RT134 Disease Processes

Def: Surfactant deficiency of the lung causing decreased lung compliance and atelectasis

Patho:
-Collapse of the alveoli after each breath
-Plasma leaks out of the lung tissue
-Forms a hyaline membrane
Lack of surfactant-Alveolar Collapse
Increased Pressures needed-leads to vasoconstriction, acidosis, hypoxemia
Capillary endothelial damage with fluid leaking into alveolar space
Diffusion of O2 and CO2 difficult due to decreased pulmonary blood flow and atelectasis
Over inflation further damages Type II cells
Formation of hyaline membrane

Premature infants

L/S ratio 2:1
PG+
Shake Test (Foam Stability Index>48) i

Intercostal retractions

Expiratory Grunting

Nasal Flaring

Tachypnea

Apnea

Decreased BS

Cyanosis

Metabolic and/or Respiratory Acidosis

Poor Peripheral Perfusion

Hypotension/shock

Oxygen Therapy

Nasal CPAP

Steroids

Exogenous Surfactant

Ventilatory Support--HFOV vs Conventional Vent

Pulse Ox/TCM

Surfactant Replacement Therapy (Prophylactic or Rescue)

Prophylactic:
.30 FiO2 to maintain PaO2>50 or O2 sat>90%
-CXR consistent with RDS

*Lung Protective strategies

Gentle suctioning prn

Minimal handling--cluster care

Fluid and electrolyte balance-keep on the dry side

Maintain blood glucose 45-120 mg%

Amp and Gent antibiotics

To do whatever I can do to avoid the use of Positive pressure ventilation.

Failure of shunts to close during transition from fetal circulation due to lack of O2

High PVR causing RightHe to Left shunt

Hypoxemia and acidemia causes further ­PVR and perpetuates the cycle

Severe Respiratory Distress

Cyanosis

Hypoxemia on 100% O2 with positive pressure

unexplained by degree of lung disease

CXR shows ¯Vascular Markings and enlarged heart

Breath sounds—rales

Severe causing RDS
congenital Heart Defect

in general, just becuase you caught PPHN doesnt mean that that is the only thing wrong. could be PNA, diaphragmatic hernia, etc.

Contrast echocardiography used to confirm shunting

Ductal blood gas, 02 hyperoxia challenge (100% for 20 mins, hyper ventilation test)

Prevent hypoxemia, acidosis and hypothermia

Correct hypoxemia by reversing R>L shunting

Drug Therapy [(INO, oxygen, Priscoline (tolazoline)] - drugs to reduce PVR

PPV with 100% Oxygen

High rate with short I-time. use just enough to move the chest

With a goal to Reduce PaCO2 to a level where PaO2 rises above 100mmHg.

Use enough FiO2 to keep PaO2 > 120mmHg if possible

iNO, oxygen, Priscoline (tolazoline)

they are drugs to reduce PVR with the goal of closing the Patent ductus arteriosis

Lungs

intrapartum

• Aspiration in utero

• Aspiration during delivery

premature rupture of the membrane (can introduce bacteria too soon)

Prolonged labor

Excessive obstrectric manipulation

Maternal GI infection

Infection (GBS, ecoli, herpes, listeria)

MOM says Baby doesn’t “look” right/“Not acting right”

Rapid Respiratory deterioration

Apnea and/or bradycardia Especially

Temp instability

hypotension/poor perfusion

Term—hyperthermia

Preterm-– hypothermia

Careful assessment and monitoring

Antibiotic Therapy

Fluid/Electrolyte support

Blood Products/volume replacement

Respiratory Support as needed

Watch out for septic shock!

Prolonged gestation >42 weeks

SGA

IUGR

Placental insufficiency (hypertension, Preeclampsia, Previa, Abruption)

Intrapartum asphyxia (Cord prolapse or Prolonged labor)

Fetal asphyxia to intestinal hypoxia then to hyperperiastalsis then anal sphincter relaxation causes merconium to enter the amniotic fluid.

this can happen before or after delivery

baby can swallow the merconium during delivery cause a reflux and aspirate it into the lungs

Tachypnea with intercostal retractions

Cyanosis, grunting, flaring

Increased AP thoracic diameter

Coarse bronchial breath sounds

Airway obstruction/Air Trapping

Complete (atelectasis)

Incomplete (ball – valve action blocking airway from exhalation)

Alert, anxious LOOK

Lung protection strategy

MOST IMPT, Do not stimulate to breathe.

If the baby is non-vigorous and flacid use merconium protocols

If the baby is vigorous and crying on their own, just treat the PNA

intubate at first breath

Direct tracheal suction below cords with DeLee suction which connects directly and uses ET tube for suction.

PPV

HFOV is recommended

If conventional, high pressures with short i-times
Hyperoxygenate with hypocapnea, Alkalosis

.30 FiO2

| maintain PaO2>50 or O2 sat>90%

Uniform reticulogranular appearance
AKA ground glass

Low lung volumes

Air Bronchograms

Atelectasis

Diffuse Bilateral infiltrates

patchy infiltrate in perihilar area

Failure of fetal lung fluid to clear causing respiratory distress

Minics clinical early RDS

Tachypnea resulting in hyperventilation

Mild respiratory alkalemia

Cyanosis

Barrel – shaped chest

Retracitons/grunting

Wet LUNG

Perihilar congestion

There may be small collections of liquid at the costophrenic angles

Progressive clearing within 48-72 hours

Supplemental Oxygen
100% by Head Hood
High flow nasal oxygen (vapotherm)

NCPAP
4 – 6 cwp
100% O2

Pulmonary Diseases

Stiff non compliant lungs

Aspriation syndromes

Hypoplastic lungs

Congenital lobar or pulmonary interstitial emphysema

Positive pressure ventilation

HFV

Permissive Hypercapnea

Keep airways clear

Pressure gauges

Recognition of infants at risk

Restless

Irritable

Lethargy

Tachypnea

Increased respiratory effort profound general cyanosis

Bradycardia

Decreased of shifted breath sounds

Chest asymmetry

Severe hypotension and poor peripheral perfusion

Cardiac arrest

Transilumination of the Chest

| CXR

Needle aspiration 2nd intercostal space midclavicular line

Oxygen therapy
HFV

A Chronic lung condition that starts with severe RDS.
has 4 stages

Presents it self in Infants requiring high ventilator settings with high FiO2 after 10 days

Use lowest ventilatory support and FiO2 to permit lung to heal.

Titrate Fi02 keeping sats 88 – 92

HFOV recommended in early stages of RDS to prevent BPD.

Good nutrition to support lung growth

Treat infections

Formation of bone that blocks ventilation through the nasal passage.

Babies are obligate nose breathers. they can only breathe through crying.

conformation with size 6 french catheter's inability to pass through nose.

it is a birth defect wherein the esophagus is narrow or absence of connection to stomach.

Esophageal atresia with distal transesophegeal Fistula.

Inability of pass OG tube (This is Very impt Point)

Excessive drooling due to inability to swallow

Aspiration of gastric secretions

Choking/coughing with first feeding

Episodes of cyanosis

Air bronchograms

Ground glass