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 1A
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/p279.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 1B
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
• 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?
-- 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 1C
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 2A
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 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
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 ,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 2C
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
(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
MODULE 4 PART 2C
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 19–11a 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 2D
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 3A
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: > 2000ML AMNIOTIC
FLUID
• CAUSE UNKNOWN 20% ASSOCIATED
WITH CONGENITAL ANOMALIES
• TWO TYPES:
– CHRONIC
– ACUTE
RISKS
• CLINICAL MANAGEMENT
True knot
MODULE 4 PART 3B
PRE-LABOR
COMPLICATIONS:
PRETERM LABOR
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
• MGSO4
• 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 3C
LABOR RELATED
COMPLICATIONS
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
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
• 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
– 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
• HEMMORHAGE