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Pediatrics Exam 2 > High Risk Infants > Flashcards

High Risk Infants Flashcards

1
Q

Level I nursery

A

normal newborn nursery

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2
Q

Level II nursery

A

Intermediate continuing care nurseries (“feeders and growers” – no ventilation)

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3
Q

Level III nursery

A

neonatal intensive care units (NICU); house the sickest and most fragile infants; provide highly specialized care

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4
Q

members of NICU care team

A

attending neonatologists, neonatology fellows, pediatric residents, medical students, nurse practitioners, neonatal nurses, respiratory therapists, discharge/care members, therapists

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5
Q

high risk infants

A

Any newborn who has a high probability of manifesting in childhood a sensory, motor, cognitive/language, or social delay later in life. Any infant at high risk should be followed for up to 1 year in a high-risk clinic. The following could place an infant in a high-risk category:

  • Prematurity
  • Birth weight
  • Pathophysiology
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6
Q

birth weight (3 types)

A

Low Birth Weight (LBW): 3.3-5.5 lbs
Very Low Birth Weight (VLBW): 2.2-3.3 lbs
Extremely Low Birth Weight (ELBW): less than 2.2 lbs

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7
Q

infants with VLBW and ELBW have higher incidence of

A

neurological problems, developmental delay, and decreased intellectual and language abilities. Small for gestational age infants have birth weights below the 10th percentile of published norms.

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8
Q

Asphyxia

A

– an interruption in the exchange of oxygen and carbon dioxide that may occur at birth due to trauma, prolonged labor or compression of the umbilical cord

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9
Q

Asphyxia may result in

A

hypoxic-ischemic encephalopathy (HIE)

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10
Q

hypoxic-ischemic encephalopathy (HIE)

A

HIE is a lesion in the brain that may cause problems later in life, depending on the severity of the HIE. HIE is the leading cause of severe, non-prgressive neurological deficits resulting from pre-natal event.

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11
Q

Brain hypoxia and ischemia from systemic hypoxemia and reduced cerebral blood flow (CBF) are the primary triggering events for HIE and can occur from any mechanism which results in poor blood flow to the fetal brain in utero including

A

1) chorioamnionitis
2) placental abruption
3) chronic maternal hypertension

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12
Q

treatment option for HIE

A

hypothermia (as soon as possible)

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13
Q

clinical signs of HIE at birth

A
  • Stupor, coma, or depressed awake state not attributed to medication
  • Seizures
  • Alternations in tone, posture, reflexes, respiration, and autonomic function
  • Low APGAR scores (ie. 1/1, 1/5, 3/10, 5/15….)
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14
Q

intraventricular hemorrhage (IVH)

A
  • bleeding in/around ventricles in the brain
  • causes: unstable respiratory status, hypoxemia, difficult deliveries, or any stresses that increase blood pressure
  • especially the germinal matrix
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15
Q

prognosis grades I and II IVH

A

generally GOOD prognosis, minimal risk for developing neurological deficits

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16
Q

prognosis grades III and IV IVH

A

higher risk of neurological deficits (cerebral palsy, intellectual disability)

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17
Q

Periventricular leukomalacia (PVL)

A

bilateral white matter lesion of premature infants

  • may result from hypotension, ischemia, and coagulation necrosis at the border of deep penetrating arteries of the middle cerebral artery
  • Decreased blood flow manifests as cystic lesions at the corners of the lateral ventricles. The site of injury affects the descending corticospinal tracts, visual radiations, and acoustic radiations.
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18
Q

risks/common occurrence/co morbidities with PVL

A
  • Other risk factors include hypotension, infections, apnea, ischemic events
  • PVL occurs most commonly in premature infants younger than 32 weeks’ gestation at birth.
  • Children may present with spastic diplegic cerebral palsy have intellectual deficits or visual problems (blindness, strabismus, nystagmus).
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19
Q

Bronchopulmonary Dysplasia (BPD)

A

A chronic lung disease (CLD) in infants. Infants who have an abnormal chest x-ray and continue to require oxygen supplementation after 28 days of life (DOL) are considered to have BPD.

  • commonly seen in ELBW infants.
  • can be caused by trauma, intubation, or prolonged mechanical venitilation.
20
Q

process of BPD

A
  • Damage to ciliary lining of bronchi leads to necrosis
  • Decreased oxygenation leads to chronic hypoxia
  • Now at risk for brain anoxia
  • May predispose infant to neurological disorders
21
Q

impacts of BPD

A
  • Potential long-term developmental problems may be seen such as mild intellectual deficits, motor coordination deficits, visual perceptual functioning
  • Most likely will affect early feeding experiences and typically infants with BPD take longer to achieve full oral feeding (by breast or bottle)
22
Q

treatment of chronic respiratory disorders

A
  • artificial surfactant, supplemental oxygen, ventilator support, and in the more severe cases extracorporeal membrane oxygenation (ECMO).
23
Q

ECMO

A

form of cardiopulmonary bypass that mechanically replaces oxygen in the blood (outside the body) allowing the lungs to rest and mature.

24
Q

Hyperbilirubinemia (jaundice)

A
  • excess accumulation of bilirubin.
  • Bilirubin is a product of the breakdown of hemoglobin from red blood cells.
  • may also be due to maternal-fetal blood group incompatibility which results in excessive hemolysis of red blood cells and, therefore, increased levels of bilirubin.
25
Q

Hyperbilirubinemia may lead

A

KERNICTERUS (Yellow staining of the brain) due to the deposition of bilirubin in the brain, especially in the basal ganglia.

Kernicterus causes neurological damage and can lead to choreoathetosis, rigidity, hypotonia, high-frequency deafness, and intellectual disability.

26
Q

treatment for Hyperbilirubinemia

A

Phototherapy is used to treat hyperbilirubinemia.

Fluorescent lamps are placed above the naked infant, whose eyes are protected by patches, to reduce serum levels of bilirubin.

27
Q

Gastroschisis or Omphalocele

A
  • the 2 most common abdominal wall defects in newborns so that the infant’s intestine or other abdominal organs are outside of the body.
    • Omphalocele – has an overlying membrane and central location
    • Gastroschisis – is typically displaced to the right of the umbilicus and does not have an overlying membrane
28
Q

treatment for Gastroschisis and Omphalocele

A

“sac” or silo protects contents until they are moved backed into the abdominal cavity with surgical closure

29
Q

Necrotizing Enterocolitis (NEC)

A
  • acute inflammatory disease of the bowel.
  • often occurs during the first 6 weeks of life in premature infants weighing less than 2000g.
  • leads to intestinal mucosal ulceration and hemorrhage, necrosis, and epithelial sloughing.
  • May lead to Short Gut Syndrome if part of the bowel must be re-sected.
Clinical signs include:
• Vomiting
• Lethargy
• Abdominal distention
• Bloody stools
30
Q

Retinopathy of Prematurity (ROP)

A
  • abnormal proliferation of blood vessels in the immature part of the retina
  • in severe cases, the blood vessels form scar tissue on the retina which may become detached, leading to severe visual problems or blindness.
  • causes: High levels of administered oxygen and vitamin E deficiency
  • leading cause of childhood blindness
    STAGE 1 = mild and goes away; STAGE V = completely detached retina
31
Q

TORCH-S infections

A

T: Toxoplasmosis
O: other infections (chicken pox, flu)
R: Rubella
C: Cytomegalovirus (common herpes type virus)
H: Herpes (can get at birth through canal; prevent with C section)
S- Syphilis (50% will result in infant death)

32
Q

HIV - pregnancy and birth

A
  • Most mother-to-child transmission (MTCT), estimated to cause more than 90 percent of infections worldwide in infants and children, probably occurs late in pregnancy or during birth.
  • Advances in HIV research, prevention, and treatment have made it possible for many women living with HIV to give birth without transmitting the virus to their babies. Today, if a woman takes HIV medicines as prescribed throughout pregnancy, labor and delivery, and HIV medicines provided to baby for 4-6 weeks, the risk of transmitting HIV can be 1% or less
33
Q

HIV - transmission

A

Without intervention, 5% to 20% of infants breastfed by mothers who are HIV-positive may acquire HIV-infection through breast-feeding

34
Q

HIV - diagnosis

A

all children born to infected mothers have antibodies to HIV, made by the mother’s immune system, that cross the placenta to the baby’s bloodstream before birth and persist for 12-18 months. Because these maternal antibodies reflect the mother’s but not the infant’s infection status, the test for HIV infection is not useful in newborns or young infants.

US guidelines recommend testing at 14 to 21 days of age, at one to two months, and at four to six months.

35
Q

progression of HIV in children

A

About 20 percent of children develop serious disease in the first year of life; most of these children die by age 4. The remaining 80 percent of infected children have a slower rate of disease progression, many not developing the most serious symptoms of AIDS until school entry or even adolescence.

36
Q

characteristics of HIV in children

A
  • Microcephaly and facial anomalies (box-like forehead, wide-spaced eyes, short nose, prominent lips)
  • Signs of infection include:
    • Failure to thrive
    • Weight loss
    • Unstable temperature
    • Opportunistic infections
    • Diarrhea
37
Q

fetal alcohol syndrome

A

most common cause of birth defects that is preventable

38
Q

characteristics of FAS

A
  • facial dysmorphology
  • high incidence of intellectual disability
  • speech and language difficulties
  • motor problems with poor motor control
  • growth deficiency
  • hyperactivity
  • learning disorders
  • minimal brain dysfunction
39
Q

cocaine exposure characteristics

A
  • LBW with intrauterine growth retardation
  • Premature birth
  • Hyper-irritability and “jittery”
  • Failure to thrive
  • Motor/sensory problems
  • Learning disabilities
40
Q

congenital heart defects

A

infant is born with abnormally structured heart or large vessels

41
Q

Ventricular Septal Defect (VSD)

A
  • *The most common cardiac defect**
  • A hole between the right and left ventricles
  • will have a loud heart murmur.
  • Usually treated with medication, but may need surgical intervention if the baby does not gain weight or the defect does not close by itself
42
Q

Hypoplastic Left Heart Syndrome (HLHS) and surgeries

A
  • The left ventricle is hypoplasic (underdeveloped or not functioning)
  • The mitral and aortic valves (semi-lunar) are stenosed or atretic (impassable).
    Multi-staged surgery is completed beginning days after birth.
    • Stage I – Norwood Procedure – at birth
    • Stage II – Glenn Procedure - at 5 to eight months
    • Stage III – Fontan procedure – at ~2 years
43
Q

Tetralogy of Fallot (TOF)

A

“Blue Baby Disease” A combination of 4 different heart defects (tetrology comes from the Greek word “four”).
• Pulmonary stenosis (narrowing)
• Ventricular septal defect
• Overriding of the aorta (the aorta is inappropriately positioned and straddles both the right and left ventricles above the ventricular septal defect)
• Right ventricular hypertrophy (the muscular wall has become thickened and enlarged)

44
Q

Transposition of the Great Vessels (TGV)

A

the origins of the aorta and the pulmonary artery are reversed from a typical presentation. The aorta rises from the right ventricle and the pulmonary artery arises from the left ventricle. Unoxygenated blood is being delivered to the body and the baby’s will appear cyanotic or “blue” soon after birth.

45
Q

Atrial Septal Defects (ASD)

A

a hole in the septum between the right and left atria. Allows a stream of oxygenated blood from the left atrium to cross over to the oxygen depleted blood in the right atrium. Spontaneous closure can occur if defect is very small. Large defects can cause exercise intolerance. Closure of large defects requires surgery, if left untreated permanent damage to the heart and lung vessels can occur.

46
Q

Patent Ductus Arteriosis (PDA)

A

Failure of the PDA to close after birth, higher incidence in premature infants. This allows oxygenated blood from the aorta to flow back through the PDA into the lung vessels producing a heart murmur. May require surgery if the PDA produces respiratory distress
• Ligation – the ductus is “tied off” and closed

47
Q

Relationship of Cardiac Defects to Feeding

A
  1. Expect the infant or child’s appetite, sleeping patterns, and behavior to be altered, especially acutely following surgery.
  2. Infants and children may initially regress in some skills acutely after cardiac surgery (ie. revert to taking the bottle after being weaned away)
  3. Recurrent laryngeal nerve – may be avulsed/stretched, or damaged during heart surgeries. This nerve innervates the vocal cords, can affect infant or child’s ability to protect the airway, especially if the cords are paralyzed in an abducted position. at greater risk for aspiration
  4. The infant child may have long-term cognitive effects from prolonged hypoxia from uncorrected cardiac defects
  5. The infant may have reduced endurance for feeding and may tire before finishing full bottle.

Pediatrics Exam 2 (9 decks)

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