Chapter 10 Complications of Pregnancy Flashcards
Exam 2 (131 cards)
1
Q
Describe the development & management of hemorrhagioc conditions of early pregnancy, including spontaneous abortion, ectopic pregnancy, & gestational trophoblastic disease.
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2
Q
Explain physiology & management of placenta previa and placental abruption.
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3
Q
Discuss the effects & management of hyperemesis gravidarum.
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4
Q
Describe the pathophysiology, effects, and management of hypertensive disorders of pregnancy.
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5
Q
Compare Rh and ABO blood incompatibilities in terms of etiology, fetal & neonatal complications, & management.
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6
Q
Describe the effects of pregnancy on glucose metabolism.
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7
Q
Discuss the effects and management of preexisting diabetes mellitus during pregnancy.
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8
Q
Explain the physiology & management of gestational diabetes mellitus during pregnancy.
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9
Q
Describe the effects of obesity during pregnancy.
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10
Q
Explain the effects of specific anemias & the required management during pregnancy.
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11
Q
Identify the effects, management, and nursing considerations of specificc preexisting autoimmune & neurologic conditions.
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12
Q
Discuss the effects of selected prenatal infections.
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13
Q
Explain nursing considerations for each complication of pregnancy.
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14
Q
high-risk pregnancy
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- jeopardy to mother, fetus, or both
- condition due to pregnancy or result of condition present before pregnancy
- essential these conditions are IDed early
15
Q
What are the 3 most common causes of hemorrhage during the first half of pregnancy?
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- abortion
- ectopic pregnancy
- gestational trophoblastic disease
16
Q
:explusion of the fetus BEFORE 20wks gestation
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abortion (AB)
17
Q
:occur naturally
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spontaneous abortion
18
Q
:caused by medical or surgical means
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induced abortion
19
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:loss of fetus AFTER 20 wks gestation
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Stillbirth
20
Q
> 20wks gestation
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viable
21
Q
categories of miscarriages
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- threatened
- inevitable
- incomplete
- complete
- missed abortion
- habitual/ recurrent abortion
22
Q
miscarriage
vaginal bleeding before 20 wks without dilation
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threatened
23
Q
miscarriage
cannot be stopped; possible see ROM and dilation of cervix; natureal expulsion of uterine contents
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inevitable
24
Q
miscarriage
some, but not all of the products of conception (retained tissue prevents contraction; D&C; Oxytocin, methylergonovine, misoprostol)
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incomplete
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# miscarriage
all fetal tissue is passed, cervix closes, slight bleeding, mild cramping
complete
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# 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
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# miscarriage
loss of three or more consecutive pregnancies
habitual/ recurrent
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Incidence/ Etiology of Spontaneous Abortions (Miscarriages)
* Chromosomal Abnormalities
* Faulty implantation of placenta
* Maternal infections/ Maternal diseases
* Placental abnormalities
* clotting disorders
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: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
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expected meds for an incomplate miscarriage (abortion)
oxytocin, methylergonovine, misoprostol (to contract and expel contents of uterus)
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risk of hemorrhage for which types of miscarriages (abortions)
inevitable, incomplete
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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)
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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)
34
T or F
Most 1st trimester spontaneous abortions result from maternal conditions.
False, chromosomal
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:implantation of a fertilized ovum in any area other than the uterus; the most common site is the fallopian tube.
ectopic pregnancy
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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
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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
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methotrexate
* given IM
* stops the division of cells
* folic acid antagonist
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education of pt: methotrexate
* NO alcohol
* cancer drug: double flush (use precautions)
* no sexual activity while on this med
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:spectrum of diseases that includes both benign hydatidiform mole & gestational trophoblastic tumors such as invasive moles & choriocarcinoma
gestatioinal trophoblastic disease
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pathologic proliferation of trophoblastic cells
gestational trophoblastic disease
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disorder of placental development
hydatidiform mole disorder
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neoplasm of trophoblast; a form of cancer
choriocarcinoma
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initially, clinical picture similar to pregnancy; embryo not viable; no circulation established; no embryonic tissue found
gestational trophoblastic disease
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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
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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
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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)
48
After 20 wks of pregnancy, what are the 2 major causes of hemorrhage?
disorders of the placenta called:
* placenta previa
* placental abruption
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:abnormal implantation of the placenta in the lower uterus at or very near the cervical os
placenta previa
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implanted in lower uterus but at least 2cm from cervical os
low lying placenta
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3 types of placenta previa
* marginal
* partial
* complete
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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
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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
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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
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:premature separation of a normally implanted placenta
placental abruption (aka: abruptio placenae)
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bleeding between the placenta and wall of uterus forming a hematoma; patietn and fetus at risk
placenta abruption
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type of Abruptio Placentae
* partial (apparent)
* partial (concealed)
* complete
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* blood passes between fetal membranes and uterine wall
* blood escapes vaginally
* placenta seperates at its edges
placenta abruption- partial (apparent)
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* placenta seperates centrally (edges intact)
* blood trapped between placenta and uterine wall
* concealed bleeding
placenta abruption- partial (concealed)
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* total separation
* massive vaginal bleeding
* both mother and fetus are in jeopardy due to hemorrhaging
placenta abruption- complete
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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
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Maternal implications of Abruptio Placentae
* Intrapartum hemorrhage- hypovolemic shock
* DIC (hemorrhage/ clotting in the wrong spots)
* Ruptured uterus from overdistention
* death
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Fetal- Neonatal Implications of Abruptio Placentae
* Sequelae of prematurity
* on monitor: late decels, decreasing baseline, absence of accels
* hypoxia
* anemia
* brain damage
* fetal demise
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:a pathological condition resulting from a prior disease, injury, or attack
sequela/ sequelae
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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
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:excessive nausea and vomiting of pregnancy
hyperemesis gravidarum (HG)
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* 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)
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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)
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Hypertensive Disorders of Pregnancy
* Gestational Hypertension (during pregnancy)
* Pre-Eclampsia
* Eclampsia
* Chronic Hypertension (prior to pregnancy)
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blood pressure elevation afte 20wks pregnancy **without** proteinuria
PIH (Pregnancy Induced Hypertension)
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PIH
Pregnancy Induced Hypertension
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:a hypertensive disorder of pregnancy characterized by new onset of hypertension after 20 wks gestation & multisystem involvement
Preeclampsia
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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)
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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
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Fetal- Neonatal Risk: Pre-Clampsia
* small for gestational age (SGA)
* premature
* hypermagnesemia (magnesium sulfate admin. to mother)
* increased morbidity & mortality
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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
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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
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Clinical Manifestations & DX: Eclampsia
* Grand Mal convulsion (seizure)
* May occur antepartum, intrapartum, or postpartum
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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
79
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
80
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)
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What is the only known cure for Pre-Eclampsia?
birth of the fetus and delivery of the placenta
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Why are corticosteroids given to the mother to manage pre-eclampsia?
(<37wk fetus) to accelerate fetal lung maturity (to increase surfacant production)
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magnesium sulfate: indications
prevention & control of seizures in pre-eclampsia with severe features, prevention of uterine contractions in preterm labor, & neuroprotection of preterm fetus
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magnesium sulfate: classification
anticonvulsant
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mag sulfate: dosage & route
* dosage: IV loading dose 4 to 6g/ 15- 30 min
1 to 2g / hr (IV piggyback)
* route: IV
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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
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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.
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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
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Goals of Mag therapy
* no seizures
* decreased BP
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:rapidly alternating muscle contraction and relaxation may occur when reflexes are hyperactive
clonus
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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?”
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assessing for DTR
the patellar or knee-jerk
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(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
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HELLP Syndrome
* **H**emolysis
* **E**levated **L**iver Enzymes
* **L**ow **P**latelets
Can happen anytime during the pregnancy (>13 wks)
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H in HELLP Syndrome:
Hemolysis- RBCs breaking down when pass through small damaged blood vessels
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EL in HELLP Syndrome:
Elevated Liver Enzymes- hepatic blood flow obstructed by fibrin deposits
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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)
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Syptoms of HELLP Syndrome
* pain in the upper right quadrant (epigastric pain; build up of waste products), N/V, possible disorientation
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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
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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
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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
102
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)
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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
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Testing: Rh factor
* Indirect Coomb's Test
* Direct Coomb's Test
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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
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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
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Conditions that complicate pregnancies
* gestational diabetes
* diabetes mellitus (pre-existing)
108
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
109
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.
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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)
111
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)
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DM effects on Neonate
* HYPOglycemia
* HYPOcalcemia
* HYPERbilirubinemia
* RDS- too much insulin, slow production of surfacant
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What percentage of pregnant clients are screened for gestational diabetes?
100%
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When is the glucose challenge test done?
around 24- 28 wks
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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
116
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.
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What is considered a positive glucose challenge test?
BS >140
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What is considered the gold standard for diagnosis of gestational diabetes?
3 hour glucose challenge
119
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
120
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
121
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**
122
TORCH infections
* T- Toxoplasmosis
* O- other (viral or non-viral
* R- Rubella
* C- Cytomegalovirus
* H- Herpes 1 & 2
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Toxoplasmosis
* protozoal infection
* transmitted through undercooked meat, infected cat feces, poor handwashing
* **Spiramycin** recommended treatment
124
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**
125
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
126
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**
127
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
128
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
129
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
130
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
