THORACIC EMERGENCIES

JOY L. COLLINS, MD, FAAP, MERCEDES M. BLACKSTONE, MD, AND MICHAEL L. NANCE, MD

INTRODUCTION

Thoracic emergencies in children often result in life-threatening alterations in cardiorespiratory physiology. A rapid, yet organized, approach to the child with a thoracic emergency is essential. The purpose of this chapter is to describe nontraumatic surgical diseases of the thorax and guide the evaluating healthcare provider in the diagnosis and treatment of these conditions. Congenital abnormalities that are usually diagnosed at birth are not included. Thoracic trauma is discussed in Chapter 123 Thoracic Trauma.

This chapter reviews the pathophysiology and clinical manifestations of thoracic emergencies, as well as the general principles of physical and laboratory assessment. Subsequent sections cover specific entities within the following categories: (i) airway obstruction, (ii) violations of the pleural space, (iii) intrinsic pulmonary lesions, (iv) mediastinal tumors, (v) diaphragmatic defects, and (vi) chest wall tumors.

GOALS OF EMERGENCY THERAPY

Children with thoracic emergencies present with a spectrum of processes and severities. Because of the potential for thoracic emergencies to be serious and even life-threatening, a rapid but organized approach to the assessment and treatment of these patients is crucial. Providers should rapidly address respiratory and hemodynamic compromise, and identify those entities that require prompt surgical consultation in the ED.

KEY POINTS

RELATED CHAPTERS

CLINICAL MANIFESTATIONS

Physical Examination

Evaluation of the child with a thoracic emergency requires a calm, orderly assessment of airway, breathing, and circulation (ABCs). In assessing the airway, the physician must evaluate the adequacy of air movement and gas exchange. Pulse oximetry should be performed upon the patient’s arrival. Anxiety or confusion in a patient with a thoracic emergency may be evidence of hypoxemia. Increased work of breathing may indicate partial airway obstruction and can be evaluated by assessing the use of intercostal, subcostal, and supraclavicular accessory muscles. Prolonged use of these accessory muscles may result in fatigue and the most common cause of cardiac arrest in children—respiratory arrest.

Breathing is best evaluated by palpation and auscultation of the chest. The trachea should be palpated to ensure that it is midline. Any lateralization of the trachea is suggestive of either unilateral volume loss or a lateral space-occupying process, such as a pneumothorax, pleural effusion, or mass. The neck and chest should be palpated for signs of subcutaneous emphysema, suggestive of a pneumothorax or airway injury with an air leak. Finally, breath sounds should be assessed via auscultation for symmetry and adequacy of inspiratory and expiratory airflow.

Evaluation of the cardiovascular system should include an assessment of the patient’s pulse for quality, rate, and regularity. The peripheral skin should be assessed for color, temperature, and capillary refill. Signs of poor perfusion often precede that of pressure instability. The neck should be assessed for signs of jugular venous distension. Finally, the heart should be examined for signs of displacement of the point of maximal impulse; shift or alteration in the heart tones; or new murmurs, gallops, or friction rubs.

Evaluation

The most important study when evaluating any patient with a thoracic emergency is a high-quality chest radiograph. The radiographs of the chest in the posteroanterior (PA) and lateral views should be performed in an upright position (unless contraindicated by the patient’s condition). The width of the mediastinum and the degree of mediastinal shift are much better seen in the upright chest radiograph. Moreover, abnormalities in the lung, pleural cavity, and diaphragm are also best appreciated in this view. When a pulmonary effusion exists, lateral decubitus anteroposterior views of the chest or an ultrasound can be obtained to determine whether the effusion layers freely or is loculated.

In interpreting the chest radiograph, the physician should distinguish between a diffuse pulmonary problem and a focal lesion. Hyperaeration of one portion of the lung suggests air trapping in the involved lobe. Hyperaeration of the entire lung field on one side is usually the result of compensatory enlargement of the lung because of atelectasis and loss of lung volume on the opposite side. Depending on the condition, laboratory studies and advanced imaging modalities may be indicated.

AIRWAY COMPROMISE

Airway compromise can occur anywhere in the respiratory tract from the nose to the alveolus. Obstructive emergencies relating to the oropharynx, larynx, and proximal trachea are discussed in Chapters 114 ENT Trauma and 126 ENT Emergencies. Compromise of the more distal tracheobronchial tree may be caused by lesions in the lumen, in the wall, or extremities to the bronchus. Intrinsic bronchial obstructions may result from compression by a tumor within the bronchial lumen (e.g., carcinoid tumor), foreign body, or a mucous plug. Obstruction from lesions in the wall of the bronchus includes collapse from tracheomalacia and stenosis after tracheostomy. Extrinsic lesions (e.g., bronchogenic cyst or inflamed lymph nodes) may be symptomatic by impinging on a bronchus. Table 132.1 lists intraluminal, mural, and extrinsic conditions that produce airway obstruction.

The anatomic level of the obstruction correlates with its effects: An obstruction of the distal tracheobronchial tree may lead to segmental lung overdistension or segmental infection. An obstruction of the proximal trachea affects both lungs, with a much greater likelihood of catastrophe for the patient. Similarly, greater degrees of obstruction, as a rule, lead to greater effects on gas exchange and severity. Infection commonly follows obstruction of bronchial drainage because the clearance of bacteria or inhaled foreign materials by the mucociliary elevator is prevented.

TABLE 132.1

TRACHEOBRONCHIAL CONDITIONS ASSOCIATED WITH AIRWAY COMPROMISE

Tracheal Obstruction

CLINICAL PEARLS AND PITFALLS

• Although wheezing and stridor are very common presentations in children with intercurrent viral illnesses, structural problems should be considered in children with recurrent presentations or significant respiratory distress that does not respond to typical therapies.

• Radiographic studies may not reveal the cause of tracheal obstruction; since these are often dynamic processes, direct laryngoscopy or bronchoscopy may be necessary.

Current Evidence

Tracheal obstruction may be produced by stenosis or lesions within the lumen of the trachea (Fig. 132.1), in the wall of the trachea, or by extrinsic compression. One of the most common causes of intrinsic obstruction in children is an aspirated foreign body (see Chapter 27 Foreign Body: Ingestion and Aspiration for details). Other causes include congenital anomalies such as subglottic stenosis, laryngomalacia, and vocal cord paralysis; acquired subglottic stenosis after tracheostomy or prolonged intubation; viral or bacterial tracheitis or any process that causes significant mucosal edema, particularly in an infant with small baseline airway diameter; or more rarely, a space-occupying lesion such as a hemangioma. Tracheomalacia, sometimes complicating lung disease of prematurity and prolonged intubation, is characterized by a floppy trachea that collapses during expiration when the intrathoracic trachea is compressed by the positive intrathoracic pressure. Laryngomalacia, or tracheomalacia outside the thoracic inlet, may produce obstruction during inspiration when the negative intraluminal pressure transmitted from the chest causes the floppy wall to collapse. Tracheomalacia often occurs in infants born with tracheoesophageal fistula (TEF) or other intrinsic anomalies. Extrinsic compression may occur both from mass lesions (Table 132.1) and as a result of anomalous arteries.

FIGURE 132.1 Acute and chronic obstruction of a bronchus owing to tumor or cyst (T) or lymph nodes (L). When the obstruction is acute, there may be bronchiectasis caused by recurrent pneumonia. The right middle lobe as shown here is particularly prone to bronchial obstruction caused by pressure from encircling lymph nodes. RUL, right upper lobe; RML, right middle lobe; RLL, right lower lobe.

Goals of Treatment

Tracheal obstruction can be caused by a variety of mechanical, infectious, and congenital abnormalities. Practitioners must rapidly assess the cause of obstruction while working toward stabilization of the airway. Surgical causes of obstruction require prompt consultation and coordination of care.

Clinical Considerations

Clinical Recognition. Tracheal compromise produces symptoms that vary from mild to severe, depending on the degree of obstruction present. When symptoms are mild, the underlying cause may not be evident. Occasional episodes of respiratory infection that are believed to result from croup or bronchiolitis may be the only symptom. Stridor, wheezing, or harsh barky cough occurs in patients with more significant obstruction, and a history of frequent hospitalizations for respiratory compromise may be obtained.

Severe tracheal compromise is usually manifested by a history of stridor at rest. Progressive cyanosis and apneic episodes may occur. On examination, a child with obstruction caused by extrinsic compression often has wheezing or stridor throughout the respiratory cycle. In contrast, a patient with the floppy trachea of tracheomalacia often wheezes only during expiration.

Radiographic evaluation of the stable patient should begin with PA and lateral chest radiographs, ideally obtained at full inspiration and again at full expiration. Lateral radiographs of the neck may be useful in showing an edematous epiglottis in patients with suspected epiglottitis. Mass lesions will require cross-section imaging (e.g., computed tomography [CT]) for evaluation. Bronchoscopy is often indicated to evaluate obstructive lesions, whether in the lumen, the wall, or extrinsic to the wall of the trachea.

Management. If the patient has a life-threatening airway obstruction, he or she should receive airway management as outlined in Chapters 1 A General Approach to Ill and Injured Children and 3 Airway. A coordinated effort between the emergency department (ED) physician, the surgeon, and the anesthesiologist or critical care physician may be necessary to establish an airway by endotracheal intubation, bronchoscopy, or tracheotomy. Intubation of the airway to within a short distance of the carina supports most patients with lesions extrinsic to the trachea or in the tracheal wall with a critical obstruction. Such a patient requires admission to an intensive care or other unit with ventilator capability. Lesions within the lumen will likely require endoscopic management in an operating room, and early involvement of an experienced surgeon is recommended.

Many inflammatory processes are controlled with antibiotics and respiratory care without airway manipulation or surgical intervention. Treatment in these cases includes the administration of humidified oxygen and inhaled racemic epinephrine, combined in some cases with the administration of oral, intramuscular, or intravascular dexamethasone. Although the procedure may be difficult, endotracheal intubation is well tolerated in the patient with epiglottitis, since the inflammation is supraglottic with no tracheal or lower respiratory tract involvement. Rarely is intubation necessary for more than 24 to 48 hours in these patients, after which antibiotics have begun to reduce the swelling associated with infection. In a patient with viral or bacterial tracheitis, however, intubation for more than 24 to 48 hours may produce tracheal injury and ulceration.

Tracheomalacia

Tracheomalacia, sometimes complicating lung disease of prematurity, is a relatively common cause of airway obstruction. It is characterized by a floppy trachea that collapses during expiration when the intrathoracic trachea is compressed by the positive intrathoracic pressure. It can be caused by intrinsic tracheal defects, extrinsic compression by surrounding structures, or from prolonged positive pressure ventilation. It commonly occurs in association with tracheoesophageal fistula repair (see TEF below).

Clinical Recognition

The clinical presentation of tracheomalacia depends on the severity and location of obstruction with more severe lesions presenting in infancy. Intrathoracic lesions typically cause expiratory wheeze that may be hard to distinguish from asthma. Extrathoracic lesions can progress to cause stridor at rest. Patients often have cough and evidence of respiratory distress. They may present with recurrent respiratory infections and episodes of severe obstruction and respiratory failure. Tracheomalacia is typically diagnosed using bronchoscopy during spontaneous respiration, which demonstrates the characteristic tracheal collapse with expiration. Although dynamic imaging studies may be useful, standard imaging modalities are typically not helpful in making this diagnosis.

Management

In general, children who are otherwise healthy will have resolution of symptoms by about a year of age as the cartilagenous tracheal structures mature. During episodes of acute illness, however, these children can present with severe work of breathing, cyanosis and respiratory failure. In addition to medical management, they may benefit from noninvasive or invasive ventilatory strategies. The subset of children with severe disease resulting in recurrent bouts of respiratory failure may require tracheal surgery or placement of a tracheal stent.

Vascular Rings

Vascular rings represent a rare and varied group of developmental anomalies of the aorta and great vessels. They may produce obstruction of the esophagus, trachea, or both. These rings are a result of failure of the normal involution of the appropriate segments of the six embryologic aortic arches. Vascular rings are characterized as complete when both the esophagus and trachea are fully encircled and incomplete when they are only partially encircled. Complete rings are typically caused by a double aortic arch or a right-sided aortic arch with an aberrant left subclavian artery and left ductus arteriosus or ligamentum. Incomplete rings are often caused by a pulmonary artery sling, innominate artery compression, or an aberrant right subclavian artery. The level of respiratory obstruction is usually the trachea, but compression of a bronchus by the ductus arteriosus, or by a pulmonary artery sling, may produce compression more distally.

Clinical Recognition

Vascular rings may be asymptomatic in infancy but lead to significant airway obstruction in childhood. The wide variety of anomalies produces varying degrees of symptoms with presentations ranging from incidental findings on imaging studies to neonates with critical airways. Vascular rings should be suspected in infants with stridor, dysphagia, failure to thrive associated with difficult feeding, or recurrent pneumonia. Esophageal obstruction can produce difficulty swallowing. A patient with esophageal compression may also have respiratory symptoms from compression on the trachea from a distended esophageal pouch. This may lead to reflex apnea during feeding, and eventually tracheomalacia in a more chronic setting.

Often, diagnosis is delayed by failure to consider these anatomic obstructions since their presentation can be quite varied and subtle. In a patient presenting with an acute airway obstruction or other medical problems requiring intubation and nasogastric tube placement, detection of a vascular ring can be even more difficult because of the presence of these tubes. Chest radiographs are the initial test of choice and may be supplemented by various diagnostic tests: contrast esophagography, angiography, echocardiography, MRI, and digital subtraction angiography are needed in some combination to define the anatomy.

Management

Although some patients with constricting anomalies improve as they grow, most will require surgical correction. Surgical treatment is usually indicated to relieve the obstruction, with predictable and immediate resolution of symptoms and excellent outcomes. Surgical repair is accomplished by dividing the vascular ring and preserving the blood supply to the aortic branches. This is usually accomplished by a left thoracotomy but more recently, video-assisted thoracoscopic surgical (VATS) techniques and endoscopic robotic-assisted techniques have been adopted in some centers for select patients.

BRONCHIAL LESIONS

Bronchial Atresia

Congenital bronchial atresia is a rare anomaly characterized by a bronchocele caused by a mucus-filled, blindly terminating segmental or lobar bronchus, with resulting hyperinflation of the distal obstructed segment of lung. Hyperaeration is believed to result from communication with the normally aerated lung via the pores of Kohn and the channels of Lambert.

Clinical Recognition

Neonates and infants with the lesion are usually seen for respiratory distress. In older patients, a history of episodic upper respiratory infection and wheezing may be elicited. Some older patients may complain of dyspnea on exertion or unilateral chest pain. Physical examination findings seldom suggest the diagnosis, but unilaterally decreased breath sounds may be evident.

Management

Often, the diagnosis is suggested by chest radiograph, but chest CT scan may be necessary to help more closely define the anatomy. Bronchoscopy is the most efficient way to identify the atretic opening to the involved bronchus. Bronchography has been used in the past, but high-resolution CT scan can often provide the same anatomic information noninvasively. Complete atresia of a main stem or lobar bronchus may lead to infectious complications or compression symptoms from overdistention of the affected lobe. This may require surgical management, such as lobectomy.

Right Middle Lobe Syndrome

Right middle lobe syndrome is the recurrence or persistence of atelectasis or pneumonitis of the right middle lobe, sometimes associated with bronchiectasis. It has been described in all age groups, in both the right middle and lower lobes concomitantly, and has also been observed in the lingula segment. This process can be caused by extraluminal or intraluminal obstruction, or by nonobstructive causes. The right middle lobe is anatomically predisposed to compression of its bronchus by the lymph nodes in the vicinity that encircle it, which can lead to sequestered areas of collapsed or infected lung. Since it is bordered by two fissures, it also receives less collateral ventilation than other lobes, making reinflation of collapsed lung more challenging. Because the right middle and lower lobes are favored sites for aspirated material (Fig. 132.1), recurrent inflammation caused by pneumonia can lead to chronic atelectasis and adenopathy. A similar situation can be seen with intraluminal tumors and other space-occupying lesions. In children, nonobstructive causes such as asthma, cystic fibrosis, and immobile cilia syndrome can also result in prolonged atelectasis, which promotes recurrent infection and eventual bronchiectasis.

Clinical Recognition

Right middle lobe syndrome is a radiographic diagnosis, so physical manifestations vary widely but commonly include persistent cough, intermittent wheezing, or dyspnea. Patients may have wheezing, rales, or decreased aeration on lung examination, particularly appreciated anteriorly. Chest radiographs typically reveal atelectasis of the right middle lobe, which may be recurrent or persistent. They may also show bronchiectasis or pneumonitis of the affected area. Recurrent episodes of pneumonia and associated atelectasis in the lingula or right middle (and often lower) lobes occur in these patients and are not responsive to chest percussion, postural drainage, or antibiotic treatment.

Management

Patients with right middle lobe syndrome may respond to conventional medical management along with chest physical therapy and postural drainage. When this is not the case, fiber-optic bronchoscopy and bronchoalveolar lavage may be helpful to restore patency of the bronchus, allow better postural drainage, and enhance antibiotic effectiveness. Although the need for resection is far less common than in the past, patients with systemic symptoms such as failure to thrive, obstructing lesions, bronchiectasis, bronchial stenosis, or failure to respond to medical management should be considered candidates for lobectomy.

ESOPHAGUS-RELATED CAUSES OF AIRWAY DIFFICULTIES

Goals of Treatment

Patients with congenital and acquired esophageal abnormalities may present with a variety of urgent complaints, the most concerning of which include significant dysphagia, impacted food or foreign bodies, and in some cases even respiratory symptoms or distress. In such patients, prompt evaluation and treatment is critical as with any primary airway issue. Familiarity with the common congenital esophageal anomalies acquired esophageal emergencies and urgencies are critical to arriving at a prompt diagnosis and delivering the appropriate treatment.

CLINICAL PEARLS AND PITFALLS

• Patients with a history of repaired esophageal atresia frequently have tracheomalacia. If severe, a child may present with episodes of respiratory distress or “death spells.”

• Patients with an H-type esophageal fistula (patent trachea and esophagus with connection between the two structures) may present after the neonatal period with symptoms of recurrent choking and congestion with feeds, or with recurrent pneumonias.

• Patients with a history of repaired esophageal atresia may present at any age with an esophageal stricture. Typical symptoms are progressive intolerance of solid food followed later by intolerance of liquids as well. In severe cases, patients may not be able to manage oral secretions.

• Esophageal injuries in older children typically present with significant symptoms (retrosternal chest pain, dysphagia, stridor, retching). Younger children may present with more subtle or vague symptoms.

Esophageal Atresia and Tracheoesophageal Fistula

TEF is typically a congenital condition but has been rarely reported as an acquired problem after suppuration of mediastinal nodes or as a result of iatrogenic injury or a complication following foreign body ingestion. The more common congenital TEF is accompanied by atresia of the esophagus in more than 85% of patients and generally presents in the immediate perinatal period with feeding intolerance and inability to handle secretions. These patients undergo repair shortly after diagnosis, typically via a right thoracotomy or thoracoscopic approach.

Approximately 3% of all patients with TEF have an “H-type” fistula, in which both the trachea and the esophagus are intact and patent but are connected by a fistula that is frequently in the cervical region or high in the thorax (Fig. 132.2). Because there is no accompanying esophageal atresia, these patients are more likely to present later in infancy or childhood with symptoms of recurrent respiratory distress or pulmonary aspiration. The acquired form is usually in the distal trachea or proximal bronchial tree, and is extremely uncommon.

H-type fistulae are notoriously difficult to diagnose, particularly if the fistula tract is small. Children generally develop recurrent pulmonary infections with no obvious source. The characteristic history of choking or gagging with swallowing that accompanies esophageal atresia with TEF may not be present, but parents may describe excessive secretions or noisy breathing after feeds. Contrast esophagram, specifically looking for an H-type TEF is necessary. Most of these fistulae are quite small in diameter (millimeters) and short (also less than 1 cm), making radiographic identification difficult.

Following repair of esophageal atresia or fistula, patients may present at any point in life with an anastomotic stricture and/or an impacted food bolus with the site of retention typically at the site of anastomosis. Patients who present to the ED with dysphagia or intolerance of solids and/or liquids in the setting of a prior history of esophageal atresia repair should undergo contrast esophagography ( e-Fig. 132.1). Patients who present with a stricture following fistula or esophageal atresia repair are typically managed with esophagoscopy under general anesthesia with removal of any impacted foreign material and bougie or balloon dilation of the stricture. Most such patients are discharged home immediately after these interventions, and some patients require multiple dilations over the course of their childhoods.

FIGURE 132.2 H-type tracheoesophageal fistula.

Esophageal Web

Rarely, a patient presents with symptoms caused by an esophageal web (Fig. 132.3). The membranous, congenital narrowing of unclear origin usually allows the passage of liquids, and symptoms often do not arise until the child begins to eat solid food. Patients may present with feeding intolerance or respiratory symptoms after drinking and eating. Recurrent aspiration pneumonia may also develop. Rarely, an esophageal web can present with associated anemia, in the form of Plummer–Vinson syndrome. An esophagram is usually diagnostic. Symptomatic patients who have respiratory symptoms or who are unable to achieve adequate oral intake should be admitted for observation and definitive management. Often, a thin membranous web may be split by esophageal dilators, cautery, or a hydraulic balloon placed endoscopically across the stenosis. If this approach is unsuccessful because the lumen is too small to transmit the dilator or the tissue is unyielding, segmental esophageal resection may be necessary via thoracotomy or thoracoscopy.

FIGURE 132.3 A child with chronic partial obstruction of the esophagus caused by a congenital web. Similar bulbous enlargement of the proximal esophagus can occur with any type of stricture and results in pressure on the trachea and recurrent regurgitation with aspiration. T4, 4th thoracic vertebrae.

Caustic Ingestion

Caustic ingestion is the leading toxic exposure in children, and can cause devastating injury to the esophagus and stomach with dire consequences. The most frequent exposures in children are to mild alkali agents such as household bleach and detergents. Button battery ingestions in children are increasingly common and can be extremely dangerous (see Chapters 99 Gastrointestinal Emergencies and 126 ENT Emergencies for a full discussion). The age distribution of pediatric ingestions is bimodal, with accidental ingestions common in children younger than 5 years and suicide attempts more common in teenagers and young adults. The extent and severity of injury depends on the type, concentration and quantity of the ingested agent, as well as the duration of exposure. Liquid agents typically cause more injury than solids, with strong alkalis being associated with very severe damage. Following the initial ingestion of an acid or alkali, a significant inflammatory response with edema, hemorrhage, and thrombosis can occur within 24 hours. Local tissue damage continues for some time after the initial exposure, causing necrosis, edema, potential perforation, and eventual fibrosis and stricture.

Clinical Recognition

Clinical findings range from a normal physical examination to respiratory distress and hemodynamic instability. Most patients will complain of oropharyngeal discomfort, odynophagia, dysphagia, and chest pain. Stridor may indicate laryngeal and epiglottic edema, and if accompanied by drooling should raise suspicion for esophageal injury. Other signs of esophageal injury include dysphagia, retrosternal pain, epigastric pain, and hematemesis. However, clinical symptoms may be poor predictors of the extent of injury. Ominous signs include hemodynamic instability, fever, tachycardia, and mental status changes; such findings raise concern for esophageal perforation and developing mediastinitis.

Management

Initial management objectives include the assessment of the severity of injury and the prevention of further injury. If possible, the type and amount of corrosive agent ingested should be identified, as this information may be useful in guiding further management. Clinicians should contact their regional Poison Control Center; this is often very helpful in determining active ingredients and the degree of concern for a given substance (see Chapter 110 Toxicologic Emergencies). The airway should be assessed and secured if necessary. Stridor should raise concern for laryngeal edema and orotracheal intubation is indicated in its presence. The airway should be visualized during this maneuver and tubes should not be passed blindly. One exception to this is in the case of ingested hydrofluoric acid, which requires immediate evacuation, best achieved by nasogastric decompression of the stomach.

Patients presenting to the ED following a caustic ingestion may become critically ill and should be closely monitored with this in mind. They should remain nil per os and large-bore intravenous lines should be placed for fluid administration. Measures to dilute or neutralize the ingested agent may cause further complications, and activated charcoal and emetic agents should be avoided. Two view radiographs of the chest and abdomen should be performed and reviewed carefully for evidence of pneumomediastinum, pneumoperitoneum, and pleural effusion. These findings raise concern for full-thickness esophageal or gastric injury.

Patients with suspected esophageal or gastric injury should receive prompt gastroenterology and/or surgical evaluation, as early endoscopy is the gold standard for the assessment of caustic injuries with suspected or known ingestion of caustic substances and in any symptomatic patient. This should be performed within the first 12 to 24 hours after ingestion. Patients with any concerning history or findings should be admitted to the appropriate inpatient ward for close monitoring thereafter, and patients with obvious perforation should receive broad-spectrum antibiotics and will likely require urgent operative management.

PLEURAL DISEASES

The lung is covered by the densely adherent visceral pleura, which moves smoothly over the parietal pleura of the chest wall. A thin fluid film and the friction created by apposition of the pleural layers (like two plates of glass held together by a film of water) contribute to the full expansion of the lung mechanically. When air, excess fluid, or purulent material comes between the two layers of the pleura, the lung may collapse or become significantly compressed and consideration needs to be given to drainage of the pleural space.

Pneumothorax

Goals of Treatment

Tension pneumothorax is a life-threatening emergency and needs to be evacuated immediately. Smaller pneumothoraces may be managed conservatively depending on hemodynamic and respiratory response. Once patients are stabilized, clinicians should investigate the etiology of the pneumothorax.

CLINICAL PEARLS AND PITFALLS

• Tension pneumothorax is a clinical diagnosis and does not require a radiograph for confirmation if there is hemodynamic compromise.

• Exercise caution in sedating patients with pneumothoraces or converting them to positive pressure ventilation since their hemodynamic status can be quite tenuous.

• Children with even small pneumothoraces require a period of ED observation and consideration of admission.

Current Evidence

A pneumothorax is a collection of air in the pleural space. It can occur for short- or long-term duration and can be static or accumulate progressively. Because atmospheric pressure is greater than intrapleural pressure, any mechanism that allows even momentary communication between the atmosphere outside the chest wall or within the tracheobronchial tree can result in a rapid shift of air into the pleural space. A pneumothorax may occur spontaneously, or it may be the result of trauma or a therapeutic intervention. Children with no known predisposing pulmonary conditions are diagnosed as having a primary spontaneous pneumothorax. Secondary spontaneous pneumothoraces occur in patients with underlying diseases such as asthma, cystic fibrosis, or structural abnormalities such as congenital blebs, pneumatoceles, or congenital cystic adenomatoid malformations (CCAMs).

Primary spontaneous pneumothoraces are thought to be the result of sudden increases in transpulmonary pressure resulting in alveolar rupture. Ruptured alveoli coalesce into blebs, which usually occur apically and can rupture into the pleural space. Varying amounts of entering air can lead to a small pneumothorax or complete collapse of the involved lung (Fig. 132.4)

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