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Pediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

How do you evaluate general appearance in a newborn?

A
  • Careful observation
    • Spontaneous activity, passive muscle tone, respirations, abnormal signs (cyanosis, intercostal muscle retractions, meconium staining)
  • Apgar scores
    • Assessment of intrapartum stress & neurologic depression at birth
    • 1-5 min after birth
    • Continue every 5 min until final score _>_7
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2
Q

What are the 5 components of the Apgars?

A
  • Heart rate
  • Respirations
  • Muscle tone
  • Reflex irritability
  • Color
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3
Q

How is the Apgars scored?

  • heart rate
  • respirations
  • muscle tone
  • reflex irritability
  • color
A
  • heart rate
    • 0 - absent
    • 1 - <100/min
    • 2 - >100/min
  • respirations
    • 0 - absent
    • 1 - slow, irregular
    • 2 - good, crying
  • muscle tone
    • 0 - limp
    • 1 - some flexion
    • 2 - active motion
  • reflex irritability (catheter in nose)
    • 0 - no response
    • 1 - grimace
    • 2 - cough, sneeze, cry
  • color
    • 0 - blue, pale
    • 1 - body pink, blue extremities
    • 2 - completely pink
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4
Q

What are the 13 variations in the newborn skin exam?

A
  • Lanugo
  • Vernix caseosa
  • Color
  • Pallor
  • Jaundice
  • Milia
  • Mongolian spots
  • Pustular melanosis
  • Erythema toxicum neonatorum
  • Nevus simplex
  • Nevus flammeus
  • Strawberry hemangiomas
  • Neonatal acne
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5
Q

Lanugo

A

thin hair that covers the skin of preterm infants

minimally present in term infants

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6
Q

Vernix caseosa

A
  • Thick, white, creamy material in term infants
  • Covers large areas of the skin in preterm infants
  • Usually absent in postterm infants
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7
Q

Describe color in newborns

What are some signs of instability?

A
  • Pink a few hrs after birth
  • Acrocyanosis
    • Cyanosis of the hands & feet
    • First 48-72 hrs
    • Cold infant: through 1st mo of life
  • Cutis marmorata
    • Mottling of the skin w/ venous prominence
  • Intermittent signs of vasomotor instability
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8
Q

Pallor

A

neonatal asphyxia, shock, sepsis, anemia

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9
Q

Jaundice

A
  • Abnormal w/i first 24 hrs of birth
  • Frequently seen during first few days after birth
  • Not associated w/ serious disease
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10
Q

Milia

A
  • Very small cysts formed around the pilosebaceous follicles
  • Tiny, whitish papules
  • Nose, cheeks, forehead, chin
  • Disappear w/i a few wks, no treatment
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11
Q

Mongolian spots

A
  • Dark blue hyperpigmented macules
  • Lumbosacral area & buttocks
  • No pathologic significance
  • Hispanic, Asian, African American infants
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12
Q

Pustular melanosis

A
  • Benign transient rash
  • Small, dry superficial vesicles
  • Dark macular base
  • African American infants
  • Differentiation from HSV & impetigo
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13
Q

Erythema toxicum neonatorum

A
  • Benign rash
  • First 72 hrs after birth
  • Erythematous macules, papules, pustules
    • “flea bites”
    • Trunk, extremities (not palms or soles)
  • 50% of full-term infants
  • Lesions filled w/ eosinophils
  • No treatment required
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14
Q

Nevus simplex

A
  • “salmon patch” or telangiectatic nevus
  • Most common vascular lesion of infancy
  • 30-40% of newborns
  • Pink macular lesion
    • Nape of neck (“stork bite”)
    • Upper eyelids
    • Glabella
    • Nasolabial region
  • Often transient
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15
Q

Nevus flammeus

A
  • “port wine stain”
  • Congenital vascular malformation
  • Dilated capillary-like vessels
    • Capillary hemangioma
    • Face or trunk
    • Darker w/ increasing post-natal age
  • Sturge-Weber syndrome
    • Area of opthalmic branch of trigeminal nerve (V1)
    • Intracranial or spinal vascular malformations, seizures, intracranial calcifications
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16
Q

Strawberry hemangiomas

A
  • Benign proliferative vascular tumors
  • 10% of infants
  • First noticed a few days after birth
  • Increase in size after birth
  • Resolve w/i 18-24 mo
  • Compromise airway or vision –> intervention
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17
Q

Neonatal acne

A
  • 20% of newborns
  • Appears after 1-2 wks of life
  • Virtually never present at birth
  • Lesions are comeones
  • Inflammatory pustules & papules may be present
  • No treatment necessary
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18
Q

What are 5 examples of newborn head abnormalities?

A
  • Microcephaly
  • Caput succedaneum
  • Cephalohematomas
  • Craniosynostosis
  • Craniotabes
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19
Q

Microcephaly

A
  • Head circumference below 10th %ile
  • Causes
    • Familial
    • Structural brain malformations
    • Chromosomal & malformation syndromes
    • Congenital infections (CMV, toxo)
    • Fetal alcohol syndrome
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20
Q

Caput succedaneum

A
  • Diffuse edema or swelling of soft tissue of scalp
  • Crosses cranial sutures & the midline
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21
Q

Cephalohematomas

A
  • Subperiosteal hemorrhages
  • Secondary to birth trauma
  • Confined & limited by cranial sutures
  • Involve parietal or occipital bones
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22
Q

Craniosynostosis

A
  • Premature fusion of the cranial sutures
  • Abnormal shape & size of skull
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23
Q

Craniotabes

A
  • Soft areas of the skull w/ “ping-pong ball” feel
  • Occur in the parietal bones
  • Not related to rickets
  • Disappear w/i wks or mo
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24
Q

How are ears inspected in a newborn?

A
  • Must be examined to assess maturity
  • Should be firm & have characteristic shape
  • Inspection for preauricular tags or sinuses
  • Inspection for appropriate shape & location
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25
Q

What does an abnormal red reflex of the retina indicate?

A
  • Cataracts
  • Glaucoma
  • Retinoblastoma
  • Severe chorioretinitis
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26
Q

The nose should be examined immediately to rule out…….

A
  • Unilateral or bilateral choanal atresia
  • Exclude by passing NG tube through nostrils
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27
Q

What are 5 newborn anomalies of the mouth?

A
  • Clefts
  • Micrognathia
  • Macroglossia
  • Neonatal teeth
  • Epstein pearls
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28
Q

What types of clefts can be present in the newborn?

A
  • Clefts of the lip & soft/hard palates
    • Inspection
  • Submucous clefts in the soft portion of the palate
    • Digital palpation
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29
Q

What is micrognathia?

A
  • Small chin
  • Pierre Robin syndrome
    • Micrognathia
    • Cleft palate
    • Glossoptosis: downward displacement or retraction of the tongue
    • Obstruction of the upper airway
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30
Q

What can macroglossia suggest?

A
  • Beckwith-Wiedemann syndrome
    • Hemi-hypertrophy
    • Visceromegaly
    • Macroglossia
  • Hypothyroidism
  • Mucopolysaccharidosis
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31
Q

Where are neonatal teeth typically seen?

A

Area of the lower incisors

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32
Q

Epstein pearls

A
  • Small, white epidermoid-mucoid cysts
  • Found on the hard palate
  • Disappear w/i a few wks
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33
Q

What are 5 abnormalities that can be found on neck & clavicle examination?

A
  • Lateral neck cysts/sinuses
    • Branchial cleft cysts
    • Cystic hydromas
  • Midline clefts or masses
  • Neonatal torticollis
  • Edema & webbing of the neck
    • Turner syndrome
  • Clavicles (rule out fractures)
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34
Q

What are midline clefts/masses caused by?

A
  • Cysts of the thyroglossal duct
  • Goiter
    • Maternal antithyroid medication
    • Transplacental passage of long-acting thyroid-stimulating antibodies
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35
Q

Neonatal torticollis

A
  • Asymmetric shortening of the SCM
  • Results from being in a fixed position in utero
  • Postnatal hematoma from birth injury
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36
Q

Accessory nipples

A
  • Anterior axillary or midclavicular lines
  • May later grow due to glandular tissue
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37
Q

What are some examples of congenital deformities of the chest?

A
  • Pectus carinatum
    • Prominent & bulging sternum
    • Benign
  • Pectus excavatum
    • Depressed sternum
    • Benign
  • Chest asymmetry
    • Absence of formation of ribs
    • More serious
  • Poland syndrome
    • Agenesis of the pectoralis muscle
    • More serious
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38
Q

How is respiratory distress diagnosed?

A
  • Tachypnea (RR >60 breaths/min)
  • Deep respirations
  • Cyanosis
  • Respiratory gruntint
  • Intercostal or sternal retractions
  • Preterm infants: periodic breathing
    • Short, apneic bursts
    • <5-10 seconds
    • No clinical significance
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39
Q

What is the cardiac exam in a newborn?

A
  • Heart rate
    • Normal: 95-180 beats/min
    • Varies during feeding, sleep, crying
  • Rhythm
  • Assessment of murmurs & peripheral pulses
  • Diminished femoral pulses
    • Coarctation of the aorta
  • Increased femoral pulses
    • Patent ductus arteriosus
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40
Q

What are 6 possible anomalies on abdominal examination of the newborn?

A
  • Diastasis recti
  • Umbilical hernia
  • Omphalocele & gastroschisis
  • Persistent urachus
  • Meconium plug, meconium ileus
  • Abdominal mass
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41
Q

The umbilical cord should be inspected to confirm the presence of _______ & _______ and the absence of the ________.

A

2 arteries & 2 vein

absence of a urachus

1 umbilical artery = congenital renal anomalies

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42
Q

What is Diastasis recti?

A
  • Separation of the L & R side of the rectus abdominus at the midline of the abdomen
  • Premature & African American infants
  • No treatment necessary
    • Diastasis recti disappears
    • Rectus abdominis muscles grow
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43
Q

What is an umbilical hernia?

A
  • Incomplete closure of the umbilical ring
  • Soft swelling beneath skin around umbilicus
  • Protrudes during crying or straining
  • African American children
  • No treatment, closes spontaneously
  • Persistance >4-5 YO
    • Surgery
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44
Q

What is a persistent urachus?

A
  • Complete failure of the urachal duct to close
  • Fistula btwn bladder & umbilicus
  • Urine drains from umbilicus (pressure)
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45
Q

Meconium plug vs. meconium ileus

A
  • Meconium plug
    • Obstruction of the L colon & rectum
    • Dense dehydrated meconium
  • Meconium ileus
    • Occlusion of the distal ileum
    • Inspissated (thick/dry) & viscid meconium
    • Deficiency of pancreatic enzymes
    • High protein content of intestinal secretions
  • Manifestations of cystic fibrosis
    • Delay in elimination: abd distension
    • Normal meconium w/i 24 hrs of birth (90%)
    • w/i 48 hrs (99%)
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46
Q

What can abdominal masses be caused by?

A
  • Hydronephrosis (most common)
  • Multicystic kidneys
  • Ovarian cysts
  • Liver on L side
    • Situs inversus
    • Asplenia
    • Polysplenia syndrome
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47
Q

The anus must be examined for……

A
  • Patency
    • Soft rubber catheter
    • Rectal thermometer
  • Imperforate anus
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48
Q

What are 2 newborn abnormalities of female genitalia?

A
  • Hypertrophied clitoris
  • Hydrometrocolpos
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49
Q

What causes a hypertrophied clitoris?

A
  • Virilization from androgen excess
  • Virilizing adrenal hyperplasia
  • Premature infants
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50
Q

What causes hydrometrocolpos?

A
  • Imperforate hymen w/ retention of vaginal secretions
  • Small cyst btwn labia at the time of birth [OR]
  • Lower midline abdominal mass during childhood
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51
Q

What are 4 newborn abnormalities of male genitalia?

A
  • Hypospadias
  • Epispadias
  • Hydrocele
  • Cryptorchidism
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52
Q

What is hypospadias?

A
  • Urethral meatus on the ventral surface of the penis in varying locations along the shaft
  • Not associated w/ increased incidence of associated urinary malformations
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53
Q

What is epispadias?

A
  • Urethral meatus located on the dorsal surface of the penis
  • Often associated w/ bladder extrophy (bladder protrusion from the abdominal wall w/ exposure of its mucosa)
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54
Q

What is a hydrocele?

A
  • Scrotal swelling caused by fluid accumulation in the tunica vaginalis adjacent to the testis
  • Isolated hydroceles do not cause clinical problems usually (resolve spontaneously)
  • Some hydroceles associated w/ inguinal hernias
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55
Q

What is cryptorchidism?

A
  • Undescended testes
  • Associated with:
    • Inguinal hernia
    • GU malformations
    • Hypospadias
    • Genetic syndromes
  • Most males have testes descend spontaneously before 12 mo
  • Testes that don’t descend by this age are predisposed to future malignancy
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56
Q

Absence or hypoplasia of the radius may be associated with……

A
  • TAR syndrome
    • Thrombocytopenia Absent Radii
  • Fanconi anemia
  • Holt-Oram syndrome
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57
Q

Polydactyly may occur as an isolated anomaly or as part of a ________.

A

genetic syndrome

58
Q

Edema of the feet w/ hypoplasia nails is characteristic of …….

A

Turner & Noonan syndromes

59
Q

Rocker bottom feet is frequently seen in…..

A

trisomy 18

60
Q

The hips of a newborn should be examined for…..

A

developmental dysplasia of the hips

61
Q

What should a newborn spine be examined for?

A
  • Spina bifida: hair tufts, lipomas, dimples in lumbosacral area
  • Sacrococcygeal pilonidal dimple
    • Identify base to rule out cutaneous sinus tract
  • Myelomeningocele
    • Hernial protrusion of the cord & its meninges through a defect in the vertebral canal
    • Anywhere along the spine
    • Obvious at birth
62
Q

What does the neuro exam of a newborn consist of?

A
  • Evaluation of muscle tone
  • Level of alertness
  • Primitive reflexes
63
Q

Preterm delivery

  • definition
  • incidence
  • complications
A
  • <37 completed wks from 1st day of last period
  • 7% of all births
  • High in lower SES populations & women w/o prenatal care
  • Complications from time of birth to 1st several wks of life
64
Q

Post-term delivery

definition

complications

A
  • _>_42 wks from 1st day of last period
  • Complications: increased incidence of fetal & neonatal mortality & death from consequences of placental insufficiency
    • Severe intrauterine asphyxia
    • Meconium aspiration syndrome
    • Polycythemia
65
Q

What are some frequent problems of pre-term infants?

A
  • Disrupted mother-father-infant interaction
  • Perinatal asphyxia
  • Hypothermia
  • Hypoglycemia
  • Hypocalcemia
  • RDS (hyaline membrane disease, surfactant deficiency syndrome)
  • Fluid & electrolyte abnormalities
  • Indirect hyperbilirubinemia
  • Patent ductus arteriosus
  • Intracranial hemorrhage
  • Necrotizing enterocolitis
  • Infections
  • Retinopathy of prematurity
  • Bronchopulmonary dysplasia
  • Anemia
66
Q

Small for gestational age infants & IUGR

definition

significance

A
  • Infants born weighing <5th %ile for corresponding gestational age as a result of IUGR
  • SGA is a sign that IUG has stopped or slowed significantly some time during pregnancy
67
Q

What are the 3 types of IUGR?

A
  • Early interference w/ fetal growth from conception to 24 wks gestation
  • Intrauterine malnutrition from 24-32 wks gestation
  • Late intrauterine malnutrition after 32 wks gestation
68
Q

Early interference w/ fetal growth from conception to 24 wks gestation

A
  • Chromosomal anomalies
    • Trisomy 21, 13-15, 18, etc.
  • Fetal infections (TORCH)
  • Maternal drugs
    • Chronic alcoholism, heroin
  • Maternal chronic illness
    • HTN, severe DM
69
Q

Intrauterine malnutrition from 24-32 wks gestation

A
  • Inadequate intrauterine space
    • Multiple pregnancies
    • Uterine tumors
    • Uterine anomalies
  • Placental insufficiency from maternal vasc. dis.
    • Renal failure
    • Chronic essential HTN
    • Collagen vascular diseases
    • Pregnancy-induced HTN
  • Small placenta w/ abnormal cellularity
70
Q

Late intrauterine malnutrition after 32 wks gestation

A
  • Placental infarct or fibrosis
  • Maternal malnutrition
  • Pregnancy-induced HTN
  • Maternal hypoxemia (lung disease, smoking)
71
Q

What are the clinical problems for small-for-gestational-age infants?

A
  • Perinatal asphyxia
  • Hypothermia
  • Hypoglycemia
  • Polycythemia
  • Thrombocytopenia
  • Meconium aspiration syndrome
  • Intrauterine fetal death
  • Hypermagnesemia
    • Mom treated w/ Mg for HTN or preterm labor
72
Q

What is the definition of a large-for-gestational-age infant?

A
  • Birth weight >90th %ile for gestational age at birth
  • Should be distinguished from those born w/ high birth weight (>4,000 g)
  • Newborn can be LGA w/ birth weight >90th %ile withouth being >4,000g
73
Q

What is the etiology of LGA infants?

What are the complications?

A
  • Causes of increased weight & LGA
    • Maternal DM
    • Beckwith-Wiedemann syndrome
    • Prader-Willi syndrome
    • Nesidioblastosis (diffuse proliferation of pancreatic islet cells)
  • Complications
    • Hypoglycemia
    • Polycythemia
    • Congenital malformations
74
Q

Cyanosis

definition

clinical significance

A
  • Bluish discoloration of skin & mucous membranes
  • Directly related to absolute concentration of unoxygenated or reduced Hgb
  • >3 g/dL of reduced Hgb in arterial blood
  • >5 g/dL in capillary blood
  • Cyanosis = EMERGENCY
75
Q

What is the etiology of cyanosis in a newborn?

A
  • Respiratory pathology (pneumothorax)
  • “5 T’s” of cyanotic congenital heart disease
    • Tetralogy of Fallot
    • Transposition of the great vessels
    • Truncus arteriosus
    • Tricuspid atresia
    • Total anomalous pulmonary venous conn.
  • CNS pathology (intraventricular hemorrhage)
  • Hematologic disorders (polycythemia)
  • Metabolic disorders (hypoglycemia, hypocalcemia, hypothyroidism, hypothermia)
76
Q

What are the initial steps in evaluation of cyanosis in a newborn?

A
  • Detailed hx & physical
  • Serum electrolytes w/ serum glucose
  • ABG, + 100% oxygen test
  • CBC, CXR
  • Sometimes:
    • Cultures
    • Pre/post-ductal PaO2
    • ECG, EKG
77
Q

What is the 100% oxygen test?

A
  • ABG performed after admin of 100% O2
  • Evaluates whether cyanosis is caused by cardiac or respiratory disease
78
Q

100% oxygen test in infants with heart disease

A
  • Reduced pulmonary blood flow (TOF)
    • Increases the PaO2 slightly
    • <10-15 mmHg
  • Normal/increased pulmonary blood flow (TA)
    • PaO2 increases >15-20 mmHg
    • Levels >150 mmHg unusual
79
Q

100% oxygen test in infants with lung disease

A
  • PaO2 increases considerably (>150 mmHg)
  • Exception
    • Severe lung disease
    • Persistant pulmonary HTN of newborn
    • Large R-L shunts through foramen ovale or ductus arteriosus
    • PaO2 may not increase by >10-15 mmHg
80
Q

How is cyanosis managed?

A
  • Administration of oxygen
  • Rapid correction of abnormalities of temperature, hematocrit, glucose & calcium levels
  • Severely cyanotic infants
    • Intubation & mechanical ventilation
81
Q

What are the 3 most common causes of respiratory distress in newborns?

A
  1. Respiratory distress syndrome (RDS)
    1. Hyaline membrane disease
    2. Surfactant deficiency syndrome
  2. Meconium aspiration syndrome (MAS)
  3. Persistent pulmonary HTN of the newborn
    1. Full-term infants
82
Q

What are the clinical features of respiratory distress?

Etiology?

A
  • Features
    • Tachypnea
    • Decreased air entry or gas exchange
    • Retractions (intercostal, subcostal, suprasternal)
    • Grunting
    • Stridor
    • Flaring of the alae nasi
    • Cyanosis
  • Many conditions that produce neonatal respiratory distress are not primary diseases of the lungs
83
Q

What is Respiratory Distress Syndrome?

A

Respiratory distress or respiratory insufficiency caused by lack of surfactant (preterm infants)

84
Q

Differential Diagnosis of Respiratory Distress

Infections

A
  • Sepsis
  • Meningitis
  • Pneumonia
85
Q

Differential Diagnosis of Respiratory Distress

Hematologic Pathology

A
  • Anemia
  • Polycythemia
86
Q

Differential Diagnosis of Respiratory Distress

Cardiovascular Pathology

A
  • Congenital heart disease
  • Cardiomyopathies
  • Myocarditis
  • Arrythmias
87
Q

Differential Diagnosis of Respiratory Distress

Respiratory Pathology

A
  • Lungs
    • BPD
    • RDS
    • MAS
    • PPHN
    • TTN
  • Airways
    • Choanal atresia
    • Pierre Robin Syndrome
    • Laryngo-tracheomalacia
    • Vocal cord paralysis
88
Q

Differential Diagnosis of Respiratory Distress

CNS Pathology

A
  • Intraventricular hemorrhage
  • Apnea
  • Congenital lesions
  • Meningoencephalitis
89
Q

Differential Diagnosis of Respiratory Distress

Abdominal Pathology

A
  • Omphalocele
  • Gastroschisis
  • Ascites
  • Diaphragmatic hernia
90
Q

Differential Diagnosis of Respiratory Distress

Metabolic Pathology

A
  • Hypoglycemia (DM)
  • Hypothermia
  • Metabolic acidosis
  • Inborn errors of metabolism
91
Q

What is the function of pulmonary surfactant?

When are infants less susceptible to RDS?

A
  • Pulmonary surfactant
    • Decreases alveolar surface tension
    • Prevents atelectasis
  • Surfactant noted at 23-24 wks gestation
  • Sufficient quantity produced at 30-32 wks gestation (RDS decreases after this period)
92
Q

How can fetal lung maturity be assessed?

A
  • Presence of surfactant in amniotic fluid obtained by amniocentesis
  • Lecithin-to-sphingomyelin (L:S) ratio >2:1 PLUS presence of phosphatidylglycerol (minor phospholipid in surfactant) are indicators of fetal lung maturity
93
Q

What is the incidence of RDS?

A
  • 0.5% of all neonates
  • Most frequent cause of respiratory distress in preterm infants
  • Higher incidence: white males
  • Risk higher the younger the gestational age
    • <30 wks = 50% risk
    • 35-36 wks = 10%
94
Q

What are the risk factors for RDS?

A
  • Low L:S ratio
  • Prematurity
  • Mother w/ previous preterm infant w/ RDS
  • Mother w/ DM
  • Neonatal hypothermia
  • Neonatal asphyxia
95
Q

What are the clinical features of RDS?

A
  • Increasing respiratory distress first 24-48 hrs
  • Tachypnea
  • Retractions
  • Expiratory grunting
  • Cyanosis
  • More severe & prolonged features in preterm infants <31 wks
96
Q

How is RDS evaluated?

A

CXR

  • Diagnostic
  • Diffuse atelectasis w/ increased density in both lungs
  • Fine, granular, ground-glass appearance
  • Small airways filled w/ air
  • Increased density of pulmonary field
  • “air bronchograms”
97
Q

How is RDS managed?

A
  • Supplemental oxygen
  • CPAP
    • Maintains positive end-expiratory pressure greater than atmospheric pressure
    • Promotes air exchange
    • Nasal prongs or nasopharyngeal tubes
  • Mechanical ventilation
    • If hypercarbia & respiratory acidosis
  • Exogenous surfactant in trachea often curative
98
Q

What are some acute complications of RDS?

A
  • Air leaks
    • Pneumothroax, pulmonary interstitial emphysema
  • Intraventricular hemorrhage
  • Sepsis
  • R-L shunt across PDA
99
Q

What are some chronic complications of RDS?

A
  • Bronchopulmonary dysplasia (BPD)
  • Retinopathy of prematurity
100
Q

What is bronchpulmonary dysplasia (BPD)?

How is it diagnosed?

A
  • Chronic lung disease
  • Progressive pathologic changes in the immature lung (affecting parenchyma & airways, altering normal lung growth)
  • Diagnosis:
    • Mechanical ventilation 1st 2 wks of life
    • Clinical signs of resp compromise
    • Need for supp O2 >28 days of life
    • Characteristic CXR
101
Q

With aggressive treatment in the NICU, >___% of infants with RDS survive

102
Q

What is Persistent Pulmonary Hypertension of the Newborn (PPHN)?

A
  • Any condition (other than congenital heart disease) associated w/ low blood flow to the lungs after birth
  • Most frequently in near-term, full-term or post-term infants
103
Q

PPHN etiology & pathophysiology

A
  • Causes: perinatal asphyxia & MAS
  • Increased pulmonary vascular resistance
  • Significant R-L shunting through foramen ovale or ductus arteriosus with resulting hypoxemia
104
Q

What are the clinical features of PPHN?

A
  • Severity is variable (cyanosis to resp failure)
  • PaO2 significantly decreased in response to minimal inspired oxygen changes or stimulation
  • Pre/post-ductal PaO2 are notably different
105
Q

How is PPHN evaluated?

A
  • CXR
    • Increased pulmonary vascular markings in infants w/ idiopathic PPHN
    • Not caused by MAS or perinatal asphyxia
  • ECG
    • Important to rule out congenital heart disease & assess the degree of pulmonary HTN & R-L shunting
106
Q

How is PPHN managed?

A
  • Prevention of hypoxemia
    • Potent pulmonary vasoconstrictor
    • O2 is the most potent pulmonary dilator
  • Mechanical ventilation
    • If O2 alone insufficient
  • High frequency ventilation & extracorporeal membrane oxygenation (ECMO)
    • Severe cases
  • Inhaled NO
    • Potent pulmonary dilator
107
Q

What is meconium?

A
  • First stools, material in fetal gut
  • Consists of:
    • Water
    • Mucopolysaccharides
    • Desquamated skin & GI mucosal epithelial cells
    • Vernix
    • Bile salts
    • Amniotic fluid
108
Q

What is Meconium Aspiration Syndrome (MAS)?

A

Acute respiratory disorder caused by aspiration of meconium in the airways of the fetus or neonate

109
Q

What is the pathophysiology of MAS?

A
  • Meconium passes as a consequence of distress (hypoxemia) in the fetus at term
  • More frequent >42 wks gestation
  • Degree of MSAF (meconium stained amniotic fluid) ranges from slighly green to dark green and thick consistency (pea soup)
  • May reach the distal airways & alveoli in utero if fetus becomes hypoxic & develops gasping or deep respiratory movements
  • May occur at time of birth w/ 1st inspirations
110
Q

What are the clinical features of MAS?

What is the evaluation?

A
  • Signs & symptoms of mild/moderate RD
  • Some have severe respiratory failure w/ severe hypoxemia & cyanosis
111
Q

How is MAS evaluated?

A
  • Hx of meconium noted at or before delivery & presence of respiratory distress
  • CXR
    • Increased lung volume
    • Diffuse patchy areas of atelectasis & parenchymal infiltrates alternating w/ hyperinflation
  • Pneumothorax or pneumomediastinum may occur
112
Q

How is MAS managed?

What are some possible complications?

A
  • Combined OB & Peds approach
  • Suctioning the perineum & direct suctioning of the trachea via endotracheal intubation
  • Generally O2 is required
    • Mechanical vent or ECMO if severe
  • Complications
    • PPHN
    • Bacterial pneumonia
    • Long-term reactive airway disease
113
Q

What is apnea of prematurity?

A
  • Respiratory pause w/o airflow lasting more than 15-20 seconds [OR]
  • Respiratory pause of any duration if accompanied by bradycardia & cyanosis or oxygen desaturation (pulse ox)
114
Q

What are the 3 categories of apnea?

A
  • Central apnea
    • Complete cessation of chest wall movements and no airflow
  • Apnea secondary to airway obstruction
    • Chest wall movements or respiratory efforts but w/o airflow
    • Apnea monitors don’t detect this
  • Mixed apnea
    • Central + obstructive
    • Most frequent type in preterm infants
115
Q

What is the etiology of apnea of prematurity?

A
  • Neonatal infections
  • Lung disease
  • Hypothermia
  • Hyperthermia
  • Hypoglycemia
  • Seizures
  • Maternal drugs
  • Drug withdrawal
  • Anemia
  • GERD
  • Idiopathic
116
Q

What is the incidence of idiopathic apnea of prematurity?

A
  • Frequency increases w/ decreasing gestational age
  • <28 wks gestation = 85%
  • 33-34 wks gestation = 25%
117
Q

What are the clinical features of idiopathic apnea of prematurity?

A
  • Absence of any identifiable cause
  • 24 hrs after birth & during 1st wk of life
  • Resolves by postconceptional age of 38-44 wks
    • Gestational age at birth + # wks postnatal
118
Q

How is idiopathic apnea of prematurity managed?

A
  • Maintenance of neutral thermal environment, treatment of hypoxia, proprioceptive stimulation
  • Respiratory stimulant medications
    • Caffeine, theophylline
  • Ventilation as needed
    • Bag & mask after severe apneic episode
  • CPAP or mechanical ventilation
119
Q

What is neonatal jaundice?

A
  • Jaundice: yellowish discoloration of mucous membranes & skin from increased bili levels
  • First wk of life, indirect (unconjugated) hyperbilirubinemia that is physiologic in nature
  • Visible jaundice: serum bili >5 mg/dL
120
Q

How is neonatal jaundice classified?

A
  • Physiologic jaundice
  • Nonphysiologic jaundice
121
Q

What is physiologic jaundice?

How is it caused?

A
  • Benign indirect hyperbilirubinemia
  • Resolves by end of 1st wk of life, no treatment
  • Causes
    • Increased bilirubin load on hepatocytes
    • Delayed activity of the hepatic enzyme glucuronyl transferase
122
Q

What are the clinical features of physiologic jaundice?

A
  • Jaundice in well-appearing infants
  • Elevated indirect bilirubin levels
  • Full-term infants
    • Peak bilirubin 5-16 mg/dL at 3-4 days of life
    • Start to decrease before 1st wk of life
  • Pre-term infants
    • Peak bilirubin after 5-7 days
    • 10-20 days before decreasing
123
Q

How is nonphysiologic jaundice classified?

A
  • Indirect hyperbilrubinemia
    • Elevated bilirubin
    • Conjugated/direct <15% of total
  • Direct hyperbilirubinemia
    • Conjugated/direct >15% of total
    • Always PATHOLOGIC in neonates
124
Q

What is the differential diagnosis of indirect hyperbilirubinemia?

A
  • Physiologic jaundice
  • Increased RBC load from bruising
  • Increased bilirubin from hemolysis
  • Upper GI obstruction (increased enterohepatic recirculation)
  • Breastfeeding jaundice
  • Breast milk jaundice
  • Sepsis
  • Inborn errors of metabolism (hypothyroidism)
  • Inherited disorders of bilirubin uptake & conjugation
125
Q

What is Breastfeeding jaundice?

A
  • First wk of life
  • Increased bilirubin levels
  • Suboptimal milk intake
  • Poor intake –> weight loss, dehydration, decreased passage of stool
  • Resultant decreased excretion of bilirubin in the stool
126
Q

What is Breast milk jaundice?

A
  • After 1st wk of life
  • Related to breast milk’s high levels of ß-glucuronidase and high lipase content
  • Elevated bilirubin is highest in the second and thrid weeks of life
  • Lower levels of bilirubin may persist until 10 wks of life
127
Q

What is the differential diagnosis of direct hyperbilirubinemia?

A
  • Obstructive jaundice secondary to choledochal cyst
  • Obstructive jaundice secondary to biliary atresia
  • Sepsis
  • Neonatal hepatitis
  • Metabolic causes
  • Cholestasis associated w/ parenteral nutrition
  • Cystic fibrosis
128
Q

Jaundice should always be evaluated under the following circumstances….

A
  • Jaundice appears <24 hrs of age
  • Bilirubin rises >5-8 mg/dL in 24 hr period
  • Rate of rise of bilirubin exceeds 0.5 mg/dL per hour (suggesting hemolysis)
129
Q

How do you evaluate for indirect hyperbilirubinemia?

A
  • CBC
  • Reticulocyte count
  • Smear (for hemolysis)
  • Evaluation for sepsis
130
Q

How do you evaluate for direct hyperbilirubinemia?

A
  • Hepatic ultrasound (choledochal cyst)
  • Serologies for viral hepatitis
  • Radioisotope scans of the hepatobiliary tree
  • Evaluation for sepsis
131
Q

How is neonatal jaundice managed?

A
  • Serial bilirubin assessments, observation, reassurance (physiologic jaundice)
  • Phototherapy
    • Water-soluble photoisomers of indirect bilirubin that are more readily excreted
    • Depends on gestational maturity, age, bili levels, risk factors, etc.
  • Exchange transfusion
    • Rapidly rising bili levels secondary to hemolytic disease
132
Q

What are the complications from neonatal jaundice?

A

kernicterus & bilirubin encephalopathy

  • Indirect bili can pass BBB (irreversible damage)
  • Bili localizes to basal ganglia, hippocampus, some brainstem nuclei
  • Clinical features
    • Choreoathetoid cerebral palsy
    • Hearing loss
    • Opisthotonus
    • Seizures
    • Oculomotor paralysis
133
Q

In approximately ___% of pregnancies in the US, fetuses are exposed to illicit drugs while in utero.

134
Q

Most women who use illicit drugs use…..

A

Compounds fetal risk if using tobacco, caffeine, prescribed drugs

  • Alcohol
  • Cocaine
  • Amphetamines
  • PCP
  • Narcotics
135
Q

What are maternal risk factors for drug abuse?

What are some obstetric complications?

A
  • Maternal risk factors
    • Inadequate prenatal care
    • Anemia
    • Endocarditis
    • Hepatitis
    • TB
    • HIV
    • STIs
    • Low self-esteem
    • Depression
  • Obstetric complications
    • Abruptio placentae
    • Precipitous delivery
    • Preterm labor & delivery
136
Q

What are the clinical features of infants of drug-abusing mothers?

Mortality rates and cause of death?

A
  • Jitteriness, hyperreflexia
  • Irritability, tremulousness, feeding intolerance, excessive weakness
  • 3-10% mortality
  • Cause of death
    • Perinatal asphyxia
    • Congenital anomalies
    • Child abuse
    • SIDS
137
Q

What is the epidemiology of esphageal atresia w/ TEF?

A
  • 1:2,000-3,000 infants
  • Associated w/ polyhydramnios
  • Most common type of esophageal atresia (>90%)
    • Atresia of the esophagus (proximal pouch)
    • Distal tracheoesophageal fistula
138
Q

What are the clinical features of esophageal atresia with TEF?

A
  • Hx of polyhydramnios
  • Copious oropharyngeal secretions
    • Increased risk of choking & aspiration pneumonia
  • Associated malformations (50%)
    • Congenital heart disease
    • Anorectal, skeletal, renal malformations
    • VACTERL association
139
Q

How is esophageal atresisa w/ TEF evaluated?

How is it managed?

A
  • Oral gastric tube inserted until meets resistance
  • Radiographs show tube in upper thorax
  • Type III
    • Air that has crosses through the distal fistula from the trachea is seen in the stomach
  • Surgical repair
    • Closure of the fistula
    • Anastomosis of the 2 esophageal segments
140
Q

What is a congenital diaphragmatic hernia?

What is the epidemiology?

Pediatrics (24 decks)

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