Complications of Pregnancy

Question 1

What is Pre-existing HTN?

Answer 1

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

Question 2

What is Gestational Hypertension (GHTN)?

Answer 2

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

Question 3

What is Severe GHTN?

Answer 3

systolic is >160 mmHg or Diastolic >110mmHg
- systole of >160 associated with increased risk of stroke in pregnancy

Question 4

What is risk for Pre-ecamplsia if they have pre-existing or gestational HTN?

Answer 4

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

Question 5

Increased BP values in pregnancy?

Answer 5

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

Question 6

Treatment in pregnancy for pre-existing & gestational HTN?

Answer 6

Beta blockers (labetalol, metropolol)

CCB (nefedipine, methyldopa - centrally acting alpha 2 adrenergic agonist)

hydralazine (direct vasodilator)

Question 7

Meds contraindicated for treatment of pre-existing or gestational HTN?

Answer 7

ACEIs & ARBs
- due to teratogenic & or fetotoxic effects

Question 8

What is Pre-eclampsia?

Answer 8

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

Question 9

Routine nursing eval for pre-eclampsia?

Answer 9

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

Question 10

Risk factors for pre-eclampsia?

Answer 10

• 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

Question 11

Treatments for pre-eclampsia?

Answer 11

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

Question 12

Pathophysiology for developing pre-eclampsia?

Answer 12

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

Question 13

Intervillious soup?

Answer 13

much of the systemic endothelial activation is primarily occuring in this intervillous space where the placental villi meet the maternal blood

Question 14

Aspirin prophylaxis in pre-eclampsia?

Answer 14

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

Question 15

Potential consequences of Pre-eclampsia?

Answer 15

left untreated can progress to eclampsia or HELLP syndrome

Question 16

What is Eclampsia?

Answer 16

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

Question 17

What is the HELLP syndrome?

Answer 17

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

Question 18

What is DIC (Disseminated Intravascular Coagulation)?

Answer 18

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

Question 19

What is Tissue Factor?

Answer 19

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

Question 20

Supportive needs for DIC?

Answer 20

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

Question 21

What is Post-Partum Hemorrhage?

Answer 21

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)

Question 22

How to manage the third stage for PPH?

Answer 22

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

Question 23

Treatment for PPH?

Answer 23

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

Question 24

what is GDM (Gestational Diabetes)?

Answer 24

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

Question 25

Screening for GDM?

Answer 25

urine dipped for glucose
- universal screenign for all pregnant women between 24-28 weeks of gestational age with 50gm oral glucose challenge ( patient doesn’t fast, drinks it & 1 hr layer the serum blood work is drawn)

Blood glucose 7.8-11mmol/L require subsequent confirmatory or diagnostic test

greater than 11.1mmol/L
- immediate diagnosis

associated with fetal hyperinsulinemia, increased birth weight, increased C section rate & increase neonatal hypoglycemia

Question 26

Treatment for GDM?

Answer 26

medical nutritional management
- client educaiton
- freq. CBG

Use of insulin to maintain normal range if it doesnt work

Promising use of oral agents (glyburide, metformin)

Question 27

Pregnancy & blood sugar

Answer 27

Mother has elevated glucose
- glucose cross placenta but insulin does not
- lead to elevated fetal glyucose & increase secretion of inculin from the fetal pancreas
- insulin acts like a GH & result in increased birth weight & incidence of macrosomia (increased case of shoulder dystonia during vaginal delivery which can lead to permanent injury of the brachial plexus)
- to avoid this injury, C section cna be used for suspected macrosomia

C section is not without its own set of potential complications (prolonged recovery time, infection, hemorrhage, damage to adjacent pelvic & abdominal contents & thromboembolism)
- other fetal effects (great risk of unexplained stillbirths but there has been a reduction in perinatal mortality especiallyin pretem labour maybe due to better surveillance & interventions)

• link between increased cases of pre-eclampsia & GDM although patho is unknown

Question 28

Neonatal complications due to GDM

Answer 28

hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia

long-term risk to children born off GDM
- higher risk for impaired glucose tolerance & obesity especially if they were larger during delivery & mother was obese
- breastfeeding mitigate some risk with a low childhood obesity rate

Strategies: return to ideal body weight after delkivery, 25% less chance of developing T2DM