FIGURE 99.5 Cor pulmonale secondary to upper airway obstruction A: This is a 2-year-old boy with tachypnea and dyspnea The chest film shows a large heart and mild interstitial edema B: The lateral view of the neck shows obstructing enlarged adenoids and tonsils C: The chest film days after adenoidectomy shows a decreased heart size and improvement in interstitial edema For children with underlying conditions, it is important to understand the status of their disease and any recent changes in therapy The possibility of acute intercurrent illness or insult should also be considered CXRs are often diagnostic, although findings may lag behind the acute clinical process Lymphatic and interstitial fluid accumulations may be visible as Kerley A and B lines (septal lines; Fig 99.6 ), which represent interstitial edema, tangential to the radiograph beam The B lines, which lie in the periphery, are often the first findings Unlike blood vessels, these radiopacities will reach the lung edge As edema progresses, Kerley A lines near the hilum may occur, and ultimately, a butterfly pattern with a central predominance of shadows can be seen Although these findings are not specific, transient changes in an appropriate clinical context usually signify edema Bedside ultrasound can also be very effective at identifying fluid in the lungs, including B lines suggested of pulmonary edema or fluid collection in the pleural space (see Chapter 131 Ultrasound ) FIGURE 99.6 Interstitial fluid from volume overload This is a 2-year-old child with paraspinal sarcoma removed months earlier Before chest radiation, he received a large fluid load The chest film shows interstitial edema with Kerley lines The distribution, symmetry, and extent of radiographic findings may also provide helpful information regarding possible etiology and severity of edema Patterns of radiographic findings in particular can be helpful in identifying underlying cause Cardiac size and increased prominence of pulmonary vasculature may suggest increased hydrostatic pressure or cardiogenic edema Conversely, presence of air bronchograms, peribronchial cuffing, and increased lung volume may suggest primary lung injury with resultant capillary leak If pulmonary edema is superimposed on another pulmonary process, the clinical and radiographic findings may be obscured by those of the primary illness Similarly, once pulmonary edema is severe enough, it may be difficult to distinguish edema, atelectasis, and inflammation on the chest film Management The management of patients with pulmonary edema includes supportive therapies and correction of the underlying disorder Initial efforts ( Table 99.9 ) should be directed toward correction of hypoxemia through the administration of supplemental oxygen In addition to satisfying the patient’s oxygen demands, reversal of hypoxemia is often useful in relieving chest pain and is important to the metabolism of vasoactive mediators that affect microvascular permeability In severe cases, HFNC, CPAP, BiPAP, or intubation and mechanical ventilation may be warranted Assisted ventilation has several beneficial effects for patients with pulmonary edema It reduces oxygen consumption by decreasing work of breathing Oxygenation is also improved through prevention of alveolar collapse In addition, positive intrathoracic pressures decrease pulmonary vascular volume and reduce fluid filtration in the lung TABLE 99.9 TREATMENT OF PULMONARY EDEMA Oxygen Diuresis Afterload reduction Morphine 0.1 mg/kg IV Furosemide mg/kg IV IV, intravenous In healthy lungs, there is a small fluid flux from pulmonary capillaries into the interstitium This fluid is actively drained by a sodium transporter in the alveolar epithelium and reenters the vascular system as lymph This process can be actively enhanced and alveolar fluid clearance augmented with β-adrenergic agonists, which may be utilized in some clinical circumstances Other therapeutic measures should be tailored to fit the patient’s underlying disease process When ventricular failure is the cause of pulmonary edema, diuretics can be used to decrease plasma volume, and inotropes can improve contractility Morphine helps physiologically by dilating the venous system and may also relieve anxiety and dyspnea Afterload reducers such as milrinone may also be helpful When decreased plasma oncotic pressure is primary, administration of colloids such as albumin is indicated Slow infusion and concomitant diuretic use will help minimize resultant increases in pulmonary vascular pressure Detailed management of ARDS is beyond the scope of this chapter, though generally it is focused on addressing underlying illness and supportive ventilatory strategies Clinical studies have shown that the use of systemic steroids does not improve outcome and may in fact increase the incidence of secondary infections and subsequent mortality Clinical Indications for Discharge or Admission Most children with pulmonary edema will require hospitalization with supportive cardiopulmonary care and evaluation for underlying conditions PLEURITIS/PLEURAL EFFUSION CLINICAL PEARLS AND PITFALLS Pleuritis without significant effusion may be associated with systemic vasculitis Most pleural effusions in pediatrics are exudative Management of effusions involves treating associated chest pain, and thoracentesis for diagnostic and therapeutic purposes Current Evidence Pleuritis or pleurisy refers to inflammation of pleural membranes, resulting from primary pleural, adjacent pneumonic, or systemic disease This inflammation is usually associated with an increased volume of fluid in the pleural space Specific references to the evaluation and management of pleural effusions in various respiratory infections are made in Chapter 94 Infectious Disease Emergencies , and the surgical approach to pleural effusions is reviewed in Chapter 124 Thoracic Emergencies The pleural membrane is thin and double layered, separating the lung from the chest wall, diaphragm, and mediastinum The outer parietal pleura is adherent to the chest wall, and the inner visceral pleura completely covers the lungs except at the hila In healthy children, the two pleural layers are opposed, separated by only a thin physiologic layer of serous fluid This pleural fluid is constantly being turned over, entering from the parietal pleura and exiting via the lymphatics and vasculature of the visceral pleura Abnormal pleural fluid accumulation can result from changes in hydrostatic or oncotic pressures (such as seen with pulmonary edema) or diseases of the pleural surface that alter capillary permeability or affect lymphatic reabsorption The underlying pathophysiology will determine if an effusion will be transudative or exudative Transudates result from increased capillary hydrostatic pressure such as congestive heart failure or decreased oncotic pressure such as hypoproteinemic states Exudates result from diseases of the pleural surface that produce increased capillary permeability or lymphatic obstruction, such as pleural infection or tumor ... without significant effusion may be associated with systemic vasculitis Most pleural effusions in pediatrics are exudative Management of effusions involves treating associated chest pain, and thoracentesis