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