MATERNAL RISK FACTORS
adolescence
increased risk during teenage pregnancy for toxemias, anemia, prematurity, low birth weight, prolonged labour, high blood pressure (preeclampsia risk), STI, and postpartum complications
poverty, education and limited family resources lead to deteriorating mental health and lack of prenatal care
MENTAL HEALTH ILLNESS
pt can be related to sbuse: physical, emotional, sexual and mental
take note of any suspicious bruising and other injuries
SUBSTANCE ABUSE
has several consequences for infant, passes easily though placenta and breast milk
includes alcohol, smoking, use of OTC and illicit drugs
marijuna and tobacco create greatest risk for stillborn
their is no save amount of alcohol during pregnancy. the first trimester is the most violable period for fetal alcohol syndrome
PRE EXISTING HEALTH ISSUES
cardiac disease, autoimmune, diabetes, renal disease
obesity leads to hypertension during pregnancy
ADVANCED MATERNAL AGE
referes to patients older than 35 years
increased risk for gestational diabetes, hypertension, infertility, c section, fetal death and Down syndrome
early screening to look for anomalies
HYPEREMESIS GRAVIDARUM
no known ethology but suspected levels of high HCG and estrogen
results in electrolyte imbalance and ketonuria, and vitamin b6 deficiency
stress can bring on symptoms
hypersensitivity and dysregulation of gastric rhythms
peaks at 8-12 weeks usually resolves by 14wks
causes decreased placental blood flow, maternal blood flow and acidosis - threats the health of mom and baby
risks to mother include pregnancy loss, activity restiction and depression
HYPEREMESIS GRAVIDARUM RISK FACTORS
young maternal age
nulliparous
low SES
unplanned pregnancy
high MBI
smoking
HG in previous pregnancy
HYPEREMESIS GRAVIDARUM TREATMENT
clear fluids
IV hydration
TPN/NPO in severe cases
electrolyte replacement
medications
diclectin, gravel, mexeran, ondansetron
NURSING CARE FOR GRAVIADRUM
psychosocial support
ins and outs
weights
oral care
quiet aroma free environment
activity as tolerated
fetal monitoring dependant on gestation
DIABETES IN PREGNANCY
type one and 2
requires adaptations to manage conditions
INCREASED RISK OF
macrosomia
congenital anomalies
spontaneous abortion
GESTATIONAL DIABETIS
carbohydrate intolerance of variable severity with onset or recognition during present pregnancy. After 20 weeks gestation.
beta cells of pancreas do not produce enough insulin, placenta produces high levels of hormones which impair action of insulin in cells, and raises blood sugars
**pregnancy insulin resistance is main cause for increase in blood sugars, and hormones peak between 24 and 28 weeks.
RISK FACTORS FOR GB
previous or fx history of gestational diabetes
previous macrosomia of >4000g
unexplained stillbirth
previous neonatal hypoglucemia
advanced maternal age
obesity BMI over 30
polyhydramnious
hypertension
at risk for ketoacidosis as the body cannot buffer acids as before pregnancy
glucose crosses the placenta = increased fetal urine production = increased volume of amniotic fluid
SCREENING FOR GB
recommended testing done at 24-28wks, >11.1 mmol confirms diagnosis
screening completed by testing one hour plasma, glucose measurement following a 50g glucose load
result between 7.8 to 11 is indication that mother has to take 75g 2 hours glucose test
undergo a hemoglobin a1c to review control of sugars 3 months previous
additional testing serum creatinine and urinalysis for micro albumin
intensive fetal monitoring done at the end of pregnancy 3rd trimester
includes fetal movement count ultrasound, NST, and doppler studies
used to reduce risk of trauma, and stillborn
GESTATIONAL DIABETIS PATHO
1st trimester:
raise in hormones stimulates insulin production and increase tissue response to insulin
insulin needs to decrease
2nd and 3rd trimester
human placental lactose causes increase resistance to insulin
ethology of beta cell destruction unknown
decrease glucose tolerance
hyperglycemia
insulin needs to increase two and 3 times
frees up glucose for fetus
FETAL IMPLICATIONS
maternal hyperglycaemia ➛ glucose crosses placenta = fetal hyperglycemia
leads to = macrosomia, congenital anomalies, intrauterine fetal demise
MANAGEMENT OF GDM IN ANTEPARTUM
diet and exercise
monitor of blood glucose
require medication (25-50%)
increase in fetal heart sounds
TREATMENT OF GDM
self assess blood sugars 5-7x a day, post prandial and preprandial
signs and symptoms of hypoglycemias
shakiness, sweating, clumsy or jerky movements, hunger, headaches, confusion
nocturnal hypoglycaemia is increased risk, may need to take blood sugars at night
evaluation q1hr during labour and birth - prevention of neonatal hypoglycemia
If patient is on insulin during labour, as energy requirements increases, extra glucose is required. Goal is to keep insulin between 4-7
POTENTIAL NURSING DIAGNOSIS FOR GDM
anxiety
deficient knowledge
ineffective health maintenance
imbalanced nutrition
ineffective coping
MANAGEMENT OF GDM IN LABOUR
goal is to maintain blood glucose between 4 and 7 during labour
continuous fetal heart survaliance
blood glusose should be higher than 7 during labour
insulin drip started with D5W infusion
HYPERTENSION IN PREGNANCY
preexisting is before 20 wks
gestational is after 20 wks
**** PREECLAMSIA IS CLASSIFIED AS HYPERTENSION AFTER 20 WKS WITH PROTEINURIA (25%) MULTIORGAN INVOLVEMENT
Hypertensive disorders
ethology not confirmed, risk increases with age over 40years
risk increased with primaparas who are obese, overweight
multipara are at risk if there is a new partner, preexisting hypertension, renal disease, diabetes or multiple gestation
PRE-ECLAMPSIA SYMPTOMS
after 20 wks gestation
PRE TRIAD - proteinuria, rising BP, edema
severe headaches
upper quadrant abd pain
naura, vomting
decreased urine output
thrombocytopenia
impaired liver function
shortness of breath
PRE ECLAMPSIA COMPLICATIONS
fetal growth restriction
pre term birth
placental abduption
HELLP syndrome
PRE ECLAMPSIA INTERVENTIONS
medications:
antihypertensives (hydralazine, labetalol, nifedipine)- BP lowered
Corticosteriroids (dexamethasone or betamethasone) - increase surfactant in fetal lungs <34 weeks. Decrease fetal lung fluid, increase surfactant
MgSo4 (magnesium sulfate) - seizure prophylaxis
assesments
neurological status - determine risk for seizures related to headaches
urinalysis - check for ptorien
blood work - K+, hematocrit, platelets, liver function
ECLAMPSIA
symptoms
S - seizures
A - acute increase of BP, multi organ involvement
I - increased liver enzymes
B - blurred vision
H - hyperreflexia
A - agitation
P - protienuria
E - epigastric or RUQ pain
L - loss of consciousness
H - headaches or muscle pain
ECLAMPSIA COMPLICATIONS
fetal growth restriction
pre term birth
placental abruption
** preeclampsia/eclampsia will NOT resolve until baby is born
HELLP SYNDROME
H - hemolysis
E - elevated liver enzymes
L - low platelet count
L - liver enzymes
P - platelet count
it can develop with or without pre existing hypertension, present with flu like symptoms, RUQ pain, weight gain and edema
** is a severe complication of gestational hypertension, syndrome may not present with high BP
ASSESMENTS INTRAPARTUM
perinatal assessment
BP readings, maintain low stimulation, assess for neurogenic symptoms, give magnesium and beta blockers
fetal assessment
continuous fetal monitoring, decreased accelerations are expected if mom is receiving magnesium sulphate
fetal assessment
fetal movement count twice a day
non stress test done 2-3 x a wk
biophysical profile 1-2 x a wk
continuous fetal monitoring while mom is in labour
ultrasounds to assess amniotic fluid volume
doppler study to determine placental blood flow
INTRAHEPATIC CHOLESTASIS OF PREGNANCY
is a pregnancy specific disorder
elevated serum bile acids, and pruitis developing ins second and third trimester
very increased risk for stillborn
diagnosis
total bile acids over 10mmol
liver panel: AST and ALT elevated
differential diagnosis
treatment
medications
delivery
ursodexycholic acid is frontline treatment for icp. Analysis has shown that udca is superior at relieving maternal symptoms, and improving fetal outcomes.
delivery is needed
PLACENTAL ANOMALIES
placenta previa
embryo implants in lower uterus that results in location of placenta over the cervical OS
bleeding condition that occurs during the last 2 trimesters of pregnancy. Placenta implants over the cervical os
serious complications arrise
hemmorage
abruption
preterm birth
emergency section
PLACENTA PREVIA NURSING IMPLICATIONS
clue is to look for malpresentation or high presentation
main symptoms is hemmoraging during last two trimesters - results in anemia, shock
end result may be premature separation of placenta, pre term birth and emergency caesarean
** these patients cannot give birth vaginally
NURSING CARE PLACENTA PREVIA
assesments
presentation
painless bleeding
home care teaching
management
fetus not yet term
close monitoring
medications
ultrasound
active management
fetus at term = safe delivery
psychosocial assessment and support is very important for mom and supports
PLACENTAL ABRUPTION
normally located placenta separates from uterus after 20wks gestation prior to birth
result is hemmorage that results in fetal and maternal mortality
can occur gradually as small parts of placenta detach, causing bleeding = clot formation = decreased maternal and fetal blood flow
classified as mild, moderate or severe
further classified as type of detachment of placenta (marginal or apparent, central or concealed, mixed or combined)
NURSING IMPLICATIONS PLACENTAL ABRUPTION
be aware of abdominal pain or backache with uterine tenderness
fetal heart sounds may be absent or abnormal
if pt experiences shock and anemia out of proportion to blood loss
result may be coagulopathy, the body’s ability to form blots is impaired
NURSING CARE PLACENTAL ABRUPTION
assesments
Presentation - malpresentation or high presentation
bleeding - hemmorage during last two trimesters = shock, anemia
active management
fluid volume replacement
PRE TERM LABOUR
true labour that begins before 37 weeks gestation
fetal implications include
intrauterine growth restriction, cerebral palsy, respiratory complications, blindness
contributing factors include
premature rupture of membranes, multiple pregnancies, cervical insufficiency, maternal infection
RISK FACTORS FOR PRE TERM LABOUR
adolescent pregnancy
antepartum hemmorage
polyhydramnous
uterine anomaly
alcohol and cocaine use
anemia
bacterial vaginosis
chrioamnionitis
diabetes
hydramnios
hypertension
malnutrition
multiple gestation
placental problems
urinary tract infections
common causes of indicated preterm birth
pre existing or gestational diabetes
chronic hypertension
preeclampsia
obstetrical disorders
placental disorders
seizures
thromboembolism
maternal hiv
obesity
advanced maternal age
fetal disorders
chronic intrauterine growth restriction
abnormal stress test
excessive or inadequate amount of amniotic fluid
birth defects
Clinically indicated pre term birth
pre eclampsia
complicated insulin dependant diabetes
abnormal fetal surveillance
intrauterine growth restriction
placenta abruption
intrauterine fetal death
chorioamnionitis
threatened pre term labour
contraindications present between 20-37wks
no cervical dilation
interventions resolve contractions
rest
hydration
UTI, STI
tocolysis
Prevention of preterm labour
primary prevention
smoking ceassation
stop maternal substance use
prenatal care
secondary prevention
screening for and treating risk factors
bacterial vaginosis in woman with prior preterm birth
asymptomatic bacteriuria
prolonging pregnancy
evidence for some efficacy
tocolytics
calcium Chanel blockers (nifedipine)
PG synthetase inhibitors (indomethacin)
nitroglycerin
no evidence for efficacy
magnesium sulphate
bedrest
fluid bolus
sedation
home uterine monitoring
Contraindications to tocolysis
any contraindication to continuing pregnancy
pre-eclampsia
chorioamnionitis
imminent delivery
abnormal fetal surveillance
significant antepartum hemmorage
Antenatal glucocorticoid theraphy
cross placenta and induce enzymes that accelerate fetal pulmonary maturity
full benefit 48hrs after dose
given at gestation between viability and 34 wks
betamethasone 12mg IM q24h x 2
dexamethasone 6mg IV/IM q12 x 4
contraindicated in gastric ulcers, TB and chorioamnionitis
MgSo4 for fetal neuroprotection
considered when managing patients at risk for imminent delivery before 31wks 6 days gestation
reduce risk of cerebral palsy and substantial motor dysfunction
4g IV over 30 mins - loading dose 1g/hr maintenance
Nursing care with Mgso4 admin
monitor vital signs
assess mom and fetus to obtain baseline vitals
ensure calcium gluconate is available
should not be given to moms with myasthenia graves
adverse effects
hot flushes, sweating, burning at iv site, nausea, vomiting, dry mouth, drowsiness, blurred vision, diplopia, headaches, weakness, lethargy, dizziness, hypocalcemia, shortness of breath and transient hypotension
fetal effects
decreased breathing movement, reduced FHR variability
COMPLICATIONS OF PREMATURITY
short term
respiratory distress syndrome: common problem in premature babies. Need extra oxygen and help with breathing
intraventricular hemmorage: bleeding inside and around ventricles in brain. Ventricles are space that hold cerebrospinal fluid. Bleeding in brain can put pressure on nerve cells, damage them and if damage is severe to cells can lead to brain injury.
necrotising enterocolitis: happens when tissues in large intestine get inflamed. The inflammation damages and kills tissues in colon. Very common in sick and premature babies. The smaller the baby the higher risk for NEC.
long term
CNS complications
Neuro developmental delay
bronchopulmonary dysplasia: chronic lung disease, results from damage to lungs caused by mechanical ventilation and long term oxygen use. Many infants can recover from BPD but some can suffer long term breathing difficulty.
RISK FACTORS PREMATURE RUPTURE OF MEMBRANES CNA PRETERM PREMATURE RUPTURE OF MEMBRANES
premature rupture of membranes
birth of baby a few days after rupture
Caesarian birth
postpartum infection
compressed umbilical cord
infection of placental tissue
placental aruption
preterm premature rupture of membranes (before 37wks gestation)
maternal and nutritional deficiencies
tobacco abuse
polyhydramnious
multiple gestations
antepartal trauma
chorioamnionitis, STI
intrauterine infection, chorioamnionitis is strongly associated with pPROM, and preterm birth at 21-24wks
fetal deformaties or fetal limb amputation )amniotic band syndrome)
ASSESMENTS RUPTURE OF MEMBRANES
report of gush, pop or leaking (date and time)
COAT (color, odour, amount, time)
inspect perineal area for fluid, odour, endovervical mucous, bloody discharge
DIAGNOSTIC TESTS RUPTURE OF MEMBRANES
nitrazine - ph of vaginal fluid (amniotic alkaline)
Ferm tests - vaginal fluid on a slide (Fern pattern indicates amniotic fluid)
fetal fibronectin - protein that glues amniotic sac. If connection is disrupted, fibronectin released into secretions near cervix. Connection can be disrupted by infection, inflammation, separation of placenta from wall of uterus, uterine contractions or shortening of cervix.
protein produced by fetal cells, found at interface of chorion and decidua. (between fetal sac and uterine lining)
ultrasound - to check amniotic levels
NURSING CARE PROM/PPROM
watch for infection fever, chills, tenderness, WBC test, changes in amniotic fluid
antenatal corticosteriroids are ordered if pregnancy is less than 34 wks but viable at least 24wks
tocolytics can be ordered
adress psycho-social issues
anxiety, stress, good communication
CERVICAL INSUFFICIENCY
occurs in 2nd trimester, defined as a structurally defective cervix, that spontaneously and painlessly dilates in absence of contractions
progress to premature rupture of membranes, preterm birth
thought to be linked to cervical damage from a congenital deformity, laceration or infection
DETECTION AND TREATMENT OF CERVICAL INSUFFICIENCY
diagnosis
transvaginal ultrasound to examine cervix
pelvic exam to see if membranes are protruding through cervix
detection
through history, has it happened before?
treatment
cervical cerclage: cervix is stitched closed with sutures. Sutures will be removed last month of pregnancy during labour
INTRAUTERINE GROWTH RESTRICTION
infants with signs of failure to thrive or hypoxia
head and body are proportionally small
results in increased risk for stillbirth, oligohydramnious, meconium aspiration, fetal distress/death
MECONIUM STAINING
meconium aspiration causes a severe form of aspiration pneumonia
before birth assess for:
assess fluid for presence of meconium after rupture of membranes
if fluid Is meconium stained, neonatal resuscitation is required
have someone perform endotracheal intubation at birth
after birth
assess respirations, heart rate and muscle tone
suction babys mouth and nose if baby has
strong respiratory efforts
good muscle tone
heart rate >100beats/min
suction trachea using endotracheal tube connected to meconium aspiration device and suction to remove meconium before respirations occur.
perform assisted ventilation if
depressed respirations
decreased muscle tone
heart rate <100beats/min
AMNIOTIC FLUID IMBALANCES
oligohydramnious
little amniotic fluid surrounding fetus and umbilical cord
diagnosed by ultrasound
caused by
renal genesis (potter syndrome)
preterm premature rupture of membranes
postdate pregnancy
uteroplacental insufficiency
hypertensive disorders in pregnancy
antepartum care
fetal wellness checks; kick counts and NST’s
serial ultrasounds to monitor amniotic fluid levels
intrapartum care
Continuous EFM, variable decelerations common
amnioinfusion can be done
polyhydramnios
excess of amniotic fluid surrounding fetus and umbilical cord
diagnosed by ultrasound: see large symphysis - fundal height
caused by
diabetes, blood glucose beyond target
fetal congenital anomalies (twin to twin transfusion syndrome, GI obstruction)
increased risk of cord prolapse with ROM
antepartum care
receive normal care
intrapartum care
monitoring for SROM
if SROM immediate cervical exam to assess cord presentation
CHORIOAMNIONIIS
organism that is part of vaginal flora ascent into amniotic cavity. Moms who have this infection can develop baceremia and can suffer from labour dystocia
is characterized by an infection of the chorion and amniotic fluid. Foul smelling, maternal temp, fetal tachycardia
prevention of maternal and neonatal complications, treatment with broad spectrum antibiotics and with of the fetus is necessary
Ampicillin, gentamycin, or penicillin are used
after section, antibiotic gives coverage for anaerobic organisms, such as clindamycin or metronidazoleshould be added
increased use to antibiotic prophylaxis who are GBS positive demonstrated decreased incidence of chorioamnionitis
ISOIMMUNIZATION
condition that occurs during pregnancy if woman is Rh- and baby has Rh+ blood
during delivery blood can intermingle
maternal body recognizes baby’s Rh protein as foreign and can begin making antibodies against baby’s Rh proteins
if second child is Rh positive, maternal anti Rh antibodies will cross placenta and cause hemolytic disease in newborn
antepartum is when pt should be tested for blood type
postpartum is when WinRho immunization should be given 72hrs of delivery to non sensitized Rh negative women who delivered Rh positive infant
NURSING CARE FOR ISOIMMUNIZATION
WinRho at 28wks
earlier winRho if trauma or antepartum bleeding occur
cord bood tested ‘if baby is Rh+ Kleihauer Betke drawn on mother baby unit