High Risk PregnancyHigh Risk Pregnancy

Lecture 10Lecture 10

Maternal MortalityMaternal Mortality: : 10/100,000 pregnant women. 10/100,000 pregnant women. Leading causesLeading causes: hemorrhage, hypertension, : hemorrhage, hypertension,

infection, preeclampsia.infection, preeclampsia.

High Risk Pregnancy:High Risk Pregnancy:A.A. Maternal Age < 15 & > 35.Maternal Age < 15 & > 35.

B. Parity Factors - 5 or more - great risk.B. Parity Factors - 5 or more - great risk. [PP hemorrhage] New preg.within 3 mos.[PP hemorrhage] New preg.within 3 mos. C. Medical-Surgical Hx - hx of previous uterine C. Medical-Surgical Hx - hx of previous uterine

surgery &/or uterine rupture, DM, cardiac dis, surgery &/or uterine rupture, DM, cardiac dis, lupus, HTN, PIH, HELLP, DIC etc. lupus, HTN, PIH, HELLP, DIC etc.

Gestational ConditionsGestational Conditions

HHyperemesis Gravidarumyperemesis Gravidarum

Persistent vomiting past first trimester or Persistent vomiting past first trimester or excessive vomiting @ anytime.excessive vomiting @ anytime.

Severe; usually 1st pregnancy. Severe; usually 1st pregnancy. Rate occurrence ^ with twins, triplets, etc.Rate occurrence ^ with twins, triplets, etc. 7 out of 1,000. Electrolyte imbalance results. 7 out of 1,000. Electrolyte imbalance results. Possible causes: ^ levels of hCG, ^ serum Possible causes: ^ levels of hCG, ^ serum

amylase, decrease gastric motility.amylase, decrease gastric motility.

Hyperemesis cont.Hyperemesis cont.S/S: S/S: dry mouth, thirst, substantial wt. loss, signs of dry mouth, thirst, substantial wt. loss, signs of

starvation, dehydration, decreased skin turgor; starvation, dehydration, decreased skin turgor; fruity breath - acidosis [metabolizing fat]. fruity breath - acidosis [metabolizing fat].

Management: admit to hospital for IV hydration. Management: admit to hospital for IV hydration. NPO then clears > full fluids> sm. solids. NPO then clears > full fluids> sm. solids. Reglan or Zofran IVPB q 6 hrs. Reglan or Zofran IVPB q 6 hrs. Hosp. for 24-48 hrs. Add Multi Vit.& K to IVF to Hosp. for 24-48 hrs. Add Multi Vit.& K to IVF to

correct electrolyte imbalance. correct electrolyte imbalance.

Use ½ NSUse ½ NS

Hydatidaform mole - "Molar preg." Hydatidaform mole - "Molar preg." Degenerative disorder of trophoblast (placenta)Degenerative disorder of trophoblast (placenta) Villi degenerate & cells fill with fluid Villi degenerate & cells fill with fluid Form clusters of vesicles; similar to “grapes” Form clusters of vesicles; similar to “grapes” Overgrowth of chorionic villi; fetus does not Overgrowth of chorionic villi; fetus does not

develop. develop. Partial or complete. Complete - no fetus; Partial - Partial or complete. Complete - no fetus; Partial -

dev. begins then stops. dev. begins then stops. Multiparous/older women.Multiparous/older women. Pathophysiology: unknown; theories: Pathophysiology: unknown; theories:

chromosomal abn., hormonal imbalances; chromosomal abn., hormonal imbalances; protein/folic acid deficiencies. protein/folic acid deficiencies.

Hydatidaform Mole cont.Hydatidaform Mole cont. S/S: S/S: from bright red spotting to bright red from bright red spotting to bright red

hemorrhage. hemorrhage. Tissue resembles grape clustersTissue resembles grape clusters Uterus appears larger than expected for gest. Uterus appears larger than expected for gest.

age. age. ManagementManagement: D&C; go to hosp. STAT; bring any : D&C; go to hosp. STAT; bring any

passed tissue. passed tissue.

“ “Gestational trophoblastic disease” - benign Gestational trophoblastic disease” - benign hydatidaform mole & gestational trophoblastic hydatidaform mole & gestational trophoblastic tumors aka & chorio tumors aka & chorio carcinoma.carcinoma.

Hemorrhagic Disorders Hemorrhagic Disorders Placenta previa:Placenta previa:

Implantation near or over cervix.Implantation near or over cervix. ~ 1/2 of all preg. start as previa then ~ 1/2 of all preg. start as previa then

placenta shifts to higher positionplacenta shifts to higher position By 35 wks. not likely to shift By 35 wks. not likely to shift Varying Degrees:Varying Degrees: Total:Total: internal cervical os completely internal cervical os completely

covered by placenta. covered by placenta. PartialPartial: os partially covered by placenta. : os partially covered by placenta. MarginalMarginal: edge @ margin of internal os. : edge @ margin of internal os. Low-lyingLow-lying: region of internal os : region of internal os nearnear

placenta. placenta.

PLACENTA PREVIA CONT…..PLACENTA PREVIA CONT…..

Cause: Cause: UnknownUnknown Risk factorsRisk factors: multiparity, AMA, multiple : multiparity, AMA, multiple

gestations, previous uterine surgerygestations, previous uterine surgery ManisfestationsManisfestations: Painless, bright red bleeding > : Painless, bright red bleeding >

20th week; episodic, starts without warning, 20th week; episodic, starts without warning, stops & starts again.stops & starts again.

PrognosisPrognosis: depends on amt. bleeding & gest.age: depends on amt. bleeding & gest.age

Management:Management: Monitor FH, maternal VS, IVF; Monitor FH, maternal VS, IVF; O2; assess I&O; amt. of bleeding, CBC, & O2; assess I&O; amt. of bleeding, CBC, & complete BR. Type & cross for poss.transfusion. complete BR. Type & cross for poss.transfusion.

Ultrasound to confirm Ultrasound to confirm No pelvic exams/no vag. del.- May lead to No pelvic exams/no vag. del.- May lead to

hemorrhagehemorrhage

Abruptio placentaAbruptio placenta: : Separation of placenta from uterine wall > 20th wk Separation of placenta from uterine wall > 20th wk

gestation (during pregnancy)gestation (during pregnancy) ““Placental Abruption”- hemorrhage results; Placental Abruption”- hemorrhage results;

Severity depends on Severity depends on degreedegree of separation. of separation. Common in multips, AMA.Common in multips, AMA. Fetal prognosis depends on blood lost & gest. age. Fetal prognosis depends on blood lost & gest. age. Grade 0Grade 0: Separation not apparent until placenta : Separation not apparent until placenta

examined > delivery. examined > delivery. Grade 1:Grade 1: minimal - causes vaginal bleeding & minimal - causes vaginal bleeding &

alterations in maternal VS. alterations in maternal VS. Grade 2Grade 2: moderate - + signs of fetal distress. : moderate - + signs of fetal distress.

Uterus tense & painful when palpated. Uterus tense & painful when palpated. Grade 3:Grade 3: extreme (total) separation. Maternal extreme (total) separation. Maternal

shock/fetal death if immediate shock/fetal death if immediate intervention not done.intervention not done.

Abruption cont.Abruption cont. Cause: Cause: Unknown; risk factors: smoking, short Unknown; risk factors: smoking, short

umbilical cord, adv. mat. age, HTN, PIH, cocaine umbilical cord, adv. mat. age, HTN, PIH, cocaine use, trauma to or near abdomen.use, trauma to or near abdomen.

ManifestationsManifestations: tenderness to severe constant : tenderness to severe constant pain; mild to moderate bleeding depending on pain; mild to moderate bleeding depending on degree of sep..degree of sep..

Total separation: tearing, knifelike sensation.Total separation: tearing, knifelike sensation. ManagementManagement: Assess amt. & control blood loss: Assess amt. & control blood loss Assess FH & mat. VS, CBC, O2, IVF [RL-volume Assess FH & mat. VS, CBC, O2, IVF [RL-volume

expander], type & cross. expander], type & cross. Neonate may be hypoxic, in hypovolemic shock Neonate may be hypoxic, in hypovolemic shock

d/t bl. loss. Prepare for emergency C/S.d/t bl. loss. Prepare for emergency C/S.

Comparison: Abruption vs. Placenta PreviaComparison: Abruption vs. Placenta Previa

Abruptio Placenta Abruptio Placenta Pathology: Sudden separation of normally Pathology: Sudden separation of normally

implanted placenta. implanted placenta. Vaginal Bleeding: may not be obvious; concealed Vaginal Bleeding: may not be obvious; concealed

behind placenta. If visible, will be dark. Bleeding behind placenta. If visible, will be dark. Bleeding into uterine cavity.into uterine cavity.

Pain: Sharp, stabbing pain in abd.Pain: Sharp, stabbing pain in abd. Uterus: hard boardlike abd. Uterus: hard boardlike abd.

Placenta Previa Placenta Previa Pathology: Abnormal implantation of placenta; Pathology: Abnormal implantation of placenta;

lower in uterine cavity.lower in uterine cavity. Vaginal Bleeding: Abrupt onset ; bright red.Vaginal Bleeding: Abrupt onset ; bright red. Completely painless.Completely painless. Uterus: Soft, unless uterine contraction is present.Uterus: Soft, unless uterine contraction is present.

Abnormal Amniotic Fluid Levels: Abnormal Amniotic Fluid Levels: AMF made up of fetal urine & fluid that is AMF made up of fetal urine & fluid that is

transported thru placenta from mat.cir.sys. transported thru placenta from mat.cir.sys. Fetus swallows AMF & excretes urine.Fetus swallows AMF & excretes urine. Waste excreted by maternal kidneys. Waste excreted by maternal kidneys. CNS or GI abnormalities inhibits uptake of AMF.CNS or GI abnormalities inhibits uptake of AMF.

PolyhydramniosPolyhydramnios: > 2,000 ml amniotic fluid. : > 2,000 ml amniotic fluid. Need ultrasound to make dx. Need ultrasound to make dx. AFI >/equal to 24= polyhydramnios. AFI >/equal to 24= polyhydramnios. AFI of 8-23 cm. normal. AFI of 8-23 cm. normal.

Visual inspection may reveal rapidly enlarging uterus. Visual inspection may reveal rapidly enlarging uterus.

Risk FactorsRisk Factors• Fetal abnormalities: neonatal macrosomia, fetal or Fetal abnormalities: neonatal macrosomia, fetal or

neonatal hydrops [swelling], ascites, pleural or neonatal hydrops [swelling], ascites, pleural or pericardial effusions. pericardial effusions.

• Skeletal malformations: congenital hip dislocation, Skeletal malformations: congenital hip dislocation, clubfoot, & limb reduction defect. clubfoot, & limb reduction defect.

• Abnormal fetal movement suggestive of neurologic Abnormal fetal movement suggestive of neurologic abnormalities (CNS)abnormalities (CNS)

• Obstruction of GI tract; prevents normal ingestion of Obstruction of GI tract; prevents normal ingestion of amniotic fluid. amniotic fluid.

• Rh iso immunization d/t mixing of maternal/fetal bloodRh iso immunization d/t mixing of maternal/fetal blood• Maternal hx DM.Maternal hx DM.• Assoc. w.spina bifida; anencephaly, hydrocephaly.Assoc. w.spina bifida; anencephaly, hydrocephaly.• Fetal death may result from severe poly. Fetal death may result from severe poly. • Not as common as oligohydramniosNot as common as oligohydramnios

Polyhydramnios cont.Polyhydramnios cont.Management: Management: Monitor wt. gain. Remove excess Monitor wt. gain. Remove excess

amniotic fluid q 1-2 wks.thru amniocentesis. amniotic fluid q 1-2 wks.thru amniocentesis. Replaced quickly. Most women with mild Replaced quickly. Most women with mild poly.deliver healthy infants.poly.deliver healthy infants.

OligohydramniosOligohydramnios: amniotic fluid < 1,000ml. : amniotic fluid < 1,000ml. Could be highly concentrated.Could be highly concentrated.Interferes w. normal fetal dev. Interferes w. normal fetal dev. Reduces cushioning effect around fetus.Reduces cushioning effect around fetus. CausesCauses: Failure of fetal kidney development; : Failure of fetal kidney development;

urine excretion blocked, IUGR, post-term preg., urine excretion blocked, IUGR, post-term preg., preterm ROM, fetal anomalies. Poor placental preterm ROM, fetal anomalies. Poor placental function.function.

Oligo cont.Oligo cont.

ManifestationsManifestations: : Facial & skeletal deformities: club foot. Facial & skeletal deformities: club foot. Fetal demiseFetal demise Pulmonary hypoplasia - improper dev. of alveoli;Pulmonary hypoplasia - improper dev. of alveoli; 22ndnd trimester oligo: higher rate of congenital trimester oligo: higher rate of congenital

anomalies (50.7 % vs. 22.1 %) and lower survival anomalies (50.7 % vs. 22.1 %) and lower survival rate (10.2 % vs. 85.3 %) than women with oligo. rate (10.2 % vs. 85.3 %) than women with oligo. in 3in 3rdrd trimester . trimester .

Prognosis: depends on severity of disease.Prognosis: depends on severity of disease.Management: Management: Careful assessment of mother/fetusCareful assessment of mother/fetus Do frequent ante-partum testing Do frequent ante-partum testing determine optimal time for delivery (early)determine optimal time for delivery (early) Antibiotics/corticosteroids with PPROMAntibiotics/corticosteroids with PPROM

Ectopic pregnancyEctopic pregnancy: : Causes: Causes: • Scarring of fallopian tubes Scarring of fallopian tubes (Chlamydia/Gonorrhea). (Chlamydia/Gonorrhea). • Implantation of ovum outside uterine cavity; Implantation of ovum outside uterine cavity; usu.usu.

upper 1/3rd fallopian tubeupper 1/3rd fallopian tube; rare on ovary, cervix, ; rare on ovary, cervix, abdominal cavity. abdominal cavity.

• Leading cause of death from hemorrhage in preg. Leading cause of death from hemorrhage in preg. • Reduces fertility Reduces fertility ~ 1 in 100 pregnancies ~ 1 in 100 pregnancies More common > infection of fallopian tubes or More common > infection of fallopian tubes or

surgery to reverse TL.surgery to reverse TL. Previous ectopicPrevious ectopic multiple induced abortions multiple induced abortions diethylstilbestrol (DES) exposure diethylstilbestrol (DES) exposure

Ectopic Ectopic

Symptoms: Symptoms: Colicky, cramping pain in lower abdomen on affected side Colicky, cramping pain in lower abdomen on affected side Tubal rupture: sharp/steady pain before diffusing thruout Tubal rupture: sharp/steady pain before diffusing thruout

pelvic region. Fetus expels into pelvic cavity. pelvic region. Fetus expels into pelvic cavity. Heavy bleeding causes shoulder pain, rectal pressure Heavy bleeding causes shoulder pain, rectal pressure N/V- 25-50% pts. think its morning sickness. N/V- 25-50% pts. think its morning sickness. Dizziness/weakness - If tube ruptures, weak pulse, clammy Dizziness/weakness - If tube ruptures, weak pulse, clammy

skin, fainting. Assess for s/s shock.skin, fainting. Assess for s/s shock.

Treatment: Treatment: Immediate surgery to remove/repair tube. Immediate surgery to remove/repair tube. If no rupture, Methotrexate - stops cellular division in fetus; If no rupture, Methotrexate - stops cellular division in fetus;

causes cell death. Conceptus expelled with bleeding. Best <6 causes cell death. Conceptus expelled with bleeding. Best <6 wks. when chance of rupture less.wks. when chance of rupture less.

Rh sensitizationRh sensitization Rh (D) Immune Globulin aka Rh (D) Immune Globulin aka “Rhogam“Rhogam”” Rh – mom: no Rh factor. Rh – mom: no Rh factor. If Rh - mom receives cells from Rh + fetus, If Rh - mom receives cells from Rh + fetus,

mother responds to (+) AGmother responds to (+) AG by producing by producing AB.AB. TreatmentTreatment: Anti-Rho (d) immune globulin @ 26-28 : Anti-Rho (d) immune globulin @ 26-28

wks. (Rhogam) & @ delivery. wks. (Rhogam) & @ delivery. Prevents antibody formation if mom is Rh -.Prevents antibody formation if mom is Rh -. Rapid RBC lysis leads to ^ bilirubin levels. Rapid RBC lysis leads to ^ bilirubin levels. 11stst exposure [Rh+ blood] IgM, antibodies exposure [Rh+ blood] IgM, antibodies

develop; too large to cross pdevelop; too large to cross placenta. . First Rh + fetus usually not harmed. First Rh + fetus usually not harmed. 22ndnd exposure, smaller IgG antibodies formed; can exposure, smaller IgG antibodies formed; can

cross placenta & destroy fetal red blood cells.cross placenta & destroy fetal red blood cells.

Maternal-Fetal Blood Group Incompatibility:Maternal-Fetal Blood Group Incompatibility:

Mom is type O & baby is A, B or AB.Mom is type O & baby is A, B or AB. Blood types A, B, & AB contain antigen not Blood types A, B, & AB contain antigen not

present in type O blood. present in type O blood. (O) blood type have anti A/anti B antibodies.(O) blood type have anti A/anti B antibodies. If exchange occurs, maternal antibodies attact If exchange occurs, maternal antibodies attact

fetal bl.cells, causing rapid lysis of RBC's. fetal bl.cells, causing rapid lysis of RBC's. Leads to byproduct bilirubin. Leads to byproduct bilirubin. Results in “jaundice”. Results in “jaundice”. ABO less severe than Rh incompatibility b/c ABO less severe than Rh incompatibility b/c

primaryprimary antibodies of ABO system are IgM which antibodies of ABO system are IgM which are too large to cross placenta.are too large to cross placenta.

Bilirubin levels done & phototherapy if ^.Bilirubin levels done & phototherapy if ^.

Hypertensive States of PregnancyHypertensive States of Pregnancy:: GGlobal lobal cause of maternal/fetal morbidity & cause of maternal/fetal morbidity &

mortality. Responsible for ~ 76,000 deaths/year .mortality. Responsible for ~ 76,000 deaths/year .

4 categories:4 categories: 1.“Chronic HTN”:1.“Chronic HTN”: ^ BP prior to pregnancy. ^ BP prior to pregnancy. Not associated w. proteinuria or end-organ Not associated w. proteinuria or end-organ

damage; continues > delivery. damage; continues > delivery. 2.2. “Preeclampsia”:“Preeclampsia”: ^ BP during preg. > 20 wks. ^ BP during preg. > 20 wks.

End-organ damage may occur. 50-70% cases.End-organ damage may occur. 50-70% cases.3.3. “ “Superimposed preeclampsia on pt. w. Superimposed preeclampsia on pt. w.

Chronic HTN”: 15-30% cases.Chronic HTN”: 15-30% cases.4. “Transient HTN”: 4. “Transient HTN”: BP >140 /90 without BP >140 /90 without

proteinuria or end-organ damage. Normotensive proteinuria or end-organ damage. Normotensive pt. may become hypertensive late in preg., pt. may become hypertensive late in preg., during labor, or 24 hours postpartum. BP normal during labor, or 24 hours postpartum. BP normal within 10 days postpartum. within 10 days postpartum.

Pre-eclampsiaPre-eclampsia

Defined As:Defined As: BP ≥ 140/90 BP ≥ 140/90 Systolic ↑ of 30mm Hg > pre-preg. levels Systolic ↑ of 30mm Hg > pre-preg. levels Diastolic ↑ of 15mm Hg > pre preg. levels. Diastolic ↑ of 15mm Hg > pre preg. levels. Presents with HTN, proteinuria, edema of face, Presents with HTN, proteinuria, edema of face,

hands, ankles. hands, ankles. Can occur anytime > 20Can occur anytime > 20thth wk of pregnancy. wk of pregnancy. Usually occurs closer to due date. Will not resolve Usually occurs closer to due date. Will not resolve

until > birth. until > birth. Can progress to HELLP syndromeCan progress to HELLP syndrome

General Signs of PREECLAMPSIA General Signs of PREECLAMPSIA Rapid weight gain; swelling of arms/face Rapid weight gain; swelling of arms/face Headache; vision changes (blurred vision, seeing Headache; vision changes (blurred vision, seeing

double, seeing spots) double, seeing spots) Dizziness/faintness/ringing in ears/confusion; Dizziness/faintness/ringing in ears/confusion;

seizures seizures Abdominal pain, ↓ production of urine; nausea, Abdominal pain, ↓ production of urine; nausea,

vomiting, blood in vomit or urine vomiting, blood in vomit or urine

MildMild: mild HTN; no end-organ damage; : mild HTN; no end-organ damage; minimal proteinuria. minimal proteinuria.

Severe:Severe: Significant HTN; severe proteinuria (>5.0 Significant HTN; severe proteinuria (>5.0

g/d); end-organ damage d/t systemic vaso- g/d); end-organ damage d/t systemic vaso- constriction.constriction.

Headache; visual changes; confusion; Headache; visual changes; confusion; abdominal pain; impaired liver function abdominal pain; impaired liver function w.hyperbilirubinemia; oliguria; w.hyperbilirubinemia; oliguria; proteinuria; pulmonary edema; hemolytic proteinuria; pulmonary edema; hemolytic anemia; thrombocytopenia; fetal growth anemia; thrombocytopenia; fetal growth retardation. retardation.

Eclampsia (seizures) may followEclampsia (seizures) may follow

EclampsiaEclampsia: :

• Seizures or coma d/t hypertensive Seizures or coma d/t hypertensive encephalopathy; most serious complication.encephalopathy; most serious complication.

Affects ~ 0.2% preg; 1 in 1000 preg. terminated. Affects ~ 0.2% preg; 1 in 1000 preg. terminated. • Major cause of maternal death d/t intracranial Major cause of maternal death d/t intracranial

hemorrhage. Maternal mortality rate is 8-36%. hemorrhage. Maternal mortality rate is 8-36%. • Deliver by C/S ASAP.Deliver by C/S ASAP.

Risk factors:Risk factors: < age 20 or > 40< age 20 or > 40 Twins, triplets; primagravidaTwins, triplets; primagravida Molar pregnancyMolar pregnancy Preexisting: HTN, Diabetes mellitus Preexisting: HTN, Diabetes mellitus Renal or vascular disease Renal or vascular disease Prior hx of preeclampsia/eclampsia Prior hx of preeclampsia/eclampsia Frequency: Frequency: 5% {all pregnancies in US}5% {all pregnancies in US}Causes:Causes: Unknown. Unknown. Theories: maternal immune reaction that leads to Theories: maternal immune reaction that leads to

systemic peripheral vascular spasm >>systemic peripheral vascular spasm >> leads to endothelial cell damage >> leads to endothelial cell damage >>

vasoconstriction> ^BP. vasoconstriction> ^BP. Affects multiple organs. Reduced bl.supply to Affects multiple organs. Reduced bl.supply to

kidneys, liver, placenta, brain. Can lead to kidneys, liver, placenta, brain. Can lead to placental abruption and fetal & maternal death. placental abruption and fetal & maternal death.

Management: Management: Usually only cure is delivery- Usually only cure is delivery- Depends on symptoms.Depends on symptoms.

Mild preeclampsiaMild preeclampsia: Bedrest. Monitor @ : Bedrest. Monitor @ home or hospital. Deliver close to EDC. home or hospital. Deliver close to EDC. Frequent BP’s, 24 hr.urine, liver enzymes, Frequent BP’s, 24 hr.urine, liver enzymes, FHR, & ultrasounds.FHR, & ultrasounds.

Severe preeclampsia: Severe preeclampsia: Goal: prevent Goal: prevent convulsions & control mat. BP. convulsions & control mat. BP.

BP = 160/110 , epigastric pain, 2-4+ BP = 160/110 , epigastric pain, 2-4+ proteinuria, ^ liver enzymes, proteinuria, ^ liver enzymes, thrombocytopenia [↓ 100,000]. thrombocytopenia [↓ 100,000].

* * Magnesium sulfate [drug of choice]Magnesium sulfate [drug of choice]

Magnesium SulfateMagnesium Sulfate

Bronchodilating effects; prevent seizures; lowers Bronchodilating effects; prevent seizures; lowers BP. BP.

Steroids to mom for fetal lung maturity if Steroids to mom for fetal lung maturity if premature delivery imminent premature delivery imminent

Infusion pump – IVPB into mainline of RL Infusion pump – IVPB into mainline of RL before/during labor & 24 hrs > delivery. before/during labor & 24 hrs > delivery.

Infuse slowly.Infuse slowly. Baseline VS & UO Baseline VS & UO before before therapy. RR @ least therapy. RR @ least

16/min16/min Mag SO4 removed Mag SO4 removed solelysolely by kidneys. by kidneys. Don’t use in pts. w.renal disease. Other drugs: Don’t use in pts. w.renal disease. Other drugs:

Dilantin & Valium. Dilantin & Valium. Patellar reflex, place foley, RR, fetal status q hr. Patellar reflex, place foley, RR, fetal status q hr.

Monitor mag.levels q 2hrs. Mag level 4-6 Monitor mag.levels q 2hrs. Mag level 4-6 meq./liter therapeutic. meq./liter therapeutic.

Magnesium ToxicityMagnesium Toxicity based on clinical signs: based on clinical signs: sharp drop in BPsharp drop in BP respiratory paralysisrespiratory paralysis disappearance of patellar reflex. disappearance of patellar reflex.

STOP infusion, give O2 & calcium gluconate STOP infusion, give O2 & calcium gluconate ASAP. ASAP.

HELLP SyndromeHELLP Syndrome: : ““HHemolysis, emolysis, EElevated levated LLiver Enzymes, iver Enzymes, LLow ow PPlatelets” latelets” Can progress to DICCan progress to DIC..

Target organ is liver. Target organ is liver. VasospasmsVasospasms cause vasoconstriction & lead to cause vasoconstriction & lead to

reduction in blood flow to uterus/other organs.reduction in blood flow to uterus/other organs. Leads to ↑ BP, visual disturbances, low UO, ↓ HCT Leads to ↑ BP, visual disturbances, low UO, ↓ HCT Anemia; Epigastric/RUQ pain & tenderness d/t liver Anemia; Epigastric/RUQ pain & tenderness d/t liver

swelling. Weakness, fatigue, jaundice.swelling. Weakness, fatigue, jaundice. Hemolysis > destruction blood cells; + anemia.Hemolysis > destruction blood cells; + anemia. ^ liver enzymes > sign of liver damage. ^ liver enzymes > sign of liver damage. Low platelets - ^ peripheral vascular destruction. Low platelets - ^ peripheral vascular destruction. CBC, platelet count, PT, PTT, LFT’s, uric acid.CBC, platelet count, PT, PTT, LFT’s, uric acid.

DIC: DISSEMINATED INTRAVASCULAR DIC: DISSEMINATED INTRAVASCULAR COAGULATIONCOAGULATION [acute disorder] [acute disorder] BBlood begins to begins to coagulate throughout entire throughout entire

body. Widespread fibrin deposits in body. Widespread fibrin deposits in capillaries/arterioles. Body depleted of capillaries/arterioles. Body depleted of platelets & & coagulation factors; ^ risk of coagulation factors; ^ risk of hemorrhage. Over . Over activation of clotting cascade. activation of clotting cascade.

Results in decreased blood flow & ^ tissue damageResults in decreased blood flow & ^ tissue damageAlways a secondary dx. Always a secondary dx. CausesCauses: ^ tissue thromboplastin d/t : ^ tissue thromboplastin d/t vascular damage vascular damage

TriggersTriggers: amniotic fluid embolism, : amniotic fluid embolism, eclampsia, , abruption, pre-eclampsia, HELLP, trauma,abruption, pre-eclampsia, HELLP, trauma,gram – sepsis.gram – sepsis.

DIC cont. Physical AssessmentDIC cont. Physical AssessmentPetechiae/ecchymotic areas on skin/mucous mem. Petechiae/ecchymotic areas on skin/mucous mem. Hemorrhaging [occult or obvious] Nose, gums, IV Hemorrhaging [occult or obvious] Nose, gums, IV site, IM inj.site, etc…site, IM inj.site, etc…

S/S shock; oligouria; ^HR; diaphoresis, seizures S/S shock; oligouria; ^HR; diaphoresis, seizures Diagnostic testsDiagnostic tests: CBC, prolonged prothrombin time: CBC, prolonged prothrombin timeLAB FindingsLAB Findings: low plts, fibrinogen, other clotting factors: low plts, fibrinogen, other clotting factors..Intervention: Intervention: Treat underlying condition. Treat underlying condition. Infection, pre-eclampsia, abruption, bleeding, shockInfection, pre-eclampsia, abruption, bleeding, shock. . IVF (RL); O2 @ 6-10 L / min.IVF (RL); O2 @ 6-10 L / min. Foley to monitor UO [30-50 ml/hr]Foley to monitor UO [30-50 ml/hr] Monitor VS; Clotting factors replaced with PRBC’s, Monitor VS; Clotting factors replaced with PRBC’s,

platelets & fresh frozen plasma.platelets & fresh frozen plasma. Heparin may be given to block coagulation cascade.Heparin may be given to block coagulation cascade.Complications: organ injury; maternal mortality.Complications: organ injury; maternal mortality.

Incompetent CervixIncompetent Cervix: : Passive dilation of cervix without contxs.Passive dilation of cervix without contxs. Usually in Usually in earlyearly pregnancy. pregnancy. hx miscarriages.hx miscarriages. Causes: congenitally short cervix; composition of Causes: congenitally short cervix; composition of

cervical tissue; DES exposure.cervical tissue; DES exposure. Dx: ultrasoundDx: ultrasound

Management:Management: Strict BR; trendelenberg position if + Strict BR; trendelenberg position if +bulging membranes; hydration IVF, tocolysis.bulging membranes; hydration IVF, tocolysis.Cerclage Cerclage bestbest if placed by 10-14 wks. – binds cervical os. if placed by 10-14 wks. – binds cervical os.

No intercourse; Remove @ 37 wks.80-90% successNo intercourse; Remove @ 37 wks.80-90% success

DiabetesDiabetes

^ 41% from 1990 - 1999 in US; 4.9 to 6.9 ^ 41% from 1990 - 1999 in US; 4.9 to 6.9 respectively. Includes gest. DM.respectively. Includes gest. DM.

Contributing factor: ^ obesityContributing factor: ^ obesity Since 1991, obesity ^ 57% in US Since 1991, obesity ^ 57% in US Perinatal mortality/morbidity 6x higher w. undx. Perinatal mortality/morbidity 6x higher w. undx.

pre-existing DM. pre-existing DM. Most common complication of pregnancy. Most common complication of pregnancy. Mexican, Puerto Rican, American Indian, Asian Mexican, Puerto Rican, American Indian, Asian

Indian, Hawaiian: higher rates than other Indian, Hawaiian: higher rates than other Hispanic, white, & black. [CDC, 1998]Hispanic, white, & black. [CDC, 1998]

Gestational Diabetes AKA “GDM”Gestational Diabetes AKA “GDM”

Glucose intolerance beginning in pregnancy.Glucose intolerance beginning in pregnancy. GDM occurs > 20GDM occurs > 20thth wk. with no ^ incidence of anomalies. wk. with no ^ incidence of anomalies. ~ 2% pts. have undx type II ~ 2% pts. have undx type II enteringentering preg. preg. Type 1 & 2Type 1 & 2 have ^ anomalies d/t organogenesis (1 have ^ anomalies d/t organogenesis (1stst

trimester). trimester). ~ 4% of preg.affected. May/may not require insulin. ~ 4% of preg.affected. May/may not require insulin. Maternal Risks: HTN disorders, PTL, Maternal Risks: HTN disorders, PTL, polyhydramnios, macrosomia (^ C/S rate). polyhydramnios, macrosomia (^ C/S rate).

Infant Risks: Birth trauma, shoulder dystocia, Infant Risks: Birth trauma, shoulder dystocia, hypoglycemia, hyperbilirubinemia, RDS, hypoglycemia, hyperbilirubinemia, RDS, thrombocytopenia, hypocalcemia, fetal death.thrombocytopenia, hypocalcemia, fetal death.

Pathophysiology: GDMPathophysiology: GDM Pregnancy hormones estrogen, HPL, Pregnancy hormones estrogen, HPL, prolactin, cortisol, progesterone, blocks prolactin, cortisol, progesterone, blocks insulin receptors insulin receptors > 20 wks. pregnancy> 20 wks. pregnancy..

Results in ^ circulating glucose; Results in ^ circulating glucose; More insulin released to attempt to More insulin released to attempt to

maintain glucose homeostasis. Pt. feels maintain glucose homeostasis. Pt. feels “hungry” d/t ^ insulin; vicious cycle of ^ “hungry” d/t ^ insulin; vicious cycle of ^ appetite & wt.gain results. appetite & wt.gain results.

Screening & Diagnosis of GDMScreening & Diagnosis of GDM screen ALL women @ 24-28 wks.screen ALL women @ 24-28 wks. HIGHER Risk pts. screened in 1HIGHER Risk pts. screened in 1stst trimester/1 trimester/1stst

prenatal visit prenatal visit && @ 24-28 wks.@ 24-28 wks.

Determining High Risk ClientsDetermining High Risk Clients: : Family hx DM; Previous hx GDMFamily hx DM; Previous hx GDM Marked obesity; GlycosuriaMarked obesity; Glycosuria Maternal Age > 30Maternal Age > 30 Hx infant > 4000gHx infant > 4000g Member of high-risk racial/ethnic groupMember of high-risk racial/ethnic group Hispanic, Native American, South or East Asian, Hispanic, Native American, South or East Asian,

African American, Pacific Islander.African American, Pacific Islander.

If results negative, repeat @ 24-28 wks.If results negative, repeat @ 24-28 wks.

Screening & Diagnosis cont.Screening & Diagnosis cont.

1st Do:1st Do: 1 hour glucose challenge test (1 hour glucose challenge test (GCTGCT) - 50g oral ) - 50g oral

glucola. No fasting needed.glucola. No fasting needed. Recommended GCT value <140mg/dL (detects Recommended GCT value <140mg/dL (detects

80%) [130 value detects 90% women w.GDM] 80%) [130 value detects 90% women w.GDM] ADA & ACOG(2003) approved.ADA & ACOG(2003) approved.

Follow GCT >/=140mg/dL with diagnostic Follow GCT >/=140mg/dL with diagnostic 3hr.GTT [glucose tolerance test] 100 g. glucola. 3hr.GTT [glucose tolerance test] 100 g. glucola.

Do fasting, 1h, 2h, 3h serum. Fast @ least 8 hrs. Do fasting, 1h, 2h, 3h serum. Fast @ least 8 hrs. with @ least 150 g. carb intake 3 days prior to with @ least 150 g. carb intake 3 days prior to test & normal activity level.test & normal activity level.

GTT Diagnostic Thresholds: [ADA 2003]GTT Diagnostic Thresholds: [ADA 2003]Fasting Blood Sugar: 95 mg/dLFasting Blood Sugar: 95 mg/dL Drink 100 g glucolaDrink 100 g glucola

1 hour: 180 mg/dL plasma level1 hour: 180 mg/dL plasma level2 hour: 155 mg/dL2 hour: 155 mg/dL3 hour: 140 mg/dL3 hour: 140 mg/dL Diagnosis of GDM made if 2 or more values ^ Diagnosis of GDM made if 2 or more values ^

than above plasma levels. than above plasma levels.

ManagementManagement *May try standard diabetic diet*May try standard diabetic diet 1 1st *dependsst *depends on lab valueson lab values

Initiate insulin for fasting > 95 & 2hr postprandial Initiate insulin for fasting > 95 & 2hr postprandial >120. >120.

Interventions: Interventions: AntepartumAntepartum

Goal: strict glucose control.Goal: strict glucose control. Provide immediate education to pt./family Provide immediate education to pt./family Standard diabetic diet [2000-2500 cal/day].Standard diabetic diet [2000-2500 cal/day].

Distribution of caloriesDistribution of calories: : 40-50% carbs, 20% 40-50% carbs, 20% protein, 30-40% fat, (< 1/3protein, 30-40% fat, (< 1/3rdrd from saturated fat, 1/3 from saturated fat, 1/3rdrd polyunsaturated, rest monounsaturated).polyunsaturated, rest monounsaturated).

Recommend:Recommend: 3 meals & 3 snacks evenly spaced 3 meals & 3 snacks evenly spaced

to avoid swings in blood glucose. Snack @ bedtime. to avoid swings in blood glucose. Snack @ bedtime.

1200 mg/day calcium, 30 mg/day iron, 400 1200 mg/day calcium, 30 mg/day iron, 400

mcg/day folate.mcg/day folate.

Antepartum Interventions Cont.Antepartum Interventions Cont. Exercise [walking, swimming] 30 min.3-4 x/wkExercise [walking, swimming] 30 min.3-4 x/wk Teach daily glucose self-monitoring & urine testing. Teach daily glucose self-monitoring & urine testing. Teach monitoring of fasting & postprandial levels.Teach monitoring of fasting & postprandial levels.

If diet can’t control glucose, start insulin.If diet can’t control glucose, start insulin. Regular & NPH insulin < breakfast & dinner. Regular & NPH insulin < breakfast & dinner. Does not cross placenta. Abdomen site.Does not cross placenta. Abdomen site. Dose based on weight & gestational age Dose based on weight & gestational age Obese pts. ^ dose.Obese pts. ^ dose.

GDM - Interventions cont.GDM - Interventions cont.Intrapartum: Intrapartum: monitor glucose levels q 2hrs. monitor glucose levels q 2hrs.

[insulin given @ 100mg/dL or <].[insulin given @ 100mg/dL or <].

Postpartum: Postpartum: Most return to normal > del. Most return to normal > del. • 50% pts. with GDM develop type II 50% pts. with GDM develop type II later in life.later in life.• 6 wk. PP serum glucose6 wk. PP serum glucose• Children of GDM pts. ^ risk for obesity/diabetes in Children of GDM pts. ^ risk for obesity/diabetes in

childhood/adolescence.childhood/adolescence.

Diabetes MellitusDiabetes Mellitus:: Disorder of fat, CH0 [carbs], protein metabolism Disorder of fat, CH0 [carbs], protein metabolism Caused by insensitivity to insulin Caused by insensitivity to insulin oror partial or partial or

complete lack of insulin secretion by beta cells of complete lack of insulin secretion by beta cells of pancreas pancreas

exposes organs to chronic hyperglycemia exposes organs to chronic hyperglycemia causing tissue damage. causing tissue damage.

Type I -Type I - IDDMIDDM predates pregnancypredates pregnancy.. Autoimmune destruction of beta cells of pancreas Autoimmune destruction of beta cells of pancreas

resulting in absolute insulin deficiency. resulting in absolute insulin deficiency. Individuals < 30 yrs.; any age. Affects ~ 1-Individuals < 30 yrs.; any age. Affects ~ 1-

3/1000 preg. 3/1000 preg. Need Need exogenous insulinexogenous insulin to prevent ketoacidosis. to prevent ketoacidosis.

Symptoms: polyuria, polydipsia, significant Symptoms: polyuria, polydipsia, significant

weight loss. Do HgbA1c ASAP to assess recent weight loss. Do HgbA1c ASAP to assess recent

serum glucose levels. serum glucose levels.

Type I contType I cont..

11stst trimester: trimester: exogenous insulin needs may drop 10-20%.exogenous insulin needs may drop 10-20%. Hypoglycemia d/t fluctuations & N/V.Hypoglycemia d/t fluctuations & N/V.

22ndnd half of pregnancy (> 20 wks.): half of pregnancy (> 20 wks.): insulin needs ^ by 50–60% for Type I & II, insulin needs ^ by 50–60% for Type I & II,

respectively compared to pre-pregnancy.respectively compared to pre-pregnancy. Have higher levels of depression which negatively Have higher levels of depression which negatively

affects glucose control.affects glucose control.

Management:Management:

Type I – Type I – Cont. insulin. Cont. insulin. incorporate exercise & diet into daily routine incorporate exercise & diet into daily routine monitor glucose levels 5-6/day. monitor glucose levels 5-6/day. Endocrinologist during pregnancy. Endocrinologist during pregnancy. Meals @ set intervals. Meals @ set intervals. Teach pt. s/s hypo & hyperglycemia. Teach pt. s/s hypo & hyperglycemia. Goal: Goal: Glucose control reduces risk of Glucose control reduces risk of

complications for pt. & fetuscomplications for pt. & fetus

Type II:Type II: More common; individuals > 30.More common; individuals > 30. Recent data [AMA 2001] 9.1% ^ in 18-29 yrs. Recent data [AMA 2001] 9.1% ^ in 18-29 yrs. &&

69.9% ^ in 30–39 yrs. [1990 to 1998] 69.9% ^ in 30–39 yrs. [1990 to 1998] Combination of insulin resistance & inadequate Combination of insulin resistance & inadequate

insulin production. insulin production. Fewer symptomsFewer symptoms Longer to dx (~ 6.5 yrs.) Longer to dx (~ 6.5 yrs.) Obesity prevalent in type II. Obesity prevalent in type II. May require exogenous insulin; may be controlled May require exogenous insulin; may be controlled

w.diet & exercise alone.w.diet & exercise alone.

Pre-Conception Planning:Pre-Conception Planning: begin during begin during reproductive years with hx of type I & II. reproductive years with hx of type I & II.

Maintain normal A1C 3-6 mos. before conception Maintain normal A1C 3-6 mos. before conception & during organogenesis (6-8 wks) - minimize risk & during organogenesis (6-8 wks) - minimize risk of spontaneous AB & congenital anomaliesof spontaneous AB & congenital anomalies

A1C level > 7: ^ risk for congenital anomalies & A1C level > 7: ^ risk for congenital anomalies &

miscarriage. Normal A1C = 4-6 %.miscarriage. Normal A1C = 4-6 %. Multidisciplinary team: nutritionist, Multidisciplinary team: nutritionist,

endocrinologist, high risk OB nurse.endocrinologist, high risk OB nurse. Educate pt.- managing diet, activity, insulin.Educate pt.- managing diet, activity, insulin. Daily food diary to assess compliance. Daily food diary to assess compliance. Home visits by RN as needed.Home visits by RN as needed.

Cardiac DiseaseCardiac Disease: :

Impaired cardiac function mainly from Impaired cardiac function mainly from

congenital/rheumatic heart disease. congenital/rheumatic heart disease.

Class DescriptionClass Description: :

Class I:Class I: unrestricted physical activity. unrestricted physical activity.

No symptoms of cardiac insufficiency.No symptoms of cardiac insufficiency.

Class II:Class II: slight limitation physical activity. slight limitation physical activity.

Class III:Class III: mod. limitation physical activity. mod. limitation physical activity.

Class IV:Class IV: No physical activity. No physical activity.

RISKS FOR MATERNAL MORTALITY CAUSED RISKS FOR MATERNAL MORTALITY CAUSED BY VARIOUS HEART DISEASES BY VARIOUS HEART DISEASES

Cardiac Disorder: Cardiac Disorder: Group 1 - Mortality (0-1 %) Group 1 - Mortality (0-1 %) ASD; VSD; PDA; Pulmonic or tricuspid disease ASD; VSD; PDA; Pulmonic or tricuspid disease Tetralogy of Fallot (corrected), Bioprosthetic valve; Mitral Tetralogy of Fallot (corrected), Bioprosthetic valve; Mitral

stenosisstenosis

Group 2 – (5-15%) Group 2 – (5-15%) Aortic stenosis; Coarctation without valve Aortic stenosis; Coarctation without valve

involvement, Tetralogy of Fallot (uncorrected), involvement, Tetralogy of Fallot (uncorrected),

previous MI, Mitral stenosis with AF, artificial valveprevious MI, Mitral stenosis with AF, artificial valve

Group 3 – (25-50%) Group 3 – (25-50%) Marfan Syndrome; MI; pulmonary HTN; Cardiomyopathy.Marfan Syndrome; MI; pulmonary HTN; Cardiomyopathy.

Group 4 – (> 50%) Group 4 – (> 50%) CHF; advanced pulmonary edemaCHF; advanced pulmonary edema

Goal: optimal uteroplacental perfusion. Goal: optimal uteroplacental perfusion. Thorough medical hx: rheumatic heart dis., Thorough medical hx: rheumatic heart dis.,

scarlet fever, lupus, renal diseasescarlet fever, lupus, renal disease Birth defects involving heart &/or valves. Birth defects involving heart &/or valves. Assess symptoms: SOB, chronic cough, Assess symptoms: SOB, chronic cough, arrhythmias, palpitations, dyspnea @ rest, arrhythmias, palpitations, dyspnea @ rest, headache, chest pain, etc. headache, chest pain, etc. Family Hx of cardiac disease. Family Hx of cardiac disease. Do PE. Do PE. Lab tests:12 lead EKG, echo, stress test, CBC, Lab tests:12 lead EKG, echo, stress test, CBC,

SMA12, uric acid levels, O2sat, CxR; ABG’s. SMA12, uric acid levels, O2sat, CxR; ABG’s. Risks ^ with maternal age & parity. Risks ^ with maternal age & parity.

ArrhythmiasArrhythmias: In Pregnancy: In Pregnancy

GGoaloal: to convert to sinus rhythm or control ventricular rate by : to convert to sinus rhythm or control ventricular rate by beta-blockers or digoxin. beta-blockers or digoxin.

Fetal-Neonatal ImplicationsFetal-Neonatal Implications::General Prognosis: proceed with pregnancy if disease General Prognosis: proceed with pregnancy if disease controlled and mild to moderate. EX. severe valve damage, controlled and mild to moderate. EX. severe valve damage, possible termination advised d/t ^ risk maternal mortality. possible termination advised d/t ^ risk maternal mortality. Correct valve lesions before preg. *Pre-conception planning.Correct valve lesions before preg. *Pre-conception planning.

Peripartum CardiomyopathyPeripartum Cardiomyopathy:: 1 in 3000-4000 pregnancies1 in 3000-4000 pregnancies. .

Findings: Findings: Cardiac failure last month of preg. or within 5 months PP Cardiac failure last month of preg. or within 5 months PP Absence of specific etiology for cardiac failure. Absence of specific etiology for cardiac failure. Absence of cardiac disease < last month of preg. Absence of cardiac disease < last month of preg.

SymptomsSymptoms: : • maternal dyspnea, cough, orthopnea [diff.breathing when maternal dyspnea, cough, orthopnea [diff.breathing when

lying down] & palpitations. lying down] & palpitations.

Management:Management: minimize decreased cardiac performance. minimize decreased cardiac performance. Give anticoagulants during/after delivery. Give anticoagulants during/after delivery. High incidence of embolic eventsHigh incidence of embolic events. .

PrognosiPrognosis: 50% pt. recover good ventricular function within s: 50% pt. recover good ventricular function within 6 mos.of delivery; 50% have persistent cardiomegaly w. 6 mos.of delivery; 50% have persistent cardiomegaly w. mortality of 80%. Must weigh risks/benefits to mom/fetus.mortality of 80%. Must weigh risks/benefits to mom/fetus.

Infections:Infections:

A. Urinary Tract InfectionsA. Urinary Tract Infections Caused by: Caused by: E coliE coli, Klebsiella, Proteus. , Klebsiella, Proteus. S&S: Asymptomatic Bacteriuria = + bacteria in S&S: Asymptomatic Bacteriuria = + bacteria in

urine cx w.no symptoms. urine cx w.no symptoms. Rx: Early pregnancy: oral sulfonomides Bactrim]; Rx: Early pregnancy: oral sulfonomides Bactrim];

Late: ampicillin, furodantin. Late: ampicillin, furodantin. if left untreated, infection lead to acute if left untreated, infection lead to acute

pyelonephritispyelonephritis. . Can cause PTL; sexual activity > UTI.Can cause PTL; sexual activity > UTI.

B.B. Cystitis (lower UTI) - Same organismsCystitis (lower UTI) - Same organisms S&S: Dysuria, urgency, frequency, low grade S&S: Dysuria, urgency, frequency, low grade

fever, clean catch leukocytes >100,000 fever, clean catch leukocytes >100,000 Same as UTI; Same as UTI Same as UTI; Same as UTI

C. Acute Pyelonephritis - infection of kidney. Caused C. Acute Pyelonephritis - infection of kidney. Caused by same.by same.

S&S: chills, fever, flank pain,dysyria, low urine S&S: chills, fever, flank pain,dysyria, low urine output, ^ B/P, N/V, WBCs, dx with + urine culture.output, ^ B/P, N/V, WBCs, dx with + urine culture.

Rx: Hospitalization, IVAB; Safe meds.during Rx: Hospitalization, IVAB; Safe meds.during pregnancy: Bactrim, a flouroquinolone (Cipro).pregnancy: Bactrim, a flouroquinolone (Cipro).

Increased risk of premature birth & IUGR.Increased risk of premature birth & IUGR.

D. Monilial Vaginal InfectionD. Monilial Vaginal Infection Caused: 80% candida albicans. Caused by Caused: 80% candida albicans. Caused by

change in normal vaginal Ph; ph < 5 - acidic. change in normal vaginal Ph; ph < 5 - acidic.

S&S: Thick white curdy discharge, severe S&S: Thick white curdy discharge, severe itching dysuria. Wet Mount: hyphae, budding itching dysuria. Wet Mount: hyphae, budding

yeast. yeast. Risk Factors: HIV, DM, pregnancy, stress, AB tx.Risk Factors: HIV, DM, pregnancy, stress, AB tx.

Tx: Intravaginal miconazole suppositories @ hs Tx: Intravaginal miconazole suppositories @ hs for 1 wk. for 1 wk.

Teach: yogurt in diet; no douching; cotton Teach: yogurt in diet; no douching; cotton underwear. underwear.

Implic: Fetus may contact thrush during Implic: Fetus may contact thrush during delivery. Tx baby w.oral nystatin 1cc q 6h.delivery. Tx baby w.oral nystatin 1cc q 6h. Infant with thrush may give it to mom when Infant with thrush may give it to mom when

breast fdg. Apply nystatin.breast fdg. Apply nystatin.

Bacterial Vaginosis & TrichomoniasisBacterial Vaginosis & Trichomoniasis

BV: Overgrowth of Gardnerella BV: Overgrowth of Gardnerella [normal vaginal flora][normal vaginal flora] Loss of protective lactobacilli bacteria. Aka vaginitis. Loss of protective lactobacilli bacteria. Aka vaginitis. Thin, watery vaginal dc with fishy odor. Clue cells seen Thin, watery vaginal dc with fishy odor. Clue cells seen

under microscope. Vaginal ph >5. under microscope. Vaginal ph >5. TX with Flagyl [Metronidazole 500mg BID x 7 days. Do not TX with Flagyl [Metronidazole 500mg BID x 7 days. Do not

take med with alcohol. Similar to Antabuse –severe N/V.take med with alcohol. Similar to Antabuse –severe N/V. Risk factor for PTL and PROM.Risk factor for PTL and PROM.

Trichomoniasis: Different organism caused by parasite Trichomoniasis: Different organism caused by parasite Trichomonas vaginalis. Vaginal discharge (thin, greenish-Trichomonas vaginalis. Vaginal discharge (thin, greenish-yellow, frothy or foamy). yellow, frothy or foamy).

An STIAn STI Same tx as above. Safe in pregnancy.Same tx as above. Safe in pregnancy. Risk factor for PTL and PROM.Risk factor for PTL and PROM.

E. STD’s E. STD’s Chlamydia Chlamydia Caused By: bacterium Caused By: bacterium Chlamydia trachomatisChlamydia trachomatis Most common STI in USAMost common STI in USA PID > infertility by blocking tubes.PID > infertility by blocking tubes. Often asymptomatic. Thin/purulent discharge, Often asymptomatic. Thin/purulent discharge,

burning & frequency w.urination, lower abd. pain. burning & frequency w.urination, lower abd. pain. Pregnant women: Zithromax 1 g single dose; Pregnant women: Zithromax 1 g single dose;

amoxicillin x 7 days. amoxicillin x 7 days.

Newborn conjunctivitis (erythromycin ointment), Newborn conjunctivitis (erythromycin ointment), neonatal pneumonia, PTL, fetal death. Perinatal neonatal pneumonia, PTL, fetal death. Perinatal transmission occurs in 50% infants where mom is transmission occurs in 50% infants where mom is infected @ time of del.infected @ time of del.

GonorrheaGonorrhea Caused by Caused by Neisseria Gonorrhea. Bacterial STI.Neisseria Gonorrhea. Bacterial STI. Can lead to PID > infertility. Green frothy dc.Can lead to PID > infertility. Green frothy dc. Often asymptomatic in females; males have Often asymptomatic in females; males have

burning with urination & penile dc.burning with urination & penile dc. Dx - vaginal or urine cx.DOH notifies partners.Dx - vaginal or urine cx.DOH notifies partners. Rx with Rocephin IM [ceftriaxone]. Zithromax Rx with Rocephin IM [ceftriaxone]. Zithromax

[azithromycin] 1 g single dose or amoxicillan po.[azithromycin] 1 g single dose or amoxicillan po. PID – caused by both. Cramping, fever, chills, PID – caused by both. Cramping, fever, chills,

purulent dc, N/V, uterine swelling, adnexal & purulent dc, N/V, uterine swelling, adnexal & cervical tenderness. Multiple sex partners, no cervical tenderness. Multiple sex partners, no condoms. Tx with Doxycycline po condoms. Tx with Doxycycline po (contraindicated in pregnancy) & Rocephin IM. (contraindicated in pregnancy) & Rocephin IM. Clinda/genta/rocephin if pregnant. May need Clinda/genta/rocephin if pregnant. May need hospitalization.hospitalization.

HerpesHerpes Viral infection – no cure.Viral infection – no cure. HSV I – oral [cold sore] outer lesion.HSV I – oral [cold sore] outer lesion. HSV 2 – genital – painful, open lesions. HSV 2 – genital – painful, open lesions. Vesicles rupture & appear right after exposure or Vesicles rupture & appear right after exposure or

within 20 days. within 20 days. Burning sensation with urination is 1Burning sensation with urination is 1stst sign. sign. Prodrome “tingling” occurs before new outbreak.Prodrome “tingling” occurs before new outbreak. Outbreaks several times/yr.Outbreaks several times/yr. Dx: vaginal cx or blood testDx: vaginal cx or blood test Rx: Acyclovir or Valtrex 500 mg once/day during Rx: Acyclovir or Valtrex 500 mg once/day during

pregnancy reduces viral load enough to deliver pregnancy reduces viral load enough to deliver vaginally. vaginally.

Syphilis: Syphilis: Treponema Palladium [SpirocheteTreponema Palladium [Spirochete] ] Primary Stage:Primary Stage: painless sores, “chancre”, approximately 2- painless sores, “chancre”, approximately 2-

3 wks > initial exposure. fever, malaise. 3 wks > initial exposure. fever, malaise. Secondary Stage:Secondary Stage: 6 wks to 6 mos. Skin eruptions, arthritis, 6 wks to 6 mos. Skin eruptions, arthritis,

liver enlarged, sore throat, liver enlarged, sore throat, Dx: VDRL, RPR, FTA-ABS (more specific), Dark field exam: Dx: VDRL, RPR, FTA-ABS (more specific), Dark field exam:

for spirochetes. for spirochetes.

Tx: Tx: <1 yr 2.4 million u benzathine penicillin x 1 dose<1 yr 2.4 million u benzathine penicillin x 1 dose >1 yr SAME MED 1x/wk x 3 wks. >1 yr SAME MED 1x/wk x 3 wks. Sexual partners screened /tx. [allergic to PCN]: tx Sexual partners screened /tx. [allergic to PCN]: tx

ceftriazone >1ceftriazone >1stst trimester. trimester. ~ 40% chance of stillbirth or death > birth. Infant may be ~ 40% chance of stillbirth or death > birth. Infant may be

born w. “congenital syphilis”. Opthalmia neonatorium: can born w. “congenital syphilis”. Opthalmia neonatorium: can cause blindness. Appears as conjunctivitis in newborn. cause blindness. Appears as conjunctivitis in newborn. Give baby PCN q day x10. Give baby PCN q day x10.

GENITAL WARTS – virus [aka condyloma] GENITAL WARTS – virus [aka condyloma] Soft pink lesions on vulva, vagina, cervix, anus. Soft pink lesions on vulva, vagina, cervix, anus.

“Cauliflower appearance”“Cauliflower appearance” HPV Types 6 and 11 cause 90% of genital warts.HPV Types 6 and 11 cause 90% of genital warts. ~ 120 strains HPV~ 120 strains HPV Tx: Trichloroacetic acid, Aldara. Category CTx: Trichloroacetic acid, Aldara. Category C Benefits (pregnancy) may be acceptable over potential Benefits (pregnancy) may be acceptable over potential

risks. risks. Contact occurs during vaginal birth. Infant may have Contact occurs during vaginal birth. Infant may have

laryngeal warts.laryngeal warts.

Gardasil Vaccine: 3 doses.Gardasil Vaccine: 3 doses. HPV Types 16 & 18 – [70% cervical cancer] and Types 6 & HPV Types 16 & 18 – [70% cervical cancer] and Types 6 &

11 – [90% genital warts] Can be given to males also. 11 – [90% genital warts] Can be given to males also.