module 4 pregnancy, childbirth, and postpartum at risk
TRANSCRIPT
PREGNANCY AT RISK PREGESTATIONAL
GESTATIONAL
CHILDBIRTH AT RISK PRE—LABOR COMPLICATIONS
LABOR—RELATED COMPLICATIONS
POSTPARTUM AT RISK
SUBSTANCE ABUSE DURING PREGNANCY
• ALCOHOL
– CNS DEPRESSANT
– INCIDENCE OF ABUSE HIGHEST IN MOTHERS 20-40 YEARS OF AGE
– PREGNANT WOMEN SHOULD AVOID ALCOHOL COMPLETELY DURING PREGNANCY—WHY?
– ADVERSE MATERNAL EFFECTS
– ADVERSE FETUS/NEONATAL EFFECTS
SUBSTANCE ABUSE DURING PREGNANCY
• COCAINE AND CRACK– PREVENTS REUPTAKE OF DOPAMINE,
NOREPINEPHRINE—LEADS TO VASOCONSTRICITION, TACHYCARDIA, HYPERTENSION
– ADVERSE MATERNAL EFFECTS– ADVERSE FETAL/NEONATAL EFFECTS
SUBSTANCE ABUSE DURING PREGNANCY
• MARIJUANA– NO STRONG RESEARCH INDICATING
TERATOGENIC EFFECTS– SOCIAL FACTORS
• HEROIN/METHADONE– ADVERSE MATERNAL EFFECTS– ADVERSE FETAL/NEONATAL EFFECTS
SUBSTANCE ABUSE DURING PREGNANCY
• BARBITURATES
• STIMULANTS
• CAFFEINE
• NICOTINE
• PSYCHOTROPICS
• METH
DIABETES MELLITUS IN PREGNANCY
• PATHOPHYSIOLOGY– INSULIN PRODUCTION DECREASE BY
PANCREAS– WITHOUT ADEQUATE INSULIN, GLUCOSE
DOES NOT ENTER CELLS, WHICH BECOME ENERGY DEPLETED
– BLOOD GLUCOSE LEVELS INCREASE– CELLS BREAK DOWN PROTEIN AND FAT
STORES FOR ENERGY
DIABETES MELLITUS IN PREGNANCY
• EARLY PREGNANCY– ESTROGEN, PROGESTERONE, OTHER
HORMONES RISE TO STIMULATE INCREASED INSULIN PRODUCTION AND INCREASED TISSUE RESPONSE TO INSULIN
– STORAGE OF GLYCOGEN IN LIVER PRODUCES ANABOLIC STATE DURING IST HALF OF PREGNANCY
DIABETES MELLITUS IN PREGNANCY
• 2ND HALF OF PREGNANCY PRESENTS WITH INCREASED RESISTANCE TO INSULIN AND DECREASED GLUSOSE TOLERANCE DUE TO:– SECRETION OF Hpl (INSULIN
ANTAGONIST) PROLACTIN, INCREASED CORTISOL AND GLYCOGEN LEVELS
– RESULTS IN CATABOLIC STATE
• DIABETOGENIC EFFECT
DIABETES IN PREGNANCY
• CLASSIFICATIONS– ETIOLOGIC
• TYPE I• TYPE II• TYPE III• TYPE IV• BASED ON CAUSE
– WHITE’S• CLASS A-T• DESCRIBES EXTENT OF DISEASE
GESTATIONAL DIABETES
• GESTATIONAL DIABETES– WHY DOES THIS OCCUR?
– WHY DOES THIS OCCUR?
– WHAT IS THE INCIDENCE OF THIS OCCURING DURING PRGNANCY?
– HOW IS IT DIAGNOSED?
DIABETES MELLITUS IN PREGNANCY
• INTRAPARTAL MANAGEMENT– WHEN TO DELIVER
– LABOR MANAGEMENT, INSULIN REQUIREMENTS
• POSTPARTAL MANAGEMENT– INSULIN REQUIREMENTS
– BREAST FEEDING
DIABETES MELLITUS IN PREGNANCY
• CLINICAL TREATMENT– GTT CRITERIA
• LAB ASSESSMENT
• ANTEPARTAL MANAGEMENT– DIET– GLUCOSE MONITORING– INSULIN REQUIREMENTS– FETAL EVALUATION
HIV IN PREGNANCY
• RISKS TO MOTHER
• RISKS TO FETUS/NEONATE
• ANTEPARTUM, INTRAPARTUM, POSTPARTUM TREATMENT & CARE
GESTATIONAL PREGNANCY RISKS• BLEEDING DISORDERS
• HYPERTENSIVE DISORDER
• Rh ALLOIMMUNIZATION
• ABO INCOMPATIBILITY
• DOMESTIC VIOLENCE
• SURGERY, TRAUMA
BLEEDING DISORDERS
• ECTOPIC PREGNANCY– TREATMENT, RISKS
• GESTATIONAL TROPHOBLASTIC DISEASE
– HYDATIFORM MOLE
– CHORIOADENOMA DESTRUENS
– CHORIOCARCINOMA
– TREATMENT, RISKS
GESTATIONAL RISKS
• INCOMPETENT CERVIX– CERCLAGE
• HYPEREMESIS GRAVIDARUM– FLUID & ELECTROLYTE ISSUES– DEHYDRATION– RISKS TO FETUS– NURSING CARE
PREGNANCY INDUCED HYPERTENSION--PIH
– PREECLAMPSIA/ECLAMPSIA
– CHRONIC HYPERTENSION
– CHRONIC HYPERTENSION WITH SUPERIMPOSED PREECLAMPSIA OR ECLAMPSIA
– TRANSIENT HYPERTENSION
PREECLAMPSIA
• DISEASE OF THEORIES
• MOST COMMON HYPERTENSIVE DISORDER IN PREGNANCY
• PATHOPHYSIOLOGY– CAUSE UNKNOWN– 5-7% OF ALL PREGNANCIES– GENERALIZED VASOSPASM, DECREASE
IN CIRCULATING BLOOD VOLUME
PREECLAMPSIA• PRENATAL FACTORS INCREASING RISK OF
PIH– PRIMIGRAVIDA– ESSENTIAL HYPERTENSION– AGE EXTREMES (UNDER 17 OR OVER 35
YEARS OLD)– UNDERWEIGHT OR OVERWEIGHT– FAMILY HISTORY OF HYPERTENSION– DIAGNOSIS OF PIH IN PREVIOUS
PREGNANCY– DIABETES MELLITUS
PREECLAMPSIA
• CHARACTERIZED BY:– DEVELOPMENT OF HYPERTENSION
• 30MM HG INCREASE IN SYSTOLIC AND 15 MM HG DIASTOLIC OVER BASELINE ON AT LEAST 2 OCCASIONS 6 OR MORE HOURS APART
– PROTEINURIA– EDEMA– MATERNAL RISKS– FETAL/NEONATAL RISKS
PREECLAMPSIA
• CLINICAL MANAGEMENT/CARE– ANTEPARTAL MANAGEMENT
• MILD PREECLAMPSIA• SEVERE PREECLAMPSIA
– INTRAPARTAL MANAGEMENT– POSTPARTAL MANAGEMENT
• HELLP SYNDROME• ECLAMPSIA
Rh SENSITIZATION
• ANTIGEN-ANTIBODY RESPONSE– IF AN Rh-NEGATIVE WOMAN IS EXPOSED
TO Rh POSITIVE BLOOD, EITHER THROUGH TRANSFUSION OR A PRIOR PREGNANCY, SHE PRODUCES IMMUNOGLOBULIN (Ig)G ANTIBODY (ANTIRhD)
– INDIRECT COOMBS TEST– DIRECT COOMBS TEST
Figure 13–5b Pregnancy with Rh-positive fetus. Some Rh-positive blood enters the mother’s bloodstream.
Figure 13–5e In subsequent pregnancies with an Rh-positive fetus, Rh-positive red blood cells are attacked by the anti-Rh-positive maternal antibodies, causing hemolysis of the red blood cells in the fetus.
Rh SENSITIZATION
• RhoGAM– PROVIDES PASSIVE ANTIBODY
PROTECTION AGAINST Rh ANTIGENS
• ERYTHROBLASTOSIS FETALIS
• HYDROPS FETALIS
• KERNICTERUS
PRE-LABOR COMPLICATIONS
• PREMATURE RUPTURE OF MEMBRANES
• PRETERM LABOR
• BLEEDING
• MULTIPLE GESTATION
• AMNIOTIC FLUID ALTERATIONS
ABRUPTIO PLACENTAE
• ABRUPTIO PLACENTAE:– PREMATURE SEPARATION OF PLACENTA
FROM UTERINE WALL– THREE TYPES:
• MARGINAL• CENTRAL• COMPLETE
– CLINICAL MANAGEMENT
PLACENTA PREVIA
• PLACENTA PREVIA: IMPLANTATION OF PLACENTA IN LOWER UTERINE SEGMENT
• THREE CLASSIFICATIONS:– LOW PLACENTAL IMPLANTATION– PARTIAL PLACENTA PREVIA– TOTAL PLACENTA PREVIA
• CLINICAL MANAGEMENT
DOMESTIC VIOLENCE IN PREGNANCY
• HOW DO WE ASSESS?
• WHEN DO WE ASSESS?
• WHAT DO WE DO IF THE WOMAN DISCLOSES ABUSE?
• MATERNAL RISKS
• FETAL RISKS
OLIGOHYDRAMNIOS
• SEVERELY REDUCED AMOUNT OF AMNIOTIC FLUID
• OCCURS IN:
– POSTMATURITY– IUGR– FETAL RENAL MALFORMATION– SOMETIMES IDIOPATHIC
OLIGOHYDRAMNIOS
• FETAL RISKS
• CLINICAL MANAGEMENT
• CRITICAL THINKING– WHAT TYPE OF DECELERATION MIGHT
YOU EXPECT TO SEE ON THE FETAL MONITOR OF A WOMAN WITH OLIGOHYDRAMNIOS? WHY?
HYDRAMNIOS
• HYDRAMNIOS: > 2000ML AMNIOTIC FLUID
• CAUSE UNKNOWN 20% ASSOCIATED WITH CONGENITAL ANOMALIES
• TWO TYPES:– CHRONIC – ACUTE
RISKS
• CLINICAL MANAGEMENT
PRETERM LABOR
• PRETERM RISK FACTORS– LABOR THAT OCCURS BETWEEN 20-37
WEEKS
– PREVELANCE
– RESEARCH
– RECURRENT
PRETERM LABOR
• TREATMENT/CARE– HOME UTERINE ACTIVITY MONITORING– TOCOLYSIS
• B-ADRENERGIC AGONISTS (B-MIMETICS)• MGSO4• NEPHEDIPINE• PROSTAGLANDIN SYNTHESIS
INHIBITORS• BETAMETHASONE (FETUS)
LABOR RELATED COMPLICATIONS
• DYSTOCIA
• POSTTERM PREGNANCY
• FETAL MALPOSITION, MALPRESENTATION
• MACROSOMIA
• FETAL DISTRESS
LABOR RELATED COMPLICATIONS
• PROLAPSED UMBILICAL CORD
• AMNIOTIC FLUID EMBOLISM
• CEPHALOPELVIC DISPROPORTION
• COMPLICATION OF THIRD OR FOURTH STAGE OF LABOR
LABOR RELATED COMPLICATIONS
• HYPERTONIC LABOR
• HYPOTONIC LABOR– LABOR MANAGEMENT– MATERNAL RISKS– FETAL/NEONATAL RISKS
• PRECIPITOUS LABOR– LABOR LESS THAN 3 HOURS
LABOR RELATED COMPLICATIONS
• MACROSOMIA– NEWBORN WEIGHT > 4000 GMS– OFTEN SEEN IN:
• DIABETIC MOTHERS• GRAND MULTIPARITY• POSTTERM GESTATION• LARGE PARENTS
– MATERNAL RISKS– FETAL / NEONATAL RISKS
POSTTERM PREGNANCY, MALPOSITION
• POSTTERM PREGNANCY– PREGNANCY 42 WEEKS PAST 1ST DAY OF LAST
MENSTRUAL PERIOD– MATERNAL RISKS– FETAL/NEONATAL RISKS
• MALPOSITION– OCCIPUT POSTERIOR– PERSISTENT OCCIPUT POSTERIOR– LABOR MANAGEMENT– MATERNAL RISKS
PROLAPSED UMBILICAL CORD
• PROLAPSED CORD: WHEN CORD PRECEDES FETAL PRESENTING PART
• DECREASED BLOOD FLOW IN CORD LEADS TO FETAL DISTRESS
• MAY RESULT WITH RUPTURE OF MEMBRANES
• CLINICAL MANAGEMENT
AMNIOTIC FLUID EMBOLISM
• AMNIOTIC FLUID EMBOLISM: AMNIOTIC FLUID MAY LEAK INTO CHORIONIC PLATE AND MATERNAL CIRCULATORY SYSTEM THROUGH: – TEAR IN AMNION OR CHORION– PLACENTAL SEPARATION– CERVICAL TEAR
AMNIOTIC FLUID EMBOLISM
• CLINICAL PRESENTATION– CHEST PAIN– DYSPNEA– CYANOSIS– HYPOTENSION– TACHYCARDIA– MASSIVE HEMORRHAGE
• CLINICAL MANAGEMENT
CEPHALOPELVIC DISPROPORTION (CPD)
• FETUS LARGER THAN PELVIC DIAMETERS
• PELVIC MEASUREMENTS
• PROLONGED LABOR
• CLINICAL MANAGEMENT
MALPRESENTATION
• MALPRESENTATION– BROW– FACE– BREECH– SHOULDER– TRANSVERSE LIE– COMPOUND PRESENTATION
MULTIPLE GESTATION
• INCREASED INCIDENCE OF MULTIPLE BIRTHS
• INCREASED INCIDENCE OF PRETERM LABOR
• FETAL AND MATERNAL IMPLICATIONS AND CARE
FETAL DISTRESS
• FETAL DISTRESS
• CONTIBUTING FACTORS:– CORD COMPRESSION– UTERO-PLACENTAL INSUFFCIENCY– PREEXISTING MATERNAL OR FETAL
DISEASE
• FETAL DISTRESS WARNING SIGNS– MECONIUM STAINED AMNIOTIC FLUID
FETAL DISTRESS
• OMINOUS FHR PATTERNS– PERSISTENT LATE DECELERATIONS
– PERSISTENT SEVERE VARIABLE DECELERATIONS
– PROLONGED DECELERATIONS
– DECREASED VARIABILITY
Figure 19–10 Intrapartum management of fetal distress. Note: bl 5 baseline; FAST 5 fetal acoustic stimulation test; SST 5 scalp stimulation test. Sources: Based on information from Strong, T. H. (1990). Fetal distress in the intrapartum period. In E. J. Quilligan & F. P. Zuspan’s (Eds.) Current Therapy in Obstetrics and Gynecology, (3rd ed.). Philadelphia: Saunders. *Huddleston, J. F. & Freeman, R. K. (1992). Estimation of fetal well-being. In A. A. Fanaroff & R. S. Martin’s (Eds.) Neonatal-Perinatal Medicine: Diseases of the fetus and newborn, (5th ed.). St. Louis: Mosby-Year Book.
FETAL DEATH
• INTRAUTERINE FETAL DEATH
• POSSIBLE CAUSES:
– PREECLAMPSIA
– ABRUPTIO PLACENTAE
– PLACENTA PREVIA
– DIABETES
– CONGENITAL ANOMALIES
– INFECTION
FETAL DEATH
• ISOIMMUNE DISEASE
• NUCAL CORD
• UNKNOWN CAUSES
• PROLONGED RETENTION OF FETUS MAY LEAD TO:
• DESSEMINATED INTRAVASCULAR COAGULATION (DIC)
COMPLICATIONS OF THE THIRD & FOURTH STAGE OF LABOR
• LACERATIONS– 1ST DEGREE– 2ND DEGREE– 3RD DEGREE– 4TH DEGREE
• SULCUS TEAR
• URETHRAL TEAR
COMPLICATIONS OF THE THIRD AND FOURTH STAGE OF LABOR
• PLACENTA ACCRETA:– ATTACHMENT OF PLACENTA DIRECTLY TO THE
UTERINE WALL WITHOUT INTEVENING DECIDUA BASALIS
– UTERINE RUPTURE
• RETAINED PLACENTA
• UTERINE ATONY