Neonatal Respiratory Pathology nSigns and Symptoms nCommon (Major) Neonatal Diseases.

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)

Page 303, Whitaker ******Comprehensive Perinatal & Pediatric Respiratory Care

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