A 7 year old girl presented with a 2 week history of a persistent dry cough, nasal congestion and mild rhinorrhea that progressed to acute onset left-sided chest pain and difficulty in breathing with a low-grade fever. She had no present or past history of wheeze, no easy fatigability or dyspnea on exertion, no body or feet swelling. No history of close contact with a patient known to have tuberculosis (TB) or severe acute respiratory syndrome coronavirus 2 disease (COVID-19) no loss of weight or poor growth, no loss of appetite nor night sweats reported. There was no known history of chest trauma.
At the onset of her symptoms she was initially managed at home as nasopharyngitis with a cough syrup with no resolution of symptoms. She was reviewed in the outpatient clinic with a diagnosis of pneumonia a few days later and standard antibiotics were prescribed. 3 days later she was reviewed by the paediatrician due to the persistent cough and difficulty in breathing. Inhaled salbutamol and oral montelukast were added as treatment for possible asthma. A further 3 days later she developed chest pain that necessitated an admission.
The birth and developmental history were unremarkable. She had no previous admission but had allergy symptoms since infancy which included eczema, history of skin eruptions with ingestion of animal proteins and allergic rhinitis with upper airway obstruction symptoms.
Her clinical examination on admission; temperature of 37.5  C, blood pressure (BP) 98/53(mean BP 63), heart rate (HR) 105, oxygen saturation (SPO2) 93% on room air and increased respiratory rate of 33 breaths per minute.
The respiratory examination revealed tracheal shift to the left side, dullness on percussion and reduced air entry on the left lung zone all indicating left lung collapse (Fig. 1). Systemic examination was positive for orbital shiners, enlarged inferior turbinates and lingual tonsils hypertrophy, dental carries and lastly mild eczema patches on her trunk.
Initial blood gas analysis done showed compensatory respiratory alkalosis and hypoxia: (pH) 7.426, partial pressure of carbon dioxide (PCO2)25.4 mmHg, partial pressure of oxygen (PO2)55 mmHg, base excess (BE)-8mmol/L, serum bicarbonate (HCO3)16.7mmol/L, total carbon dioxide (TCO2)17 mmHg, oxygen saturation (SPO2)90% and lactate 0.65mmol/L. Normal values for Abbott  blood gas analysis machine i-STAT CG8+: pH (7.35-7.45), PaO2 (80-105 mmHg), PaCO2 (35-45 mmHg), BE (-2 to +3 mmol/L), HCO3 (22-26 mmol/L), TCO2 (23-27 mmHg), SPO2 (95-98%), lactate 0.36-1.25mmol/L.
The patient was admitted to the high dependency unit (HDU) due to features of compensated respiratory failure for monitoring, oxygen supplementation, intravenous fluids and intravenous antibiotics.
A working diagnosis of features of lung collapse/consolidation, pneumonia and possible foreign body aspiration.
Initial investigations were as follows: Haemogram and serum biochemistry were normal, the inflammatory/infective markers C-reactive protein (CRP) and Pro-calcitonin (PCT) were low and blood culture was negative. Multiplex respiratory panel polymerase chain reaction test (PCR) was negative for viruses and atypical bacteria tested, tuberculosis microbiology and PCR was also negative. COVID-19 test was also negative. Vitamin D levels were low at 22.9 (30-100) U/L.
Based on her clinical and laboratory findings, an additional diagnosis of; upper airway obstruction, due to adenotonsillar hypertrophy, dental carries, eczema and Vitamin D deficiency was made. She was started on intravenous ceftriaxone and flucloxacillin, skin emollients and Vitamin D supplementation. By the second day she had increased work of breathing and was started on continuous positive airway pressure (CPAP) non-invasive ventilation by mask alternating with a non-rebreather high flow oxygen mask (NRM).
A multidisciplinary consult was sought that included the ear, nose and throat specialist (ENT), pulmonologist and the cardiothoracic surgeon. A plan was made for a computerized tomography (CT) scan of the chest, upper airway endoscopy and bronchoscopy with a possible open surgical approach if needed (Fig. 2).
Rigid bronchoscopy was done on day 3 of admission and removal of a small fat like consistency foreign body from the left main bronchus. It was noted that there was minimal mucus in the trachea and no features of major lower airway inflammation of the visualized segment. Grade 3 fibrotic tonsils and enlarged adenoids were confirmed.
Further history revealed that she had choked on chewing gum 2 months prior to presentation but had not experienced any significant respiratory symptoms warranting a review.
She was maintained on oxygen supplementation by NRM on that day, which was being weaned off gradually as tolerated and remained clinically and vitally stable.
By the second day post-bronchoscopy, we managed to wean off oxygen to 1Litre/min via nasal prongs with no respiratory distress. However, there was still minimal air entry on the left upper and mid lung zones. A repeat CXR done 24 hours after the procedure showed a persistent lung collapse with no interval change. She was initiated on aggressive chest physiotherapy and incentive spirometry to recruit the lung for up to 3 days and continued on antimicrobials despite no sign of obvious infection, with no clinical improvement.
A case conference held with the multi-disciplinary team suggested a second CT scan or a repeat rigid and flexible bronchoscopy to investigate cause of the airway obstruction or endobronchial lesion with a possibility of a thoracotomy and open surgical approach.
Flexible bronchoscopy done on day 8, found an endobronchial lesion completely occluding the left main bronchus slightly below the carina that could not be suctioned. The right bronchial tree was normal. Rigid bronchoscopy was done and we found a tenacious mass, soft to firm in consistency extending to the segmental branches with attendant bronchial wall inflammation throughout. Mucoid discharge was noted from the left basal inferior segment. Multiple segments of thick mucoid/lipoid like material and bronchial casts suggestive of PB were extracted by use of forceps through the rigid bronchoscope and eventual bronchial toilet to conclude the procedure.
Immediate post bronchoscopy period there was minimal oxygen requirements, no respiratory distress, marked improvement in air entry on the left lung zone and we managed to wean off oxygen within 24 hours (Fig. 3).
The team began a regime of combined inhaled corticosteroid with a long-acting beta-agonist (ICS/LABA) and a 3-day course of intravenous methylprednisolone, continuation of chest physiotherapy and incentive spirometry as a deep breathing exercise to improve her lung capacity after lung collapse, antimicrobials and other supportive management. She remained hemodynamically stable with no respiratory distress, vitally stable off oxygen, alert and ambulant. Cardiac sonography was done to also rule out complications from the upper airway obstruction and was normal.
Microscopy showed a suppurative and mixed inflammatory cellular debris with mainly neutrophils and eosinophils. Necrotic debris and flakes of squamous epithelium were also noted. No foreign body material could be discerned (Fig. 4).
Further tests for Immunoglobulin E (IgE) 0.53Ku/l (<90) and Aspergillus Fumigatus IgE were negative.
She was discharged on day 12 on the ICS/LABA and a plan to complete 3 more courses of monthly pulsed methylprednisolone with possibility of adeno-tonsillectomy if upper airway symptoms of obstruction persists. Post discharge she's doing well, no further symptom and normal chest exam and x-ray after the 3rd course of methylprednisolone, her dental carries were filled and no further upper or lower airway symptoms persist.
CT scan chest before bronchoscopy. (A) Coronal section shows a soft tissue density lesion obstructing the left main bronchus (arrow).