MODULE 4 PREGNANCY, CHILDBIRTH, AND POSTPARTUM AT RISK

MODULE 4 PREGNANCY, CHILDBIRTH, AND POSTPARTUM AT RISK

PREGNANCY AT RISK PREGESTATIONAL

GESTATIONAL

CHILDBIRTH AT RISK PRE—LABOR COMPLICATIONS

LABOR—RELATED COMPLICATIONS

POSTPARTUM AT RISK

MODULE 4 PART 1APREGESTATIONAL RISKS

SUBSTANCE ABUSE

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


• COCAINE AND CRACK– PREVENTS REUPTAKE OF DOPAMINE,

NOREPINEPHRINE—LEADS TO VASOCONSTRICITION, TACHYCARDIA, HYPERTENSION

– ADVERSE MATERNAL EFFECTS– ADVERSE FETAL/NEONATAL EFFECTS


• MARIJUANA– NO STRONG RESEARCH INDICATING

TERATOGENIC EFFECTS– SOCIAL FACTORS

• HEROIN/METHADONE– ADVERSE MATERNAL EFFECTS– ADVERSE FETAL/NEONATAL EFFECTS


• BARBITURATES

• STIMULANTS

• CAFFEINE

• NICOTINE

• PSYCHOTROPICS

• METH

MODULE 4 PART 1BPREGESTATIONAL RISKS:

DIABETES

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


• 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


• 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?

COMPARISON OF DIABETES MELLITUS AND GESTATIONAL DIABETES


• INTRAPARTAL MANAGEMENT– WHEN TO DELIVER

– LABOR MANAGEMENT, INSULIN REQUIREMENTS

• POSTPARTAL MANAGEMENT– INSULIN REQUIREMENTS

– BREAST FEEDING

DIABETES IN PREGNANCY

• CHALLENGES, INFLUENCES

• MATERNAL RISKS

• FETAL, NEWBORN RISKS


• CLINICAL TREATMENT– GTT CRITERIA

• LAB ASSESSMENT

• ANTEPARTAL MANAGEMENT– DIET– GLUCOSE MONITORING– INSULIN REQUIREMENTS– FETAL EVALUATION

MODULE 4 PART 1CPREGESTATIONAL RISKS

INFECTIONS

HIV/AIDS IN PREGNANCY

• HIV

• AIDS

• PATHOPHYSIOLOGY

• INCIDENCE

HIV IN PREGNANCY

• RISKS TO MOTHER

• RISKS TO FETUS/NEONATE

• ANTEPARTUM, INTRAPARTUM, POSTPARTUM TREATMENT & CARE

TORCH• TOXOPLAMOSIS

• OTHER– GBS

• RUBELLA

• CYTOPMEGLIVIRUS

• HERPES

TORCH

• MATERNAL RISKS

• FETAL RISKS

• ANTEPARTUM, INTRAPARTUM, POSTPARTUM TREATMENT AND CARE

GROUP B STREPTOCOCCUS

• INCIDENCE

• TESTING

• TREATMENT

• NURSING INTERVENTIONS

GESTATIONAL PREGNANCY RISKS• BLEEDING DISORDERS

• HYPERTENSIVE DISORDER

• Rh ALLOIMMUNIZATION

• ABO INCOMPATIBILITY

• DOMESTIC VIOLENCE

• SURGERY, TRAUMA

MODULE 4 PART 2AGESTATIONAL ONSET

COMPLICATIONS:BLEEDING DISORDERS

BLEEDING DISORDERS

• ECTOPIC PREGNANCY– TREATMENT, RISKS

• GESTATIONAL TROPHOBLASTIC DISEASE

– HYDATIFORM MOLE

– CHORIOADENOMA DESTRUENS

– CHORIOCARCINOMA

– TREATMENT, RISKS

BLEEDING DISORDERS

• SPONTANEOUS ABORTION

• MISSED ABORTION

• THREATENED ABORTION

GESTATIONAL RISKS

• INCOMPETENT CERVIX– CERCLAGE

• HYPEREMESIS GRAVIDARUM– FLUID & ELECTROLYTE ISSUES– DEHYDRATION– RISKS TO FETUS– NURSING CARE

GESTATIONAL RISKS

• PREMATURE RUPTURE OF MEMBRANES

– PROM

– PPROM

– NST, BPP

RISKS

NURSING CARE

MODULE 4 PART 2B GESTATIONAL

COMPLICATIONS AND RISKS:PREGNANCY REDUCED

HYPERTENSION

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

MODULE 4 PART 2CGESTATIONAL RISKS &

COMPLICATIONS: Rh ISOIMMUNIZATION

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 13–5d Anti-Rh-positive antibodies (triangles) are formed.

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

MODULE 4 PART 2CBLEEDING

COMPLICATIONS

ABRUPTIO PLACENTAE

• ABRUPTIO PLACENTAE:– PREMATURE SEPARATION OF PLACENTA

FROM UTERINE WALL– THREE TYPES:

• MARGINAL• CENTRAL• COMPLETE

– CLINICAL MANAGEMENT

Figure 19–11a Abruption placentae. Marginal abruption with external hemorrhage.

Figure 19–11c Complete separation.

Figure 19–11b Central abruption with concealed hemorrhage.

PLACENTA PREVIA

• PLACENTA PREVIA: IMPLANTATION OF PLACENTA IN LOWER UTERINE SEGMENT

• THREE CLASSIFICATIONS:– LOW PLACENTAL IMPLANTATION– PARTIAL PLACENTA PREVIA– TOTAL PLACENTA PREVIA

• CLINICAL MANAGEMENT

Figure 19–12a Placenta previa. Low placental implantation.

Figure 19–12c Total placenta previa.

Figure 19–12b Partial placenta previa.

MODULE 4 PART 2DSURGERY TRAUMA

INFECTIONDOMESTIC VIOLENCE

SURGERY

TRAUMA FROM AN ACCIDENT

INFECTION AFFECTING THE FETUS

– MATERNAL RISKS

– FETAL RISKS

DOMESTIC VIOLENCE IN PREGNANCY

• INCIDENCE

• RESEARCH

• STATISITICS

• SIGNS AND SYMPTOMS

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

MODULE 4 PART 3APRE-LABOR COMPLICATIONS

AMNIOTIC FLUID ALTERATIONS

OLIGOHYDRAMNIOS

• SEVERELY REDUCED AMOUNT OF AMNIOTIC FLUID

• OCCURS IN:

– POSTMATURITY– IUGR– FETAL RENAL MALFORMATION– SOMETIMES IDIOPATHIC

OLIGOHYDRAMNIOS

• FETAL RISKS


• 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


MODULE 4 PART 3BPRE-LABOR

COMPLICATIONS:PRETERM LABORLABOR RELATED COMPLICATIONS

PRETERM LABOR

• PRETERM RISK FACTORS– LABOR THAT OCCURS BETWEEN 20-37

WEEKS

– PREVELANCE

– RESEARCH

– RECURRENT

PRETERM LABOR

– NONRECURRENT

– SCREENING

– FACTORS CORRELATED WITH PRETERM LABOR

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


• PROLAPSED UMBILICAL CORD

• AMNIOTIC FLUID EMBOLISM

• CEPHALOPELVIC DISPROPORTION

• COMPLICATION OF THIRD OR FOURTH STAGE OF LABOR


• HYPERTONIC LABOR

• HYPOTONIC LABOR– LABOR MANAGEMENT– MATERNAL RISKS– FETAL/NEONATAL RISKS

• PRECIPITOUS LABOR– LABOR LESS THAN 3 HOURS


• 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

MODULE 4 PART 3CLABOR RELATED COMPLICATIONS

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


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


CEPHALOPELVIC DISPROPORTION (CPD)

• FETUS LARGER THAN PELVIC DIAMETERS

• PELVIC MEASUREMENTS

• PROLONGED LABOR


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

COMPLICATIONS OF THE FOURTH STAGE OF LABOR, 24 HOURS

POSTPARTUM• HEMMORHAGE

Documents

MODULE 4 PREGNANCY, CHILDBIRTH, AND POSTPARTUM AT RISK