Complications of Pregnancy Flashcards
(28 cards)
What is Pre-existing HTN?
when systolic is >140mmHg or diastolic >90 & this is diagnosed before 20 weeks gestational age
- older literature referes to this as chronic HTN & accounts for 1% pregnancis requiring ongoing medical monitoring
What is Gestational Hypertension (GHTN)?
diastolic >90 mmHg or systolic >140 occurs after 20 weeks gestation
- diastolic is better predictor of Adverse pregnancy outcomes compared to systolic but both are important to monitor during the antenatal period during each visit
- leading cause of maternal morbidity & mortality in Canada with aprx. 15% of maternal deaths attributed
What is Severe GHTN?
systolic is >160 mmHg or Diastolic >110mmHg
- systole of >160 associated with increased risk of stroke in pregnancy
What is risk for Pre-ecamplsia if they have pre-existing or gestational HTN?
HTN & increasing proteinuria
-women with pre-existing HTN have 10-20% risk or if they develop GHTN before 34 weeks they have 35% risk developing pre-eclampsia
Increased BP values in pregnancy?
increase mom’s risk for MI, stroke, heart failure, renal failure
fetus: increased risk for placental complications; poor O2 transfer, placental abruption, fetal growth restriction, preterm birth, death
Treatment in pregnancy for pre-existing & gestational HTN?
Beta blockers (labetalol, metropolol)
CCB (nefedipine, methyldopa - centrally acting alpha 2 adrenergic agonist)
hydralazine (direct vasodilator)
Meds contraindicated for treatment of pre-existing or gestational HTN?
ACEIs & ARBs
- due to teratogenic & or fetotoxic effects
What is Pre-eclampsia?
affects aprx. 1-2% of pregnancies & is a progression of HTN with clinically significant proteinuria (dipstick of >2+ or >30mg/mmol urinary creatinine in a random urine sample or >0.3 g/day in a 24 hr urine)
- adverse conditions such as new/unusual headache, visual disturbances, persistent epigastric pain, chest pain, dyspnea, changing liver enzymes, decreasing platelets
- edema no longer associated with perinatal morbidity or mortality
Routine nursing eval for pre-eclampsia?
dipstick urinalysis for presence of protein & BP measurement at every antenatal visit
- changes in amount of protein from baseline should be documented
-changes suggest progession towards gestational HTn with new onset proteinuria (add exam of the deep tendon reflexes & testing for the presence of clonus, sign of CNS irritabiity)
- clonus serves as predictor of seizure activity
- If G-HTN is suspected, increased fetal surveillance required
- in instances of sudden onset or severe disease, mother may be hospitalized for monitoring (Bp monitoring, I&O & continuous fetal monitoring
Risk factors for pre-eclampsia?
- advanced maternal age (over 40 yrs)
- first continuing pregnancy
- obesity, excessive weight gain in pregnancy
- family or personal history
-interpregnancy interval less than 2 yrs or greater than 10 yrs - use of reproductive tech
- multiple gestation
- elevated Bp at initial prenatal visit
Abotu 35% of women who develop G-HTN before 34 weeks will progress to pre-eclampsia with high perinatal & maternal complications
Treatments for pre-eclampsia?
can begin in the pre-conception period by counseling women considering pregnancy to adopt healthy lifestyle including diet, exercise, controlling any pre-existing hypertension
- depends on gestational age & disease severity, only cure for this is delivery of fetus
Although bedrest is commonly recommended, there is limited evidence to support
control of Bp can be done with use of beta blockers or methyldopa
with addition of pre-eclampsia especially is before 34 weeks gestation (antenatal corticosteroid therapy should be given to all women)
- betamethasone IMx2 to facilitate fetal lung maturation
if after 37 weeks the woman presents with pre-eclampsia often, she proceeds to induciton & delivery to be safe
despite correct treatment some will progress to more serious stage & declien may occur rapidly
Pathophysiology for developing pre-eclampsia?
complex process leads to uteroplacental mismatch
- there is an incomplete trophoblastic invasion & placental implantation causing shallow vessel development
- immunological maladaptation between maternal/paternal & fetal tissue & some state it is suggestive of acute graft rejection which leads to overall poor placentation
- with this mismatch, high #’s of leukocytes. inflammatory cytokines (TNF-alpha, ILs), prostaglandins, with free radicals such as ROS all contribute to oxidative stress
mismatch where feto-placental demands are higher than the maternal supply promotes the inflammatory & anti-angiogenic mediators leading to endothelial activation
- endothelial cells promote a pro-thrombotic & pro-inflammatory state leading to maternal syndrome causing potential end organ damage
Intervillious soup?
much of the systemic endothelial activation is primarily occuring in this intervillous space where the placental villi meet the maternal blood
Aspirin prophylaxis in pre-eclampsia?
Daily low dose aspirin (60-150mg), after the first trimester, reduces incidence of pre-eclampsia in women at risk by at least 10%
- No increase in adverse maternal/fetal health outcomes such as PPH, maternal blood loss, neonatal intercranial or interventricular bleeding
- beenfits include a reduction in IUGR (Intrauterine growht restriction), avg. increase in birth weight of aprx. 130g
- increased risk of placental abruption could not be ruled out
Potential consequences of Pre-eclampsia?
left untreated can progress to eclampsia or HELLP syndrome
What is Eclampsia?
occurs in 1-3 out of 1000 pre-eclamptic patients & includes all features of pre-eclampsia with the addition of seizure activity
- obstetrical emergency
- immediate goal: to stop the seizures & deliver baby
-when mother seizes, uterus is seizing as well
can result in placental abruption (shearing og the placenta from wall of uterus, effectively ending fetu’s blood supply & lifeline)
- prolonge seizure activity can have neurological consequences for mother depending on length
prevention of seizure can be done with magnesium sulfate- non-specific muscle relaxant
peak postnatal occurence is at 3-6 days
What is the HELLP syndrome?
further progression of HTN state of pregnancy which can occur in 10-20% of patients with severe pre-eclampsia & eclampsia
Hemolysis
Elevated Liver Enzymes: inflammation of liver, pain under right ribcage caused by inflammed liver capsule
Low Platelets
- signal impending diroder of clotting status that if kleft unchecked can progress to DIC (disseminated intravascular coagulopathy)
treatment is effecting delivert in safe & timely manner
- vaginalk or c/section delivery occurs ASAP even if fetus is premature as this can progress to DIC
Maternal corticosteroids given for fetal & maternal benefits, blood prodycts such as platelts given if values under 50x10 9?L
What is DIC (Disseminated Intravascular Coagulation)?
major medical complication can occur with pregnancy as well as in sepsis & major trauma
- imbalance between coagulation- ability to clot or make thrombi with fibrinolysis or ability to break down fibrin clots
- both processes are normal & for homeostasis to occur these must balance each other
- coagulation is over-activated, promoting thrombin generation, body consumes clottign factors & platelets leading to abnormal bleeding & even severe hemorrhage
In case of DIC with pre-eclampsia or other obstetrical complications, main initiating factor is over expression of Tissue factor
What is Tissue Factor?
TF with other pro-inflam mediators such as IL-1, IL-6, IL-8 or adhesion molecules continue to facilitate secretion of TF from endothelial cells or monocytes
- Tf is responsible for activating coag cascade (with activation of thrombin)
- normally plasmin works in conjunction with thrombin limiting the fibrin clot as with any injury
- TNF-A stimulates PAI (plasminogen activator inhi=bitor)= limiting plasmis from breaking up any fibrin clots
- continuing witht his spiraling process any inflammation continues to activate more monocytes by a variety of cytokines further expressing TF leading to more fibrin deposition
- microvascular clots in organs & small vessels leading to ischemia or necrosis which further activates inflammatory cytokines, if clots persist, organ failure may result
-direct link with inflammation to the kinin & complement systems (lead to increased vascular perm., decreased BP, shock, further platelet activsation inducing more TF & cytokines)
= overall overwhelming consumption of platelets & clottign factors,m body cant clot, leading to hemorrhage
- can be identified by small petichiae or large hematomas to bleeding from every orifice
Obstetrical populations:
- the risk of placental abruption or PP hemorrhage becomes uncontrollable is high
- if mom deliverys baby & supportive care is available the outcome can be favourable
Supportive needs for DIC?
freq. BP & vital signs, bloodwork, IV access (2 or more large bore catheters, oxygenation, often large #s of blood prodcuts- including packed RBC’s (PRBC), fresh frozen plasma (FFP), platelets & cryoprecipitate, fluids such as NS or RL ensure mom stays warm especially with large numbers of fluids
monitor blood loss
What is Post-Partum Hemorrhage?
excessive bleeding that occurs in the first 24 hrs after delivery
cause by:
- abnormal tone in uterine atony
- over-distention of the uterus, as wilth multiple gestation
-polyhydramnios
- fetal macrosomia
- bladder distension preventing uterine contraction
-prolonged labour
- retained placental tissue
- obestetrical lacerations or trauma
- maternal intrinsic bleeding defects (Von Willebrand’s disease, ITP)
How to manage the third stage for PPH?
third stage (delivery of placenta)
- adminster a dose of oxytocin with the delivery of the anterior shoulder, which can be given IM, IV, IV bolus
- each delivery attendant will have a preferred delivery method & advise nurses prior delivery
monitor vital signs at regular intervals following the delivery
- if excessive bleed occurs, monitor amount by number of pads, towels saturates, weight of items used to staunch flow or by volume should suction be used
Treatment for PPH?
resuscitation to ensure adequate perfusion of O2 to tissues
- assess circulation
- ensure patient IV
- equip. freq. monitor vital signs
uterine massage may be done by experience HCP to promote production of prostaglandins & lead to uterine contractions
Most meds given are uterotonics that promote uterine contractions (oxytocin, ergotamine, misoprostol)
if bleeding cant be stopped, the obstetrician may need to provide direct compression on the uterine wall with uterine packing or using a balloon device
if none of these work, surgery will be needs often needing a hysterectomy as last resort
what is GDM (Gestational Diabetes)?
a;ltered glucose metabolism
- untreated GDM leads to increased maternal/perinatal morbidity while intensive treatment is associated with outcomes similar to general population
In Canada, prevalence is 4% in non-indigenous & 8-18% in indigenous populations
risk factors: previous GDM, previous delivery of macrosomic infant(>4000gm at birth), high risk ethnicity (Hispanic, southeast asian, african) age >35 yrs, Obesity, PCOS
