Respiratory Distress in Pediatric Age

Respiratory Distress and Failure in Pediatric Age

Introduction

Respiratory distress and failure represent a spectrum of clinical conditions that can rapidly progress to cardiopulmonary arrest if not promptly recognized and managed. In children, respiratory issues are the most common cause of cardiac arrest, underscoring the importance of early intervention. The unique anatomy, physiology, and pathology of the pediatric respiratory system necessitate age-specific approaches to assessment and treatment.

Definitions

Respiratory Distress: A clinical state characterized by increased work of breathing, with the patient able to compensate and maintain adequate oxygenation and ventilation.
Respiratory Failure: Inability to maintain adequate gas exchange, resulting in hypoxemia (PaO₂ <60 mmHg) and/or hypercarbia (PaCO₂ >50 mmHg). Can be classified as:
- Type I (Hypoxemic): Characterized primarily by hypoxemia
- Type II (Hypercapnic): Characterized by hypercarbia, with or without hypoxemia
- Type III (Perioperative): Due to atelectasis from hypoventilation during anesthesia
- Type IV (Shock): Associated with hypoperfusion in septic or hypovolemic shock

Pediatric Respiratory Anatomy and Physiology

Several factors make children, especially infants, more susceptible to respiratory compromise:

Airways:
- Proportionately narrower lumens; resistance increases exponentially with decreased radius (Poiseuille's law)
- Softer cartilaginous support, more compliant chest wall, leading to easier collapse
- Proportionately larger tongue, superior larynx (C3-C4 vs. C5-C6 in adults)
- Funnel-shaped larynx with narrowest point at cricoid (vs. vocal cords in adults)
Chest Wall and Diaphragm:
- More compliant chest wall provides less recoil for passive exhalation
- Diaphragm prone to fatigue; principal muscle of respiration
- Horizontal rib orientation less effective for expanding chest volume
Respiratory Dynamics:
- Higher metabolic rate and oxygen consumption
- Lower functional residual capacity (FRC); desaturate more quickly
- Higher closing capacity relative to FRC; prone to atelectasis

Etiology

Causes of pediatric respiratory distress/failure can be categorized by anatomic location:

Upper Airway

Croup (laryngotracheobronchitis)
Epiglottitis (rare since Hib vaccine)
Bacterial tracheitis
Angioedema, anaphylaxis
Foreign body aspiration
Peritonsillar/retropharyngeal abscess

Lower Airway

Asthma
Bronchiolitis
Pneumonia (viral, bacterial, aspiration)
Foreign body in bronchus

Parenchymal

Acute respiratory distress syndrome (ARDS)
Pulmonary edema (cardiogenic, non-cardiogenic)
Pulmonary hemorrhage

Extrapulmonary

Neurologic/Neuromuscular: Central hypoventilation, spinal cord injury, Guillain-Barré syndrome, botulism
Chest Wall: Flail chest, pneumothorax
Abdominal: Diaphragmatic hernia, abdominal compartment syndrome
Metabolic: Diabetic ketoacidosis, inborn errors of metabolism
Toxicologic: Opioid overdose, organophosphate poisoning

Clinical Assessment

History

Key elements include:

Onset and progression of symptoms
Associated symptoms: fever, cough, stridor, wheezing
Recent illnesses, exposures, vaccinations
Past medical history: prematurity, asthma, congenital anomalies
Response to any pre-hospital interventions

Physical Examination

The Pediatric Assessment Triangle (PAT) provides a rapid, global assessment:

Appearance: Tone, interactiveness, consolability, look/gaze
Work of Breathing: Abnormal airway sounds, retractions, flaring, positioning
Circulation to Skin: Pallor, mottling, cyanosis

Detailed examination should note:

Vital Signs: Tachypnea often the earliest sign; heart rate, blood pressure, oxygen saturation
Mental Status: Agitation may indicate hypoxemia; lethargy suggests hypercapnia or fatigue
Airway Sounds:
- Stridor: Upper airway obstruction; inspiratory (extrathoracic), expiratory (intrathoracic), biphasic (fixed)
- Wheezing: Lower airway obstruction; differentiates from stertor (snoring), snoring (nasopharyngeal)
- Grunting: Attempt to provide auto-PEEP; ominous in infants
Retractions: Suprasternal, intercostal, subcostal; degree correlates with severity
Nasal Flaring: Attempts to decrease airway resistance
Head Bobbing: Accessory muscle use in infants
Lung Auscultation: Air entry, breath sound quality, adventitious sounds
Perfusion: Capillary refill, peripheral pulses, liver edge (right heart failure)

Diagnostic Studies

Pulse Oximetry: Continuous, non-invasive; may be less reliable in poor perfusion, motion artifact
Capnography: End-tidal CO₂ monitoring; useful for intubated patients, can indicate hypoventilation earlier than SpO₂
Blood Gas Analysis:
- Arterial: Gold standard for gas exchange; pH, PaO₂, PaCO₂, HCO₃⁻, base excess
- Venous/Capillary: Adequate for pH, PvCO₂; PvO₂ not reliable
Chest Radiograph: Evaluate for pneumonia, atelectasis, pneumothorax, pulmonary edema
Laboratory: CBC, electrolytes, glucose, blood culture if sepsis suspected
ECG/Echocardiography: If cardiac etiology considered

Management

Initial Stabilization (ABCs)

Airway:
- Position: Sniffing position (infants), head tilt-chin lift, jaw thrust if trauma
- Suctioning: Bulb for infants, Yankauer for copious secretions
- Adjuncts: Nasopharyngeal/oropharyngeal airways if no gag reflex
Breathing:
- Oxygen: Titrate to SpO₂ 94-98% (90-94% if risk of hyperoxic injury)
- Non-invasive support: High-flow nasal cannula (HFNC), CPAP, BiPAP
Circulation:
- Vascular access: IO if immediate need and no IV
- Fluid resuscitation for signs of shock

Respiratory Support

Non-invasive Ventilation (NIV):

HFNC: Up to 50-60 LPM flow, provides some PEEP, decreases work of breathing
CPAP: 5-10 cmH₂O; improves FRC, reduces atelectasis
BiPAP: Added inspiratory pressure support; useful in neuromuscular disease, obstructive lung disease

Invasive Mechanical Ventilation: Indications include:

Apnea or impending respiratory arrest
Refractory hypoxemia (PaO₂ <60 mmHg on FiO₂ >0.6) or hypercarbia (PaCO₂ >50 with pH <7.25)
Inability to protect airway (GCS ≤8)
Hemodynamic instability

Initial settings:

Mode: Usually start with synchronized intermittent mandatory ventilation (SIMV) or assist-control (AC)
Rate: Varies by age; often start near physiologic rate
Tidal Volume: 6-8 mL/kg ideal body weight (lower if lung injury)
PEEP: 5 cmH₂O, titrate up for hypoxemia
FiO₂: Start 100%, wean to minimum needed for target SpO₂

Pharmacotherapy

Targeted to underlying etiology:

Bronchodilators: β₂-agonists (albuterol), anticholinergics (ipratropium) for bronchospasm
Corticosteroids: For laryngeal edema (e.g., croup), reactive airway disease exacerbations
Epinephrine: Nebulized for croup, IM for anaphylaxis, IV for shock
Magnesium Sulfate: IV for severe asthma; bronchodilator, anti-inflammatory
Antibiotics: For bacterial pneumonia, sepsis
Antivirals: Oseltamivir for influenza if <48 hours symptomatic
Surfactant: Consider in neonates/infants with ARDS, meconium aspiration

Adjunctive Therapies

Heliox: 70:30 helium:oxygen mixture; reduces airflow resistance in upper airway obstruction
Inhaled Nitric Oxide (iNO): Pulmonary vasodilator; may improve V/Q matching in ARDS
Prone positioning: Improves V/Q matching, recruitability in ARDS
ECMO (Extracorporeal Membrane Oxygenation): Rescue therapy for refractory hypoxemia despite maximal ventilatory support

Disease-Specific Considerations

Status Asthmaticus

Continuous or intermittent nebulized β₂-agonists ± ipratropium
Systemic corticosteroids (prednisone, methylprednisolone)
Consider IV magnesium sulfate, terbutaline, aminophylline
Avoid routine use of antibiotics unless clear infection
Intubation if needed; caution for air-trapping, dynamic hyperinflation

Bronchiolitis

Supportive care: hydration, oxygen, suctioning
Trial of nebulized hypertonic saline
Most guidelines recommend against routine bronchodilators, corticosteroids
High-flow nasal cannula may reduce intubation rates

Croup

Mild: Optional dexamethasone (0.15-0.6 mg/kg)
Moderate-Severe: Dexamethasone + nebulized epinephrine (0.5 mL of 2.25% solution)
Humidified air/oxygen controversial; avoid upsetting child
Monitor for post-treatment rebound; may need multiple epinephrine doses

Monitoring and Complications

Ongoing Assessment:

Continuous cardiorespiratory and SpO₂ monitoring
Serial blood gases (initially q2-4h, then as needed)
Daily chest radiographs if intubated
Assess for vent asynchrony, auto-PEEP
Titrate respiratory support to maintain pH >7.25, PaO₂ >60, SpO₂ >88%

Potential Complications:

Ventilator-Associated Pneumonia (VAP): Use VAP bundle (head-of-bed elevation, oral care, subglottic suctioning)
Barotrauma: Pneumothorax, pneumomediastinum; minimize peak inspiratory pressures
Volutrauma: Alveolar overdistension; use lung-protective strategies (low tidal volumes)
Atelectrauma: Repetitive alveolar collapse; adequate PEEP
Oxygen Toxicity: Especially in neonates; target minimum FiO₂ for adequate oxygenation
Post-extubation Stridor: Consider dexamethasone pre-extubation if high-risk (prolonged intubation, multiple attempts, large tube)
Sedation-related: Delirium, withdrawal, ventilator asynchrony; use validated sedation scales, daily interruption when possible

Special Populations

Neonates

Unique pathologies: respiratory distress syndrome (RDS), meconium aspiration, persistent pulmonary hypertension of the newborn (PPHN)
More prone to apnea, especially if premature
Consider caffeine for apnea of prematurity
Exogenous surfactant often beneficial
Vulnerability to hyperoxic injury; target SpO₂ 90-95% in preterm infants

Congenital Heart Disease

May present with respiratory distress from pulmonary overcirculation or edema
Cyanotic lesions may have baseline hypoxemia; know acceptable SpO₂ range
"Tet spells" in Tetralogy of Fallot: knees-to-chest position, morphine, phenylephrine
Caution with positive pressure ventilation in lesions with pulmonary hypertension or single-ventricle physiology

Neuromuscular Disease

Often develop hypercapnic respiratory failure due to muscle weakness
May need lower threshold for non-invasive support (e.g., nocturnal BiPAP)
Aggressive pulmonary toilet, assisted cough techniques
Consider tracheostomy for chronic ventilation

Weaning and Extubation

Prerequisites for extubation readiness:

Resolution or improvement of underlying cause
Adequate oxygenation: FiO₂ ≤0.5, PEEP ≤5-7 cmH₂O
Adequate ventilation: Low ventilatory requirements, normal PaCO₂ (or baseline)
Hemodynamic stability, no significant electrolyte disturbances
Able to protect airway: Adequate cough, gag reflex, manageable secretions
Successful spontaneous breathing trial (SBT): 30-120 minutes on minimal support (PS 5-8, CPAP, or T-piece)

Extubation Procedure:

Pre-oxygenate with 100% FiO₂
Suction airway, consider cuff leak test
Administer post-extubation corticosteroid if high-risk for stridor
After extubation, provide supplemental oxygen, monitor closely
Consider prophylactic NIV in high-risk patients

Ethical and End-of-Life Considerations

Establish goals of care early, especially for children with life-limiting conditions
Involve palliative care for symptom management, family support
Consider quality of life, projected outcomes when discussing chronic ventilation
Allow for care conferences with family, subspecialists, ethics committee if needed
Respect do-not-intubate (DNI) orders; offer alternative comfort measures
Provide compassionate extubation when appropriate, with adequate anticipatory symptom management

Prevention and Follow-up

Immunizations: Particularly influenza, pneumococcus, Hib, pertussis
Tobacco Exposure: Counsel caregivers on smoking cessation, avoid secondhand smoke
Asthma Management: Asthma action plans, controller medications, trigger avoidance
Technology-dependent Children: Ensure home equipment (oxygen, suction, monitors), caregiver training
Post-discharge Follow-up: Primary care, pulmonology, neurodevelopmental screening after critical illness