Dr. Kavya Chikkam (Little Lung Children’s Clinic)

Yes  -  and the answer to this question matters enormously for a child's physical health, social participation, and self-confidence. Asthma, when well controlled, should not prevent a child from participating in sports and physical activity at the same level as their peers. Many elite athletes have asthma and manage it successfully. The condition that concerns families about sport is exercise-induced bronchoconstriction  -  EIB  -  where physical activity triggers airway narrowing, producing cough, wheeze, chest tightness, or breathlessness during or after exercise. EIB is common in children with asthma but it is manageable: a short-acting bronchodilator inhaler taken 10 to 15 minutes before exercise prevents EIB in most children, and a warm-up period of 10 to 15 minutes of moderate exercise before more intense activity also reduces the bronchoconstriction response. Swimming is often said to be the best exercise for children with asthma because the warm humid air at pool level is less provocative for the airways than cold dry outdoor air. In children whose asthma is poorly controlled, exercise limitation may reflect undertreated background disease rather than inevitable exercise intolerance  -  better daily controller therapy often resolves EIB by reducing the underlying airway inflammation. If your child is avoiding sport because of asthma, that is a signal that their asthma is not yet as well controlled as it should be, not a reason to accept limitation.

Primary ciliary dyskinesia and cystic fibrosis are both genetic chronic lung conditions that produce recurrent respiratory infections and bronchiectasis, but they have different underlying mechanisms, different diagnostic pathways, and different treatments  -  and distinguishing between them matters because the management of each is specific. Cystic fibrosis is caused by mutations in the CFTR gene that produce abnormally thick, sticky mucus in the lungs, pancreas, and other organs. It is diagnosed by a sweat chloride test (elevated chloride concentration in sweat is characteristic) and confirmed with CFTR genetic testing. Modern CFTR modulator therapies have transformed outcomes for patients with certain mutations. Primary ciliary dyskinesia is caused by mutations in genes responsible for the structure and function of cilia  -  the tiny hair-like projections that line the airways and move the mucus layer that traps inhaled particles and pathogens. When cilia are dysfunctional, mucus accumulates and infection recurs, damaging the airways and producing bronchiectasis over time. Unlike cystic fibrosis, PCD does not produce abnormally thick mucus  -  it produces normal mucus that is not cleared because the machinery for clearing it is broken. PCD is diagnosed by nasal nitric oxide measurement (characteristically very low in PCD), followed by ciliary biopsy and electron microscopy and genetic testing. Situs inversus  -  the mirror-image arrangement of the organs  -  occurs in approximately half of PCD patients and is part of Kartagener syndrome. Treatment for both conditions centres on optimising airway clearance, treating infections early, and monitoring lung function longitudinally.

Snoring in a child that is associated with observed pauses in breathing, gasping, or very laboured respiratory effort during sleep is the classic presentation of obstructive sleep apnoea  -  a condition where the upper airway collapses during sleep, interrupting breathing and fragmenting sleep quality. This is not a normal finding and should not be attributed to a cold or tolerated as a phase the child will grow through without evaluation. The immediate step is a specialist consultation where the clinical features  -  the frequency and pattern of snoring, observed apnoea events, mouth breathing, restless sleep, night sweating, and daytime symptoms including morning headache, excessive daytime sleepiness, and behavioural or attention difficulties  -  are assessed systematically. A formal sleep study, polysomnography, is the gold standard investigation, measuring oxygen levels, airflow, chest and abdominal movement, heart rate, and arousal events throughout the night to confirm the diagnosis and quantify its severity. In children without comorbidities, enlarged tonsils and adenoids are the most common anatomical cause, and adenotonsillectomy typically produces significant or complete resolution. In obese children, weight management is an important component alongside surgical assessment. For children with persistent or residual OSA after surgery, or those who are not surgical candidates, CPAP therapy delivered through a mask during sleep is effective and well-tolerated with appropriate support. The consequences of untreated OSA in children  -  impaired growth, neurocognitive deficit, and cardiovascular risk  -  are avoidable with early diagnosis and treatment.

A child's cough warrants Paediatric Pulmonologist evaluation when it is chronic  -  defined as lasting longer than 8 weeks  -  when it recurs repeatedly after antibiotic treatment without a full resolution period, when it is associated with wheeze, shortness of breath, chest tightness, or exercise limitation, or when it has not responded as expected to standard management for the most likely diagnosis. The clinical situations I encounter most frequently where pulmonologist input changes the outcome are: chronic wet cough that produces mucus and may indicate underlying bronchiectasis or an impaired airway clearance mechanism; dry persistent cough that may represent cough-variant asthma not yet confirmed with spirometry; cough in a child with recurrent pneumonias who may have an immune deficiency, structural abnormality, or primary ciliary dyskinesia as the underlying cause; and cough in a child who has had prolonged antibiotic courses for diagnoses of pneumonia where the diagnosis itself may not have been correct. A general paediatrician provides excellent care for acute respiratory illness, but a cough that is chronic, recurrent, or unresponsive to standard treatment is precisely the pattern where a Paediatric Pulmonologist's diagnostic tools  -  spirometry, lung function testing, allergy evaluation, bronchoalveolar lavage via flexible bronchoscopy  -  add diagnostic precision that changes the treatment plan.