The Breathless Child: A Systematic Approach

Definition

The evaluation of a breathless child is a critical, time-sensitive challenge. Understanding the clinical spectrum is vital for effective communication, triage, and timely escalation. This spectrum represents a continuum of physiological compromise, from mild difficulty in breathing to imminent cardiorespiratory arrest.

• Breathlessness (Dyspnoea): This is the subjective sensation of difficult or laboured breathing. In older children who can verbalise, they may complain of being "unable to catch their breath."

  • In infants and pre-verbal children, this state must be inferred from observable behaviours that signal an inability to cope with the work of breathing. These signs can be subtle and include a weak, shortened, or hoarse cry; an inability to complete a feed without pausing for breath (as feeding requires coordination of sucking, swallowing, and breathing); and a general look of anxiety or distress (1).

• Respiratory Distress: This is a state of active compensation, where the child expends significant physiological energy to maintain adequate oxygenation and ventilation. The body is successfully meeting its metabolic demands, but at a significant cost.

  • Key Signs: The signs of distress are direct manifestations of this increased effort. They include tachypnoea (an increased respiratory rate), nasal flaring (to decrease nasal resistance and draw in more air), and retractions. Retractions are the inward pulling of the chest wall due to the high negative intrathoracic pressure generated to overcome airway obstruction or poor lung compliance. Their location can indicate the level of obstruction: subcostal and intercostal retractions are common, but suprasternal and supraclavicular retractions signify more severe obstruction, as the child recruits accessory muscles of the neck (2).

• Respiratory Failure: This is a state of decompensation and a life-threatening emergency. It is a condition where the respiratory system can no longer maintain adequate gas exchange, resulting in hypoxaemia (insufficient oxygen in the blood) and/or hypercapnia (excess carbon dioxide in the blood).

  • Critical Transition: The transition from distress to failure is often perilous and can be missed. It is frequently marked by a paradoxical decrease in the visible work of breathing as the child's respiratory muscles fatigue.

  • ⚠️ The quiet, lethargic, or drowsy child who was previously agitated and working hard to breathe is a pre-terminal sign. This change from a "noisy, distressed" state to a "quiet, tired" state signals impending collapse. This state is marked by signs of end-organ dysfunction due to hypoxia and hypercapnia, such as altered mental status and poor peripheral perfusion (cool, clammy, mottled skin) (3, 4).

Epidemiology

Acute respiratory infections (ARIs) represent a formidable and persistent public health challenge in Malaysia, consistently ranking as a leading cause of morbidity and mortality in children under five (16).

• Burden of Disease: The gravity of the situation is underscored by national statistics. In 2021, pneumonia was the third leading cause of death in this vulnerable age group. This is not a rare occurrence; national survey data from 2022 revealed that 1.4% of all Malaysian children under five had experienced symptoms of an ARI within the preceding two weeks, a figure that translates to a significant and constant burden on primary care clinics and emergency departments (16). Consequently, diseases of the respiratory system are a primary driver of hospitalisations, accounting for a substantial 13.86% of admissions to government hospitals and an even higher 18.73% to private hospitals in 2018 (34).

• Antimicrobial Stewardship Challenge: A particularly concerning local trend is the disconnect between aetiology and practice in antimicrobial use. Despite the vast majority of ARIs being viral in origin, the antibiotic prescription rate for children with ARI symptoms surged alarmingly from 58.9% in 2016 to 74.6% in 2022. This practice, often driven by diagnostic uncertainty or parental pressure, not only fails to treat the underlying viral cause but also fuels the growing threat of antimicrobial resistance, a major public health crisis. It also exposes the individual child to unnecessary risks like diarrhoea, allergic reactions, and disruption of their gut microbiome (16).

• Local Viral Patterns: The viral landscape in tropical Malaysia is relentless and differs significantly from temperate regions. While Western textbooks describe a distinct "respiratory season," key pathogens like Enterovirus/Rhinovirus, Influenza, and Adenovirus circulate year-round, with no significant seasonal variation.

  • Only Respiratory Syncytial Virus (RSV) demonstrates predictable seasonality, with a primary peak between July and September, often followed by a smaller wave towards the end of the year (November-December) (20, 35). This perennial circulation means clinicians must maintain a high index of suspicion for respiratory illness at all times, as there is no "off-season." The COVID-19 pandemic also temporarily altered these patterns, leading to a concept of "immunity debt," with a significant rebound surge of RSV in 2022 after restrictions were lifted.

Etiology

The cause of respiratory distress is intrinsically linked to the child's age. This age-stratified diagnostic approach is a powerful tool for clinical reasoning, helping to prioritize the differential diagnosis at the bedside (11).

• Neonate (<28 days): The immediate postnatal period is dominated by issues of cardiorespiratory transition.

  • Common: Transient Tachypnoea of the Newborn (TTN), caused by delayed clearance of fetal lung fluid, is common in term infants delivered by Caesarean section. Respiratory Distress Syndrome (RDS), resulting from surfactant deficiency, is the hallmark of prematurity (27).

  • Must Not Miss: Infectious causes like sepsis (especially from Group B Streptococcus) and pneumonia must be aggressively sought and treated. Critical congenital anomalies that require immediate recognition include congenital heart disease (CHD) presenting with failure, congenital diaphragmatic hernia, and structural airway issues like choanal atresia (bilateral posterior nasal passage blockage) (12).

• Infant (1-12 months): This age is the epicentre of viral respiratory illnesses, driven by waning maternal antibodies and increased environmental exposure.

  • Common: Viral Bronchiolitis, most often caused by RSV, is exceedingly common and a leading cause of hospitalization in this group. Viral Pneumonia and Croup (laryngotracheobronchitis) are also frequent (19, 20).

  • Consider: Congenital issues like laryngomalacia often present in the first few months. The first episodes of episodic viral wheeze (a precursor to asthma) and the possibility of Foreign Body Aspiration (FBA) emerge as the infant becomes more mobile and begins to explore objects with their mouth (18, 36).

• Toddler (1-3 years): This age is defined by increased mobility, curiosity, and an immature swallowing mechanism.

  • Peak Age For: Croup and Foreign Body Aspiration (FBA). The combination of oral exploration, molar teeth that are not yet fully developed for effective grinding, and a tendency to run and play while eating creates the perfect storm for FBA (36).

  • Common: Asthma becomes an increasingly important diagnosis, often triggered by viral infections. Pneumonia (both viral and bacterial) remains a frequent cause of admission.

• Preschool (3-5 years):

  • Most Common: Asthma solidifies as the most common cause of recurrent respiratory distress in this age group (36).

  • Also Common: Pneumonia remains prevalent, with Adenovirus being a notable pathogen known for causing more severe disease (20).

  • Consider in Toxic Child: Complications of upper respiratory infections like retropharyngeal abscess and the life-threatening bacterial tracheitis should be considered in a toxic-looking child with stridor who is not responding to standard croup therapy.

• School-Age (>5 years):

  • Most Common: Asthma is the dominant diagnosis (36).

  • Also Common: Pneumonia, including atypical pathogens like Mycoplasma pneumoniae, becomes more frequent (20).

  • Other Causes: Consider exercise-induced bronchoconstriction, complications like pleural effusion, and important non-pulmonary causes of breathlessness such as Diabetic Ketoacidosis (DKA), which presents with deep, sighing Kussmaul respirations as a compensation for metabolic acidosis.

Pathophysiology

Understanding the underlying mechanism of obstruction or compromise is key to interpreting clinical signs and directing therapy. The location of the problem dictates the sound produced and the pattern of distress.

• Upper Airway Obstruction (Produces Stridor):

  • Croup: A viral infection inflames the subglottic region. This area, encircled by the rigid cricoid cartilage, is the narrowest part of the paediatric airway. According to Poiseuille's law, resistance is inversely proportional to the radius to the fourth power (resistance ∝ 1/r⁴). This means that even 1mm of oedema can increase airway resistance 16-fold, causing turbulent airflow and the characteristic inspiratory stridor and barking cough (13).

  • Laryngomalacia: A structural, congenital issue where immature supraglottic tissues (like the arytenoid cartilages and aryepiglottic folds) are "floppy" and collapse inward during the negative pressure of inspiration, creating a dynamic, fluttering obstruction and an inspiratory stridor that is often worse when supine or agitated (18).

• Lower Airway Disease (Produces Wheeze):

  • Viral Bronchiolitis: RSV infection of the small airways (bronchioles) leads to a cascade of inflammation, oedema, necrosis of epithelial cells, and a slough of mucus and cellular debris. This creates a "ball-valve" obstruction: air is drawn past the plug during inspiration but becomes trapped during expiration as the airway naturally narrows. This leads to progressive lung hyperinflation, a flattened diaphragm (reducing its efficiency), and a severe ventilation/perfusion (V/Q) mismatch, which is the primary driver of hypoxaemia (19).

  • Asthma: The underlying pathology is a triad of reversible processes: bronchoconstriction (hyperresponsive smooth muscle contracts excessively), airway inflammation (chronic eosinophilic inflammation causes airway wall oedema), and mucus plugging (goblet cells produce thick, tenacious mucus). Together, these cause widespread airflow obstruction, leading to the classic polyphonic expiratory wheeze and dynamic hyperinflation (22).

• Parenchymal Disease (Affects Gas Exchange):

  • Pneumonia: The alveoli fill with inflammatory exudate (consolidation), effectively turning air-filled sacs into solid, fluid-filled ones where gas exchange is impossible. Blood perfusing these non-ventilated areas returns to the left heart deoxygenated. This phenomenon, where deoxygenated blood mixes with arterial blood, is called an intrapulmonary shunt and is the principal cause of hypoxaemia in pneumonia (26).

  • Paediatric ARDS (PARDS): This is the most severe form of acute lung injury, representing a final common pathway of overwhelming lung inflammation. A direct (e.g., severe pneumonia) or indirect (e.g., sepsis, pancreatitis) insult triggers diffuse damage to the alveolar-capillary barrier. This leads to catastrophic, protein-rich pulmonary oedema, inactivation of surfactant (leading to widespread alveolar collapse or atelectasis), and profoundly stiff, non-compliant lungs. The result is massive intrapulmonary shunting and severe, refractory hypoxaemia (hypoxaemia that does not respond well to supplemental oxygen) (6).

• Foreign Body Aspiration (FBA):

  • This is a purely mechanical obstruction. A large object lodged in the larynx or trachea can cause complete obstruction and rapid asphyxiation. More commonly, a smaller object (like a peanut or bead) travels down into a mainstem bronchus (usually the right, due to its wider and more vertical orientation). Here, it can create the classic ball-valve effect, leading to unilateral air trapping, hyperinflation, and a localized wheeze. Organic matter (like nuts) can also incite a severe local inflammatory reaction (granuloma), leading to post-obstructive pneumonia or bronchiectasis if not removed (31, 33).

Clinical Presentation

A meticulous clinical evaluation, often performed rapidly using the Paediatric Assessment Triangle (Appearance, Work of Breathing, Circulation), often provides the diagnosis before any tests are ordered.

• Classic Presentations:

  • Croup: A toddler with a 1-2 day history of coryza and low-grade fever who develops a characteristic barking cough and inspiratory stridor, which are classically worse at night (14).

  • Bronchiolitis: An infant (<2 years) with several days of coryza and low-grade fever, progressing to tachypnoea, fine inspiratory crackles, and widespread expiratory wheezing (19).

  • FBA: A sudden onset of choking, violent coughing, and unilateral wheeze in a previously well toddler. The history of a witnessed choking event is classic but may be absent (32).

• Diagnostic Clues:

  • A barking, "seal-like" cough is pathognomonic for croup (14).

  • The triad of new-onset unilateral wheeze, cough, and unilaterally diminished air entry is highly specific for a bronchial foreign body (32).

• Common Symptoms (>50%):

  • Tachypnoea is a sensitive but non-specific sign of distress, present in almost all cases (1).

  • Cough and fever are common across most infectious aetiologies (41).

• Less Common Symptoms (10-50%):

  • Hoarseness of the voice or cry points towards laryngeal inflammation as seen in croup (13).

  • Poor feeding is a very sensitive indicator of significant respiratory distress in infants, as they cannot coordinate sucking, swallowing, and breathing (1).

⚠️ Red Flag Signs & Symptoms

These signs indicate impending respiratory failure and require immediate senior help.

• Altered Mental Status: Lethargy, drowsiness, or inconsolable irritability are direct consequences of hypoxia and/or hypercapnia affecting the central nervous system. Hypercapnia acts as a narcotic, causing drowsiness (3).

• Cyanosis: A late and ominous sign indicating severe deoxygenation of haemoglobin (at least 5 g/dL of deoxygenated haemoglobin). Its presence means profound hypoxia is already established (2).

• Diminished Respiratory Effort: Bradypnoea (a slow respiratory rate) or shallow breathing in a tired-looking child indicates respiratory muscle fatigue. The child can no longer sustain the work of breathing and is on the verge of respiratory arrest (3).

• A "Silent Chest": In a child with a history of severe asthma, the disappearance of wheeze is a life-threatening sign. It indicates that airflow is so poor that it is insufficient to even generate a sound. This requires immediate, aggressive intervention (40).

• Head Bobbing or Grunting: Head bobbing signifies the use of neck accessory muscles (sternocleidomastoids) to overcome severe obstruction. Grunting is a physiological manoeuvre where the child exhales against a partially closed glottis to create positive end-expiratory pressure (PEEP), attempting to keep alveoli from collapsing (1).

• Inability to Speak or Cry: Suggests a severely obstructed airway that prevents air from passing through the vocal cords (53).

Complications

• Acute: The most feared acute complication is cardiorespiratory arrest, which in children is almost always secondary to progressive, uncorrected hypoxia. Other acute issues include hypoxic brain injury with potential for long-term neurological deficit, pneumothorax (from severe air trapping in asthma or barotrauma from positive pressure ventilation), and secondary bacterial infection of a primary viral illness (12).

• Chronic: Untreated FBA or recurrent, severe, or poorly managed pneumonia can lead to permanent lung damage in the form of bronchiectasis (a permanent, abnormal widening of the airways). A significant proportion of infants hospitalized with severe RSV bronchiolitis will go on to develop a recurrent post-viral wheeze, sometimes referred to as reactive airway disease. Survivors of severe PARDS can suffer from long-term pulmonary fibrosis, reduced exercise tolerance, and significant neurocognitive impairment (33).

Prognosis

While the prognosis for the vast majority of children with common viral illnesses like croup and bronchiolitis is excellent with appropriate supportive care, the stakes for severe disease remain high.

• Pneumonia remains a leading cause of death in Malaysian children under five, a stark reminder of its potential lethality (16).

• PARDS, though less common, carries a very high mortality rate, with severe infection (septicaemia and pneumonia) being the primary driver of this outcome in the local Malaysian setting (7).

• For asthma, the prognosis is heavily influenced by management and risk factors; a history of a previous PICU admission for asthma dramatically increases the risk for a future life-threatening attack (39). Risk factors for poor outcomes in bronchiolitis include prematurity, underlying congenital heart disease, and chronic lung disease.

Differential Diagnosis

Distinguishing between common causes of respiratory distress is a key clinical skill.

• [Croup vs. Asthma]:

  • Croup: Presents with inspiratory stridor and a barking cough, indicating upper airway obstruction. It does not respond to salbutamol (13).

  • Asthma: Presents with expiratory wheeze, indicating lower airway obstruction. It typically shows a good clinical response to inhaled bronchodilators like salbutamol. A personal or family history of atopy (asthma, eczema, allergic rhinitis) strongly favours this diagnosis (22).

• [Bronchiolitis vs. Pneumonia]: These conditions often overlap.

  • Bronchiolitis: Typically affects infants <2 years and is characterized by diffuse inflammation of the small airways, leading to widespread wheeze and fine inspiratory crackles on a background of coryzal symptoms (19).

  • Pneumonia: Should be strongly suspected if the child presents with a high fever (>39°C), appears toxic, or if there are focal chest signs on auscultation (focal crackles, reduced air entry, bronchial breathing). A chest X-ray is the key investigation to differentiate the two if the clinical picture is ambiguous (50).

• [Foreign Body Aspiration]: This diagnosis must be entertained in any toddler with a sudden onset of respiratory symptoms, particularly choking or coughing, without a preceding viral prodrome.

  • The cardinal distinguishing features are the unilaterality of the physical signs (localized wheeze, asymmetric air entry) and a complete lack of response to medical therapies like bronchodilators or steroids (32). A witnessed choking event is highly suggestive but may be absent in up to 50% of cases (41).

Investigations

Investigations should be judiciously targeted to answer specific clinical questions, confirm a diagnosis, or assess severity, not ordered as a routine panel.

Immediate & Bedside Tests

• Pulse Oximetry (SpO2): This is the fifth vital sign in paediatrics. It is an essential, non-invasive bedside tool to objectively quantify the severity of hypoxaemia (the action), which directly guides the need for supplemental oxygen therapy and the decision for hospital admission (the rationale). In Malaysian hospitals, an SpO2 <94% is a common threshold for intervention (19).

• Peak Expiratory Flow Rate (PEFR): In cooperative children (typically >5-6 years), this provides a simple, objective measure of airflow obstruction (the rationale). It is invaluable for quantifying the severity of an asthma exacerbation at presentation and for tracking the response to bronchodilator therapy (the action) (39).

Diagnostic Workup

• First-Line (Chest X-ray): A CXR is indicated for severe distress, diagnostic uncertainty, or suspicion of complications (pneumonia, FBA, pneumothorax). It provides crucial diagnostic information, revealing focal consolidation in pneumonia, signs of hyperinflation (flattened diaphragms, increased lucency) in asthma/bronchiolitis, or the classic "steeple sign" (subglottic narrowing) in croup (19, 51). For suspected FBA, an expiratory film can unmask unilateral air trapping not visible on an inspiratory film.

• Gold Standard:

  • For FBA: Rigid bronchoscopy under general anaesthesia is the gold standard for both diagnosis and treatment (the action), as it provides direct visualization and a means for removal of the object (the rationale) (18).

  • For PARDS: The diagnosis is confirmed by meeting the specific PALICC criteria, which require objective evidence of severe, non-cardiogenic hypoxaemic respiratory failure on imaging and blood gas analysis (the action), thereby identifying this specific, severe phenotype of lung injury that mandates specialized ICU-level care (the rationale) (6).

• Nasopharyngeal Aspirate (NPA) for Viral PCR: This test is highly useful to identify the specific viral pathogen (e.g., RSV, Influenza) causing an ARI (the rationale). Its primary utility is for infection control purposes, allowing for the cohorting of patients on the ward to prevent nosocomial spread, and for epidemiological surveillance. It also guides therapy in specific cases, such as the use of oseltamivir for influenza (the action) (20).

Monitoring & Staging

• Blood Gas Analysis: This is performed in any child with moderate-to-severe distress to formally quantify the degree of hypoxaemia (PaO2) and, most importantly, ventilation (PaCO2) and acid-base status (pH) (the action). It helps differentiate between Type 1 (hypoxaemic) and Type 2 (hypercapnic) respiratory failure. A rising PaCO2 on serial measurements is a critical indicator of respiratory muscle fatigue and impending respiratory failure, signalling an urgent need to escalate respiratory support (the rationale) (7).

• Full Blood Count (FBC): While not routinely helpful in differentiating viral from bacterial causes, an FBC is indicated in a child who appears septic or has severe pneumonia (the action). It helps to assess for significant neutrophilic leukocytosis or thrombocytopenia, which may point towards a severe bacterial infection and guide management decisions (the rationale) (19).

Management

The management of a breathless child is a dynamic process that begins with immediate life-saving interventions based on the systematic ABCDE approach, followed by aetiology-specific treatments guided by the Malaysian Paediatric Protocols (19).

Management Principles

1. Correct life-threatening hypoxaemia.

2. Reduce the excessive work of breathing to prevent exhaustion.

3. Treat the underlying cause.

Acute Stabilisation (The First Hour)

• A - Airway:

  • Action: Ensure the airway is patent. Open the airway with simple manoeuvres like a head-tilt-chin-lift or jaw thrust (in case of potential cervical spine injury) and suction secretions (53).

  • Rationale: To relieve simple positional obstruction and clear occluding material that may be causing the distress.

• B - Breathing:

  • Action: Administer high-flow oxygen immediately to any child with significant distress or hypoxaemia. Use a non-rebreather mask at 10-15 L/min to deliver the highest possible fraction of inspired oxygen (FiO2) and maintain SpO2 ≥94% (49).

  • Rationale: To prevent tissue hypoxia, which is the final common pathway to cardiac arrest in children.

• C - Circulation:

  • Action: Secure vascular access promptly. In a severely ill or shocked child, this means establishing intravenous (IV) or, if that fails after two attempts, intraosseous (IO) access. If in shock (tachycardia, prolonged CRT, hypotension), give a rapid fluid bolus of IV Normal Saline 10-20 mL/kg over 5-10 minutes and reassess (54).

  • Rationale: To provide a reliable route for the administration of emergency fluids and medications and to restore tissue perfusion.

Definitive Therapy

• Asthma (Moderate-Severe):

  • Action: Management is stepwise and aggressive. For moderate-to-severe exacerbations, treatment involves back-to-back or continuous nebulised Salbutamol (0.15mg/kg) combined with Ipratropium Bromide (250-500mcg) for the first three doses, alongside early administration of systemic corticosteroids like oral Prednisolone (1-2mg/kg) or IV Hydrocortisone (4-5mg/kg) (19).

  • Rationale: This combination approach targets both bronchoconstriction (salbutamol/ipratropium) and airway inflammation (steroids) simultaneously for maximal effect.

• Croup (Moderate-Severe):

  • Action: The cornerstone of therapy is a single dose of Dexamethasone (0.15-0.6mg/kg oral/IM/IV) and nebulised Adrenaline (0.5mL/kg of 1:1000 solution) (19).

  • Rationale: Adrenaline acts as a potent alpha-adrenergic vasoconstrictor, rapidly reducing subglottic oedema to relieve obstruction within minutes, while the steroid provides a more sustained anti-inflammatory effect that reduces symptom severity and duration.

• Community-Acquired Pneumonia (CAP):

  • Action: Antibiotic choice is guided by the National Antimicrobial Guideline and severity. For non-severe suspected bacterial CAP managed as an outpatient, high-dose oral Amoxicillin is first-line. For hospitalised, non-severe cases, IV Benzylpenicillin is preferred. For severe CAP, broad-spectrum coverage with IV Ceftriaxone or Cefotaxime is required (52).

  • Rationale: To effectively target the most likely and potentially resistant pathogens, such as Streptococcus pneumoniae.

Supportive & Symptomatic Care

• Oxygen Therapy: The method of oxygen delivery should be escalated to meet the child's needs. This can range from low-flow nasal prongs to a simple face mask, or increasingly, High-Flow Nasal Cannula (HFNC) therapy. HFNC is particularly beneficial in bronchiolitis as it delivers heated, humidified oxygen at high flow rates, which reduces anatomical dead space, provides a small amount of PEEP, and decreases the overall metabolic work of breathing (43).

• Fluid Management: Maintain meticulous fluid balance. Children in significant distress cannot feed safely and require nasogastric (NG) tube feeding or IV fluids to prevent dehydration. However, in children with or at risk of PARDS, a restrictive fluid strategy is crucial to avoid iatrogenic fluid overload, which can worsen pulmonary oedema and clinical outcomes (19).

• Analgesia & Antipyretics: Treat fever and discomfort with paracetamol or ibuprofen. This is not just for comfort; reducing fever lowers the child's metabolic rate and oxygen consumption, thereby decreasing the demand on their already strained respiratory system.

Key Nursing & Monitoring Instructions

• Continuous cardiorespiratory and SpO2 monitoring is mandatory for any admitted child with significant distress.

• Maintain a strict input/output chart, with particular attention to urine output as an indicator of renal perfusion.

• Perform regular assessments of the work of breathing (retraction score, respiratory rate) and neurological status (AVPU/GCS).

• For any child who has received nebulised adrenaline for croup, a minimum 4-hour observation period is required to monitor for rebound stridor as the drug's effect wears off.

• Clear instructions must be given to inform medical staff immediately if there is any sudden deterioration, a drop in SpO2 below target, or any change in mental status.

Long-Term Plan & Patient Education

Discharge planning is a crucial part of management and a key safety-netting intervention. For a child with a new diagnosis of asthma, this involves establishing a clear asthma action plan, providing extensive education on trigger avoidance, and ensuring correct inhaler and spacer technique. For children recovering from severe infections like pneumonia or PARDS, appropriate follow-up is necessary to ensure complete clinical and radiological recovery. For all parents, education on recognizing red flag signs (such as those listed in the Clinical Presentation section) and understanding when to seek immediate medical attention is vital.

When to Escalate

Knowing when to call for help is a critical skill for a house officer. The decision should be made early, not when the child is already arresting.

• Call Your Senior (MO/Specialist) if:

  • The patient shows signs of tiring (e.g., slowing respiratory rate, shallowing breaths) or has a deteriorating level of consciousness.

  • There is a rising oxygen requirement to maintain target SpO2, or the child fails to maintain saturation despite high-flow oxygen.

  • A repeat blood gas analysis shows a rising PaCO2 or worsening acidosis.

  • The child fails to respond to standard first-line treatment within a reasonable timeframe (e.g., no improvement after 3 doses of back-to-back nebulisers for severe asthma).

  • You have a high suspicion of a life-threatening diagnosis that requires immediate specialist intervention, such as FBA, epiglottitis, or myocarditis.

• Referral Criteria:

  • Refer to PICU for any child requiring, or likely to require, advanced respiratory support such as non-invasive ventilation (CPAP/BiPAP) or invasive mechanical ventilation.

  • Refer to ENT urgently for any child with a suspected FBA or severe upper airway obstruction that is not responding to medical management for croup.

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