Wk 6: High risk pregnancies Flashcards
Define high-risk pregnancy and identify factors that
categorize a pregnancy as high risk: WHAT CAN INFLUENCE A HIGH RISK PREGNANCY? (4)
*preexisting condition (ill b4 or during preg)
*complications at fertilization
*complications at any time during pregnancy
*external complications affecting mom/fetus (changes in mom can affect fetus and vice versa)
factors impacting high risk (4)
*maternal age (adolescent preg (<20) or geriatric (>35))
*maternal parity
*maternal obstetric/gyno hx
*maternal med hx
cues nurse might see: preeclampsia/other hypertensive disorders (non-severe and severe and eclampsia)
*non-severe: > 140/90, 300 mg protein in 24hr urine or 2+ urine on dipstick
*severe: >160/110, platelets >100,000, LFT >2 times upper limit of norm (URQ), pulmonary edema, vision/mental changes
*eclampsia is either condition plus seizures
Most common HTN disorder of pregnancy
HELLP Syndrome
HELLP Syndrome def:
A subtype of preeclampsia w/ severe features
*liver and kidneys are not doing their part
*more sick than preeclampsia
HELLP syndrome includes (3)
*Hemolysis
*Elevated LHTs
*Low platelets
HELLP syndrome labs
*Hemolysis: elevated bili >1.2
*elevated liver enzymes: AST >70, LDH >600
*low platelets: <100000
PREECLAMPSIA risks
- Chronic hypertension
- Diabetes – both type 1 and 2
- Hx of preeclampsia
- Multiple fetuses
Presentation PreE
◦ Progressive disorder; most commonly seen:
◦ Last 10 weeks of gestation
◦ During labor
◦ First 480 postpartum
◦ Preeclampsia is a multi-system, vasospastic disease process
Eclampsia
*The presence of new onset grand mal seizures in a woman with preeclampsia.
*Rule-out other causes of seizures such as bleeding, idiopathic seizure disorders, etc.
PreE: why, may lead to
*Why: Rejection of genetic material – primip, twins, new FOB
*Leads to…
1. Placental abruption
2. Fetal intolerance of labor
3. Activation of the coagulation cascade – DIC
Patho: PreE
- placental ischemia ->leading to…
2.widespread vasospasms -> leads to… - endothelial injury -> leads to…
- edema -> leads to…
- decreased plasma volume -> leads to…
- Hemoconcentration -> leading to…
- decreased perfusion to mom’s organs
PreE: what’s happening in the systems (cues)
vasospasm leads to edema, leading to…
*Cardiac: endothelial damage (increased cap permeability, hemoconcentration, HTN
*Resp: Narrow upper airway: crackles, low o2 sat
*Neuro: H/A, clonus, brisk reflexes, low LOC
*Renal: low urine output, high proteinuria, uric acid, BUN, serum creatinine
*Hematology: low platelets, DIC (Disseminated intravascular coagulation), high Hct
*Hepatic: High LFTs, RUQ pain, N/V
PreE’s: Effect on hematologic system
*low platelets (thrombocytopenia: <100,000): rush to where vasospasm has caused injury
*DIC: failure of the normal coagulation system (no clotting -> leading to hemorrhage and shock)
*high HCT
DIC: lab values
Platelet count = decreased
Fibrinogen = decreased
Prothrombin time = prolonged
partial thromboplastin time = prolonged
D-dimer - increased
PreE’s: Effect on Renal symptoms and NRSG intervention
*Decreased GFR: less kidney function
*BUN (waste product) increases: signaling that kidneys are not working
*Uric acid increases
*Urine output decreases: Edema will increase bc of this
*High proteinuria
NRSG intervention: Strict I&O, listen to breath sounds
PreE’s: Effect on Hepatic and NRSG intervention
*Elevated LFT (liver function test)
*subscapular hematoma (Glisson’s capsule): leads to edema -> this leads to liver swelling, pressure within Glisson’s capsule
NRSG intervention: Pt may complain of RUQ pain and nausea (this is a sign of both of these complications)
PreE’s: Effect on NEURO and NRSG intervention
*cerebral ischemia, edema: very bad bc the skull prevents expansion
* this ^ leads to blurred vision, scotoma (holes in vision), hyperflexia, HA, exhausting, seizures
NRSG interventions: if seizure, averageFHR decel is 9 min. DO NOT GO TO C/S (best place for bb in mom’s belly)
Adolescent pregnancy: age
under 20 when conceives
Adolescent pregnancy: reproductive risk >15 yo (what happens in delivery/to baby)
1) Intrauterine growth restriction (IUGR)
2) Premature Birth
3) Preeclampsia
4) Stillbirth
5) Death
Reproductive risks for a woman over 35
1) Placenta previa
2) Fraternal twins or infants with genetic abnormalities (i.e. Down syndrome)
3) Hydatidiform mole (growth inside the womb)
4) Perinatal morbidity and mortality
High risk factor: Maternal parity (2 points and explanations)
- 5+ pregnancies lasting >20wks: weak muscles have trouble contracting and can contribute to postpartum HEMORRHAGE
- current preg w/i 3mon of last delivery: nutritional status low
High risk factors: Obstetric and Gyno Hx (8)
- 1+ stillbirths at term: (what is going on inside?)
*uterine/cervical incompetency (not staying closed/dilating too soon)
*prior placenta or amniotic fluid abnormalities (previa/abruption)
*prior poot wt gain (nutrition)
*prior GBS, HTN, infection (premature rupture)
*prior post-term bbs, shoulder dystocia, prolonged labor, PPH
*lack of prenatal care
High risk factors: maternal medical hx (5)
- Cardiac or metabolic disease
- Sexually transmitted diseases (STD’s)
- Endocrine disorders (DM type 1: no insulin being made = easily get ketoacidosis)
- Pulmonary disease (extra fluid)
- Surgery during current pregnancy (should be prepared to watch baby during mom’s surgery)
Fetal high risk factors (4)
- birth defects (heart, lungs, etc)
- chromosome probs (down syndrome)
- fetal growth restriction (fetus grows mom slowly)
- fetal anemia (Rh factor?)
most common high risk conditions
- HTN disorders (Preeclampsia)
- GDM
- Placenta issues (placenta previa, abruption, accreta)
- Preterm labor
- oxytocin induction at a high risk interval
HTN disorder: < 20 wks gest.
chronic HTN (pregnancy hasn’t done this to her)
HTN disorders: > 20 wks gest
*1. preeclampsia
*gestational HTN
*Chronic HTN w/ imposed preeclampsia
Gold standard for anti-convulsants
Magnesium Sulfate
Mag sul: initial dose, infusion rate, therapeutic level
*initial dose: 4-6 gm over 20 min
*infusion rate: 1-2 gm/hr
*therapeutic level: 5-8 mh/dl
which anti-hypertensive meds are used in L&D and NRSG consideration
*Apresoline (Hydralazine)
*Labetol (Normodyne, Trandate)
*Nifedipine (Procardia)
(only one would be given with the mag sul)
When would you notify physician about magnesium sul SE
*pulse >120
*urine output < 30 mL/hr for 2 hrs
*brisk reflexes (deep tendon and clonus)
GDM: maternal effects and complications (3)
*infection r/t hyperglycemia (bacteria likes to eat sugar)
infection can manifest as…
*UTI
*Chorioamnionitis: corion layer infection (while mom is still pregnant)
*Postpartum endometriosis: inner lining of the placenta left inside mom (after pregnancy…duh)
Blood sugar between meals: effects
- blood sugar between meals (sleeping) has basal insulin
- this triggers the pancreas to break down glucagon
- glucagon is broken down in the liver (glycogenolysis)
- causing high blood sugar
Blood sugar after meals: effects
- high blood sugar after a meal
- stimulates the pancreas to produce insulin
- in the liver glucose becomes glycogen and is stored. Excess releases into the blood
- cells take up the glucose and lower the blood sugar
Blood sugar after meals: effects
- high blood sugar after a meal
- stimulates the pancreas to produce insulin
- in the liver glucose becomes glycogen and is stored. Excess releases into the blood
- cells take up the glucose and lower the blood sugar
T1DM
*absolute insulin deficiency “juvenile diabetes”
*B-cell destruction
T2DM
*relative insulin deficiency “adult onset diabetes”
*insulin resistance and/or secretory defect
GDM
*develops during pregnancy
*not a disease but a higher range of normal insulin resistance in pregnancy
*usually goes away after pregnancy
impaired Glucose Tolerance
hyperglycemia not sufficient to meet diagnostic criteria
Diff between GDM and other DMs
*occurs during preg/not DXed prior to preg
*usually disappears after preg
*suggests risk of future T2Dm w/i 5-10 years after GDM
similarities between all types of Dms
*inadequate (or absent) insulin for glucose load
approach to TX for DM
balance avaliable insulin w/ glucose intake (avoid large glucose (carb) loads))
?Diabetic conditions?
Liver continues production of glucose after meal starts
when and what is the anabolic state in pregnancy
*when: first 1/2 of preg
*what: building fat stores
when and what is the diabetogenic state in pregnancy
*when: second half of preg
*what: placenta “fogs up” the insulin receptors, glucose ingested into the fetus, mom burns fat for energy
who is at risk for GDM
*ethnicity
*fam hx (1st gen) w/ DM
*obesity
*late maternal age >40yo
*if there is glycosuria
*previous delivery hx such as stillbirth and macrosomia
When are moms screened for GDM
24-28 wks typically
screening process for GDM
- 50 gram glucose drink
- don’t need to fast
- blood is drawn 1 hr after first sip
- if > 140 mg/dl, scheduled 3hr OGTT
Diagnostic process for GDM
- fasting for 8-12 hr
- 100 gm glucose drink
- fasting blood sample is drawn
- additional blood samples x3
- if glucose is elevated at 2 or more times, pt gets Dx of GDM
GDM: fetal effects
*neural tube defects: Meningomyelocele, encephalocele, anencephaly
*cardio effects
Maternal A1C values at 14wks can predict risk: <7%: no greater risk than non-GDM baby
Fetal oxygenation: effects of maternal hyperglycemia
*fetal hypoxemia: resulting in fetal death, metabolic acidosis, polycythemia (Jaundice risk)
placental vascular disease risk related to hyperglycemia
*vascular aging accelerated by glucose -> risk of late decels in labor
*shortens effective life span & capacity of placenta -> risk of preterm labor and delivery
GDM: short term goals
*protect pancreas
*protect your fetus
GDM: long term goals
*prevent T2DM
*improve existing insulin resistance
*permanent lifestyle changes
most common high risk Labor interventions
cervical ripening and oxytocin induction
indications to induce labor: Maternal
*Abruptio placentae
*Chorioamnionitis
*preg induced hypertension
*maternal conditions (DM, renal disease, chronic pulmonary disease)
*PreE, eclampsia
*Post-term preg
indications to induce labor: fetal
*fetal comp (IUGR)
*Fetal demise
induction
stimulation o uterine contractions where there are none (initiated)
augmentation
improving the frequency or strength of contractions (Hastened)
cervical ripening
process of effecting physical softening and distensibility of the cervix in prep for labor
Preferred pharmacologic agent for inducing labor when cervix is ripe r favorable
oxytocin
what is the dosing for oxytocin
starting 2mU/min, increasing 1-2 mU/min every 20-30 min
goal of oxytocin
contractions Q2-3 min, 60 sec duration w/ reassuring FHR
when does 2nd RN double-check and document pump set-up
- at initiation of infusion
- at start of shift
- When hanging new bag
NRSG interventions for non-reassuring FHR
*tocin off
*give o2 at 10L/min non-rebreather mask
*notify Dr (SBAR include tocin off)
*run 500 mL IV bolus unless contraindicated
*change mom’s position to other side
most common high risk condition
multiple gestation
Monozygotic monochorionic diamniotic twins
*1 sperm, 1 egg, so “mono-zygotic”
*1 chorion, “mono-chorionic”
*2 amniotic sacs “Di-amniotic”
*1 placenta, so higher risk for complications
Monozygotic monochorionic monoamniotic twins
*identical twins
*1 sperm, 1 egg
*1 chorion and 1 amnion so “mono/mono”
*one placenta
*one amniotic sac so higher risk for death due to entanglement of cords
Dizygotic Dichorionic Diamniotic twins
*most common twin pregnancy
*fraternal twins
*2 sperm, 2 eggs = “Di-zygotic”
*separate amniotic sacs = “Di-chorionic” and “di-amniotic”
*Separate placentas
*may be different sex
most common high risk placenta issues
*implantation
*detachment
*abnormal invasion into uterine wall
placenta implantation issues
- Placenta Previa
- Placental Abruption
- Placental Accreta
placenta previa
*Implantation of the placenta in the lower uterine segment
◦ Near or covering the cervical os
placenta previa classicifations
- Complete (total) - Covers entire cervical os
- Incomplete (partial) – Partially covers internal cervical os
- Low-lying (marginal) – placental border reaches the border of the internal os
placenta previa: related/risk factors (9)
◦ Previous placenta previa
◦ Previous uterine surgery: Cesarean section
◦ Multiparity (80%)
◦ Advanced Maternal Age (>35 yrs)
◦ Smoking
◦ Multiple gestation
◦ Macrosomia (lg placenta)
◦ Uterine fibroids
◦ SAB’s involving suction curettage
placenta previa: clinical findings
*bright red, PAINLESS BLEEDING
*1st bleed >30 wks, some not till after labor
*1st bleed NOT OFTEN life-threatening
*usually continue to spot after 1st bleed
placenta previa: NRSG implacations
*bedrest till after pregnancy
*no sex rest of pregnancy
Placenta Abruption: what, when, blood loss
*detachment of part/all placenta from implantation site b4 delivery
*typically >20 wks
*blood loss may be revealed (external), or concealed (internal)
placental abruption: partial (2)
◦ Bleeding concealed or apparent
◦ May continue pregnancy if abruption is small and fetus is stable
placental abruption: marginal (3)
◦ Only “edge” involved
◦ Usually bright red bleeding
◦ “Irritable” uterus contraction pattern on EFM
placental abruption: complete (5)
*fetal distress
◦ Uterine hypertonus
◦ Uterine hyperstimulation
◦ Maternal vital sign changes
◦ STAT c-section
what conditions put moms at a high risk of having a placental abruption?
PreE or eclampsia
