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Neonatal Diseases

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Neonatal Diseases RC 290 Respiratory Distress Syndrome (RDS) Also known as Hyaline Membrane Disease (HMD) Occurrence 1-2% of all births 10% of all premature births ... – PowerPoint PPT presentation

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Title: Neonatal Diseases


1
Neonatal Diseases
  • RC 290

2
Respiratory Distress Syndrome(RDS)
  • Also known as Hyaline Membrane Disease
  • (HMD)

3
Occurrence
  • 1-2 of all births
  • 10 of all premature births
  • Greatest occurrence is in the premature and low
    birth weight infant

4
Etiology Predisposing Factors
  • Prematurity
  • Immature lung architecture and surfactant
    deficiency
  • Fetal asphyxia hypoxia
  • Maternal diabetes
  • Increased chance of premature birth
  • Possible periods of reflex hypoglycemia in the
    fetus causing impaired surfactant production

5
Pathophysiology
  • Surfactant deficiency
  • Decreased FRC
  • Atelectasis
  • Increased R-L shunt
  • Increased W.O.B.
  • Hypoxemia and eventually hypercapnia because of
    V/Q mismatch

6
Pathophysiology (cont.)
  • Atelectasis keeps PVR high
  • Increased PAP
  • Lung hypoperfusion
  • R-L shunting may re-occur across the Ductus
    Arteriosus and the Foramen Ovale

7
Hypoxia/hypoxemia results in anaerobic metabolism
and lactic acidosis
  • This damages the alveolar-capillary membrane
    causing formation of hyaline membranes. Hyaline
    membranes perpetuate all of the problems in the
    lung

8
The cycle continues until surfactant levels are
adequate to stabilize the lung
  • Symptoms usually appear 2-6 hours after birth
  • Why not immediately?
  • Disease peaks at 48-72 hours
  • Recovery usually occurs 5-7 days after birth

9
Clinical findings Physical
  • Tachypnea (60 BPM or gt)
  • Retractions
  • Nasal flaring
  • Expiratory grunting
  • Helps generate autoPEEP
  • Decreased breath sounds with crackles
  • Cyanosis on room air
  • Hypothermia
  • Hypotension

10
Clinical Findings Lab
  • ABGs initially respiratory alkalosis and
    hypoxemia that progresses to profound hypoxemia
    and combined acidosis
  • Increased Bilirubin
  • Hypoglycemia
  • Possibly decreased hematocrit

11
CXR Normal
12
RDS CXR Ground Glass Effect
13
RDS CXR Air Bronchograms Hilar Densities
14
Time constant is decreased since elastic
resistance is so high
  • Increased elastic resistance means decreased
    compliance!

15
RDS Treatment Primarily supportive until lung
stabilizes
  • NTE, maintain perfusion, maintain ventilation and
    oxygenation
  • O2 therapy, CPAP or mechanical ventilation
  • May require inverse IE ratios if oxygenation can
    not be achieved with normal IE ratio
  • Surfactant instillation!!!
  • May cause a sudden drop in elastic resistance!

16
Prognosis/Complications
  • Prognosis is good once infant makes it past the
    peak (48-72 hours)
  • Complications possible are
  • Intracranial Bleed
  • BPD (Bronchopulmonary Dysplasia)
  • PDA (Patent Ductus Arteriosus)

17
Transient Tachypnea of the Newborn (TTN)
  • Also known as Type II RDS or Retained Lung Fluid

18
Occurrence Similar to RDS
  • More common in term infants!

19
Etiology Predisposing Factors
  • C-section
  • These infants do not have the fluid expelled from
    their airways as occurs in vaginal delivery
  • Maternal Diabetes
  • Increased chance of C-section due to LGA
  • Cord Compression
  • Anesthesia

20
TTN Pathophysiology
  • Primary problem retained lung fluid
  • Fluid not expelled from airways because of
    C-section
  • Poor absorption of remaining fluid by pulmonary
    capillaries and lymphatics
  • If retained fluid is in interstitial spaces,
    compliance and TC are decreased
  • If retained fluid is in airways,airway resistance
    and TC are increased
  • TTN can be restrictive , obstructive, or both!
  • Fluid usually clears by itself after 24-48 hours
    after birth

21
Clinical Signs
  • Tachypnea (usually rate is greater than seen in
    RDS)
  • Minimal (if any) nasal flaring or expiratory
    grunting
  • ABGs mild hypoxemia. PaCO2 depends on whether
    problem is restrictive or obstructive

22
TTN CXR
  • Coarse peri-hilar streaks
  • Prominent lung vasculature
  • Flattened diaphragms if fluid is causing
    obstruction/air-trapping

23
TTN Treatment Like RDS, it is primarily
supportive
  • Monitoring and O2 therapy
  • Possibly CPAP or mechanical ventilation

24
Prognosis/Complications
  • Prognosis is very good
  • Main complication is pneumonia
  • Often initial diagnosis

25
Lab Time!
26
Patent Ductus Arteriosus-PDA_
  • Failure of the D.A. to close at birth or a
    re-opening of the D.A. after birth. Allows
    shunting between the pulmonary artery and the
    aorta

27
Occurrence
  • 1 per 2000 term babies
  • 30-50 of RDS babies

28
Etiology Predisposing Factors
  • Prematurity
  • D.A. not as sensitive to increasing PaO2
  • Hypoxia
  • Decreasing PaO2 allows it to re-open for up to
    three weeks after birth
  • Thus, a PDA can occur in a premature infant who
    is NOT hypoxic or in a term baby who is hypoxic
  • Worst case is a premature infant who is hypoxic!

29
Pathophysiology
  • D.A. fails to close or it re-opens
  • Then shunting occurs between the pulmonary artery
    and the aorta
  • The direction of the shunt depends on which
    vessel has the higher pressure
  • A PDA can cause L-R shunting or R-L shunting!
  • Clinically, most PDAs refer to a L-R shunt

30
Clinical Signs
  • Tachypnea, bounding pulses, hyperactive
    pre-cordium
  • Decreased breath sounds and possibly some
    crackles
  • Possible murmur over left sternal border
  • Murmur is loudest when D.A. just starts opening
    or when it is almost closed

31
Clinical Signs (cont.)
  • ABGs hypoxemia with respiratory acidosis
  • If R-L shunting, the PaO2 in the upper
    extremities, ie pre-ductal, will be greater than
    the PaO2 in the umbilical artery, ie post-ductal!
  • TC decreased if L-R shunting causes pulmonary
    edema increased if fluid spills into airways and
    increases airway resistance
  • CXR if L-R shunt, butterfly pattern of
    pulmonary edema with possible cardiomegaly

32
PDA Treatment
  • Basic NTE, O2, may require CMV if not already
    on the ventilator
  • Medical
  • L-R shunt that fails to close Indomethacin
    (Indocin)
  • R-L shunt Priscoline (Tolazoline) to decrease
    PVR also nitric oxide
  • Surgical if medical treatment fails, the PDA may
    be surgically ligated

33
Prognosis/Complications
  • Good prognosis when baby responds to medical
    treatment
  • May develop
  • Shock
  • CHF
  • Necrotizing Enterocolitis (NEC)

34
Meconium Aspiration Syndrome-MAS-
  • Syndrome of respiratory distress that occurs when
    meconium is aspirated prior to or during birth

35
Occurrence
  • 10-20 of ALL births show meconium staining
  • 10-50 of stained babies may be symptomatic
  • More common in term and post-term babies

36
Etiology Predisposing Factors
  • Intra-uterine hypoxic or asphyxic episode
  • Post-term
  • Cord compression

37
Pathophysiology Check Valve Effect
Causes gas trapping (obstruction) If complete
obstruction, then eventually atelectasis
occurs Irritating to airways, so edema and
bronchospasm Good culture ground for bacteria,
so pneumonia possible
38
Pathophysiology (cont.)
  • V/Q mismatch leads to hypoxia and acidosis which
    increases PVR
  • TC increases because it increases airway
    resistance
  • Meconium is usually absorbed in 24-48 hours
    there are still many possible complications

39
Clinical Signs
  • Respiratory depression or distress at birth
  • Hyperinflation
  • Pallor
  • Meconium stained body
  • Possible cyanosis on room air
  • Moist crackles
  • ABGs hypoxemia with combined acidosis
  • CXR coarse, patchy infiltrates with areas of
    atelectasis and areas of hyperinflation
  • May see flattened diaphragms if obstruction is
    severe

40
M.A.S. Treatment
  • Amnioinfusion artificial amniotic fluid infused
    into uterus to dilute meconium
  • Proper resuscitation at birth(clear meconium from
    trachea before stimulating respiration)
  • Oro-gastric tube
  • NTE
  • O2
  • NaHCO3 if severe metabolic acidosis
  • Broad spectrum antibiotics
  • Bronchial hygiene
  • May need mechanical ventilation
  • Slow rates and wide IE ratios because of
    increased TC
  • Low level of PEEP may help prevent check valve
    effect
  • May need HFO

41
Prognosis Complications
  • Good prognosis if there are no complications
  • Complications
  • Pneumonia
  • Pulmonary baro/volutrauma
  • Persistent Pulmonary Hypertension (PPHN)

42
Persistent Pulmonary Hypertension-PPHN-
  • Also known as Persistent Fetal Circulation
  • -PFC-

43
Failure to make the transition from fetal to
neonatal circulation or a reversion back to the
condition where pulmonary artery pressure exceeds
aortic pressure
  • Results in R-L shunting across the D.A. and the
    Foramen Ovale

44
Occurrence
  • Usually term and post-term babies
  • Females more often than males
  • Symptoms may take 12-24 hours after birth to
    develop

45
Etiology Predisposing Factors
  • M.A.S most common
  • Hypoxia and /or acidosis, eg RDS
  • Any condition that causes PVR to increase

46
Pathophysiology
  • Primary problem is pulmonary artery hypertension
  • Infants arterial walls are thicker and they are
    more prone to vasospasm
  • If pulmonary artery pressure gets high enough,
    blood will shunt R-L across the D.A. and Foramen
    Ovale
  • Remember, conditions that drive up PAP usually
    make the D.A. open
  • Lung is hypoperfused resulting in refractory
    hypoxemia and hypercapnia

47
Clinical Signs
  • Refractory hypoxemia and cyanosis
  • Shock and tachypnea
  • Murmur possible
  • Pre-ductal PaO2 gt post-ductal PaO2
  • Hypoxemia with combined acidosis
  • CXR usually OK when compared to infants condition

48
PPHN Treatment
  • NTE and O2
  • Nitric Oxide
  • Often in conjunction with HFO
  • Priscoline, Indocin may also be used
  • If completely unresponsive to therapy ECMO may be
    tried

49
Prognosis Complications
  • Prognosis depends on how well infant responds to
    treatment
  • Complications
  • Shock
  • Intracranial bleed
  • Internal bleeding
  • Especially a problem if Priscoline is used

50
Wilson Mikity Syndrome-Pulmonary Dysmaturity-
  • Respiratory distress that develops after the
    first week of life and presents with definite CXR
    changes

51
Occurrence
  • Usually in lt36 weeks gestational age and birth
    weight lt1500 grams
  • After first week of life
  • No prior symptoms

52
Etiology Predisposing Factors
  • Exact etiology unknown
  • Appears to be due to immature lung and airways
    trying to function
  • Not due to O2 toxicity or mechanical ventilation!

53
Pathology
  • Immature alveoli and T-B tree causes V/Q mismatch
  • Areas of atelectasis and hyperinflation develop

54
Pathology (cont.)
  • 3 Stages
  • Stage 1
  • 1-5 weeks after birth
  • Diffuse areas of atelectasis and hyperinflation
  • Stage 2
  • 1-5 months after birth
  • Cystic (hyperinflated) areas coalesce and cause
    flattening of the diaphragms
  • Stage 3
  • 5-24 months after birth
  • Cystic areas start to clear up

55
Clinical Signs
  • Tachypnea
  • Cyanosis on room air
  • Some retractions and/or nasal flaring
  • Decreased breath sounds with crackles
  • ABGs respiratory acidosis with hypoxemia
  • CXR consistent with the stage of the disease

56
Wilson Mikity Treatment
  • Is purely supportive-there is no medicinal or
    surgical treatment
  • O2 and NTE
  • Some cases require mechanical ventilation
  • Maintain fluids/electrolytes and caloric intake
  • Watch for infection

57
Prognosis Complications
  • Prognosis good if infant survives stage 2
  • Complications
  • PDA
  • Cor Pulmonale
  • CNS damage

58
Bronchopulmonary Dysplasia-BPD-
  • A result of RDS and/or its treatment that results
    in areas of fibrosis, atelectasis, and
    hyperinflation

59
Etiology Predisposing Factors
  • RDS and prematurity
  • Triad of O2, ET tube, and mechanical ventilation

60
Pathology 4 Stages
  • Stage 1
  • Acute phase of RDS
  • Stage 2
  • 4-10 days after the onset of RDS
  • Areas of atelectasis and hyperinflation
  • Stage 3
  • 2-3 weeks after RDS
  • Hyperinflated areas start to coalesce
  • Fibrosis starts to develop
  • Stage 4
  • 1 month after the onset of RDS
  • Diaphragms start to flatten
  • Interstitial fibrosis evident on CXR
  • PPHN may start to develop
  • O2 dependency develops

61
Clinical Signs
  • Tachypnea
  • Persistent retractions
  • A-B spells
  • Cyanosis on room air
  • Decreased breath sounds with crackles
  • ABGs respiratory acidosis (may be compensated)
    with hypoxemia
  • CXR consistent with stage of disease

62
BPD Stage 4 CXR
Interstitial fibrosis and flattened diaphragms
63
BPD Treatment
  • Prevention is best! Use the least amount of
    intervention for the least amount of time!
  • Supportive care
  • O2, NTE, bronchial hygiene, maintain
    fluids/electrolytes
  • Diuretics if needed to prevent fluid overload and
    heart failure
  • Possibly vitamin E

64
Prognosis Complications
  • Good if infant survives to age 2
  • 50 mortality if PPHN develops
  • Complications
  • PHTN
  • Cor Pulmonale
  • Respiratory Infections
  • CNS damage

65
Diaphragmatic Hernia
  • Congenital malformation of the diaphragm that
    allows abdominal viscera into the thorax

66
Occurrence
  • 1 per 2200 births

67
Etiology Predisposing Factors
  • Exact unknown but may be related to vitamin A
    deficiency

68
Pathology
  • Usually occurs during the 8-10th week of
    gestation
  • 80 occur on the left at the Foramen of Bochdalek
  • Abdominal viscera enters thorax and compresses
    developing lung
  • As baby attempts to breathe after birth, the
    stomach and bowel fill with air and cause further
    compression of the lung
  • Severe restriction!

69
Clinical Signs
  • Cyanosis
  • Severe respiratory distress with retractions and
    nasal flaring
  • Bowel sounds in chest
  • Uneven chest expansion
  • Decreased breath sounds on affected side
  • ABGs profound hypoxemia with combined acidosis
  • CXR loops of bowel in chest with shift of
    thoracic structures towards unaffected side, eg
    dextrocardia

70
Diaphragmatic Hernia CXR
71
Diaphragmatic Hernia Treatment
  • Immediate ET tube and NG tube
  • No BVM it will make things worse!
  • Surgical repair
  • Post operative ECMO and/or HFO
  • May need NO with HFO

72
Prognosis Complications
  • 50 mortality
  • Complications
  • Pneumothorax
  • PDA
  • Hypoplastic lung

73
Pulmonary Barotrauma Air Leak Syndromes
74
4 Main Types
  • Pneumothorax
  • Pneumomediastinum
  • Pneumopericardium
  • PIE (Pulmonary Interstitial Emphysema)
  • Gas from ruptured alveoli dissects along
    perivascular and interstitial spaces
  • Causes airway compression (obstruction) and
    alveolar compression (restriction)
  • May lead to pneumothorax, pneumomediastinum, or
    pneumopericardium

75
Occurrence
  • 1-2 of all births
  • (not all are symptomatic)

76
Etiology Predisposing Factors
  • Positive pressure ventilation
  • Increased airway resistance/airway obstruction
  • RDS

77
Clinical Signs
  • Sudden cyanosis (except with PIE)
  • Respiratory distress
  • Mediastinal shift
  • Sudden hypotension (except with PIE)
  • Crepitus (if sub-Q emphysema develops)
  • Unequal chest expansion
  • Decreased breath sounds and hyperressonance
  • ABGs hypoxemia with respiratory acidosis
  • Transillumination

78
Transillumination
Small Pneumothorax
79
Transillumination
Big Pneumothorax
80
CXR Pneumothorax
81
CXR Pneumomediastinum
Note how air does NOT outline the apex of the
heart
82
CXR Pneumopericardium
Note how air completely outlines the heart
83
CXR PIE
84
Air Leak Syndrome Treatment
  • Prevention! Use the least amount of intervention
    for the shortest time possible!
  • Chest tube for pneumothorax
  • HFO may help prevent and/or resolve PIE

85
Prognosis and Complications
  • Good as long as shock and/or cardiac tamponade
    does NOT occur
  • PIE puts infant at risk for BPD

86
Necrotizing Enterocolitis-NEC-
  • Necrosis of the intestinal mucosa

87
Occurrence
  • 20 of all premature births
  • Males Females
  • Most common in low birth weight babies who
    experience perinatal distress

88
Etiology Predisposing Factors
  • Exact cause unknown but seen with the following
  • Intestinal ischemia
  • Bacterial colonization
  • Early formula feeding

89
Pathology
  • Intestinal ischemia due to hypoperfusion, eg
    shock, or vascular occlusion, eg, clot from
    umbilical artery catheter
  • Bacterial colonization after ischemia starts
    necrosis
  • Early formula feeding may provide substrate
    needed for further bacterial growth and further
    necrosis

90
Clinical Signs
  • Abdominal distention
  • Poor feeding
  • Blood in fecal material
  • Lethargy
  • Hypotension
  • Apnea
  • Decreased urine output
  • Bile stained emesis
  • CXR bubbles in intestinal wall

91
NEC Treatment
  • NPO and NG suction
  • IV hydration and hyperalimentation
  • Broad spectrum antibiotics
  • Ampicillin, Gentamycin
  • Minimum pressure on abdomen
  • No diapers or prone positioning
  • Monitor for/treat sepsis
  • Necrotic bowel may need surgical resection

92
Prognosis Complications
  • Mortality is 20-75
  • Best prognosis if infant does NOT require any
    surgery
  • Main complication is sepsis
  • Infants who have bowel resection may develop
    malabsorption syndrome

93
Congenital Cardiac Anomalies
94
Tetralogy of Fallot
  • VSD
  • Over-riding aorta
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
  • Significant cyanosis because of R-L shunt

95
Complete Transposition of the Great Vessels
  • Pulmonary artery arises from left ventricle and
    Aorta arises from right ventricle
  • R-L shunt through PDA, ASD, or VSD needs to be
    present for infant to survive until corrective
    surgery
  • Balloon septostomy during cardiac catheterization

96
Truncus Arteriosus
  • Aorta and pulmonary artery are the same vessel
  • Large VSD
  • Requires MAJOR surgical repair
  • Mortality is 40-50

97
Case Study Time
98
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