BACKGROUND Foreign body aspiration (FBA) is a life-threatening pediatric emergency, most common in 1-3-year-olds due to immature swallowing reflexes and exploratory oral behaviors. Common aspirated items include nuts, food particles and small toys, presenting with variable symptoms such as cough, dyspnea, wheezing or acute respiratory failure. Delayed diagnosis or improper management causes severe complications like post-obstructive pneumonia, atelectasis, bronchiectasis and irreversible airway stenosis, increasing morbidity and treatment complexity. CASE REPORT A 16-month-old girl was admitted with persistent cough, progressive dyspnea, intermittent fever, hoarseness, and occasional cyanosis that developed 6 days after accidental pine nut ingestion. Initial flexible bronchoscopy at a local hospital failed due to the foreign body's rigid texture and deep impaction in the right lower lobe basilar bronchus. Chest CT confirmed a pine nut shell in the B9/B10 segmental bronchus with surrounding inflammation. She was transferred for combined rigid-flexible bronchoscopy to establish a secure airway and enable precise visualization before holmium laser fragmentation broke the shell into retrievable fragments for complete removal. Two-week follow-up showed symptomatic B9/B10 stenosis, which improved significantly after sequential 3.5 mm and 4.0 mm balloon dilation. Her respiratory symptoms resolved and imaging confirmed restored lobar ventilation. CONCLUSIONS Rigid-flexible bronchoscopy synergy benefits removal of large rigid foreign bodies in sub-main bronchi by combining rigid bronchoscopy's airway security with flexible bronchoscopy's maneuverability and visualization. Holmium laser safely fragments hard foreign bodies with minimal airway trauma, and sequential balloon dilation effectively treats post-FBA stenosis. Individualized application guided by clinical assessment and imaging optimizes pediatric FBA outcomes.

A newborn infant with pulmonary atresia, intact ventricular septum, and moderately hypoplastic right ventricle underwent radiofrequency perforation and balloon dilation of the pulmonary valve immediately after birth, followed by one-and-one-half ventricle (1.5 V) repair at 5 months of age. At 7 years of age, the patient developed worsening cyanosis and exercise intolerance with increasing right-to-left shunting through the atrial septal defect (ASD). Due to the combination of tricuspid regurgitation and such ASD shunting, the pulmonary regurgitation fraction reached 110%. Consequently, the advantages of utilizing the right ventricle as an additional antegrade source of pulmonary blood flow in the 1.5 V circuit were not achieved. This case report highlights the importance of phase-by-phase assessment of blood flows using phase-contrast magnetic resonance imaging for understanding the complex hemodynamics.

Abernethy malformation is a rare congenital portosystemic shunt. A type 2 Abernethy malformation is characterised by a side-to-side shunt between the extrahepatic portal vein and the inferior vena cava. Unmetabolised toxins that bypass hepatic circulation lead to intrapulmonary vascular dilatation. Approximately 3%-12% of portosystemic shunts present with features of hepatopulmonary syndrome, often presenting with progressive hypoxaemia and cyanosis.While endovascular device closure represents the preferred therapeutic approach for most cases, rarely, large or anatomically unfavourable shunts may necessitate surgical ligation that is met with unique anaesthetic challenges surrounding maintenance of adequate oxygenation and haemodynamic stability. We report the noteworthy anaesthetic concerns faced during successful surgical closure of Abernethy shunt in a boy in mid childhood.

Heterotaxy syndrome comprises a spectrum of laterality defects frequently associated with complex congenital heart disease and extracardiac anomalies. We report a 2-year-old male who presented with persistent cyanosis, recurrent respiratory infections, and failure to thrive. Cardiac computed tomography demonstrated ambiguous situs with dextrocardia, reversed atrial arrangement, L-looped ventricles, large atrial and ventricular septal defects, hypoplastic right ventricle, absent right ventricular outflow tract, and double-outlet left ventricle. Additional findings included polysplenia, right-sided aortic arch with mirror branching, aortopulmonary collaterals, and a left posterolateral Bochdalek hernia. This case highlights the value of comprehensive cross-sectional imaging in defining complex heterotaxy anatomy and underscores the clinical implications of associated extracardiac anomalies in surgical planning and prognosis.

The Spanish influenza pandemic of 1918 caused well over fifty million deaths. The epicentre undoubtedly was China, where gene mixing of different virus strains occurred amongst aquatic, migrant birds. But where and when did the virus first infect (or spill over to) a human being? We take, as our starting point, a paper demonstrating that an infection causing the same symptoms as the influenza virus was widespread in New York during the winter of 1917-1918. The authors of that paper went on to suggest that the virus had probably reached North America from Europe, in the context of troop movement during World War I. Our own researches have focussed on this point. We show that outbreaks of serious respiratory disease, local in nature but causing unusual patterns of mortality, were indeed reported by scientists and doctors in army hospitals in England and in France, well before the first wave of the pandemic had arrived. We use the records of these hospitals, now held in the National Archives, to trace the progress of this disease amongst the individuals who fell ill. We examine contemporary reactions to this minor epidemic - an epidemic, we suggest, which acted as a herald wave of the pandemic yet to come. The latter part of our paper addresses the second question, as to how troop movement across the North Atlantic, once the United States had entered into war, may well have enabled the virus to spread from Europe to North America.

Methemoglobinemia is a rare but potentially life-threatening condition caused by oxidation of hemoglobin iron from the ferrous to ferric state, impairing oxygen delivery to tissues; early recognition is crucial as clinical manifestations may be disproportionate to pulse oximetry readings. We describe a case of a three-year-old female child who presented with acute onset cyanosis and hypoxia unresponsive to supplemental oxygen, despite a normal cardiopulmonary examination and persistently low oxygen saturation on pulse oximetry. Blood gas analysis revealed a discrepancy between low oxygen saturation and oxygen levels, raising suspicion of methemoglobinemia, which was subsequently confirmed by elevated methemoglobin levels. The child was managed with prompt supportive care, including high-flow oxygen therapy, followed by intravenous methylene blue, due to significant symptoms and elevated methemoglobin levels, which resulted in rapid clinical and biochemical improvement. She made a complete recovery without residual complications. This case underscores the importance of considering methemoglobinemia in young children presenting with unexplained hypoxia refractory to oxygen therapy, as timely diagnosis and appropriate treatment can be life-saving.