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A previously healthy 7-month-old boy presents to an outside hospital’s emergency department in severe respiratory distress after a fall. The patient’s mother reported that she was in the other room when she heard his fall and his immediate cry. When she arrived to the room, she noted cyanosis and respiratory difficulty. She believed the patient was on the floor trying to pull to a stand when he fell over, striking his eye on the bedpost and landing on the carpeted floor. There was no reported vomiting, loss of consciousness, or bleeding. The family brought him to the emergency department for evaluation immediately.Prior to the fall the patient experienced 1 day of nasal congestion and cough without fever. His past medical history was significant for hospitalization at 3 months of age for acute respiratory failure secondary to viral bronchiolitis requiring high-flow nasal cannula and intravenous fluid resuscitation. Following this hospitalization, he had complete resolution of his symptoms. His family history is significant for asthma in his 2 older brothers and a paternal grandmother who died at age 38 from unknown cardiac causes.On arrival to the emergency department, the patient’s vital signs were significant for hypertension with blood pressure 139/75, tachycardia with heart rate 176, tachypnea with respiratory rate 50, afebrile with temperature 98.9, and desaturation with oxygen saturation 92% in room air. The physical examination was significant for a distressed infant with suprasternal, subcostal, and intracostal retractions, head-bobbing, and peri-oral cyanosis. The child was noted to have erythematous swelling of the left forehead and left-sided periorbital ecchymosis. Cardiac examination showed sinus tachycardia with normal S1 and S2, and no murmurs, rubs, or gallops. Respiratory auscultation was significant for tachypnea, diffuse wheezing, and diminished air entry bilaterally. No stridor, rhonchi, or crackles were present.Initial laboratory results were concerning for a respiratory acidosis with a peripheral venous blood gas pH 7.15 (normal: 7.31–7.41), pCO2 75 mm Hg ([10.0 kPa], normal: 41–51 mm Hg), pO2 67 mm Hg ([8.9 kPa], normal: 30–50 mm Hg), HCO3− 24.6 mEq/L ([24.6 mmol/L], normal: 22–29 mEq/L), and lactate 2.8 mmol/L (normal: 0.5–2.2 mmol/L). A basic metabolic panel and serum transaminase levels were within normal limits. Complete blood count was significant for leukocytosis of 25 × 103/uL ([25 × 109/L]) with neutrophil percentage 76%, segmented neutrophils 7%, monocytes 4.7%, eosinophils 2.1%, bands 1%, Hgb 12.8 g/dL ([128 g/L]), Hct 40.2% ([0.402]), and platelet count 750 000 /μL ([750 × 109/L]). The respiratory viral panel was positive for rhinovirus and enterovirus.Chest radiography revealed well-expanded lungs without focal consolidation. The patient was treated presumptively for status asthmaticus with epinephrine, albuterol, and high-flow nasal canula oxygen therapy. His acidosis improved, and he was admitted to the outside hospital’s pediatric intensive care unit for further management.Upon admission, the patient developed worsening respiratory distress, hypoxia, and hypercapnia. A terbutaline infusion was initiated, and continuous albuterol was administered. Overnight the patient remained hypertensive (blood pressure: 118/57) likely secondary to distress and medication effects. Bilevel positive airway pressure was trialed but was poorly tolerated by the patient. On neurologic examination, the patient appeared less alert. Due to worsening hypoxemic and hypercapnic respiratory failure, the decision was made to proceed with endotracheal intubation. Following intubation, the patient was transferred to our institution for further management. At the time of transfer, the patient’s blood pressure and heart rate normalized.On arrival at our facility, physical examination revealed poor air entry diffusely with prolonged expiratory phase. Given the history of trauma and inability to obtain a neurologic examination due to sedation, a head computed tomography (CT) scan was performed and showed no hemorrhage, shift, or hydrocephalus. Chest radiography was repeated and showed bilateral hyperinflation.Overnight, the patient developed worsening hypoxia and respiratory acidosis despite aggressive treatment with bronchodilators and use of high positive end-expiratory pressure. Physical examination at this time revealed absent breath sounds on the left side. Chest radiography was significant for diffuse left hemithorax opacity and leftward mediastinal shift consistent with atelectasis (Figure 1). Over the next 24 hours, alternating hyperinflation and left-sided collapse were visible on chest imaging. Hypoxia and severe respiratory acidosis persisted despite continued optimization of mechanical ventilator settings.The patient’s respiratory distress, recent history of upper respiratory symptoms, past admission for viral bronchiolitis and positive viral testing initially raised suspicion for viral bronchiolitis. However, the degree of leukocytosis in this patient would be unusual in a case of viral bronchiolitis. Other possible explanations considered were reactive leukocytosis from steroid administration or acute stress given the severity of illness at presentation. His family history and his history of albuterol responsiveness increased concern for asthma but the severity of disease and intermittent left-sided lung collapse raised concerns for another process. Given that the patient’s respiratory distress coincided with a fall, it was important to consider traumatic causes for his respiratory distress. The mechanism of trauma was mild and not consistent with injury to the upper airway, there was no stridor or evidence of subcutaneous emphysema, pneumomediastinum, or pneumothorax on physical examination or imaging. Given the patient’s age, nonaccidental trauma was considered but ultimately deemed unlikely given that the patient was known to pull to stand prior to this event, the visible injuries were consistent with the history, and the family sought immediate medical care. Additionally, the family was evaluated by a social worker and no concerns were identified. Congenital airway malformation was also considered given the patient’s history of prior respiratory failure and persistent distress despite initial treatments. However, upon radiology review of the chest radiography images, this was considered unlikely. Given the patient’s failure to improve with aggressive treatment and repeated left lobar collapse, decision was made to pursue bronchoscopy to evaluate for mucous plug or foreign body.The pulmonology team performed a bedside bronchoscopy (Figure 2). A piece of red yarn was seen in the left mainstem bronchus and removed successfully (Figure 3). Copious amounts of mucous were seen distal to the foreign body and were suctioned out. No anatomical abnormalities of the airway were seen. A respiratory culture from the endotracheal tube retrieved via bronchoalveolar lavage grew methicillin-sensitive Staph aureus (MSSA). Repeat chest radiography conducted after bronchoscopy and removal of the foreign body showed left lung re-inflation with patchy areas of atelectasis.Foreign body aspiration is a common cause of pediatric respiratory distress. It is most commonly seen in children aged 6 months to 3 years of age.1 Aspirations can have a variable presentation, from asymptomatic to respiratory distress, depending on the size and character of the object and its final anatomical location. Food is the most frequently aspirated item.2 In many cases, choking events are witnessed by a caregiver and can be brought to prompt medical attention. However, when an aspiration goes unwitnessed or complications develop, patients can present days to weeks after an inciting incident.2 Patients with delayed diagnosis of foreign body aspiration may present with fever, dyspnea, wheezing, chronic cough, or recurrent pneumonia that may improve but not completely resolve with therapy.3 Nonaccidental foreign body insertion is also a cause of aspiration in children and should be ruled out through a history and physical examination. In this case, the acute onset of respiratory distress following a fall was a hint that infectious etiology was less likely.Children with foreign body aspiration most often present with partial airway obstruction. In this case, the foreign body acts as a mobile, one-way ball valve.4 Changes in intrathoracic pressure allow air entry during the inspiratory phase but prevent exhalation during the expiratory phase. This leads to subsequent air trapping and hyperinflation.5 When the foreign body causes complete obstruction, atelectasis occurs.4 As the foreign body moves, the degree of obstruction changes leading to the characteristic cycle of hyperinflation and collapse.A classic triad of wheeze, cough, and diminished breath sounds is used to describe foreign body aspiration, but is only present in 57% of cases.6 Additional signs include tachypnea, stridor, cyanosis, and decreased air entry. Focal differences in ventilation are often noted on physical exam.7 In children, the right and left mainstem bronchi are the most likely locations for foreign body aspiration.8 When the diagnosis of foreign body aspiration is delayed, the risk of airway infection increases.In the setting of acute respiratory distress secondary to a foreign body aspiration, the first step is management of the airway. A complete airway obstruction requires back slaps and chest thrusts in the head down position for an infant. Partial airway obstruction may require the placement of an advanced airway. After stabilizing the patient, a plain chest radiograph can confirm suspicion for a foreign body aspiration. Radiographs should include posteroanterior, lateral, inspiratory and expiratory views. Common findings include hyperinflation of the affected lung, atelectasis, mediastinal shift, and pneumonia.9 However, 30% of confirmed foreign body aspiration cases present with a normal chest radiograph.10 Therefore, a lack of these findings does not rule out the condition and CT can be considered in cases with moderate suspicion and inconclusive chest radiographs including three views.11 If suspicion is high, a bronchoscopy should be conducted as soon as possible to identify the foreign object and guide removal. In cases when bronchoscopy is not conducted promptly, morbidity and mortality are increased.6,12 Complications can arise due to delayed diagnosis and treatment, including pneumonia, abscess formation, atelectasis, and bronchiectasis. Additionally, there is a risk of iatrogenic injury secondary to treatments given for an incorrect diagnosis.1After foreign body removal, the patient initially required high ventilator settings, raising concern for acute respiratory distress syndrome secondary to infection. Lung protective ventilation strategies and prone placement were used to improve ventilation and recruitment. He was treated with cephalexin for MSSA tracheitis given bronchoalveolar lavage results, fever, and leukocytosis. Ventilator settings were slowly weaned, and the patient was extubated to noninvasive ventilation on hospital day 12. He was transferred to the inpatient floor for sedation wean and feeding therapy and was eventually discharged home on hospital day 36.Foreign body aspiration should be suspected in children with a presentation of respiratory distress, even in atypical circumstances.A normal chest radiograph does not have a high negative predictive value for foreign body aspiration. If there is high suspicion for foreign body aspiration, bronchoscopy should be performed.Alternative diagnoses should be sought in children with respiratory distress who do not respond to therapy.Occam’s razor—the principle that the simplest explanation for an observation is usually the best—can cause physicians to unify a patient’s presentation under one diagnosis. However, it is important to consider Hickam’s dictum—that patients can have multiple diagnoses explaining their presentation.