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Women's Health Test III > Chapter 30: High Risk Newborn: Acquired and Congenital Conditions > Flashcards

Chapter 30: High Risk Newborn: Acquired and Congenital Conditions Flashcards

1
Q

asphyxia in the newborn

A
  • insufficient O2 and excess CO2 in the blood and tissue
    • can occur in utero, at birth, or after birth
  • many causes:
    • maternal: HTN, infection drug use
    • placental conditions: placenta previa, abruption, or postmaturity
    • fetal causes: cord problems, infection, prematurity, multifetal gestation
  • lack of O2 to the cells–>lactic acid production and metabolic acidosis develops when inadequate bicarb available
    • results in ischemia to major organs
  • quick intervention is needed to prevent brain damage and death
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2
Q

what are problems that may occur as a result of asphyxia?

A
  • asphyxia leads to ischemia of major organs; therefore, pulmonary ischemia occurs which results in the inability to produce surfactant–>inc risk of RDS,
  • intrauterine stress may cause passage of meconium and meconium aspiration syndrome
  • hypoglycemia
  • feeding and thermoregulation problems
  • seizures
  • hypoTN
  • pulmonary HTN
  • metabolic acidosis
  • renal problems
  • fluid and electrolyte imbalances
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3
Q

manifestations of asphyxia

A
  • rapid respirations followed by cessation of respirations and a rapid fall in HR
    • stimulation (alone or with O2) may restart respirations
  • if no intervention, gasping respirations may resume until the infant enters a period of secondary apnea
    • in secondary apnea, O2 levels continue to dec, infant loses consiousness, and stimulation is ineffective
  • resuscitative measures must be started immediately
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4
Q

infants at risk for asphyxia

A
  • if complications occurred during pregnancy, labor, or birth
  • if mother received narcotics for analgesia, may depress infant’s CNS
    • if infant has a normal color and HR but depressed respirations, and the mother received opiates w/in 4 hours of birth, given naloxone
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5
Q

neonatal resuscitation

A
  • ABC’s and prevent heat loss
  • ventilate over nose and mouth at 40-60/min
  • do compressions if HR<60 at 90/min
  • maintain thermoregulation
    • warm infant slowly over 2-4 hours as rapid warming can cause apnea
  • umbilical line
  • administer sodium bicarb (to help with acidosis) and epinephrine as ordered
  • use the lowest O2 concentration possible
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6
Q

transient tachypnea of the newborn (TTN)

A
  • infants develop rapid respirations soon after birth from inadequate absorption of fetal lung fluid
    • usually resolves in 24-48 hours
  • risk factors: C/S, macrosomia, multiple gestation, excessive maternal sedation, prolonged or precipitous labor, male gender, maternal diabetes or asthma
  • cause unknown: possibly delay in absorption of fetal lung fluid which means decreased lung compliance and air trapping
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7
Q

manifestation of TTN

A
  • tachypnea w/in 6 hours of birth
  • grunting
  • retractions
  • nasal flaring
  • mild cyanosis
  • CXR: shows hyperinflation, perihilar streaking
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8
Q

TTN: management and nursing considerations

A
  • oxygen
  • gavage feeding when RR is high in order to prevent aspiration and conserve energy
  • watch for signs of sepsis and RDS
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9
Q

meconium aspiration syndrome (MAS)

A
  • condition in which there is obstruction, chemical pneumonitis, and air trapping caused by meconium in the lungs
  • risk factors: asphyxia, post-term, SGA, being compromised with placental insufficiency with decreased amniotic fluid and cord compression
  • causes: MAS occur when hypoxia causes inc peristalsis of the intestines and relaxation of the anal sphincter, so meconium is passed and it is aspirated into the lungs
    • airways can be complete or partially blocked and the obstruction may occur in utero or at birth
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10
Q

severe MAS

A
  • when meconium is below the vocal cords which results in respiratory distress
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11
Q

complications of MAS

A
  • atelectasis: if small airways are completely blocked
  • pneumothorax or pneumomediastinum: occurs when overdistended alveoli (due to air being inhaled but being blocked from exhalation by meconium in the airway) have a leak
  • inhibition of surfactant production–>resp distress
  • chemical pneumonitis
  • persistent pulmonary HTN
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12
Q

manifestations of MAS

A
  • respiratory distress can be mild to severe:
    • tachypnea
    • cyanosis
    • retractions
    • nasal flaring
    • grunting
    • rales
    • barrel shaped chest r/t hyperinflation
  • radiography: patchy infiltrates, atelectasis, consolidation, hyperexpansion
  • yellow green nails, skin, umbilical cord
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13
Q

MAS: management and nursing considerations

A
  • if good APGARs, routine care
  • if poor APGARs, warmed O2, endotracheal tube to remove meconium, ventilation
  • may have to use ECMO if severe MAS which oxygenates blood while bypassing the lungs ot allow the infant’s lungs to rest
  • nurse should notify physician during labor is meconium in fluid
    • NICU RN/neonatologist may be needed for birth
    • be sure O2 and suction are working before birth
  • monitor baby for infection and monitor thermoregulation
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14
Q

Persistent Pulmonary HTN of the Newborn (PPHN)

A
  • condition in which pulmonary vasoconstriction occurs after birth and elevates vascular resistance of the lungs, so it causes a rise in pressure on the right side of the heart–>R to L shunt of unoxygenated blood that flows thru foramen ovale–>aorta: so this blood bypasses lungs and metabolic acidosis occurs which makes for more pulmonary vasoconstriction
    • causes changes to neonatal circulation
    • develops w/in 12 hours
  • causes:
    • most often in term or preterm infants
    • abnormal lung development, maternal use of NSAIDs or SSRIs
    • also assoc with hypoxemia and acidosis from asphyxia, MAS, sepsis, polycythemia, hernia, RDS
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15
Q

PPHN: manifestations

A
  • tachypnea
  • respiratory distress
  • progressive cyanosis that becomes worse with handling/stimulation
  • O2 sats are dec, PaCO2 is inc, acidosis is present
  • echocardiogram indicates R to L shunting of the blood
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16
Q

PPHN: management and nursing considerations

A
  • tx underlying cause of poor oxygenation and relieve vasoconstriction
    • sedation, ventilation, surfactant therapy
    • can use inhaled NO to dilate vessels
    • ECMO
  • maintain thermoregulation to prevent cold stress which will require need for more O2
  • keep handling and noise to a minimum to prevent inc hypoxia
  • assess for hypoglycemia, anemia, acidosis
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17
Q

what is hyperbilirubinemia (pathologic)?

A
  • when total serum bilirubin is >5-6, then jaundice appears
    • it is considered abnormal when the TSB rises more rapidly or to a higher level than expected or remains elevated
  • usually seen during 1st 24 hours
  • may lead to bilirubin encephalopathy which can lead to kernicterus (brain damage from bilirubin toxicity)
    • more likely in infants who have had hypoxemia, resp acidosis, infection, dehydration
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18
Q

causes of hyperbilirubinemia

A
  • hemolytic dz of the newborn is more common cause: caused by Rh or ABO incompatibility of the mom and baby
    • erythroblastosis fetalis: occurs when Rh incompatibility causes the Rh antibodies the mom has formed to cross the placenta, attach to the fetal RBCs, and hemolyze them–>causes severe anemia
      • hydrops fetalis: can result from this if too many RBCs destroyed, causes HF and edema
  • infection
  • hypothyroidism
  • polycythemia
  • G6PD deficiency
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19
Q

therapeutic management of hyperbilirubinemia

A
  • need to prevent bilirubin encephalopathy and kernicterus
  • Rh negative mother has indirect Coombs test to check for antibodies against fetal blood
  • if an infant is jaundiced, a direct coombs test is done using cord blood
    • if positive, this means mother’s antibodies have attached to infant’s RBCs
  • TC bilirubinometers are used to screen the TC bili level–noninvasive
  • frequent feedings–every 2-3 hours
  • phototherapy (infant wears only diaper and covers over the eyes, monitor hydration and temp)
  • exchange transfusions
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20
Q

what are side effects of phototherapy?

A
  • frequent, loose, green stools that result from inc bile flow and peristalsis–>more rapid excretion of bilirubin, but damaging to the skin and causes rapid fluid loss
    • so need to inc fluids in infant by 25% during therapy
  • macular skin rash
  • bronze baby syndrome: grayish brown discoloration of skin and urine
  • rebound TSB of 1-2 when phototherapy ends, but monitor for 24 hours and should not inc more
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21
Q

explain exchange transfusions to treat hyperbilirubinemia

A
  • used when phototherapy cannot reduce bili levels enough quickly
  • this tx removes maternal Abs, unconjugated bilirubin, and antibody coated (sensitized) RBCs
  • provides fresh albumin with binding sites for bilirubin and helps correct severe anemia
  • if Rh incompatibility: use type O, Rh negative blood
  • if ABO incompatibility: use type AB blood, so that there are not A/B antibodes to destroy RBCs
  • complications: electrolytes and acid base imbalance, infection, dysrhythmias, NEC, bleeding, thrombosis, thrombocytopenia, air embolism
  • nurse: prepare equipment, assess infant: cardiac monitor/temperature/etc., teach parents
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22
Q

signs of bilirubin encephalopathy

A
  • lethargy
  • inc or dec muscle tone
  • poor feeding
  • dec or absent Moro reflex
  • high pitched cry
  • opisthotonos
  • seizures
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23
Q

infection in newborns

A
  • can be acquired before, during, and after birth
    • during pregnancy: rubella, CMV, syphilis, HIV, and toxoplasmosis can pass across placenta
      • type of vertical infection
    • during labor: GBS, herpes, hepatitis
      • type of vertical infection
    • after birth: from hospital staff or contaminated equipment, family, visitors
      • type of horizontal infection
      • ie. MRSA
24
Q

sepsis neonatorum

A
  • infection that occurs during or after birth may result in this systemic infection from bacteria in the bloodstream
  • newborns have immature immune systems that react more slowly to invaders
    • they have fewer Abs and are less able to localized infection, so the organism can spread easily from one organ to the next
    • BBB is less effective in preventing entrance of organisms–>CNS infection
25
Q

common causes of sepsis neonatorum

A
  • GBS
  • E. coli
  • coagulase negative Staphylococcus
  • Staph aureus
  • Haemophilus influenze
  • fungi like Candida albicans
26
Q

early vs. late onset of sepsis neonatorum

A
  • early:
    • acquired during birth: from complications of labor like prolonged ROM, prolonged labor, or chorioamnionitis
    • show signs during 1st hours after birth, 90% in 24 hours
    • rapidly progressive, multisystem, high mortality
    • pneumonia and meningitis are often present
  • late:
    • occurs from 8-90 days after birth in healthy term infants or after 72 hours of life in VLBW infants
    • acquired during or after birth
    • usually localed infection such as meningitis
    • serious long term effects
27
Q

diagnosit testing of sepsis neonatorum

A
  • CBC count: will show inc immature neutrophils, sudden change in number of leukocytes
    • elevated IgM
  • cross reactive protein: sign of inflammatory process
    • can check rise and fall as infection improves
  • CXR: differentiate b/w sepsis and RDS
  • glucose levels: unstable with sepsis
28
Q

treatment of sepsis neonatorum

A
  • if GBS +, women receive abx during labor
  • if develop signs of infection, then treat with IV broad spectrum abx
    • and do a culture and sensitivity test in order to determine how to better treat the specific organism
    • commonly use: ampicillin, aminoglycoside, cephalosporin, vancomycin
  • oxygen
  • fluid maintenance
  • monitor glucose
29
Q

complications of sepsis neonatorum

A
  • shock
  • hypo/hyperglycemia
  • electrolyte imbalances
  • problems with thermoregulation
30
Q

risk factors for sepsis neonatorum

A
  • prematurity and low birth weight: MOST IMPORTANT
  • prolonged ROM or labor
  • chorioamnionitis
  • foul smelling amniotic fluid
  • being in the NICU
    • risk of infection in as gestational age and birth weight decrease
31
Q

S/S of infection in the newborn

A
  • early signs are subtle:
    • temp instability
    • respiratory problems
    • changes in feeding or behavior
32
Q

how to prevent infection in a newborn

A
  • handwashing
    • teach parents/visitors also to use good handwashing
  • disinfect equipment
  • sterile technique during invasive procedures
  • minimize handling and trauma to the skin
  • use separate equipment on each infant
  • place infant in incubator which is used as a physical separation
33
Q

nursing considerations with sepsis neonatorum

A
  • prevent infection
  • provide abx
    • obtain labs
    • start IV fluids and administer abx (7-14 days for sepsis, 14-21 days for meningitis)
  • provide supportive care: O2, fluid maintenance, monitor V/S, urine output, gavage feeding
  • support parents
34
Q

infants of diabetic mothers (IDM)

A
  • risk depend on type of diabetes and if well controlled or not
  • high risk of mortality
  • most common problems: cardiac, urinary, GI anomalies; neural tube anomalies; sacral agenesis
    • cardiomegaly is common and may lead to HF
  • insulin acts as a growth hormone–>macrosomia
  • if mom is hyperglycemic, glucose crosses placenta, but the insulin does not, so the glucose causes the fetus to secrete insulin
    • when infant is born, the mother’s glucose no longer is available but insulin remains high, so inc risk of hypoglycemia during first 4 hours
  • higher risk of asphixia, RDS, hypocalcemia, polycythemia, jaundice, and prematurity
35
Q

characteristics of IDM

A
  • infant’s with macrosomia is different from LGA
    • IDM: infant’s size from fat deposits and hypertrophy of liver, spleen, and heart, but the brain and kidneys are normal in size
      • length and head circumference are normal
    • LGA: no enlargement of organs, long with large heads
  • IDM:
    • round face
    • red skin obese body
    • poor muscle tone at rest but becomes irritable and may have tremors when disturbed
36
Q

therapeutic management of IDM

A
  • controlling mother’s diabetes throughout pregnancy to dec complications
  • if infant is large, monitor for shoulder dystocia or cephalopelvic disproportion which may require C/S
37
Q

nursing interventions for IDM

A
  • assess for signs of complications, trauma, and congenital anomalies
  • monitor for hypoglycemia: jitteriness, tremors, hyporeflexia
    • feed infants early and often to prevent this, b/c glucose levels are lowest at 1-3 hours after birth
    • keep glucose above 40 (should be 40-60 mg/dL during first 24 hours)
  • be alert for signs of RDS, cold stress
  • if infant has polycythemia, make sure to provide adequate hydration to prevent sluggish blood flor
  • support parents
38
Q

polycythemia in newborns

A
  • hemoglobin greater than 22 and hematocrit greater than 65%
    • inc viscosity of the blood causes resistance in the blood vessels and dec blood flow to organs–>organ damage from ischemia
    • results in hyperbilirubinemia due to inc RBC breakdown
  • cause: poor intrauterine oxygenation–>fetus makes more RBCs
  • most common in infants who are postterm, LGA, SGA, or have fetal growth restriction
    • also in infants of mothers who smoke, have HTN, or DM
39
Q

manifestations of polycythemia in newborns

A
  • most commonly asymptomatic
  • if symptomatic: plethoric color, lethargy, irritability, poor tone, tremors
    • abdominal distention, dec bowel sounds
    • poor feeding
    • hypoglycemia
    • respiratory distress
    • jaundice
40
Q

polycythemia: management and nursing considerations

A
  • if asymptomatic: observe and administer hydration
  • if HCT above 70%, mayneed partial exchange transfusion
  • phototherapy to tx jaundice
  • monitor bilirubin levels
  • hydrate infants adequately
41
Q

Prenatal drug exposure

A
  • if infants exposed to drugs before birth, may have neonatal abstinence syndrome (NAS)–experience withdrawal
  • most drugs cross placenta
    • early abuse of drugs–>congenital anomalies
    • later abuse of drugs–>poor development or function of organs
  • higher risk of long term cognitive, emotional problems, and SIDS
42
Q

how to identify drug exposed infants

A
  • note lack of prenatal care
  • NAS occurs most often in infants who had opiate exposure prenatally
    • esp if use of heroin, codeine, hydroxyzine, amphetamines, and antidepressants
  • signs are usually present 24-48 hours after birth, but may not occur for up to 4 weeks depending on specific drug, dose, and time of last use
43
Q

NAS

A
  • infants are irritable, have hyperactive muscle tone, and have a high pitched cry
  • they have tremors, but blood glucose is normal
  • infants appear hungry and suck vigorously on fits, but have poor coordination of suck and swallow
  • frequent regurgitation, vomiting, and diarrhea are common
  • restless, excessive energy
  • failure to gain weight
  • seizures may occur
44
Q

therapeutic management of prenatal drug exposure

A
  • rule out other conditions with testing: test for sepsis, hypoglycemia, hypocalcemia, neuro disorders
  • deal with complications like respiratory problems
  • meds: oral morphine, methadone, phenobarbital
    • med dosage is gradually tapered until the infant doesn’t need it anymore
  • gavage/IV feeds b/c suck and swallow reflex is poor
    • may need excess calories due to excessive activity
  • nursing should obtain a urine sample to test for drug exposure if ordered
    • the 1st urination is best!!!
45
Q

nursing care with feeding for drug exposure

A
  • infants often suck frantically on their fists but are unable to coordinate feeding
  • assess the infant’s ability to coordinate suck and swallow with breathing
  • administer gavage feedings if infnat is agitated, breathing rapidly
    • may have inc caloric need due to excess energy, poor sleep
  • quiet, low activity area for feedings to prevent distractions
  • swaddle infants to help prevent startling
  • position infant on right side with HOB elevated to 30-45 deg after feeding
46
Q

nursing care with rest for drug exposed infants

A
  • excessive activity and poor sleep patterns interfere with ability to rest
    • excess muscle tone, tremors, and tendency for excessive energy should be assessed
    • assess what inc or dec irritability
  • keep stimuli to a minimum
    • place crib in quietest corner
  • swaddle infant in flexed position to prevent startling and agitation
  • add new stimuli gradually as able to withstand
  • organize nursing care to preduce handling and disturbances–cluster care
  • use pacifiers for nonnutritive sucking
47
Q

alterations in behavior states of drug exposed infants

A
  • periods of activity delayed for several days
  • disorganized sleep/wake patterns
  • unable to attend to human face and objects
  • exhibits gaze aversion with over stimulation
  • neurologically weaker responses: suck, muscle tone, states of arousal
48
Q

fetal exposure to tobacco

A
  • most common form of substance abuse
  • nicotine causes vasoconstriction, transfers across placenta, and reduces placental blood criculation
    • reduce O2 delivered to fetus
  • maternal effects: dec maternal appetite–>less weight gain, higher risk of abortion, placenta abruption, premature ROM, placenta previa, perinatal mortality
  • infant risks: prematurity, LBW, learning disabilities, asthma, obesity, colic, RDS, nicotine withdrawal, SIDS
49
Q

fetal exposure to caffeine

A
  • causes vasoconstriction of mother’s vessels
  • the half life is 3x longer in pregnancy
  • causes fetal stimulation
    • but teratongenic effects are undocumented
50
Q

fetal exposure to marijuana

A
  • active ingredient: THC–>crosses placenta and accumulates in fetus
  • frequently paired with other drugs
  • reduces O2 available to fetus
  • causes tachycardia and euphoria
  • maternal: anemia, less weight gain
  • infant: tremors, possible motor skill problems, sleep disturbances
51
Q

fetal exposure to antidepressants (SSRIs)

A
  • SSRIs include: prozac, zoloft, celexa
  • prescribed legally for depression and anxiety
    • have to weigh the risks vs benefits
  • Paroxetine is not longer recommended for use b/c of reports of congenital malformations
  • neonatal effects:
    • transient respiratory distress
    • poor tone
    • irritbility
    • PPHN
52
Q

fetal exposuse to alcohol

A
  • most commonly used drug–>easily crosses placenta
  • can cause spontaneous abortion and placental abruption
  • teratogen that can cause FAS: a group of abnormalities resulting from alcohol exposure as a fetus
  • amount and timing influence effects:
    • first trimester: structural defects
    • third trimester: CNS problems
  • binge drinking most dangerous, but no amount of alcohol is safe
53
Q

FAS diagnosis triad

A
  • facial abnormalities
    • microcephaly, short palpebral fissures (openings b/w eyelids), epicanthal folds, flat midface w/ low nasal bridge, indistinct philtrum, thin upper lip
  • prenatal and postnatal growth restrictions
    • noted in length, weight, head circumference
  • CNS impairment
    • includes intellectual disability, learning disability, high activity levels, short attention span, poor short term memory
54
Q

symptoms in neonate of FAS

A
  • sleepiness
  • inconsolable crying
  • abnormal reflexes
  • hyperactivity
  • jitteriness
  • excessive mouthing behaviors
  • hyperactive rooting
  • inc non-nutritive sucking
55
Q

possible long term complication of FAS

A
  • failure to thrive
  • dec ability to block out repetitive stimuli
  • severe mental retardation
  • impulsivity
  • cognitive impairment
  • speech/language abnormalities
56
Q

fetal exposure to cocaine

A
  • powerful short acting CNS stimulant that blocks the reuptake of NE and dopamine which causes hyperarousal, euphoria, sexual excitement, inc alertness
    • causes cardiovascular stimulation and vascoconstriction–>HTN, tachycardia, tremors, anemia, anorexia
    • when euphoria wears off, irritability, exhaustion, lethargy, depression occurs
  • maternal effects:
    • inc risk of STDs and HIV b/c trading sex for drugs
    • b/c of the vasoconstriction–>placental abruption
    • stimulates uterine contractions–>abortion, premature ROM, preterm labor, preeclampsia, fetal hypoxia, meconium staining
  • neonatal effects: CNS signs like lethargy, alternating b/w sleep and agitation, LBW, prematurity, tremors, tachycardia, long term mental/motor/developmental problems
57
Q

fetla exposure to opioids

A
  • these drugs are CNS depressants that cause mental dullness, drowsiness, dtupor
  • intrauterine asphyxia occurs during maternal withdrawal–>fetal withdrawal–>hyperactivity–>inc O2 consumption–>asphyxia
  • mother often has poor health, malnourished, anemic, high risk for STDs/HIV
  • fetal effects: MAS, hypoxia, fetal growth restriction, preterm labor, premature ROM, fetal distress
  • neonatal effects: NAS, LBW, SIDs, neglect/abuse
  • methadone use causes fewer infections, larger birth weight
    • but withdrawal symptoms may be more severe in methodone exposed infants

Women's Health Test III (7 decks)

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