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Maternal- Newborn & Women's Health Nursing > Chapter 10 Complications of Pregnancy > Flashcards

Chapter 10 Complications of Pregnancy Flashcards

Exam 2

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1
Q

Describe the development & management of hemorrhagioc conditions of early pregnancy, including spontaneous abortion, ectopic pregnancy, & gestational trophoblastic disease.

A
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2
Q

Explain physiology & management of placenta previa and placental abruption.

A
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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.

A
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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

A
  • jeopardy to mother, fetus, or both
  • condition due to pregnancy or result of condition present before pregnancy
  • essential these conditions are IDed early
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15
Q

What are the 3 most common causes of hemorrhage during the first half of pregnancy?

A
  1. abortion
  2. ectopic pregnancy
  3. gestational trophoblastic disease
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16
Q

:explusion of the fetus BEFORE 20wks gestation

A

abortion (AB)

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17
Q

:occur naturally

A

spontaneous abortion

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18
Q

:caused by medical or surgical means

A

induced abortion

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19
Q

:loss of fetus AFTER 20 wks gestation

A

Stillbirth

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20
Q

> 20wks gestation

A

viable

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21
Q

categories of miscarriages

A
  • threatened
  • inevitable
  • incomplete
  • complete
  • missed abortion
  • habitual/ recurrent abortion
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22
Q

miscarriage

vaginal bleeding before 20 wks without dilation

A

threatened

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23
Q

miscarriage

cannot be stopped; possible see ROM and dilation of cervix; natureal expulsion of uterine contents

A

inevitable

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24
Q

miscarriage

some, but not all of the products of conception (retained tissue prevents contraction; D&C; Oxytocin, methylergonovine, misoprostol)

A

incomplete

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25
Q

miscarriage

all fetal tissue is passed, cervix closes, slight bleeding, mild cramping

A

complete

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26
Q

miscarriage

fetus has died in utero, miscarriage has not occurred yet (uterus emptied by most appropriate method for gestational age/ size); <20 wks

A

missed abortion

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27
Q

miscarriage

loss of three or more consecutive pregnancies

A

habitual/ recurrent

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28
Q

Incidence/ Etiology of Spontaneous Abortions (Miscarriages)

A
  • Chromosomal Abnormalities
  • Faulty implantation of placenta
  • Maternal infections/ Maternal diseases
  • Placental abnormalities
  • clotting disorders
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29
Q

: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)

A

chorioamnionitis

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30
Q

expected meds for an incomplate miscarriage (abortion)

A

oxytocin, methylergonovine, misoprostol (to contract and expel contents of uterus)

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31
Q

risk of hemorrhage for which types of miscarriages (abortions)

A

inevitable, incomplete

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32
Q

Assessment question for Spontaneous Abortion (miscarriage)

A
  • 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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33
Q

Management of Spontaneous Abortions (miscarriage)

A
  • 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)
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34
Q

T or F
Most 1st trimester spontaneous abortions result from maternal conditions.

A

False, chromosomal

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35
Q

:implantation of a fertilized ovum in any area other than the uterus; the most common site is the fallopian tube.

A

ectopic pregnancy

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36
Q

physiology of ectopic pregnancies

A
  • 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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37
Q

Ectopic Pregnancy (rupture)

A
  • 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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38
Q

methotrexate

A
  • given IM
  • stops the division of cells
  • folic acid antagonist
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39
Q

education of pt: methotrexate

A
  • NO alcohol
  • cancer drug: double flush (use precautions)
  • no sexual activity while on this med
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40
Q

:spectrum of diseases that includes both benign hydatidiform mole & gestational trophoblastic tumors such as invasive moles & choriocarcinoma

A

gestatioinal trophoblastic disease

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41
Q

pathologic proliferation of trophoblastic cells

A

gestational trophoblastic disease

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42
Q

disorder of placental development

A

hydatidiform mole disorder

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43
Q

neoplasm of trophoblast; a form of cancer

A

choriocarcinoma

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44
Q

initially, clinical picture similar to pregnancy; embryo not viable; no circulation established; no embryonic tissue found

A

gestational trophoblastic disease

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45
Q

Classic signs of gestational trophoblastic disease

A
  • 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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46
Q

therapy for gestational trophoblastic disease

A
  • 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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47
Q

F/U after therapy gestational trophoblastic disease

A
  • 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)
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48
Q

After 20 wks of pregnancy, what are the 2 major causes of hemorrhage?

A

disorders of the placenta called:
* placenta previa
* placental abruption

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49
Q

:abnormal implantation of the placenta in the lower uterus at or very near the cervical os

A

placenta previa

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50
Q

implanted in lower uterus but at least 2cm from cervical os

A

low lying placenta

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51
Q

3 types of placenta previa

A
  • marginal
  • partial
  • complete
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52
Q

What are the clinical manifestations of placenta previa?

A
  • 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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53
Q

Implications of Placenta Previa

A
  • 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
54
Q

Nursing plan for Placenta Previa

A
  • No vaginal exams!
  • Objectively & subjectively assess blood loss, pain, uterine contractility
  • Continuous external monitoring of FHR & uterine activity- NO INTERNAL MONITORING
55
Q

:premature separation of a normally implanted placenta

A

placental abruption (aka: abruptio placenae)

56
Q

bleeding between the placenta and wall of uterus forming a hematoma; patietn and fetus at risk

A

placenta abruption

57
Q

type of Abruptio Placentae

A
  • partial (apparent)
  • partial (concealed)
  • complete
58
Q
  • blood passes between fetal membranes and uterine wall
  • blood escapes vaginally
  • placenta seperates at its edges
A

placenta abruption- partial (apparent)

59
Q
  • placenta seperates centrally (edges intact)
  • blood trapped between placenta and uterine wall
  • concealed bleeding
A

placenta abruption- partial (concealed)

60
Q
  • total separation
  • massive vaginal bleeding
  • both mother and fetus are in jeopardy due to hemorrhaging
A

placenta abruption- complete

61
Q

Signs of a placenta abruption

A
  • vaginal bleeding- dark red
  • severe abdominal pain
  • uterine hyperactivity with poor relaxation between contractions (tachy contractions)
  • uterine tenderness
  • “board-like” abdomen
  • FHR non-reassuring
62
Q

Maternal implications of Abruptio Placentae

A
  • Intrapartum hemorrhage- hypovolemic shock
  • DIC (hemorrhage/ clotting in the wrong spots)
  • Ruptured uterus from overdistention
  • death
63
Q

Fetal- Neonatal Implications of Abruptio Placentae

A
  • Sequelae of prematurity
  • on monitor: late decels, decreasing baseline, absence of accels
  • hypoxia
  • anemia
  • brain damage
  • fetal demise
64
Q

:a pathological condition resulting from a prior disease, injury, or attack

A

sequela/ sequelae

65
Q

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

A

d. relaxed uterus

66
Q

:excessive nausea and vomiting of pregnancy

A

hyperemesis gravidarum (HG)

67
Q
  • 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
A

Hyperemesis Gravidarum (HG)

68
Q

Aim of Tx: HG

A
  • 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)
69
Q

Hypertensive Disorders of Pregnancy

A
  • Gestational Hypertension (during pregnancy)
  • Pre-Eclampsia
  • Eclampsia
  • Chronic Hypertension (prior to pregnancy)
70
Q

blood pressure elevation afte 20wks pregnancy without proteinuria

A

PIH (Pregnancy Induced Hypertension)

70
Q

PIH

A

Pregnancy Induced Hypertension

71
Q

:a hypertensive disorder of pregnancy characterized by new onset of hypertension after 20 wks gestation & multisystem involvement

A

Preeclampsia

72
Q

Pathophysiology: Pre-Eclampsia

A
  • vasospasms of blood bessels impeding bloodflow to plancenta, kidneys, other organs
  • characterized by proteinuria and htn
  • edema from endothelium disruption (increases capillary permeability)
73
Q

Maternal Risks of Pre-Eclampsia

A
  • 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
74
Q

Fetal- Neonatal Risk: Pre-Clampsia

A
  • small for gestational age (SGA)
  • premature
  • hypermagnesemia (magnesium sulfate admin. to mother)
  • increased morbidity & mortality
75
Q

Clincial Manifestations & DX: Mild Clampsia

A
  • BP 140/90 mm Hg or higher
  • 1+ proteinuria may occur
  • Liver enzymes may be elevated minimally
  • Edema may be present
76
Q

Clinical Manifestations & DX: Preclampsia with Severe Features

A
  • 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
77
Q

Clinical Manifestations & DX: Eclampsia

A
  • Grand Mal convulsion (seizure)
  • May occur antepartum, intrapartum, or postpartum
78
Q

mag toxicity

A

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
Q

Home Management of Mild Pre-Eclampsia

A
  • 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
Q

Management of Pre-Eclampsia with Severe Features

A

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)

81
Q

What is the only known cure for Pre-Eclampsia?

A

birth of the fetus and delivery of the placenta

82
Q

Why are corticosteroids given to the mother to manage pre-eclampsia?

A

(<37wk fetus) to accelerate fetal lung maturity (to increase surfacant production)

83
Q

magnesium sulfate: indications

A

prevention & control of seizures in pre-eclampsia with severe features, prevention of uterine contractions in preterm labor, & neuroprotection of preterm fetus

84
Q

magnesium sulfate: classification

A

anticonvulsant

85
Q

mag sulfate: dosage & route

A
  • dosage: IV loading dose 4 to 6g/ 15- 30 min
    1 to 2g / hr (IV piggyback)
  • route: IV
86
Q

Nursing Implications: Mag sulfate admin. for Pre-Eclampsia

A

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

87
Q

magnesium sulfate: mech of action

A

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.

88
Q

Management: Eclampsia

A
  • Anticonvulsants: Bolus of Mag Sulfate
  • Sedation & other anticonvulsants: Dilantin
  • Diuretics to treat pulmonary edema
  • Strict monitoring of I&Os
  • Vigilant fetal monitoring/ contraction pattern
89
Q

Goals of Mag therapy

A
  • no seizures
  • decreased BP
90
Q

:rapidly alternating muscle contraction and relaxation may occur when reflexes are hyperactive

A

clonus

91
Q

Questions to ask client during an assessment for Pre-Elampsia

A
  • “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?”
92
Q

assessing for DTR

A

the patellar or knee-jerk

93
Q

(DTR) Deep Tendon Reflex Rating Scale

A
  • 0: reflex absent
  • +1: reflex present, hypoactive
  • +2: normal reflex
  • +3: brisker than average reflex
  • +4: hyperactive reflex; clonus may also be present
94
Q

HELLP Syndrome

A
  • Hemolysis
  • Elevated Liver Enzymes
  • Low Platelets

Can happen anytime during the pregnancy (>13 wks)

95
Q

H in HELLP Syndrome:

A

Hemolysis- RBCs breaking down when pass through small damaged blood vessels

96
Q

EL in HELLP Syndrome:

A

Elevated Liver Enzymes- hepatic blood flow obstructed by fibrin deposits

97
Q

LP in HELLP Syndrome:

A

Low Platelets- vascular damage resulting from vasospasm –> platelet aggregation at the site of damage
(endothelieal damage caused by ELEVATED, PROLONGED BP)

98
Q

Syptoms of HELLP Syndrome

A
  • pain in the upper right quadrant (epigastric pain; build up of waste products), N/V, possible disorientation
99
Q

Treatment for HELLP Syndrome

A
  • Delivery of Baby!
    -induction but anesthesia choices are tricky
    -magnesium sulfate to prevent seizures
    -BP meds if pre-eclampsia is involved
100
Q

Incompatibility Between Maternal & Fetal Blood

A
  • 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
101
Q

Rh incompatibility

A
  • 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
Q

ABO incompatibility

A

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)

103
Q

Rh- Mother/ Rh+ Father

A
  • 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
104
Q

Testing: Rh factor

A
  • Indirect Coomb’s Test
  • Direct Coomb’s Test
105
Q

Indirect Coomb’s Test

A

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

106
Q

Direct Coomb’s Test

A

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

107
Q

Conditions that complicate pregnancies

A
  • gestational diabetes
  • diabetes mellitus (pre-existing)
108
Q

Gestational Diabetes

A

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
Q

Diabetes Mellitus (pre-existing)

A
  • 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.
110
Q

DM Effects on Pregnant Client

A
  • 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
Q

DM effects on Fetus

A
  • 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)
112
Q

DM effects on Neonate

A
  • HYPOglycemia
  • HYPOcalcemia
  • HYPERbilirubinemia
  • RDS- too much insulin, slow production of surfacant
113
Q

What percentage of pregnant clients are screened for gestational diabetes?

A

100%

114
Q

When is the glucose challenge test done?

A

around 24- 28 wks

115
Q

What is a glucose challenge test (gct)?

A

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
Q

What is a 3 hr oral glucose tolerance test (OGTT)?

A

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.

117
Q

What is considered a positive glucose challenge test?

A

BS >140

118
Q

What is considered the gold standard for diagnosis of gestational diabetes?

A

3 hour glucose challenge

119
Q

Plasma glucose levels are determined at 1, 2, 3 hrs. How is a dx of GDM made?

A

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
Q

Gestational DM Management

A
  • 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
Q

Obesity and pregnancy effects

A
  • 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
Q

TORCH infections

A
  • T- Toxoplasmosis
  • O- other (viral or non-viral
  • R- Rubella
  • C- Cytomegalovirus
  • H- Herpes 1 & 2
123
Q

Toxoplasmosis

A
  • protozoal infection
  • transmitted through undercooked meat, infected cat feces, poor handwashing
  • Spiramycin recommended treatment
124
Q

Group B Streptococcus Infection (group beta strep)

A
  • 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
Q

Cytomegalovirus

A
  • 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
Q

Rubella

A
  • 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
Q

Varicella- Zoster virus

A
  • 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
Q

Herpes simplex virus

A
  • 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
Q

HIV

A
  • 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
Q

COVID-19

A
  • 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

Maternal- Newborn & Women's Health Nursing (19 decks)

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