Neonatal Respiratory Pathology
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Transcript Neonatal Respiratory Pathology
Neonatal Respiratory Pathology
Signs and Symptoms
Common (Major) Neonatal Diseases
Normal Neonatal Vital Signs
Smaller = faster
Normal heart rate 120-160/minute
Normal respiratory rate 40-60/minute
Normal blood pressure
– pre term 50/30 mm Hg
– increases with size
Signs & Symptoms of Respiratory
Distress
Tachypnea
Nasal flaring
Expiratory grunting
Retractions
See saw breathing
Central cyanosis (as opposed to
acrocyanosis)
Apnea
Periodic Breathing vs Apnea
Periodic breathing
– normal in preterm
– seen in 25 to 50% of all preterms
– cessation of breathing for 10 seconds with no
changes
Apnea
– cessation of breathing for 20 seconds with
changes
– deteriorating color, SaO2, bradycardia
Common Neonatal Respiratory
Diseases
Hyaline Membrane Disease
Transient Tachypnea of the Newborn
Bronchopulmonary Dysplasia
Meconium Aspiration Syndrome
Persistent Fetal Circulation
Retinopathy of Prematurity
Hyaline Membrane Disease
Abbreviated HMD
Also known as RDS type I
Seen in premature infants
Caused by immature surfactant system
HMD Pathology
Restrictive lung disease
HMD Pathology
Restrictive lung disease
Decreased lung compliance
– increased elastic recoil
– increased surface tension
– increased work of breathing
HMD Pathology (cont.)
Atelectasis
– decreased diffusion due to surface area
– Increased AaDO2 (aA ratio)
– increased intrapulmonary shunting (Qs/Qt)
HMD Pathology (cont.)
Atelectasis
– decreased diffusion due to surface area
– Increased AaDO2 (aA ratio)
– increased intrapulmonary shunting (Qs/Qt)
Formation of hyaline membrane
– decreased diffusion secondary to thickness
HMD Histology
Surfactant helps keep lung dry
HMD, alveolar leakage
Fluid rich in protein, fibrin, dying epithelial
cells
Forms a hyaline membrane
Membrane forms within first 24 to 48 hours
Around 72 hours, phagocytosis begins
HMD Clinical Findings
Premature infant
Grunting and retractions
“Crash” within first 24 to 48 hours
HMD Chest X Ray
Hypoinflated
(diaphragm less than 8 ribs)
Reticulogranular pattern
(Ground glass, frosted glass)
Air Bronchograms
HMD Treatment
Artificial Surfactants
“Textbook Management”
– Increasing Severity - Hood O2 to CPAP to Vent
– Weaning - Vent to CPAP to Hood
Disease runs course 5 to 7 days
Transient Tachypnea of the
Newborn
Also known as RDS type II
Also known as Wet Lung Syndrome
Abbreviated as TTN, TTNB
Seen in infants delivered via C sections
A disease of retained Fetal Lung Liquid
TTNB Pathology
Interstitial edema
Increased Raw (until fluid absorbed)
TTNB Clinical Findings
C-section infants
Good Apgars at birth
Mild hypoxemia within first 24 hours
TTNB Chest X Ray
Lymphatic engorgement
(white strings)
Hyperinflation
(diaphragm greater than 10 ribs)
TTNB
TTNB Treatment
Hood O2 within first 24 to 48 hours
Infant on room air
Bronchopulmonary Dysplasia
Abbreviated as BPD
Obstructive disease
Definition - O2 useage, 28 days post partum
Causitive factors:
– O2
– Airway Pressure
– Time of exposure
BPD Pathology
Stage I - same as HMD
BPD Pathology
Stage I - same as HMD
Stage II
– occurs at 3 to 4 days
– alveolar necrosis, development of smooth
muscle
BPD Pathology (cont.)
Stage III
– continued smooth muscle development
– interstitial fibrosis
– emphysematous bullae
BPD Pathology (cont.)
Stage III
– continued smooth muscle development
– interstitial fibrosis
– emphysematous bullae
Stage IV
– around one month
– emphysema, interstitial fibrosis, pulmonary
hypertension
Summary BPD Pathology
Increased Raw
Areas of increased and decreased Clt
Hyperinflated
Interstitial edema
many have PDA (L to R)
BPD Chest X Ray Stages
Stage I - HMD like
Stage II - increased ‘white out’
Stage III - ‘sponge like’, bullae and white
out
Stage IV - ‘honeycomb’
BPD Treatment
Supportive
Steroids
Meconium Aspiration Syndrome
Abreviated as MA, MAS
Meconium is infant stool
Presence indicates delivery stress
Found in approx. 10% of all deliveries
MAS Pathology
Check valve, ball valve effect
(Increased incidence of pneumothorax)
Chemical (aspiration) pneumonitis
MAS Clinical Findings
Commonly post mature
– larger infants
– long fingernails, peeling skin
Delivered through stained amniotic fluid
Yellow or greenish nails, chord
MAS Chest X Ray
Increased patchy density
Hyperinflation
MAS Treatment
Deep tracheal suctioning at birth
Supportive
Chest physiotherapy
Persistent Fetal Circulation
Also known as Persistent Pulmonary
Hypertension of the Newborn
Abbreviated as PFC, PPH, PPHNB
Page 81, Whitaker
******Comprehensive
Perinatal & Pediatric
Respiratory Care*****
PFC Pathology
Continuance of Fetal Circulation post
partum
R to L shunting through PDA
R to L shunting through FO
Severe hypoxemia
PFC Clinical Findings
Infants tend to be term
Non responsive hypoxemia
Right sided PaO2 (preductal) 15 torr higher
than left
Differential Diagnosis of PFC
Hyperoxia test (100% hood)
– PaO2 > 100 is lung disease
– PaO2 = 50 to 100 is either lung or heart disease
– PaO2 < 50 is fixed right to left shunt
Differential Diagnosis of PFC
(cont.)
If fixed R to L shunt is suspected
– Obtain pre and post ductal PaO2
– Difference < 15 torr, no ductal shunting
– Difference > 15 torr, ductal shunting present
Differential Diagnosis of PFC
(cont.)
Perform Hyperoxic - Hyperventilation Test
– Hyperventilate with 100% O2 until PaCO2 20
to 25 torr
– If PaO2 > 100 torr, then PFC is present
– If PaO2 < 100 torr, then congenital heart disease
PFC Treatment
High vent settings (shoot for PaCO2 20-25
torr)
? Paralysis
Allow PaO2 to be 80 to 100 torr
Use vasodilator Priscolene (Tolazoline)
– Nitric Oxide
Use of ECMO
Retinopathy of Prematurity
Also known by older name of Retrolental
Fibroplasia (RLF)
Whitaker
******Comprehensive Perinatal
& Pediatric Respiratory Care
Page 303,
Abbreviated as ROP
Visual disturbances secondary to O2 use
ROP Pathology
Stage I - vascoconstrictive response of
immature retinal vessels when PaO2 is
increased
Stage II - (proliferative stage), new vessels
form to oxygenate retina, retinal
hemorrhage
Causative Factors of ROP
PaO2
Retinal Maturity
Duration of Hyperoxia
ROP Treatment
Closely monitor PaO2 or SaO2
Closely monitor FiO2
‘Cryo’ therapy
Ophthalmic examination at discharge