Chapter 10 Complications of Pregnancy Flashcards
Exam 2
Describe the development & management of hemorrhagioc conditions of early pregnancy, including spontaneous abortion, ectopic pregnancy, & gestational trophoblastic disease.
Explain physiology & management of placenta previa and placental abruption.
Discuss the effects & management of hyperemesis gravidarum.
Describe the pathophysiology, effects, and management of hypertensive disorders of pregnancy.
Compare Rh and ABO blood incompatibilities in terms of etiology, fetal & neonatal complications, & management.
Describe the effects of pregnancy on glucose metabolism.
Discuss the effects and management of preexisting diabetes mellitus during pregnancy.
Explain the physiology & management of gestational diabetes mellitus during pregnancy.
Describe the effects of obesity during pregnancy.
Explain the effects of specific anemias & the required management during pregnancy.
Identify the effects, management, and nursing considerations of specificc preexisting autoimmune & neurologic conditions.
Discuss the effects of selected prenatal infections.
Explain nursing considerations for each complication of pregnancy.
high-risk pregnancy
- jeopardy to mother, fetus, or both
- condition due to pregnancy or result of condition present before pregnancy
- essential these conditions are IDed early
What are the 3 most common causes of hemorrhage during the first half of pregnancy?
- abortion
- ectopic pregnancy
- gestational trophoblastic disease
:explusion of the fetus BEFORE 20wks gestation
abortion (AB)
:occur naturally
spontaneous abortion
:caused by medical or surgical means
induced abortion
:loss of fetus AFTER 20 wks gestation
Stillbirth
> 20wks gestation
viable
categories of miscarriages
- threatened
- inevitable
- incomplete
- complete
- missed abortion
- habitual/ recurrent abortion
miscarriage
vaginal bleeding before 20 wks without dilation
threatened
miscarriage
cannot be stopped; possible see ROM and dilation of cervix; natureal expulsion of uterine contents
inevitable
miscarriage
some, but not all of the products of conception (retained tissue prevents contraction; D&C; Oxytocin, methylergonovine, misoprostol)
incomplete
miscarriage
all fetal tissue is passed, cervix closes, slight bleeding, mild cramping
complete
miscarriage
fetus has died in utero, miscarriage has not occurred yet (uterus emptied by most appropriate method for gestational age/ size); <20 wks
missed abortion
miscarriage
loss of three or more consecutive pregnancies
habitual/ recurrent
Incidence/ Etiology of Spontaneous Abortions (Miscarriages)
- Chromosomal Abnormalities
- Faulty implantation of placenta
- Maternal infections/ Maternal diseases
- Placental abnormalities
- clotting disorders
:inflammation of the amniotic sac (fetal membranes); usually caused by bacterial and viral infections. (also called amnionitis or Triple I-intrauterine infection or inflammation of both)
chorioamnionitis
expected meds for an incomplate miscarriage (abortion)
oxytocin, methylergonovine, misoprostol (to contract and expel contents of uterus)
risk of hemorrhage for which types of miscarriages (abortions)
inevitable, incomplete
Assessment question for Spontaneous Abortion (miscarriage)
- s/s = vaginal bleeding? Color and amount? Cramping? Back pain?
- passage of tissue = save any tissue or clots passes and bring with you to facility (appointment)
Management of Spontaneous Abortions (miscarriage)
- could be hospitalized for IVF or blood administration
- dilatation & curettage (D&C)
- Rhogam IF mom is Rh -
- bedrest & abstinence from sex (esp. a threatened)
- psychological needs (grief, guilt)
- cerclage (weak cervix- sewn closed)
T or F
Most 1st trimester spontaneous abortions result from maternal conditions.
False, chromosomal
:implantation of a fertilized ovum in any area other than the uterus; the most common site is the fallopian tube.
ectopic pregnancy
physiology of ectopic pregnancies
- initial symptoms of pregnancy
- postive HCG present in blood and urine and ultrasound to visualize the pregnancy
- chorionic villi (back of the placenta) grow into tube wall or implantation site & establish blood supply
- unilateral severe pain, rupture & bleeding into the abdominal cavity
Ectopic Pregnancy (rupture)
- result is sharp unilateral pain and syncope
- referred shoulder pain or scapular pain
- lower abdominal pain
- HALLMARK SIGN: abdominal pain with spotting within 6-8 wks after missed menses
- DX: transvaginal U/S or laparoscopy
- Medical therapy: intramuscular methotrexalate if tube unruptured
- Surgical therapy: Salpingostomy; Salpingectomy
methotrexate
- given IM
- stops the division of cells
- folic acid antagonist
education of pt: methotrexate
- NO alcohol
- cancer drug: double flush (use precautions)
- no sexual activity while on this med
:spectrum of diseases that includes both benign hydatidiform mole & gestational trophoblastic tumors such as invasive moles & choriocarcinoma
gestatioinal trophoblastic disease
pathologic proliferation of trophoblastic cells
gestational trophoblastic disease
disorder of placental development
hydatidiform mole disorder
neoplasm of trophoblast; a form of cancer
choriocarcinoma
initially, clinical picture similar to pregnancy; embryo not viable; no circulation established; no embryonic tissue found
gestational trophoblastic disease
Classic signs of gestational trophoblastic disease
- Uterine enlargement greater than gestational age; U/S shows vesicles & absence of fetal sac
-
Vaginal bleeding
* Hyperemesis gravidarum- from high hCG levels
therapy for gestational trophoblastic disease
- CXR to detect metastatic disease (risk of it traveling to the lungs)
- uterine curettage for removal of placental fragments (D&C) or vacuum aspiration
- Hysterectomy for excessive bleeding
F/U after therapy gestational trophoblastic disease
- evaluation of hCG levels every 1-2 wks until no longer detectable
- then monthly hCG levels
- No pregnancy for 1 yr! (ed pt- birth control methods)
After 20 wks of pregnancy, what are the 2 major causes of hemorrhage?
disorders of the placenta called:
* placenta previa
* placental abruption
:abnormal implantation of the placenta in the lower uterus at or very near the cervical os
placenta previa
implanted in lower uterus but at least 2cm from cervical os
low lying placenta
3 types of placenta previa
- marginal
- partial
- complete
What are the clinical manifestations of placenta previa?
- bleeding is BRIGHT RED, PAINLESS because it is not occurring in a closed cavity & does not cause pressure on adjacent tissue
- it may be scanty or profuse, and it may cease and recur latert
Implications of Placenta Previa
- if low-lying = woman is allowed labor
- conservative management (considered a high risk pregnancy)
- if profuse bleeding = stat c/s
- changes to FHR
- fetal compromise (hypoxia)
- cesarean birth
Nursing plan for Placenta Previa
- No vaginal exams!
- Objectively & subjectively assess blood loss, pain, uterine contractility
- Continuous external monitoring of FHR & uterine activity- NO INTERNAL MONITORING
:premature separation of a normally implanted placenta
placental abruption (aka: abruptio placenae)
bleeding between the placenta and wall of uterus forming a hematoma; patietn and fetus at risk
placenta abruption
type of Abruptio Placentae
- partial (apparent)
- partial (concealed)
- complete
- blood passes between fetal membranes and uterine wall
- blood escapes vaginally
- placenta seperates at its edges
placenta abruption- partial (apparent)
- placenta seperates centrally (edges intact)
- blood trapped between placenta and uterine wall
- concealed bleeding
placenta abruption- partial (concealed)
- total separation
- massive vaginal bleeding
- both mother and fetus are in jeopardy due to hemorrhaging
placenta abruption- complete
Signs of a placenta abruption
- vaginal bleeding- dark red
- severe abdominal pain
- uterine hyperactivity with poor relaxation between contractions (tachy contractions)
- uterine tenderness
- “board-like” abdomen
- FHR non-reassuring
Maternal implications of Abruptio Placentae
- Intrapartum hemorrhage- hypovolemic shock
- DIC (hemorrhage/ clotting in the wrong spots)
- Ruptured uterus from overdistention
- death
Fetal- Neonatal Implications of Abruptio Placentae
- Sequelae of prematurity
- on monitor: late decels, decreasing baseline, absence of accels
- hypoxia
- anemia
- brain damage
- fetal demise
:a pathological condition resulting from a prior disease, injury, or attack
sequela/ sequelae
Which of the following would the nurse expect to assess in a woman with placenta previa?
a. dark red vaginal bleeding
b. uterine tenderness
c. fetal distress
d. relaxed uterus
d. relaxed uterus
:excessive nausea and vomiting of pregnancy
hyperemesis gravidarum (HG)
- exact cause is unclear
- increased levels of hCG may play a role
- severe cases: causes dehydration
-fluid electrolyte imbalance
-muscle wasting, ketones in urine
-decreased urine output
-ruptured esophagus
Hyperemesis Gravidarum (HG)
Aim of Tx: HG
- control vomiting: antiemetics
-Vit B6 (pyridoxine), Metoclopramide, Ondansetron - Correct fluid & electrolyte imbalance- potassium chloride
- Correct dehydration: IVF with thiamine or multivitamins (banana bag)
- Control enviromental factors (smells, foods, light, sound, temp)
- Diet: clear liquids –> bland foods –> non greasy (encourage frequent, small meals) (ginger, ginger ale)
Hypertensive Disorders of Pregnancy
- Gestational Hypertension (during pregnancy)
- Pre-Eclampsia
- Eclampsia
- Chronic Hypertension (prior to pregnancy)
blood pressure elevation afte 20wks pregnancy without proteinuria
PIH (Pregnancy Induced Hypertension)
PIH
Pregnancy Induced Hypertension
:a hypertensive disorder of pregnancy characterized by new onset of hypertension after 20 wks gestation & multisystem involvement
Preeclampsia
Pathophysiology: Pre-Eclampsia
- vasospasms of blood bessels impeding bloodflow to plancenta, kidneys, other organs
- characterized by proteinuria and htn
- edema from endothelium disruption (increases capillary permeability)
Maternal Risks of Pre-Eclampsia
- Hyperreflexia & headache; visual disturbances
- Decreased renal perfusion: BUN/Cr elevation
- Reduced liver circulation leads to hepatic edema (epigastric pain/ right-sided under ribs; not getting rid of waste well)
- Edema from loss of Protein
Fetal- Neonatal Risk: Pre-Clampsia
- small for gestational age (SGA)
- premature
- hypermagnesemia (magnesium sulfate admin. to mother)
- increased morbidity & mortality
Clincial Manifestations & DX: Mild Clampsia
- BP 140/90 mm Hg or higher
- 1+ proteinuria may occur
- Liver enzymes may be elevated minimally
- Edema may be present
Clinical Manifestations & DX: Preclampsia with Severe Features
- BP 160/110 mm Hg or higher (measurements, 6 hrs apart)
- Proteinuria 300mg in a 24-Hr urine colletion
- Dipstick urine protein 2+ to 3+
- Visual or cerebral disturbances (headaches, seeing spots, blurred vision)
- Epigastric pain
Clinical Manifestations & DX: Eclampsia
- Grand Mal convulsion (seizure)
- May occur antepartum, intrapartum, or postpartum
mag toxicity
hypotension, lethargy, mental confusion, slurred speach, visual distrubances, depressed DTRs, respiratory depression or arrest, adventitous lung sounds, and electrocardiogram changes leading up to cardiac arrest; urine output <30mL/hr; unresponsive
* antedote: Calcium Gluconate
Home Management of Mild Pre-Eclampsia
- Client monitors her BP
- Measures weight daily
- Tests urine protein daily
- Remote NSTs (non-stress test 15/15) performed daily or bi-weekly
- Advised to report signs of worsening pre-eclampsia
Management of Pre-Eclampsia with Severe Features
IN-PT Hospitalization
* Bed rest
* Diet: High-protein, moderate-sodium
* Antihypertensives (Labetalol, Hydralazine, Nifedipine)
* Anticonvulsants: IV Magnesium Sulfate
-Mag level: 4-7 (want a high value)
-Adverse Effects: Toxicity (hypotension, lethargy, mental confusion, slurred speech, visual disturbances, depressed DTRs, respiratory depression or arrest, adventitious lung sounds and electrocardiogram changes leading up to cardiac arrest)
* Corticosteroids
-for baby- to increase surfacant production, as birth is imminent (naturally, artificially, surgically)
What is the only known cure for Pre-Eclampsia?
birth of the fetus and delivery of the placenta
Why are corticosteroids given to the mother to manage pre-eclampsia?
(<37wk fetus) to accelerate fetal lung maturity (to increase surfacant production)
magnesium sulfate: indications
prevention & control of seizures in pre-eclampsia with severe features, prevention of uterine contractions in preterm labor, & neuroprotection of preterm fetus
magnesium sulfate: classification
anticonvulsant
mag sulfate: dosage & route
- dosage: IV loading dose 4 to 6g/ 15- 30 min
1 to 2g / hr (IV piggyback) - route: IV
Nursing Implications: Mag sulfate admin. for Pre-Eclampsia
Monitor: BP closely during admin.
Assess: respiratory rate above 12 bpm, clear bilateral lungs sounds, presence of DTRs, and urinary output greater than 30mL/hr (before admin mag sulfate); after admin- hourly assessments (urine, DTR & clonus, RR, mag levels, decrease environmental stimulation)
Maintain: strict I&Os
Notify provider: insufficient urine output or signs of toxicity occur
Place: resuscitation equipment (suction & oxygen) in the room
Ensure: Calcium Gluconate is readily available
magnesium sulfate: mech of action
blocks neuromuscular transmission of acetylcholine, which decreases the amount liberated & reduces CNS irritability, blocks cardiac conduction, & relaxes smooth muscle, including the uterus, and thus reduces vasoconstriction, possibly resulting in modest BP reduction; decreased vasoconstriction promotes circulation to the vital organs of the pregnant client and increases placental circulation; increased circulation to the kidneys leads to diuresis as interstitial fluid is shifted into the vascular compartment and excreted.
Management: Eclampsia
- Anticonvulsants: Bolus of Mag Sulfate
- Sedation & other anticonvulsants: Dilantin
- Diuretics to treat pulmonary edema
- Strict monitoring of I&Os
- Vigilant fetal monitoring/ contraction pattern
Goals of Mag therapy
- no seizures
- decreased BP
:rapidly alternating muscle contraction and relaxation may occur when reflexes are hyperactive
clonus
Questions to ask client during an assessment for Pre-Elampsia
- “Do you have a headache? Describe it for me.”
- “Do you have any pain in the abdomen? Show me where it hurts, and describe it.”
- “Do you see spots before your eyes? Flashes of light?”
- “Do you have double vision? Is your vision blurred? Does the light bother you?”
- “Are you still able to wear your rings? Did you remove them because your hands were swollen? When did that happen?”
assessing for DTR
the patellar or knee-jerk
(DTR) Deep Tendon Reflex Rating Scale
- 0: reflex absent
- +1: reflex present, hypoactive
- +2: normal reflex
- +3: brisker than average reflex
- +4: hyperactive reflex; clonus may also be present
HELLP Syndrome
- Hemolysis
- Elevated Liver Enzymes
- Low Platelets
Can happen anytime during the pregnancy (>13 wks)
H in HELLP Syndrome:
Hemolysis- RBCs breaking down when pass through small damaged blood vessels
EL in HELLP Syndrome:
Elevated Liver Enzymes- hepatic blood flow obstructed by fibrin deposits
LP in HELLP Syndrome:
Low Platelets- vascular damage resulting from vasospasm –> platelet aggregation at the site of damage
(endothelieal damage caused by ELEVATED, PROLONGED BP)
Syptoms of HELLP Syndrome
- pain in the upper right quadrant (epigastric pain; build up of waste products), N/V, possible disorientation
Treatment for HELLP Syndrome
- Delivery of Baby!
-induction but anesthesia choices are tricky
-magnesium sulfate to prevent seizures
-BP meds if pre-eclampsia is involved
Incompatibility Between Maternal & Fetal Blood
- when a mother is exposed to a RBC antigen that is not on THEIR RBCs, they develop antibodies against it = sensitization
- the antibodies attack & destroy any RBC with that foreign antigen
- in pregnancy, concern is Rh antigen & ABO antigens
Rh incompatibility
- mother is Rh- & baby is Rh +
- problem that affects fetus not mother
- Rh- mother who is sensitized, develops antibodies to destroy Rh+ antigen (therefore, whole RBC destroyed)
- mother has to receive RHOGAM (passive immunity)!!
- if not, erythroblastosis fetalis develops- ANTIBODIES cross placenta and destroy fetal RBCs, causing severe anemia & fetal hydrops
ABO incompatibility
Occurs when pregnant client is type O & the fetus is A, B, or AB
* Types A, B & AB have an antigen that is not present on type O red blood cells
* Mom’s blood contains anti-A & anti-B crosses placenta and attacks baby
* Cord blood taken at delivery to determine blood type of the newborn (direct Coomb’s test)
Rh- Mother/ Rh+ Father
- 1 or 2 drops of fetal blood in the maternal circulation initiates production of antibodies
- During the 3rd stage of labor, damaged placental vessels allow exchange of maternal & fetal blood
- The mother’s body forms additional antibodies after birth
- The mother’s antibodies affect subsequent Rh+ fetuses
Testing: Rh factor
- Indirect Coomb’s Test
- Direct Coomb’s Test
Indirect Coomb’s Test
antibody screen to see if pregnant Rh- patients are sensitized or if there are circulating antibodies in a woman’s blood
* if NEGATIVE- then mom receives Rhogam (no antibodies are present)
* All Rh- women receive Rhogam between 28-32 wks prophylactically
Direct Coomb’s Test
cord blood is taken at delivery to test infant’s blood type, Rh factor
* If baby is Rh+, then mother receives Rhogam again within 72hrs of delivery
Conditions that complicate pregnancies
- gestational diabetes
- diabetes mellitus (pre-existing)
Gestational Diabetes
first recognized during pregnancy, but these patients have a great risk of developing TYPE 2 diabetes later in life
* dx after the 1st trimester
Diabetes Mellitus (pre-existing)
- early pregnancy: n/v occur & cause hypoglycemia
- late pregnancy, placental hormones (estrogen, progesterone, HPL) cause insulin resistance (insulin doesn’t bind to glucose) = hyperglycemia
- blood sugar needs to be CONTROLLED.
DM Effects on Pregnant Client
- hyperglycemia can lead to spontaneous abortion
- UTIs are more common from glucose in urine
- Polyhydraminos: fetus hyperglycemia leads to more urination in utero (increasing amniotic fluid)
DM effects on Fetus
- Congenital malformations (neural tube defects, cardiac defects, & caudal regression syndrome)
- Macrosomia (LGA)- fetus produces extra insulin, acts as growth hormone & extra fat deposits
- Shoulder dystocia at birth- leads to broken clavicle(s)
DM effects on Neonate
- HYPOglycemia
- HYPOcalcemia
- HYPERbilirubinemia
- RDS- too much insulin, slow production of surfacant
What percentage of pregnant clients are screened for gestational diabetes?
100%
When is the glucose challenge test done?
around 24- 28 wks
What is a glucose challenge test (gct)?
a screening procedure only and requires no fasting before the client drinks a 50-g glucose solution and has a serum glucose drawn 1 hour later. No special client instructions are required; to test for gestational diabetes
What is a 3 hr oral glucose tolerance test (OGTT)?
is performed to diagnose diabetes mellitus, including gestational diabetes. The OGTT requires measurement of a fasting blood glucose level followed by intake of 100 g of glucose solution. Blood glucose levels are determined hourly after the solution is taken at 1, 2, and 3 hours. Prior to the test, the client should be instructed to have 3 days of unrestricted diet and activity followed by an 8 hour fast. They should not eat or smoke throughout the test.
What is considered a positive glucose challenge test?
BS >140
What is considered the gold standard for diagnosis of gestational diabetes?
3 hour glucose challenge
Plasma glucose levels are determined at 1, 2, 3 hrs. How is a dx of GDM made?
if two or more of the values meet or exceed the threshold:
* Fasting 95 mg/dL
* 1 hour, 180 mg/dL
* 2 hours, 155 mg/dL
* 3 hours, 140 mg/dL
Gestational DM Management
- not at risk for congenital abnormalities
- fetal affects of hyperglycemia: LGA birth trauma all exist
- Ed pt on diet, glucose monitoring
- Insulin preferred treatment
- NST & more frequent prenatal visits, same as w/ pre-existing DM
- consult a dietician
Obesity and pregnancy effects
- obesity could impact fertility
- increased risk of GDM, c-section, pre-eclampsia
- Recommended weight gain 11-20lbs
- Special equipment needed for labor & delivery
- External monitoring is difficult (due to adipost tissue)
- Risk of venous thromboembolism on PP, poor wound healing
remain respectful & considerate
TORCH infections
- T- Toxoplasmosis
- O- other (viral or non-viral
- R- Rubella
- C- Cytomegalovirus
- H- Herpes 1 & 2
Toxoplasmosis
- protozoal infection
- transmitted through undercooked meat, infected cat feces, poor handwashing
- Spiramycin recommended treatment
Group B Streptococcus Infection (group beta strep)
- colonized vagina, rectum, & urethra in pregnant & nonpregnant pts
- vaginal or rectal culture around 34- 36 wks gestation
- if +, treated DURING labor with PCN G or Cephazolin
Cytomegalovirus
- close personal contact, usually through saliva & urine of children
- daycare centers most common for transmission
- infants with congenital infection could have hearing loss, jaundice, growth restriction, intellectual & physical disabilites
- No treatment, just prevention
Rubella
- congenital rubella spread through droplet/ nasopharyngeal secretions
- cross placenta: cause deafness & growth restriction- most dangerous during first trimester when miscarriage & rubella syndrome are likely
- infants born to patients who had rubella during pregnancy, shed the virus for several months
- MMR vaccine so important
Varicella- Zoster virus
- causes chicken pox, spread through direct contact or respiratory tract
- lays dorment & could cause shingles
- acute infection could cause varicella pneumonia, miscarrriage
- * live vaccine,* so can’t receive during pregnancy
Herpes simplex virus
- gential heropes (simplex 2) but could be caused by type 1
- if pregnant pt has active lesioins, must have C/S
- those with past hx of herpes should be offered antiviral therapy at 36 wks to decrease transmission to neonate
HIV
- no breastfeeding per CDC
- attacks immune system
- transmission can occur during pregnancy, during labor, or breatfeeding
- all patients are tested, if found after conception, start antiretroviral therapy (ART) ASAP
- vaginal birth if viral load low, C/S if viral load high
- newborn & mother should continue with ART after birth
- breastfeeding avoided to prevent transmission
COVID-19
- spread by respiratory droplets
- effects on the fetus still being studied, can become infected after birth if exposed
- breastfeeding is supported as maternal antibodies pass
