Respiratory Distress in the Newborn: Recognition and

Treatment

Respiratory Distress

• Hyaline Membrane Disease= Respiratory Distress Syndrome- major cause

– Pathophysiology– Surfactant and ventilator therapy

Must distinguish from other causes:• Transient Tachypnea of the Newborn• Pneumonia/sepsis

Evaluation of respiratory distress

• History and Physical• Chest X-Rays• Hematocrit• Blood Glucose• Blood pressure• Blood gas status

RDS

Diffuse reticulogranular pattern

Air bronchograms

Moderate to low inflation

Clinical Features aid in diagnosis

• Gestational age• Historical risk factors for infection• Type of distress- grunting,flaring, retractions,

tachypnea• Associated anomalies• Radiographs

Transient Tachypnea of the Newborn

• Mild and self-limited• Increased RR, no retractions, mild cyanosis• FiO2 < 0.4

• Usually term infants, C/S and maternal IV fluids associated

• CXR with prominent vascular markings

Transient Tachypnea of the Newborn

Lungs hyperinflated.

Prominent markings dueto interstitial fluid.

Flat diaphragmNormal heart size

Transient Tachypnea of the Newborn

• Delayed resorption of fetal lung fluid• Must consider, and rule out pneumonia• Treat with antibiotics if diagnosis is uncertain

– Oxygen need beyond six hours– Oxygen need increasing– Worsening symptoms

Meconium aspiration syndrome

• MSF in 10-15% of births• Rare before 34 weeks gestation• More likely with thick staining or particulate

MSF• Thin staining in vigorous infant requires no

special Rx• Can’t prevent all MAS

Meconium Aspiration

• CXR- increased density, irregular [patchy] infiltrates– areas of hyper-expansion, areas of collapse– Fluffy non-homogeneous infiltrates

• May be hard to distinguish from retained fluid, pneumonia

Meconium Aspiration Syndrome

Hyperinflation but patchy

Patchy flocculant infiltrate

Pneumomediastinum

Neonatal Respiratory Disease

• Not every infant with respiratory symptoms has respiratory disease

• Consider Extra-pulmonary causes:– Heart disease

[cardiac]– Hypovolemia, polycythemia, anemia [Blood]– Acidosis, hypoglycemia, hypothermia [Metabolic]– CNS hemorrhage, drugs, muscle disease [CNS]

Respiratory Distress Syndrome (RDS)

• Once the major cause of mortality in premature infants

• Progress in treatment mirrors advances in neonatal medicine

• Effective treatment has improved survival at gestational ages as low as 24 weeks

RDS - Clinical features

• It’s a Disorder of premature infants• Respiratory distress:

– tachypnea, grunting, flaring, retractions

• Difficult to distinguish from pneumonia• Severity peaks at 24-48 hours, resolution by

72-96 hours (without surfactant therapy)• Recovery prolonged by barotrauma or

oxidative injury!!!

RDS - Pathologic features

• Characteristic injury to terminal airways beginning within the first few breaths

• Lungs are solid, congested, with destruction of epithelium of terminal conducting airways

• Hyaline membranes: coagulum of sloughed cells and exudate,plastered against epithelial basement membrane

RDS- Pathophysiology

• Instability of terminal airspaces due to elevated surface forces at liquid-gas interfaces

• Stable alveolar volume depends on a balance between: 1) surface tension at the liquid-gas interface, and 2) recoil of tissue elasticity

RDS - Pathophysiology

• Some alveoli remain collapsed, some are ventilated but collapse during expiration, and some remain ventilated during inspiration and expiration

• Reduction in FRC • Lung Compliance is reduced • Lung resistance is significantly increased

Clinical Presentation

• Tachypnea may be initial symptom- especially at higher gestational age

• Grunting Flaring and Retractions (subcostal, substernal) are hallmark clinical signs

• Always consider other causes of respiratory distress

Initial Care

• Maintain warmth- cold stress will mimic other causes of distress

• Monitor blood glucose levels- assure they are normal

• Provide oxygen to keep the baby pink

Temperature ControlFirst things first:

– Dry the baby– Keep the baby warm

• Warmer beds• Incubators

– Use shields to decease evaporative and convective losses

– USE A HAT!

Initial Care

Ensure adequate hydration:• Start fluids at 70-80 ml/kg/d 10% glucose

solution• Smaller babies may need more fluid !!!• Add electrolytes by the second day• On day 3-4 watch for diuresis

Assess circulation

• Monitor heart rate• Assess Blood pressure• Check peripheral perfusion and capillary refill• Avoid excessive blood sampling

Initial Care

Consider other etiologies:• Make sure it is not INFECTION

– Evaluate– Begin antibiotic therapy as prophylaxis– Continue as clinically indicated

• Anatomic malformations

Acute Complications• Air Leak Syndromes

– Consider with sudden change in condition– More common if baby receiving ventilatory support– Pneumothorax most common

• Therapy– None required if baby is stable– Oxygen 100% [so that nitrogen diffuses

out]– Thorocentesis: Needle or tube

Complications

Right Tension pneumothorax

Pneumomediastinum

Acute Complications

• Intracranial Hemorrhage– High risk if HMD is severe– More common at lower gestational ages– Rare above 33 weeks gestation

• Suspect if sudden change in condition• May coincide with air leak• Change in fontanel, perfusion

Acute Complications• Patent Ductus arteriosus

– Usually evident during resolution phase

• Signs of Congestive Heart Failure– Increased oxygen need– Cardiomegaly– Acidosis, decreased urine output

• Therapy:– Decrease fluid intake– Indomethacin or Ibuprofen

Anatomic abnormalities

• Major– Congenital Diaphragmatic hernia– Airway obstruction– Lung malformation

• Other– Choanal Atresia

Underlying Mechanisms of Disease

• RDS, Pneumonia and Retained fluid all result in degrees of atelectasis

• For RDS and pneumonia, atelectasis may worsen and become increasingly difficult to treat

• Early institution of therapy improves short and long term outcome

• Retained fluid is usually mild, resolves slowly on its own

Therapeutic Goals

• Support the patient during the illness, aid the patient’s own respiratory drive

• Prevent progression from worsening atelectasis

• Avoid complications, such as pneumothorax• Treat infection, avoid nosocomial infection

Additional Support

• Oxygen is key- as much as it takes• Continuous Positive Airway Pressure

– Usually 5-7 cm H2O

– Variety of delivery devices– Simplicity is good-Water bottles

• Mechanical Ventilation– Bag and mask / endotracheal tube– Ventilator if available

Surfactant replacement

• Targets root cause of RDS, aids treatment of pneumonia

• Works with CPAP and mechanical ventilation• Expensive US$5-600/dose, total course up to

US$2400.• Must be stored cold, expires• Requires technical skill for administration

Surfactant replacement

• May be ultimate standard in US, but drawbacks and cost limit use to tertiary centers

• As alternative delivery systems are developed, cost may decrease and ease of use increase

• Not a realistic universal goal for either Ethiopia or United States

Mechanical Support of Ventilation

• Mechanical Ventilation• CPAPPhilosophy of Respiratory Therapy • The Machine doesn’t make the

patient better. It optimizes their condition while they recover

• These are tools- must decide on the right tool for the problem at hand

Mechanical Ventilation- highly effective therapy:

• Relative Indications– FiO2 more than 0.35 -0.4 on CPAP

– Condition is deteriorating– Increased “work of breathing”– Frequent apnea– Plan to give surfactant therapy**

• Absolute Indications– Prolonged apnea– Hypoxemia in absence of heart disease

Significant risk of pneumothoraxUse primarily limited to tertiary centers

Mechanical Ventilation

• Technically complex to use. Can be started easily, but safety requires radiographs, increased skill of Physicians and Nurses, use in tertiary centers

• Expensive Equipment• Difficult to maintain and clean• Numerous and expensive disposable

components

Mechanical ventilation - risks

• Airleaks , especially pneumothoraces as compliance improves

• High risk of nosocomial infection• May increase risk of chronic lung disease

among premature infants due to baro-volutrauma

• May require sedation, reducing spontaneous respiration

CPAP

• Very effective• Available for much lower cost• Technically less complex• May be safely started very early- no

radiograph is required• Lower risk of pneumothorax• Lower risk of nosocomial infection, chronic

lung disease

CPAP

• First used by mask in 1936 for acute ventialtory insufficiency

• First used in 1940s in high altitude flying• Introduced in treatment of Adult Respiratory

Distress Syndrome in 1967• First applied to infants with HMD in 1971,

improved survival from 25% to 80%

Continuous Positive Airway Pressure(CPAP)

Can correct ventilatory insufficiency by;

•Diminishing atelectasis•Improving Functional residual capacity•Correcting ventilation-perfusion abnormalities•Decreasing pulmonary edema•Reducing INTRAPULMONARY SHUNTING

CPAP - Mechanism of action

•CPAP prevents collapse of unstable alveoli upon expiration

•Facilitates recruitment of unventilated alveoli

•Reduces right to left shunting across foramen ovale

•Reduces left to right shunting across the Ductus Arteriosus, improving cardiac output and blood pressure

Pulmonary Effects

• Improved oxygenation through increased FRC and recruitment of alveoli

• Compliance is improved as airways and alveoli are distended

• Further alveolar collapse is prevented, improving surfactant conservation

Cardiovascular Effects

• May decrease venous return and blood pressure, if patient is hypovolemic

• May increase pulmonary vascular resistance, except in HMD, where it is decreased

• Cardiac output may be compromised

Delivery Devices

• Many variations but can be inexpensively built:

• All devices employ:– continuous gas flow (blended air/oxygen) supply

to inspiratory side– a reservoir bag if necessary to monitor flow– an expiratory valve or submerged tubing

• The result is the production of expiratory pressures that exceed ambient levels

Delivery Devices

CPAP device - Colombia Presbyterian

Delivery Devices

• Gas delivered to circuit with adequate flow • CPAP maintained by either underwater tube

or a valve- which creates a set amount of resistance or pressure

• Gas flow must be adequate to keep reservoir distended

Fluid Dynamics

Flow through a tube = Pressure/ Resistance

Resistance α Viscosity x Length/Radius4

Flow = ΔP x π R 4 / Length x Viscosity Since viscosity of gas is constant:

Flow α ΔP x R 4 / Length

Delivery of CPAP

• Small R or long length: • Decreased flow on inspiratory side due to

increased resistance = ↓ CPAP• Increased resistance on expiratory side

obstructs flow = ↑ CPAP• Wider and shorter tubing means lower

resistance, greater flow, so CPAP to be reliably set by depth to which tube end is submerged.

CPAP Delivery

• Endotracheal tube: simple and efficient, but increases work of breathing and airway resistance by reducing radius

• Face mask: Easy to apply, inexpensive, but difficult to regulate, causes abdominal distention

CPAP Delivery- Nasal Prongs

• Simple to apply and use • Low cost, especially if “home made”• Short length minimizes resistance due to low

radius prongs• Mouth leaks prevents excess but do hamper

efficacy

Application

• Need humidification mechanism, except for very short term use

• “Water Bottle” pressure control is simple to adjust and maintain, can not “breakdown”

• New evidence suggests that the “BUBBLE” effect may aid in ventilation

Rationale for development of locally made units vs. Imported

• Equally effective in treating patients• Simpler mechanism decreases breakdowns,

simplifies cleaning and maintenance• Made with locally available parts, manufactured in

country, so more readily repaired, committed service• BUBBLE aspect may be superior• Lower cost allows broader deployment, readily

available resource even for smaller hospitals

KSE CPAP- The Vietnam experience

KSE=Kirk S Evans, engineer

Device and nasal catheters

Nasal catheter

CPAP Indications

• FiO2 above 0.3 with clinical distress

• FiO2 above 0.4

• Significant retractions after extubation• Hypoventilation: CPAP may be helpful

• Used most often at 4-6 cm of H2O

CPAP risks

• Hard to control in spontaneously breathing baby, especially if vigorous

• Potential for airleak• Can’t give surfactant• May worsen ventilation

Beginning Therapy

• Start at CPAP of 6 cm H2O. Look for increase in pO2 within 10-15 minutes

• If pCO2 increases reduce pressure

• If no response, may increase to 8 cm H2O

• Optimal level may correlate with the point of initial rises in esophageal pressure measured with a feeding tube

Failure

• No response to increased level of CPAP• Rise in CO2 level or drop in O2 level on CPAP• If noninvasive system fails, may consider

endotracheal CPAP• If acidosis persists, change to mechanical

ventilation.

Weaning

• Decrease Oxygen as long as color maintained, or measured levels are normal

• When FiO2 is < .40, wean CPAP by 1 cm. Monitor color, work of breathing

• Wean to 4 cm H2O If tolerated, wean to hood oxygen and then to air

• Monitor as oxygen is weaned

Other considerations

• May not work for all babies- observation and assessment are necessary

• For some patients, intubation and mechanical ventilation are required

• Adjuvant or parallel therapies remain important

Steroids and surfactant

Conclusions

• The understanding of the root cause and pathophysiology of hyaline membrane disease has made successful treatment a reality

• CPAP and mechanical ventilation have been refined to provide support while minimizing complications

• Antenatal steroids minimize incidence and severity of RDS

Conclusions

• CPAP is a key part of the treatment array• Delivery can be accomplished by simple, easily

made devices• Many babies, especially those 1500 gm and

above can be helped by CPAP• Continued progress begins with these basic

steps