Module 5 Flashcards
Hypertensive disorders of pregnancy
pre-existing HTN (essential vs. secondary)
gestational HTN
pre-eclampsia
severe pre-eclampsia
eclampsia
HELLP
gestational HTN
occurs after 20 weeks
1) with proteinuria (with or without adverse conditions)
2) without proteinuria (with or without adverse conditions)
pre-eclampsia
HTN + proteinuria (+1 or greater) OR end-organ dysfunction OR severe consequences (eclampsia)
RF for HTN in pregnancy
family hx
extremes of reproductive age (<20 or >35)
primigravida
multiple gestation
diabetes, renal dx, prior HTN
collagen vascular dx
no mid-trimester fall in BPO
excessive weight gain (>2 lb/week)
finger/facial edema
Patho of pre-eclampsia
poor placentation
first stage: cytotrophoblast invades endometrium & remodels spiral arteries
second stage: cytotrophoblast invades myometrium & remodels arteries –> wider, low pressure system
pre-eclampsia occurs when this remodeling does not occur. placental ischemia –> release of inflammatory cytokines/factors that get released into maternal circulation and cause endothelial dysfunction
Adverse outcomes of pre-eclampsia
vascular remodeling/endothelial vasospasm = HTN
kidney damage = proteinuria, liver damage = elevated enzymes
RBC traveling through damaged blood vessels sheared = hemolysis
clotting activated by endothelial injury/turbulent blood flow thrombocytopenia s/t systemic clotting –> DIC edema (increased capillary permeability)
eclampsia/headache/hemiplegia/visual disturbance (cerebral vasospasm)
cardiomyopathy
ARDS
Nursing mgmt of pre-eclampsia
bed rest
fetal assessment (ultrasound/nonstress test)
weight gain
blood pressure measurements
proteinuria
fetal movement
general symptoms
Severe pre-eclampsia
gestational HTN with or without proteinuria with 1+ adverse conditions
Severe pre-eclampsia adverse conditions
severe N/V
frontal headache
visual disturbance
epigastric/RUQ pain
chest pain
SOB
leukocytosis
abnormal coagulation
thrombocytopenia
increased creatinine/uric aid
increased liver enzymes (AST, ALT, LDH, bili)
decreased albumin
fetoplacental (abnormal FHR, IUGR, oligohydramnios, absent/reversed end-diastolic flow)
Maternal signs of severe pre-clampsia
DBP > 110
oliguria <500/day
pulmonary edema
suspected abruptio placenta
Maternal labs for severe pre-eclampsia
platelets <100
elevated liver enzymes (AST/ALT)
plasma albumin <18
heavy proteinuria 3+ or greater
Fetal signs of severe pre-eclampsia
IUGR
oligohydramnios
absent/reversed end diastolic flow of doppler
S/S of eclampsia
**often not observed prior to seizures
severe headache/occipital headache
brisk reflexes
visual disturbances
Severe pre-eclampsia treatment
1:1 nursing
calm, quiet environment
transfer to specialized unit
increased monitoring (HR/BP Q15min/4 hours until stabilized –> Q30min)
oral HTN medication
IV insertion
indwelling catheter (monitor output)
proteinuria testing
I&O documentation
O2 supplementation
VTE prophylaxis
seizure precautions (padded rails)
ensue calcium gluconate/maternal resuscitation equipment ready
Pharmacologic management of severe pre-eclampsia
nifedipine (CCB)
labetolol (beta blocker)
hydralazine (vasodilator)
methyldopa
Magnesium sulfate
seizure prophylaxis
Magnesium sulfate MOA
decreases CNS irritability
blocks Ach release –> blocking neuromuscular conduction
relaxes smooth muscle of uterus (competes w/ calcium)
peripheral vasodilation
increased uterine/renal perfusion
increased prostacyclin from endothelial cells (vasodilation)
reduced platelet aggregation
inhibits RAAS
Magnesium sulfate antidote
calcium gluconate IV
Magnesium sulfate side effects
flushing of skin
hypotension
metallic taste
N/V
palpitations
sweating
Magnesium sulfate toxicity
absent deep tendon reflexes
cardiac arrhythmia
CNS depression
excessive drowsiness
muscle weakness, ataxia
respiraotry depression (<12)
slurred speech
hypocalcemia + tetany (competes with calcium which is needed for muscle contraction)
Eclampsia
new onset generalized tonic-clonic seizures assoc w/ pre-eclampsia
can occur up to 24 hours postpartum
Gestational diabetes
insulin resistance –> diabetes after 20 weeks
Human placental lactogen
produced ~6-30 weeks
antagonist to insulin
increases insulin resistance
GDM & fetal development
macrosomia (>90th percentile)
hyperinsulinemia = decreased surfactant production
increased fetal BMR = fetal hypoxemia = metabolic acidosis
increased erythropoiesis = polycythemia = decreased iron for developing organs = cardiomyopathy, altered neurodevelopment, cardiac remodeling
RF for GDM
age >25
non-white people
PCOS (higher testosterone)
HTN
multiple gestation
family hx
previous macrosomia
Maternal complications of GDM
increased r/o HTN/pre-eclampsia
polyhydramnios
increased r/o future T2DM
Fetal complications of GDM
macrosomia
hypoglycemia
respiratory distress syndrome
hyperbilirubinemia
stillbirth
future obesity
HDN
hemolytic anemia caused by isoimmunization
maternal IgG antibodies attack fetal RBC d/t incompatibility of surface antigens
Types of blood incompatibility
ABO
RH
ABO incompatibility
mild
usually resolves on its own
dose not typically result in severe hyperbilirubinemia
**most common with O- mom
Rh- incompatibility
caused by Rh- mom & Rh+ baby
first pregnancy: maternal IgG antibodies form when mom blood exposed to fetal blood
second pregnancy: maternal IgG antibodies attack fetal RBC
HDN treatment
rhogam (prevention)
phototherapy
exchange transfusion
IV immunoglobulin (reduces hemolysis)
centesis for hydrops fetalis
in utero RBC transfusion
When is rhogam given
28 days
72 hours after birth
Causes of maternal sensitization (HDN)
normal delivery
spontaneous/induced abortion
chorionic villlus sampling
amniocentesis
prenatal hemorrhage
maternal trauma
idiopathic
**only .1 mL needed to activate maternal immune response
HDN complications
anemia
hyperbilirubinemia
kernicterus
growth restriction
hydrops fetalis
HDN complications
hyperbilirubinemia –> acute encephalopathy/kernicterus
symptomatic anemia (pallor, lethargy, tachycardia, tachypnea)
hydrops fetalis
IUGR
HDN tests
DAT (coombs test) measures IgG antibodise
cord blood
IAT
CBC
TCB/serum bili
peripheral blood smear
Maternal hormones that act as insulin antagonists
human sommatotropic hormone (human placental lactogen)
estrogen
progseterone
prolactin
cortisol
insulinase (degrading enzyme)
When does fetus begin secreting insulin
10-14 weeks gestation
Hypoglycemia in pregnancy
<3.2 mmol
Pharmacotherapy GDM
insulin (first-line, doesn’t cross placenta)
metformin (may cross placenta)
glyburide (last resort if intolerant to metformin & refusing insulin)
Hyperglycemia in pregnancy
> 11
Target blood glucose levels in pregnancy
3.8-5.2
(S/S of hypoglycemia may present at <3.8)
Fetal consequences of GDM
hyperinsulinemia –> decreased surfactant/lung maturation, increased growth (macrosomia)
increased O2 demand = increased erythropoiesis = decreased iron (cardiac myopathy/impaired neural development), increased r/o jaundice
abnormal placenta –> preterm, IUGR
perinatal asphyxia/hypoglycemia upon birth
neonatal respiratory distress syndrome
Maternal consequences of GDM
higher longterm r/o of T2DM
DKA
macrosomia –> dystocia –> C/S or hemorrhage
pre-eclampsia/HTN
infection
hypoglycemia (higher risk in early 1-2 trimesters as insulin need decreases)
GDDC
gestational diabetes diet controlled
low glycemic diet
exercise (30 min/daily)
decreased fat/carbs
GDID
gestational diabetes insulin dependent
insulin indicated when glucose targets cannot be maintained on diet/exercise alone
Blood glucose targets in pregnancy
FBG <5.3
1 hour postprandial <7.8
2 hours postprandial <6.7
Ferritin target in pregnancy
> 15
Hemoglobin target in pregnancy
> 105
Entonox
nitrous oxide
Stages of PPH
Stage 1
Stage 2
Stage 3
Stage 1 PPH
> 500 SVD or >1000 CS with continued bleeding + HR higher than SBP
Stage 2 PPH
1000-1500 and HR higher than SBP
Stage 3 PPH
> 1500 blood loss or hemodynamically unstable
anticipated need for 3+ PRBCwithin 1 H or fibrinogen level <2.5 g/L
S/S of neonatal adaptation syndrome
**caused by exposure to SSRI/SNRi in utero
respiratory distress
feeding difficulty
jitteriness
irritabiilty
temperature instability
sleep problems
tremors
shivering
restlessness
convulsions
jaundice
rigidity
hypoglycemia
Onset of NAS
0-3 days
duration 2 weeks
NAS interventions
quiet, low-light enivronment
STS
if s/s toxicity present:
respiratory support
fluid replacement
anticonvulsant therapy
Persistent pulmonary hypertension
failure of pulmonary vasculature to relax after extrauterine transition –> right-to-left shunting of blood thru fetal circulatory pathways
can cause hypoxemia refractory to treatment
SSRI newborn complications
neonatal adaptation syndrome
congenital heart defects
persistent pulmonary hypertension
is breastfeeding contraindicated with SSRIs?
no
NESTS self-care acronym
nutritious food
exercise (daily)
sleep
time for self-care
support
