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Pediatrics Exam 1 > Perinatology & Neonatology > Flashcards

Perinatology & Neonatology Flashcards

1
Q

Early term

A

37 0/7 weeks of gestation through 38 6/7 weeks

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2
Q

Full term

A

39 0/7 weeks of gestation through 40 6/7 weeks

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2
Q

Late term

A

41 0/7 weeks of gestation through 41 6/7 weeks

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3
Q

Post term

A

42 0/7 weeks of gestation and beyond)

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3
Q

Perinatal Period:

A

After 28 weeks gestation up to 28 days following birth

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4
Q

Neonatal Period:

A

First 28 days (4 weeks) of life

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5
Q

Ductus venosus

A

O2 rich blood from maternal placenta enters
circulation (bypasses liver) via inferior vena cava
* Connects umbilical vein to
inferior vena cava

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6
Q

Ductus arteriosus

A

~90% of blood bypasses the pulmonary
vasculature directly to the aorta
* Connects the pulmonary
artery & aorta

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7
Q

Foramen ovale

A

O2 rich blood from the Right Atrium directly
to the Left Atrium (right-to-left shunting)
* Opening between the two atria of the fetal heart

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8
Q

Median closure time of ductus arteriosus

A

13.5 hours

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9
Q

Clamping the umbilical cord ___ preload to the left ventricle & ___ cardiac output = _____

A

↓; ↓ ; bradycardia

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10
Q

Delayed cord clamping =

A

After the lungs have aerated
- 30-60 seconds
- Cardiac output should not fall
- Delayed cord clamping should be performed in preterm & term newborns not requiring resuscitation at birth

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11
Q

Delayed umbilical cord clamping in term infants

A

↑ Hgb levels at birth
↑ iron stores during infancy
↑ neurodevelopment at 4 yo

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12
Q

Delayed umbilical cord clamping in pre-term infants

A

↓ need for blood transfusion
↓ intraventricular hemorrhage
↓ necrotizing enterocolitis

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13
Q

When to not delay cord clamp

A
  1. Resuscitation is required
  2. Placental circulation is disrupted by:
    * Abruption
    * Cord avulsion
    * Bleeding placenta previa
    * Vasa previa
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14
Q

Neonates are sensitive to

A

heat loss & retention

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15
Q

How do neonates thermoregulate at birth?

A
  • Temperature has been tightly regulated for 9 months
  • Now dependent mainly on metabolic heat from brown adipose tissue
    Limited, esp. preterm
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16
Q

When is surfactant produced?

A

3rd trimester (28-40 weeks)

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17
Q

Surfactant

A
  • Phospholipid & protein substance ↓ surface
    tension at the liquid-air interface
  • Produced by Alveolar type II cells
  • Without surfactant, ↑ pressure is required
    to inflate & ventilate the lungs
    –Without surfactant → alveoli collapse
  • Production minimally sufficient by 34 weeks gestation
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18
Q

Following birth, the neonate MUST transition from placental to pulmonary
gas exchange, meaning these things must occur:

A
  • Pulmonary vascular resistance must ↓
  • Pulmonary perfusion must ↑
  • Fetal vascular shunts must close to separate systemic & pulmonic circulation
  • Patent Ductus arteriosus & Foremen Ovale
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19
Q

At term, fetal lungs contain _____ of fluid

A

~90 mL (~3 1/8 oz)

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20
Q

How is the fluid from fetal lungs removed?

A
  • Uterine contractions & vaginal birth
    squeeze this from the lungs
    ~1/3 of fluid through nose & mouth
  • Fetal adrenaline stimulates pulmonary
    epithelial cells to stop secreting & start
    reabsorbing lung fluid via Na+ channel
    activation
    -Lung aeration changes the transpulmonary
    pressure gradient & the remaining fluid is
    reabsorbed via capillaries & lymphatics
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21
Q

T/F Pre-mature neonates &/or cesarean born do not experience the “vaginal squeeze” &
experience greater respiratory difficulty

A

T

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22
Q

Neonatal breathing begins within ____
seconds of birth & should be sustained
by ____ seconds

A

30; 90

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23
Q

Steps for newborn resuscitation

A
  1. Dry infant & place under radiant heat, monitor temp.
  2. Position infant to open airway, gentle suction of mouth/nose
  3. Assess respiratory effort (apneic v. gasping v. regular)
  4. Assess heart rate (>100 or <100 beats/min)
    * ↓ HR is the MOST RELIABLE indicator for resuscitation
  5. Gently stimulate (back rub, heel flick) if HR <100 or irregular respiration
  6. If stimulation fails within a few seconds begin bag & mask ventilation
    * More to come in Pediatric Advanced Life Support
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24
Q

How many newborns need resuscitation?

A

~10% require active resuscitation & 1% need extensive care

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25
Q

The APGAR Score

A
  • Time honored method in evaluating the
    newborn infant at time of delivery
  • NOT predictive of long-term outcomes
  • Description of the severity of perinatal
    depression & the need for & response to
    resuscitative efforts
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26
Q

APGAR Levels

A

Assessed at 1 & 5 minutes following birth
7-10 = stable infant
<7 = resuscitative measures continue &
scores assigned q 5 minutes until infant
stabilized
<7 after 3-4 intervals = consider ICU

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27
Q

Ophthalmia neonatorum

A
  • Mucopurulent conjunctivitis of
    newborns
    12% of neonates
    Gonococcal & Chlamydial
    infections = MOST COMMON
  • 1% Silver Nitrate solution or
    0.5% erythromycin ointment
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28
Q

First immunization a newborn will recieve

A

Routine immunization against
hepatitis B
Standard practice prior to d/c for all
medically stable newborns with
birthweights >2000 g

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29
Q

What if the mother is seropositive
for Hepatitis B surface antigen?

A

Neonate is also passively
immunized with Hep
B immune globulin

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30
Q

Vitamin K supplementation in newborns

A
  • Single, IM dose of Vitamin K 0.5 - 1 mg given within 1 hour of birth
    Prevents Vitamin K dependent hemorrhagic disease of the newborn
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31
Q

3 part newborn screening for rare disorders includes

A
  1. Blood sample (heel stick) collected on filter paper
  2. Pulse Oximetry
  3. Hearing Screen

60+ asymptomatic conditions including:
Phenylketonuria (PKU), galactosemia,
hemoglobinopathies, hypothyroidism, cystic fibrosis,
hearing,

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32
Q

Consequences for failure to screen for PKU

A

Phenylketonuria (PKU) → inability to break down the amino acid phenylalanine
Left untreated, PKU → brain damage or death

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33
Q

Consequences for failure to screen for galactosemia:

A
  • Galactosemia → inability to digest galactose, a sugar found in milk
    Builds up in the blood
    Left untreated → seizures, sepsis, liver damage, or death
34
Q

Consequences for failure to screen for hemoglobinopathies

A
  • Hemoglobinopathies → Variety of inherited conditions affecting the number or
    shape of RBCs.
    Some cause life-threatening symptoms, while others do not cause medical
    problems or even signs of the condition
35
Q

Consequences for failure to screen for hypothyroidism

A

Hypothyroidism → thyroid gland does not produce enough thyroid hormone
(What does thyroid hormone do?)
Left untreated → sluggishness, slow growth, & learning delays

36
Q

Consequences for failure to screen for Cystic fibrosis

A
  • Cystic Fibrosis → an inherited disorder of the mucus glands
    Causes excess, abnormally thick, sticky mucus production → variety of
    health problems
    Left untreated → serious lifelong morbidity & early mortality
37
Q

Consequences for failure to screen for hearing loss

A
  • Hearing loss can occur when outer ear,
    middle ear, inner ear, or acoustic nerve do
    not work appropriately
  • Left untreated, hearing loss affects
    development of:
    Speech
    Language
    Social skills
38
Q

Why is there a loss of body weight occurs first
few postnatal days?

A
  • Weight loss of 5-12% is normal
    in first week after birth
  • Predominantly loss of
    extracellular water
  • Inadequate nutritional intake
  • Lag time for maternal breast milk
    engorgemen
39
Q

SGA

A

Small for gestational age or Intrauterine growth restriction (IUGR):
<10th percentile in weight

40
Q

AGA

A

Appropriate for gestational age

41
Q

LGA

A

Large for gestational age or fetal macrosomia
>90th percentile in weight

42
Q

What does it mean when there is a symmmetric growth restriction?

A
  • Weight, length, & head circumference
    ALL ≤10th percentile
  • Symmetric implies an event in EARLY
    pregnancy such as:
    Chromosomal abnormalities
    Drug or alcohol use
    Congenital viral infections
43
Q

What does it mean when there is an asymmetric growth restriction?

A
  • ONLY WEIGHT ≤10th percentile
    Asymmetric implies problem LATE in
    pregnancy such as:
    Pregnancy-induced hypertension
    Preeclampsia
    Placental insufficiency
44
Q

Causes for LGA babies

A
  • Infant of a diabetic mother (IDM)
  • Normal variants:
    Genetic predisposition
    Male fetus
    Post-dates gestation
    Multiparity
45
Q

Effects of LGA on the baby

A

Birth injury (fractures, shoulder dystocia, subdural hemorrhage)
Respiratory Distress Syndrome
Asphxia

45
Q

Infants of diabetic mothers

A

In utero, ↑ flow of nutrients from
hyperglycemia
High glucose loads → fetal
pancreas secretes excessive
amounts of insulin to maintain
neonatal euglycemia

46
Q

All LGA infants should be screened for
_____ while in the hospital

A

hypoglycemia

46
Q

Normal-term infant blood glucose stabilizes at ___ mg/dL 3 hours after birth

A

50-80

47
Q

If signs of hypoglycemia are present, they
are often relatively nonspecific & may be
subtle including

A

Lethargy
Poor feeding
Irritability
Tremulousness/jitteriness
Apnea
Seizures

48
Q

T/F SGA (IUGR) infants can also have hypoglycemia

A

T
Different mechanism = ↓ glucose stores

49
Q

Infant respiratory distress syndrome

A
  • 1% of pregnancies in the US
    50% of deliveries at 26-28 weeks
    30% of deliveries at 30-31 weeks
    More common in premature, Caucasian neonates (m/f)
50
Q

Infant respiratory distress syndrome clinical presentation

A

Progressive, respiratory distress after birth
Tachypnea
Expiratory grunting
Subcostal & intercostal retractions
Cyanosis
Nasal flaring
Possible apnea &/or hypothermia

51
Q

IRDS diagnosis

A
  1. CBC & Blood cultures
  2. Blood gases
  3. Pulse oximetry → should be 90-95%
  4. . CXR
  5. Echocardiogram
52
Q

IRDS management

A
  1. Continuous positive airway pressure
    (CPAP) if spontaneously breathing
  2. Surfactant administration ↓
    mortality rate by 50%
  3. Tx other complications
    (Eg. Pneumothorax)
  4. Fluid & metabolic management to
    ↓ energy & O2 consumption
  5. Possible empiric antibiotics
    (ampicillin & gentamicin)
53
Q

CXR findings for IRDS

A
  1. Bilateral, diffuse, reticular granular or ground-glass appearances
  2. Air bronchograms
    * air-filled brochii on a background of airless lung
  3. Poor lung expansion
54
Q

Meconium composition

A

Sterile, thick, black-green (from bile),
& odorless material in the fetal intestine
Composed of debris
Desquamated cells from the intestine & skin
Gastrointestinal mucin & other intestinal secretions
Lanugo hair
Vernix caseosa
Amniotic fluid

55
Q

Meconium aspiration syndrome epidemiology

A

0.1 - 0.4 of all births
2 - 10% with meconium-stained amniotic fluid
- Etiology (Theory)
Fetal distress → meconium passage in utero followed by aspiration

56
Q

Meconium aspiration pathogenesis

A
  • Aspirated during fetal gasping/initial
    breaths after delivery.
  • Prolonged hypoxia stimulates fetal
    breathing & gasping that can lead
    to inhalation of amniotic in the
    hypopharynx or trachea
57
Q

Meconium aspiration clinical presentation

A
  • Meconium-stained amniotic fluid (often can see staining under finger nails)
    Similar to Respiratory distress syndrome
    Cyanosis
    End-expiratory grunting
    Alar (nasal) flaring
    Intercostal retractions
    Tachypnea
    ↑ anteroposterior chest diameter
    (“Barrel chest”) 2° air trapping
    Auscultated rales & rhonchi
    (in some cases)
58
Q

MAS diagnosis

A
  1. ABGs
  2. Pulse Oximetry
  3. CBC c/ Diff
  4. Blood cultures
  5. CXR
  6. Echocardiogram
59
Q

What would you see on a CXR for meconium aspiration?

A

Air space opacities “Fluffy infiltrates”

60
Q

Echo findings for meconium aspiration

A
  • Pulmonary consolidation with air
    bronchograms
  • Pleural line anomalies & absence
    of the A-line
  • Alveolar-interstitial syndrome or
    B-lines in nonconsolidated regions
61
Q

MAS management

A

Baby → NOT vigorous (depressed respiratory effort or poor muscle tone)
Baby to radiant warmer
Clear the secretions with a bulb syringe
Proceed with the normal steps of newborn resuscitation

62
Q

Start positive pressure ventilation if, after these initial steps are taken, when

A

the baby is:
Not breathing OR
Heart rate is <100 bpm

63
Q

MAS management

A
  • Oxygen therapy with monitoring of blood gases
  • May administer artificial surfactant
  • CPAP or mechanical ventilation
  • Administration of antibiotics may be considered for possible occurrence of
    secondary bacterial pneumonia
64
Q

Persistent pulmonary HTN of newborn (PPHN)

A

Failure to transition to normal circulation, aka persistent fetal circulation

65
Q

PPHN epidemiology

A

0.4-6.8 per 1000 live births
- Etiology
Sustained ↑ pulmonary vascular resistance → pulmonary hypertension
Right to left shunting of desaturated blood through fetal pathways
Patent foramen ovale OR
Patent ductus arteriosus otherwise structurally normal heart

66
Q

PPHN clinical presentation

A

Clinical Presentation
Respiratory distress, 1st 24 hrs
Tachypnea
Retractions
Grunting
Cyanosis

67
Q

Management of PPHN

A
  • Maintain normal body temperature
  • Correction abnormal electrolytes &/or glucose
  • Correct metabolic acidosis
  • Maintain adequate systemic blood pressure
  • ↓ pulmonary vascular resistance
  • Ensuring O2 release to tissues
  • Minimize barotrauma from ↑ O2 & high ventilator pressure settings
68
Q

Transient tachypnea of the newborn (TTN) Epidemiology

A

~1% of newborns some general respiratory distress
33 - 50% have TTN
- Benign, self-limiting condition
- Delayed resorption/clearance of fetal alveolar fluid
- Often occurs in term or near-term infants (Esp. those not “vaginally squeezed”)

69
Q

TTN clinical presentation

A

Signs of respiratory distress shortly after birth
Tachypnea
nasal flaring
grunting
Retractions
Hypoxia
↑ O2 requirement
Cyanosis (extreme cases)

70
Q

CXR findings for TTN

A

↑ lung volume & flat diaphragm
Prominent vascular markings
(sunburst pattern) originating
from the hilum
Fluid in interlobar fissures
Alveolar edema (“Fluffy densities”)

71
Q

When does physiologic jaundice of newborn occur?

A

Begins AFTER 24 hours of life!

72
Q

Physiologic jaundice of newborn pathogenesis

A

Neonate → immature liver → impaired ability to conjugate bilirubin

73
Q

Neonate gut is ____ so very little urobilin is created

A

sterile

74
Q

Symptoms of Acute Bilirubin Encephalopathy

A

Sleepy
Hypotonia
High pitched cry
Retrocollis (arches neck & trunk)
Bicycling/twitching of the hands & feet
Death (respiratory failure or seizure)

75
Q

Remove bilirubin from blood = _____

A

Prevent neurotoxicity (Kernicterus)

76
Q

1st line treatment for physiologic jaundice of the newborn

A

Phototherapy

77
Q

ABO & Rh hemolytic disease is caused by what combination of blood in the mother/baby?

A

Maternal type O blood
+
Baby type A or B

78
Q

Treatment for breastfeeding failure jaundice

A
  • Frequent feeds & adequate hydration
  • Consider phototherapy
    Depends on total serum bilirubin
  • Exchange transfusion, prn
79
Q

SIDS defined

A

Unexplained death < 1 year of age

80
Q

Leading cause of infant
mortality 1 to 12 mo

A

SIDS

81
Q

Risk factors for SIDS

A

Sleeping position & Co-sleeping
Bottle feeding
Maternal smoking (pre & postnatal)
Infant overheating
Soft sleeping surface
Car seat napping (not car travel)

Pediatrics Exam 1 (6 decks)

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