risks: previous gdm familial hx of gdm, type 2 or type 1 diabetes previous macrosomial infant...

RISKS: Previous GDM Familial Hx of GDM, type 2 or type 1 diabetes previous macrosomial infant unexplained stillbirth congenital anomalies advanced maternal age

Gestational Diabetes Melitus

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 sugarPeoria is lower than book, frequent blood glucose checking & injections ofInsullin

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 hormoneMany 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 fluidsK+ 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 bedrestTendency 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 cardiacwork 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 &

hemoglobinTx. 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-greenvegetables 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 crisesTX: 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 RBCMom: 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 excessFetal: 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 presentFetus: 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 abortionEAB = 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 486Morning after pill

Adolescent Pregnancy

Legal Tips - emancipated minorconfidentiality

parents of PG patientcontraceptionretaining child custodyadoption

FOLLOW UP CARE IS VIP !!!!

Terbutaline or Brethine is the medication we see used the most

If doesn’t work go toMagnesium Sulfate

Don’t worry about dosages

Effects on mother

Effects on mother

Tachyphylaxis:a phenomenon inwhich repeatedadministration ofdrug results in marked decreasewithin drug effectiveness

More effects on mom

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 calledForelying

Nursing care when postpartum hemorrhage occurs

Most causes:Uterine atony LacerationsHematomas

Who is at a higher risk?Why?

Nursing care when postpartum hemorrhage occurs

Most causes:Uterine atony LacerationsHematomas

Uterine atony

Uterine message

MyometriumDecidua 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 periodEtiology: 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, DICTX: may need tocolytic to relax uterus, increase fluid, possible hysterectomy

Any incision C-section episiotomy

Any insertion site IV epidural

CatheterizationVag 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 sizeTOO 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