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 1 A PREGESTATIONAL 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

Fetal Alcohol Syndrome Retrieved from: http: //www. aafp. org/afp/2005/0715/p 279. html

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

MODULE 4 PART 1 B PREGESTATIONAL 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

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 • 2 ND 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 III • TYPE IV • BASED ON CAUSE – WHITE’S • CLASS A-T • DESCRIBES EXTENT OF DISEASE

GESTATIONAL DIABETES • GESTATIONAL DIABETES – WHY DOES THIS OCCUR? -- WHEN DOES THIS OCCUR? – WHAT IS THE INCIDENCE OF THIS OCCURING DURING PRGNANCY? – HOW IS IT DIAGNOSED?

COMPARISON OF DIABETES MELLITUS AND GESTATIONAL DIABETES

DIABETES MELLITUS IN PREGNANCY • 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

DIABETES MELLITUS IN PREGNANCY • CLINICAL TREATMENT – GTT CRITERIA • LAB ASSESSMENT • ANTEPARTAL MANAGEMENT – DIET – GLUCOSE MONITORING – INSULIN REQUIREMENTS – FETAL EVALUATION

MODULE 4 PART 1 C PREGESTATIONAL RISKS INFECTIONS

HIV IN PREGNANCY • RISKS TO MOTHER • RISKS TO FETUS/NEONATE • ANTEPARTUM, INTRAPARTUM, POSTPARTUM TREATMENT & CARE

TORCH • TOXOPLAMOSIS • OTHER – GBS • RUBELLA • CYTOMEGALIVIRUS • 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 2 A GESTATIONAL ONSET COMPLICATIONS: BLEEDING DISORDERS

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

Cerclage Retrieved from: www. drlindagalloway. wordpress. com

GESTATIONAL RISKS • PREMATURE RUPTURE OF MEMBRANES – PROM – PPROM – NST, BPP RISKS NURSING CARE

Positive Fern Test Retrieved from: commons. wikimedia. org

MODULE 4 PART 2 B GESTATIONAL COMPLICATIONS AND RISKS: PREGNANCY REDUCED HYPERTENSION

PREGNANCY INDUCED HYPERTENSION--PIH – PREECLAMPSIA/ECLAMPSIA – 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

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 • 30 MM HG INCREASE IN SYSTOLIC AND 15 MM HG DIASTOLIC OVER BASELINE ON AT LEAST 2 OCCASIONS 6 OR MORE HOURS APART – PROTEINURIA , HYPERREFLEXIA – EDEMA – MATERNAL RISKS – FETAL/NEONATAL RISKS

PREECLAMPSIA • CLINICAL MANAGEMENT/CARE – ANTEPARTAL MANAGEMENT • MILD PREECLAMPSIA • SEVERE PREECLAMPSIA – INTRAPARTAL MANAGEMENT – POSTPARTAL MANAGEMENT • HELLP SYNDROME • ECLAMPSIA

H E L L P Syndrome • H – hemolysis- distortion and rupture of RBCs • E – elevated • L – liver enzymes- fibrin deposits obstruct blood flow • L – low • P – platelet count

MODULE 4 PART 2 C GESTATIONAL 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 (ANTIRh. D) – INDIRECT COOMBS TEST – DIRECT COOMBS TEST

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

Figure 13– 5 b Pregnancy with Rh-positive fetus. Some Rh-positive blood enters the mother’s bloodstream.

Figure 13– 5 e 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 • Rho. GAM – PROVIDES PASSIVE ANTIBODY PROTECTION AGAINST Rh ANTIGENS • ERYTHROBLASTOSIS FETALIS • HYDROPS FETALIS • KERNICTERUS

MODULE 4 PART 2 C BLEEDING COMPLICATIONS

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

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

Figure 19– 11 c Complete separation.

Figure 19– 11 b 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– 12 a Placenta previa. Low placental implantation.

Figure 19– 12 c Total placenta previa.

Figure 19– 12 b Partial placenta previa.

MODULE 4 PART 2 D SURGERY TRAUMA INFECTION DOMESTIC 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 3 A PRE-LABOR COMPLICATIONS AMNIOTIC FLUID ALTERATIONS

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: > 2000 ML AMNIOTIC FLUID • CAUSE UNKNOWN 20% ASSOCIATED WITH CONGENITAL ANOMALIES • TWO TYPES: – CHRONIC – ACUTE RISKS • CLINICAL MANAGEMENT

True knot

MODULE 4 PART 3 B PRE-LABOR COMPLICATIONS: PRETERM LABOR RELATED COMPLICATIONS

PRETERM LABOR – NONRECURRENT – SCREENING – FACTORS CORRELATED WITH PRETERM LABOR

PRETERM LABOR • PRETERM RISK FACTORS – LABOR THAT OCCURS BETWEEN 20 -38 WEEKS – PREVELANCE – RESEARCH – RECURRENT

PRETERM LABOR • TREATMENT/CARE – HOME UTERINE ACTIVITY MONITORING – TOCOLYSIS • MGSO 4 • NEPHEDIPINE • PROSTAGLANDIN SYNTHESIS INHIBITORS • BETAMETHASONE (FETUS)

LABOR RELATED COMPLICATIONS • DYSTOCIA • POSTTERM PREGNANCY • FETAL MALPOSITION, MALPRESENTATION • MACROSOMIA • FETAL DISTRESS

LABOR RELATED COMPLICATIONS • HYPERTONIC LABOR • HYPOTONIC LABOR – LABOR MANAGEMENT – MATERNAL RISKS – FETAL/NEONATAL RISKS • PRECIPITOUS LABOR – LABOR LESS THAN 3 HOURS

LABOR RELATED COMPLICATIONS • PROLAPSED UMBILICAL CORD • AMNIOTIC FLUID EMBOLISM • CEPHALOPELVIC DISPROPORTION • COMPLICATION OF THIRD OR FOURTH STAGE OF LABOR

Uterine Tachysystole

LABOR RELATED COMPLICATIONS • MACROSOMIA – NEWBORN WEIGHT > 4000 GMS – OFTEN SEEN IN: • • DIABETIC MOTHERS GRAND MULTIPARITY POSTTERM GESTATION LARGE PARENTS – MATERNAL RISKS – FETAL / NEONATAL RISKS

MODULE 4 PART 3 C LABOR RELATED COMPLICATIONS

POSTTERM PREGNANCY, MALPOSITION • POSTTERM PREGNANCY – PREGNANCY 42 WEEKS PAST 1 ST 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

Nurse and Prolapsed cord

AMNIOTIC FLUID EMBOLISM • CLINICAL PRESENTATION – CHEST PAIN – DYSPNEA – CYANOSIS – HYPOTENSION – TACHYCARDIA – MASSIVE HEMORRHAGE • 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

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 • 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

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 – 1 ST DEGREE – 2 ND DEGREE – 3 RD DEGREE – 4 TH 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 • HEMMORHAGE