When the level of airway obstruction is at the lower airway, chest X-ray findings may include hyperinflation, atelectasis, pneumonia, and mediastinal shift. Hyperinflation occurs when there is a “ball-valve” mechanism secondary to partial airway obstruction, allowing air to flow in during inspiration but not out during expiration, resulting in air trapping. Hyperinflation of the unaffected airway may also occur in some instances because of preferential ventilation of the unobstructed airway (least resistance of airflow). Atelectasis eventually develops as a result of complete obstruction of the affected airway. Mediastinal shift may be prominent or may be subtle. Pneumonia may eventually develop, with the FB as a nidus of infection. This usually manifests as a persistent infiltrate. Lung abscess or bronchiectasis could be a late finding for an undiagnosed and retained FB.

Additional radiographic procedures may be helpful if the standard chest X-ray does not reveal abnormal findings. For older cooperative children, an expiratory chest X-ray may reveal hyperinflation of the affected area because of air trapping distal to the FB. In addition, mediastinal shift away from the affected side (where the FB is) may manifest in an expiratory film. For younger children and infants, a lateral decubitus film could be obtained. Normally, the side that is down (the side the child or infant is lying) will be of smaller volume because of the effect of gravity. Persistent hyperinflation of the side that is down suggests the presence of an FB on that side. It is important to remember that the absence of any of these findings on chest X-ray does not rule out the diagnosis of FBA.

Computed tomography (CT) scan or magnetic resonance imaging (MRI) of the chest is used only when the chest X-ray is nonconclusive but the presentation is very suspicious for FBA. These procedures tend to take longer to perform compared to the chest radiographs, may require sedation, and expose the patient to an increased amount of radiation.

Complications

The most serious complication of FBA is complete airway obstruction, which may lead to death. This is almost always at the laryngeal level. Death tends to occur in infants and younger children because of their small airway size. Delayed removal of the FB may also lead to severe hypoxia and neurological injury.

Retained FB, when it remains undiagnosed, may lead to infection, such as persistent pneumonia. Unresolved pneumonia with persistent infiltrate on chest X-ray series warrants visualization of the airway to rule out FBA. Late manifestations may include lung abscesses and bronchiectasis, leading to chronic lung disease.

Management

Complete airway obstruction with life-threatening symptoms (i.e., severe respiratory distress, no cough, inability to communicate, cyanosis, altered mental status) is a medical emergency. Dislodgement of the FB to relieve the airway obstruction should be attempted immediately. Knowledge of basic life support maneuvers is very important. Heimlich maneuver for older children, back blows, and chest compressions for infants and younger children are recommended. Children who can cough and speak should be allowed to relieve the obstruction themselves because Heimlich or back blows may convert a partial to a complete airway obstruction.

Establishment of an airway is of primary importance. If the obstruction is deemed to be at the laryngeal level, cricothyrotomy may be performed to bypass the obstruction. For lower obstruction, intubate the trachea, force the FB down into one of the mainstem bronchi, and ventilate the patient through the unobstructed lung while awaiting endoscopic removal of the FB.

FB removal in children is performed using rigid bronchoscopy under general anesthesia (Ciftci, Bingol-Kologlu, Senocak, Tanyel, & Buyukpakcu 2003). Rigid bronchoscopy provides the ability to ventilate the patient during the procedure, a wider angle visualization of the airway, and the ability to pass instruments such as forceps for extraction of the FB.

Flexible bronchoscopy may be initially performed to scout for possible FB. It is a relatively safe procedure that can be performed under conscious sedation. When an FB is visualized, a rigid bronchoscopy is then performed.

Nursing Care of the Child and Family

FBA is completely preventable. Education is the key to its prevention. It is the responsibility of nurses to provide education to parents about the risk factors for FBA. The risk of aspiration should be discussed in the context of a growing and developing child that is exploring the world. Caregivers should be educated about the following:

• Safe and developmentally appropriate foods (in young children, encourage the avoidance of foods in shapes, sizes, and textures that the children are not ready to handle, such as hotdogs, grapes, popcorn, nuts, candy, and gum).
  
• Developmentally appropriate toys (emphasize the dangers associated with batteries and magnets).
  
• Childproofing their home (remind parents about risks associated with small, attractive parts when decorating for holidays or outside).

All parents should also be educated on early detection and initial management of FBA.

PNEUMOTHORAX

Pneumothorax is the accumulation of air in the pleural space. Air enters into the pleural space either from the alveoli or from the atmosphere. Pneumothorax can be traumatic or spontaneous when it occurs in the absence of trauma. The spontaneous form will be discussed in this chapter.

Spontaneous pneumothorax can be primary (i.e., with no underlying lung pathology) or secondary (i.e., when there is identified lung pathology). Risk factors for the development of pneumothorax include asthma, cystic fibrosis, chronic lung disease, certain congenital anomalies, and presence of apical blebs. Pneumothorax is more common in tall, thin individuals. The upper lobes of the lungs are normally more expanded compared with the dependent lower regions due to the more negative transalveolar pressures in the apices. The difference in transpulmonary pressures is exaggerated in thin, tall individuals, which predisposes them to the formation of apical blebs and, eventually, pneumothorax.

Pneumothorax could be life threatening but can result in a good prognosis with careful and immediate attention. Recurrence is common in patients diagnosed with pneumothorax particularly if the pneumothorax is spontaneous.

Epidemiology

Pneumothorax is less common in the general pediatric population compared to adults (Davis, Wensley, & Phelan, 1993; Poenaru, Yazbeck, & Murphy, 1994; Wilcox, Glick, Karamanoukian, Allen, & Azizkhan, 1995). The reported incidence of pneumothorax in adults is about 5–10 per 100,000 populations/year. The exact incidence of pneumothorax in children in the general population is not reported in the literature. There are few published reports of cohorts of pneumothorax in children, most of which are observed cases over a period of time from large institutions like children’s hospitals (Davis, Wensley, & Phelan, 1993; Poenaru, Yazbeck, & Murphy, 1994; Wilcox, Glick, Karamanoukian, Allen, & Azizkhan, 1995). Demographics, clinical course and response to treatment have been described, and differences were compared to pneumothorax in adults. Underlying pathology is more frequently observed in children and recurrence is less common. Pneumothorax is more common in males (Kirby & Ginsberg, 1992; Paape & Fry, 1994; Sahn & Heffner, 2000; Weissberg & Refaely, 2000). Studies in young children also report a male preponderance (Davis 1993; Wilcox, Glick, Karamanoukian, Allen, & Azizkhan, 1995).

The rate of pneumothorax is relatively high in newborns. A report of spontaneous pneumothorax in term newborns was 0.17 per 1,000 live births (Al Tawil et al., 2004). The incidence rate of spontaneous pneumothorax in preterm newborns with birth weights of 500–1,500 g is even higher at 6.3% of 26,007 infants (Horbar et al., 2002). Reasons may include the fact that the majority of preterm neonates develop lung disease, such as respiratory distress syndrome, and are placed on positive pressure ventilation. Chronic lung disease of infancy and bronchopulmonary dysplasia (BPD) are also associated with a higher risk for pneumothorax. Other risk factors for developing pneumothorax during the newborn period and infancy include meconium aspiration syndrome (Wiswell & Henley, 1992; Wiswell, Tuggle, & Turner, 1990), transient tachypnea of the newborn, pulmonary hypoplasia and other congenital anomalies, pneumonia, and infection.

Risk factors associated with spontaneous pneumothorax apart from body habitus are smoking, marijuana smoking, and cocaine inhalation (Feldman, Sullivan, Passero, & Lewis, 1993; Luque, Cavallaro, Torres, Emmanual, & Hillman, 1987). There were familial cases of spontaneous pneumothorax, namely, autosomal dominant and X-linked recessive inheritance described in the literature (Abolnik, Lossos, Zlotogora, & Brauer, 1991; Morrison, Lowry, & Nevin, 1998). A rare genetic disorder, Birt–Hogg–Dubé syndrome, may cause spontaneous pneumothorax in families as a result of lung cyst formation (Menko et al., 2009).

The underlying pulmonary conditions associated with secondary spontaneous pneumothorax found in children and adolescents are cystic fibrosis, asthma, acute respiratory infections especially necrotizing pneumonia and lung abscess, FBA, congenital malformations such as congenital cystic adenomatoid malformation and congenital lobar emphysema, lung diseases including interstitial lung disease, sarcoidosis, and Langerhans cell granulomatosis; and connective tissue disorders including Marfan’s syndrome and Ehlers–Danlos syndrome (Robinson, Cooper, & Ranganathan, 2009). Catamenial pneumothorax (occurring in relation to the menstrual cycle) with endometriosis in the chest may be found in adolescent females (Johnson, 2004; Joseph & Sahn, 1996).

Pathophysiology

Air leak through the visceral and/or parietal pleura results in pneumothorax. Significant transalveolar pressures (i.e., the difference between the alveolar pressure and the intrapleural pressure) cause the alveoli to distend and eventually to rupture. These pressure differences typically occur with increases in alveolar pressure such as during positive pressure ventilation or Valsalva maneuver, or with more negative intrapleural pressure such as with severe asthma exacerbation.

Subpleural blebs, when present, are usually found in the apices of the lungs due to the difference in transalveolar pressure between the apices and the bases of the lungs (West, 2007; Jenkinson, 1985). The blebs can rupture directly into the pleural space leading to a pneumothorax. Occasionally, blebs can rupture into other anatomical spaces such as the mediastinum, soft tissues, and peribronchial tissues leading to pneumomediastinum, subcutaneous emphysema, and pulmonary interstitial emphysema, respectively.

Pneumothorax could also occur as a result of direct injury to the visceral pleura. This commonly occurs secondary to an underlying lung disease such as infections (e.g., lung abscess, necrotizing pneumonia, tuberculosis, and exacerbation/infection in cystic fibrosis) or malignancies. Bronchopleural fistula may occur as a result of a persistent connection between the airways and pleural space.

Physiological disturbances depend on the size of the pneumothorax. A small amount of air leak is usually tolerated with minimal symptoms. The air leak is eventually resorbed without any interventions. When the pneumothorax is large, the buildup of pressure in the intrapleural space leads to lung collapse. This is called tension pneumothorax. The significantly increased intrapleural pressure shifts the mediastinum away from the affected side, leading to compromised venous return, decreased ventricular size during diastole, decreased cardiac output, and cardiovascular collapse (Leigh-Smith & Harris, 2005; Montgomery, 2006).

The signs and symptoms of a pneumothorax may be attenuated by preexisting adhesions in the pleural space. Despite its size, lung collapse and the accompanying effects of a tension pneumothorax may not occur when the visceral pleura is tethered to the parietal pleura due to the adhesions.

Signs and Symptoms

The signs and symptoms of a pneumothorax may be subtle with nonspecific chest pain or vague symptoms of feeling uncomfortable, or may present with acute respiratory distress with cardiopulmonary compromise. The clinical presentation depends on a number of factors including the size of the pneumothorax (amount of air leak in the pleural space), the degree of lung collapse, the speed of equilibration (rapid vs. slow), the presence of tension within the pleural space (increased intrathoracic pressure), and the patient’s underlying condition (including age and severity of illness).

History

Sudden onset of chest pain and dyspnea is the usual complaint of a patient with a large pneumothorax. The pain is described as sharp or stabbing, and can even be preceded by a sensation of “popping” on the affected side. The pain typically is diffuse on the affected side with radiation to the ipsilateral shoulder. A small pneumothorax may present with minimal to no symptoms and may be an incidental finding on a chest imaging for another indication. Patients presenting with spontaneous pneumothorax should always be investigated for potential underlying conditions that may predispose them to develop the pneumothorax.

Physical Examination

Physical findings associated with a large pneumothorax may include decreased breath sounds, decreased chest rise during inspiration, and hyperresonance on percussion on the affected side. Respiratory compromise may include tachypnea, increased work of breathing, and cyanosis. Patients should be examined for signs of tension pneumothorax, such as tracheal shift to the opposite side, decreased heart sounds, and apical impulse shifted to the opposite side. Crepitations usually imply the presence of subcutaneous emphysema and can be palpitated on the chest wall and the neck.

Diagnosis

Chest X-ray confirms the diagnosis of pneumothorax. Both anteroposterior and lateral views will be helpful in delineating the pleural air especially for the small pneumothorax. Intrapleural air presents on a chest X-ray with a pleural line that outlines the visceral pleura (see Figure 11.2) together with a hyperlucent area devoid of lung and vascular markings. A large pneumothorax presents with more obvious findings including a hyperlucent area surrounding the collapsed lung on the affected side, flattening of the diaphragm on the affected side, and tracheal and/or mediastinal shift to the opposite side of the pneumothorax. A lateral decubitus film with the affected side up may also be helpful, especially in an infant.

Figure 11.2 Chest X-ray (PA view) showing a small pneumothorax (<25% of the left hemithorax). Note the pleural line (white line) outlining the visceral pleura on the left apex with a small area of hyperlucency with no lung and vascular markings (as compared to the rest of the lung fields). There is also the presence of pneumomediastinum, with note of air (black line) outlining the mediastinal area.

Courtesy of Dr. Jeffrey Hellinger.

A CT of the chest is not usually needed to diagnose a pneumothorax. However, CT is most helpful in determining the underlying lung pathology (Choudhary, Sellar, Wallis, Cohen, & McHugh, 2005). In newborns, transillumination of the chest in a darkened room may help make the diagnosis of pneumothorax immediately, especially in an emergency. A high-intensity fiber-optic probe is placed against the chest wall of the neonate. Positive transillumination is highly suggestive of a pneumothorax (Kuhns, Bednarek, Wyman, Roloff, & Borer, 1975).

Complications

Tension pneumothorax is a life-threatening medical emergency. The prognosis significantly improves with immediate diagnosis and intervention.

The recurrence of spontaneous pneumothorax is common. In adults, recurrence of spontaneous pneumothorax is about 30% (Kirby & Ginsberg, 1992; Paape & Fry, 1994). Reports in children are limited (Davis, Wensley, & Phelan, 1993; Wilcox, Glick, Karamanoukian, Allen, & Azizkhan, 1995). In a report of 58 children with spontaneous pneumothorax, the risk of recurrence was 50%, with each recurrence increasing the risk of further recurrences (Poenaru, Yazbeck, & Murphy, 1994).

Activities associated with drastic changes in pressure like scuba diving and flying in unpressurized aircrafts should be avoided to decrease recurrence. In addition, patients are advised to avoid contact sports, playing wind musical instruments, or air travel at least 4 weeks after an episode of pneumothorax (Montgomery, 2006).

Management

Management depends on the severity of symptoms, size of the pneumothorax, and the underlying lung problem. Ideally, children with pneumothorax should be observed in the hospital initially.

Conservative Management

For a small pneumothorax (i.e., less than 25% of the affected hemithorax) with minimal symptoms, treatment is conservative, mainly with supplemental oxygen and close observation. Treatment of the underlying lung disease, if any is identified, should be addressed.

Supplemental oxygen is usually used to enhance the resorption of the intrapleural air. Unless the patient is inhaling supplemental oxygen when the pneumothorax occurred, air in the intrapleural space is room air with 21% oxygen and 79% nitrogen. Inhalation of 100% oxygen creates a steep gradient for nitrogen absorption from the intrapleural space into the alveolar space. Eventually, the air in the intrapleural space gets converted into 100% oxygen, which is more easily resorbed by the body compared with nitrogen. Oxygen at 100% can only be delivered to a nonventilated patient via a non-rebreather mask. Pain control with analgesics and supportive care should be provided.

Evacuation of the Pleural Air

For children with a large pneumothorax (i.e., more than 25% of the affected hemithorax) who typically present with more significant symptoms such as dyspnea, hypoxemia, and pain, evacuation of the pleural air is needed. Needle aspiration and chest tube placement are options for evacuation of the pleural air (Camuset et al., 2006). In an emergency, air can be evacuated from the intrapleural space with a large-bore intravenous catheter placed anteriorly in the second intercostal space of the affected site. The catheter can be connected to a large syringe via a three-way stopcock or to a tubing with the opposite end submerged in water. Air can be easily withdrawn with the syringe until resistance is felt. In this case, the pneumothorax has been evacuated. This method provides an estimate of the size of the pneumothorax. If the latter method is used, where the tubing is submerged in water, bubbles should form until the pneumothorax is completely evacuated. The temporary catheter is typically converted into a chest tube (pigtail catheter or thoracostomy tube) until the source of the air leak is identified and addressed or no more air leak is present.

The chest tube uses a one-way Heimlich valve or water seal device to prevent reaccumulation of air. Suction is applied to a water seal device if the lung does not fully expand after the drainage. The chest tube is usually clamped when no bubbles are seen on the water seal from the patent tube after approximately 12 hours. The chest tube is then removed after 24 hours if there is no radiographic or clinical evidence of recurrence of the pneumothorax.

Pleurodesis

Pleurodesis is the injection of sclerosing agents at the time of thoracostomy tube placement to decrease the risk of recurrence. Agents used are talc, tetracycline, and fibrin glue (Cardillo et al., 2006; Chen et al., 2006). Pleural abrasion with dry gauze has also been used (Casadio et al., 2002). In a report of about 200 spontaneous pneumothorax cases, the recurrence rate in the intrapleural tetracycline group (25%) was significantly less than that in the control group (41%)(Light et al., 1990).

Surgical Intervention

Surgery is indicated for persistent air leaks and is needed more often in secondary rather than in primary pneumothorax. Surgical approaches include video-assisted thoracoscopic surgery (VATS), minithoracotomy, and conventional thoracotomy (Chan, Clarke, Daniel, Knight, & Seevanayagam, 2001; Hatz et al., 2000; Lang-Lazdunski, Kerangal, Pons, & Jancovici, 2000; Nazari, Buniva, Aluffi, & Salvi, 2000; Yamamoto et al., 2000). Thoracoscopic treatment of spontaneous pneumothorax is safe and effective in children. Recently, VATS has been used often, especially in children, because it provides adequate exposure for resection or stapling (Ozcan, McGahren, & Rodgers, 2003). Surgical intervention includes stapling or oversewing of ruptured blebs or tears, and resection of abnormal lung tissue, if found.

Nursing Care of the Child and Family

Nursing care of the child with a pneumothorax requires a comprehensive understanding of normal respiratory anatomy and physiology in order to understand the process that led to the accumulation of air in the pleural space and the rationale for the treatment in an individual patient. Needle aspiration or chest tube placement may be needed to remove the air, restore negative pressure, and re-expand the lung.

Chest tube insertion requires pain management. Once a chest tube is placed, the nurse should consult with the medical team to confirm that a chest X-ray was performed and should document proper placement of the tube. The nurse must also ensure the tube is secure to prevent displacement. In the event of tube displacement, the site should be covered with a sterile petroleum dressing to prevent ambient air from entering the pleural space and from enlarging the pneumothorax. If displacement occurs, the physician should be contacted immediately. Furthermore, if the tube becomes disconnected, place the end of the tube in a bottle of sterile water until a new unit is established (Verger & Lebet, 2008).

When treating a small pneumothorax with 100% supplemental oxygen, the nurse must ensure that the non-rebreather mask is maintained in place and that it has adequate flow from the oxygen flow meter. Nursing care of the patient with a chest tube includes managing and monitoring the chest tube system function. A chest tube is connected to a drainage system and the specific system used varies according to the institution. Nurses should consult their institution’s policy and procedure manual for operational information about the chest tube system.

Wall suction may or may not be ordered. The amount of sterile water in the water seal chamber and negative pressure are dictated by the manufacturer. Constant bubbling in the water seal chamber indicates an air leak. The tubing should be kept in a dependent position free of loops that could impede the evacuation of air. Milking or stripping chest tubes causes large fluctuations in intrapleural pressure and may cause air leak, bleeding from entrapment of pleural tissue in the drainage system, or worsening of the pneumothorax (Halm, 2007).

The integrity of the suture made at the time of tube placement should be assessed. Care must be taken to limit the risk of displacing the tube. The chest tube insertion site should also be evaluated on a regular basis. Assessment includes observing the insertion site for signs of infection such as redness, swelling, warmth, and drainage (color and amount). An occlusive petroleum dressing is applied to the insertion site to prevent air leaks. The frequency of dressing changes depends on institutional policy.

All patients with pneumothorax require continuous cardiopulmonary and pulse oximetry monitoring. The nurse must monitor vital signs and respiratory status including auscultation of breath sounds in all lung fields. Auscultation helps to determine progress or signs of deterioration.

A tension pneumothorax is a medical emergency, and the nurse must communicate signs of a tension pneumothorax to the child’s physician immediately. Signs of a tension pneumothorax include tachycardia, hypotension, dyspnea, chest pain, decreased oxygen saturation, and tracheal deviation (a relatively late finding).

Nursing care of patients with a pneumothorax also includes regular encouragement of deep breathing and position changes. Pain management should be ongoing to prevent the child from splinting (especially during coughing or deep breathing), which could prevent optimal lung re-expansion.

As children are recovering from a pneumothorax, education should be provided cautioning patients against certain activities. Children should avoid flying, contact sports, scuba diving, and playing musical wind instruments.

RESPIRATORY FAILURE

Respiratory distress occurs often in children and is one of the most common complaints in an emergency room (Krauss, Harakal, & Fleisher, 1991). Infants and younger children with respiratory problems can deteriorate quickly. Therefore, it is very important to be able to recognize early signs immediately and to intervene appropriately.

There are several anatomical and physiological differences in the respiratory system in infants and younger children as they develop. These differences may explain the higher incidence of respiratory failure in the younger age group. The upper airway is funnel shaped, with its narrowest portion at the subglottic area. This is a likely site for obstruction as in the case of croup. The infant’s thoracic cage is soft, with the ribs more horizontally positioned, resulting in a disadvantage for chest expansion. Another disadvantage is the infant’s diaphragm, which is more flattened. In addition, the younger child’s diaphragm has a higher percentage of type II respiratory muscle fibers (responsible for bursts of motor activity) than type I fibers (responsible for sustained muscle activity), making the diaphragm easier to fatigue. The nervous system of the infant is immature and, thus, more prone to apnea. Finally, the infant’s lower airways are smaller and more prone to significant airway obstruction during illness as in the case of bronchiolitis.

Respiratory failure occurs when the respiratory system cannot sustain adequate gas exchange, particularly oxygen and carbon dioxide. A partial pressure of oxygen (paO₂) is decreased below 60 mmHg (hypoxemia), or a partial pressure of carbon dioxide (paCO₂) above 50 mmHg (hypercarbia) with blood pH below 7.35 is frequently used to define respiratory failure (Pope & McBride, 2004). Even with significant impairment in gas exchange, children may be clinically stable until rapid deterioration happens.

Respiratory failure can be “acute” or “chronic.” Acute respiratory failure presents with rapid onset (i.e., minutes to hours), such as in toxic inhalation, whereas chronic respiratory failure presents with an insidious onset (i.e., weeks to months), such as in muscular dystrophy. Some patients may have an acute-on-chronic respiratory failure. High-risk children with chronic respiratory insufficiency (as seen in neuromuscular disease) may have acute deterioration during an intercurrent respiratory infection.

Epidemiology

Respiratory failure can be caused by abnormalities of one or any combination of the following three main categories:

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