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Anemia
HgB <11 g/dl pregnant women : lower then normal d/t hemodilution
Affected by race, altitude, smoking, nutrition, and medications
causes during pregnancy:
Insufficent Hgb production (decrease iron and folic acid intake)
Hgb destruction (inherited disorders)
Important to test at first appointment
Maternal risk of anemia
May be asymptomatic
more susceptible to infection
tire easily
increase risk of preeclampsia and postpartum
healing may be delayed
poor toleration of even minimal blood loss
Fetal risks of anemia
low birth weight
prematurity
stillbirth/death
Prevention/treatment of anemia
First goal is prevention
Iron-rich diet
27 mg supplement daily (most prenantal vitamins have this)
education
may cause constipation: bowel regimen
Treatment
65 mg iron BID/ 325 mg ferrous sulfate
large doses can cause Gi symptoms
may give parenterally in severe cases
Patient self-monitoring
fetal kick counts
fetus should kick at least 10x in 2 hrs during the final months of pregnancy)
Awareness of fetal routines
report vaginal bleeding, leakage of fluid, contractions ( 5 or more in one hour)
BP/glucose monitoring at home when indicated
educate about warning s/s, when to call the provider and seek care (reinforced at every visit)
Fetal growth assessment
U/S
frequent growth (size and weight) measurements
Leopolds
amniotic fluid measurements
fetal growth restriction
<10th %
feto-placental or materal
macrosomia >400g
Umbilical artery dopplers
ordered for babies with abnormal fetal growth, high risk patient
abnormal values can indicate fetal risk
Non-stress test (NST)
Indicated for risk factors, post-dates, or any concerns about fetal well-being
decreased fetal movement
highly predictive of fetal well-being
Fetal activity marker utilized (by Mother)
button she can push
Non-stress test (NST) reactive
What we want to see, reassuring baby is well oxygenated
2 or more fetal heart accelerations within a 20-minute period (may extend to 40 minutes)
FHR acceleration >15 beats/min above the baseline, lasting at least 15 seconds
Moderate variablity
Non-stress test (NST) nonreactive
Can’t definitvely say something is wrong, need more information
lacks sufficient FHR acceleration over a 40 minute period
Biophysical profile (BPP)
Non-invasive assessment of fetus based on acute and chronic markers of disease
Ultrasound and NST (often done following a non-reactive NST)
Amniotic fluid volume
fetal breathing movements
fetal movements
fetal tone
FHR reactivity: non-stress test
10 possible points, anything less than 8 is concerning, less than 4 terminate
Amniotic fluid index (AFI)
Amniotic fluid volume determined by
fetal swallowing
fetal urine output
Oligohydramnios: AFI <5cm
Polyhydramnios: AFI > 25cm
Contraction stress test (CST)
Evaluated uteroplacental function
identifies intrauterine asphyxia
observes fetal heart rate response to contractions
Contraction stress test (CST) indications
IUGR
Diabetes
Postdates
Nonreactive NST
Abnormal biophysical profile
Contraction stress test (CST) results
must have 3 uterine contractions of at least 40 seconds duration in 10 minutes
FHR assessed in comparison to contractions
Contractions may be sponatenous or induced
oxytocin administration
nipple stimulation
Normal: negative
Abnormal: positive
Chronic Hypertension
defined as hypertension present prior to the start of the pregnancy or that develops during the first 20 weeks of the pregnancy
Gestational hypertension
onset at or after 20 weeks of pregnancy, without proteinuria
fine during first part of pregnancy, then develops
2 readings of 140/90 or greater at least 4 hrs apart, in women normally normotensive
usually resolves within the first postpartum week
can progress to preeclamsia, so careful monitoring is necessary
Preeclampsia
onset at or after 20 weeks of pregnancy, with proteinuria or other severe systemic symptoms
high BP + proteinuria
2 readings of 140/90 at least 4 hrs apart, in women who were previously normotensive
progressive : can quickly move from mild to severe
Chronic hypertension considerations
Important to obtain BP reading during first trimester
2 readings of 140/90 or greater, at least 4 hrs apart
Ratings are increasing, especially among African American and other minority women
Maternal risk of chronic HTN
counseling on weight loss, diet and lifestyle modifications
limit dietary salts
initate low-dose aspirin after 12 weeks
frequent prenatal visits
increased fetal surveillance
blood pressure monitoring
Medications
Labetalol or nifedipine
Risk factors of Preeclampsia
High risk
Previous pregnancy with preeclampsia
mutlifetal gestation
renal disease
autoimmune disease
diabetes mellitus
Moderate risk
first pregnancy
age 35 or olders
BMI >30
family history
race
low socio-econmoic status
Physiology of preeclampsia
progressive, widely believed that the placenta is the root cause
likely caused by disruption in plcaental perfusion and endothelial cell dysfunction
develops long before symptoms appear
lack of vascualr remodeling leads to decreased placental perfusion
placental ischemia causes release of substance toxic to endothelial cells
generalized vasospasm leads to poor tissue perfusion in all organ systems
Biggest organ affected by Preeclampsia
Placental dysfunction
anti-angiogenic and inflammatory factors released into the maternal circulation
Systemic vasoconstriction
leading to maternal hypertension
Fetal growth restriction
impaired blood supply to the fetus can compromise fetal growth
Major organ damage
impaired blood supply to major organs including the kidney, brain and heart
Symptoms of Preeclampsia
Headache
RUQ pain
liver is the most vascular organ, causes discomfort because the liver is so swollen
Visual disturbances
inflammation of the brain
Edema
SPECIFICALLY HANDS/FACE….NOT NORMAL!
Hyperreflexia
clonus, patellar reflex will have a huge response
diagnosis of Preeclampsia
BP 140/90 or greater, at least 4 hrs apart
and
Proteinuria >300 mg in 24 hr urine or protein/creatinine ratio >.3 or urine dip > 1+
or
thrombocytopenia
renal insufficency
increased liver enzymes
pulmonary edema
cerebral or visual changes
Nurse should anticipate for Preeclampsia
Labwork
CBC: platelets
Liver enzymes
Serum BUN and creatinine
Serum uric acid
24 hr urine or P/C ratio or urine dip
Non stress test
if NST is. non-reactive, BPP
Preeclampsia treatment
no actual cure
mild forms can be treated at home with frequent BP monitoring, prenatal visits, and fetal assessment
severe preeclampsia or signs of fetal compromise necessitate inpatient care and/or delievery (consider cortiosteriods in case early delivery is indicted)
Magnesium Sulfate
not a cure for Preeclampsia but a treatment to prevent seizures d/t neurological irritability
IV bolus of 4-6g in 100ml over 20 minutes, followed by IV infusion of 2g/hr: continue for 24 hrs postpartum
Antidote: Calcium Gluconate 1g IV push over 3-5 minutes
Magnesium Sulfate monitoring
Respiratory rate
BP, HR
LOC
Fetal assessment
Deep tendon reflexes
Clonus
Hourly urine output
use Foley catheter with urometer for accurate measurement
kidneys are effected by preeclampsia, not putting out enough urine= mg sulfate isnt being properly excreted
Magnesium Sulfate toxicity
Decreased LOC
RR <12
Urine output <30ml an hr
Diminished and absent DTRS
slurred speech
feeling flushed or hot
chest pain
IMMEDIATELY
discontinue magnesium sulfate drip
administer calcium gluconate
continue careful fetal monitoring
notify provider
Eclampsia
the convulsive manifestation of the hypertensive disorders of pregnancy: among the more severe manifestations of the disease
defined by new-onset tonic-clonic, focal, or multifocal seizures in the absence of other causative conditions
HELLP Syndrome
Hemolysis, elevated liver enzymes, low platelets
Severe form of preeclampsia
can occur in absence of hypertension or proteinuria
can occur anytime between 20 weeks gestation through postpartum
Life threatening for patient and fetus
HELLP Syndrome s/s
Nausea, extreme fatigue, chest pain, RUQ pain, difficulty breathing, shoulder pain, malalise