx. Iron supplements (give with vit C) and what foods are high in iron
folic acid deficiency or megaloblastic anemia: results in presence of large,
immature erythrocytes (megaloblasts)
mom: folic acid requirement doubles in PG. Dilatin, hemolytic anemias &
malabsorption entities will contribute
fetus: spontaneous abortion, abruptio placentae, and fetal anomalies, esp.
neural tube defects
TX. Supplements and foods liver, kidney beans, lima beans & fresh dark-green
vegetables and now added to many cereals, breads, etc
Anemias continued:
Sickle cell hemoglobinopathy: autosomal recessive genetic. Defect in hemoglobin
causes RBC to become shaped like sickle or crescent. Low O2 – RBC cannot
pass through small arteries and capillaries & tend to clump together & occulde
the blood vessel.
Mom: temporary cessation of bone marrow function, hemolytic crises with
RBC destruction resulting in jaundice, severe pain, pyelonephritis, bone
infection, heart disease
fetus: prone to serious complications including prematurity & IUGR.
Fetal death is common especially in those moms that have a sickle cell crises
TX: S&S of sickle cell crises and treat
Thalassemia: is a genetic disease that involves abnormal synthesis of a of B
chains of hemoglobin. Leads to alterations in RBC membranes and decreased
life span of RBC
Mom: minor types often are mildly anemic – but have to be careful not to give
large doses of iron because they absorb & store iron in the bodies excessively
& must take a chelating agent to rid the excess
Fetal: may inherit the problem due to genetics
Cholecytitis & cholelithiasis: increase during PG, but often
absent or decrease after delivery
Inflamatory bowel disease: may actually improve WHY?
may vary from person to person
Neurologic disorders:
Epilepsy seizure: 0.3 to 0.6% of PG women affected. Effect on PG is
variable & unpredictable
higher incidence of stillbirth, preterm labor.
teratogenic effects of anticonvulsant meds – fetal hydantoin syndrome
includes craniofacial abnormalities, limb reduction defects, growth
restriction, mental retardation, cardiac anomalies.
TX preconception plan with neurologists very risky
Bell’s palsey: thought to be caused by a virus, 3 X’s more common in PG
90% recover within weeks to months.
TX. Steroids within the first few days., facial massage, cream.
Autoimmune disorders:
Systemic Lupus Erythematosus (SLE): increased abortion and fetal death
during the first trimester, the prognosis for live birth is as high as 90%
if no active flare ups occur, 50% if hypertensive renal disease is present
Fetus: congenital heart block which is permanent & will require a pacemaker
Rheumatoid arthritis: marked improvement often during PG. (suppression of
immune inflammatory response). Most relapse within 6 wks to 6 mos after
delivery. In contrast to SLE, the risk of abortion does not increase.
Multipe Scerosis: basically follows RH. Some women report an improvement
of their MS while PG others will have more symptoms
Trauma in PG: as with any other trauma but now have fetus to
worry about. FHM
TAB = therapeutic abortion
EAB = elective abortion
First trimester:
D & C – dilation & curretage
Second trimester:
transabdominal intrauterine injection of hypertonic solution ofter
sodium chloride
D&C
injection of urea solution after amniocentsis
protaglandins – pitocin
abdominal hysterotomy
Complications
RU 486
Morning after pill
Adolescent Pregnancy
Legal Tips - emancipated minor
confidentiality
parents of PG patient
contraception
retaining child custody
adoption
FOLLOW UP CARE IS VIP !!!!
Terbutaline or Brethine
is the medication we see
used the most
If doesn’t work go to
Magnesium Sulfate
Don’t worry about dosages
Effects on mother
Effects on mother
More effects on mom
Tachyphylaxis:
a phenomenon in
which repeated
administration of
drug results in
marked decrease
within drug
effectiveness
Used for stopping preterm labor & preeclampsia - eclampsia
Magnesium sulfate continued:
Calcium gluconate must be at bedside or readily available
counteracts effects of MgSo4
MgSo4
continued
Magnesium sulfate effects on fetus and neonate
Magnesium sulfate
Abnormal uterine types, cervical problems
May help with shoulder dystocia
Version
Prolapse of cord 1:200
May also be called
Forelying
Nursing care when postpartum hemorrhage occurs
Most causes:
Uterine atony
Lacerations
Hematomas
Who is at a higher risk?
Why?
Nursing care when postpartum hemorrhage occurs
Most causes:
Uterine atony
Lacerations
Hematomas
Uterine atony
Uterine message
Myometrium
Decidua basalis
Decidua spongiosa
Amnion
A = normal
B = placenta accreta:
placental tissue is
adherent to myometruim
C = placenta increta:
placenta has penetrated
into uterine muscle
D = placenta percreta:
placenta has penetrated
through the uterine
muscle
rare 1: 7000 births
Uterine prolapse 1:15,00 May occur after placenta delivered or in PP period
Etiology: bearing down, precipitous delivery, pulling on cord, fundal pressure,
vigorous message of uterus, manual extraction of placenta
S&S: pain, fear, blood loss, shock, infection, DIC
TX: may need tocolytic to relax uterus, increase fluid, possible hysterectomy
Any incision
C-section
episiotomy
Any insertion site
IV
epidural
Catheterization
Vag exams
polyhydramnios
•idiopathic (60%)
•maternal (20%)
•diabetes
•Rh incompatibility (fetal hydrops)
fetal (20%)
•Neural tube defect GI obstruction
(prox. to ileum)
•cardiac
•dwarfism
•Placental chorioangioma see also:
oligohydramnios
oligohydramnios
•prerenal
•placental insufficiency
•low-output cardiac failure
•Fetal demise
•renal
•Renal agenesis
•Polycystic disease
•Multicystic dysplasia
•postrenal
•UPJ obstruction
•megaureter
•posterior urethral valves
•urethral agenesis
abnormal placental size
TOO BIG (>5cm in sections obtained at right angles to the long axis)
•maternal disease
•diabetic mothers (= villous edema)
•Intrauterine infections
•anemic mothers (= normal histology)
•fetal disease
•Erythroblatosis fetalis (= villous edema and hyperplasia)
•umbilical vein obstruction
•fetal high output failure
•large chorioangioma
•sacrococcygeal teratoma
•arteriovenous fistula
TOO SMALL
•preeclampsia (a/w placental infarcts in 33-60%)
placental chorioangioma
•most common benign tumor of placenta
•incidence: 0.7%
•DDx:
•hydatidaform mole
•large leiomyoma
•chorioepithelioma
•complications:
•IUGR, fetal anomaly,
polyhydramnios, hemorrhage, heart
failure, premature labor