Chapter 11: Imaging of the Critically Ill Patient: Radiology

Imaging is an essential tool in the clinical assessment and management of critically ill patients. Although bedside ultrasound and chest radiography are the mainstays of initial assessment, an extensive variety of imaging options are available to the physician in the ICU, including CT, magnetic resonance imaging (MRI), and nuclear medicine studies. Interventional procedures, either at the bedside or in the radiology suite, are also playing an increasingly important role in the management of critical illness.

The choice of a particular imaging modality is occasionally difficult and should be based on recommendations in the literature, local expertise, type of equipment available, and the experience of the radiologists. Given the increasing emphasis on cost-effective practice, clinicians and radiologists must maximize the diagnostic and therapeutic yield of procedures while minimizing costs. The main indications, strengths, and weaknesses of imaging modalities used in common ICU scenarios are reviewed in this chapter. Although abdominal, neurologic, and musculoskeletal imaging studies play an important role in the care of the critically ill patient, this chapter will focus primarily on imaging of the chest and devices used in the ICU.

Plain Radiography

Portable chest radiographs are the most commonly requested imaging examination in the ICU. Despite their limitations, these films play an important role in the management of ICU patients. Chest radiographs are used to identify and follow pulmonary and cardiac disorders as well as evaluate the positions of and complications from catheters and support devices used in the care of critically ill patients.

Imaging of the abdomen can also often begin with plain radiographs, which provide a readily accessible means of diagnosing perforation, bowel obstruction, and ileus. However, because the overall sensitivity of plain radiographs remains low, further imaging with CT is frequently necessary to confirm suspected pathology and to inspect the features of the bowel walls and surrounding fat. Supine radiographs are appropriate for verifying nasogastric or feeding tube placement and for initial investigation of renal stones and ileus or bowel obstruction. Additional views obtained with the patient in a semiup-right or lateral decubitus position are used to show air-fluid levels in the gastrointestinal tract or free intraperitoneal gas and may be helpful in patients with suspected bowel perforation or obstruction.

Ultrasound

Ultrasound examination at the bedside in the ICU is relatively inexpensive and does not use ionizing radiation. In the thorax, ultrasound is useful in imaging lung consolidation, pleural-based masses and effusions, pneumothorax, and diaphragmatic dysfunction. It can identify complex or loculated effusions and be used as a guide to thoracentesis or thoracostomy tube insertion.

In the abdomen, ultrasound provides for rapid evaluation of hepatobiliary and genitourinary disease, as well as assessment of vascular structures such as the aorta and the inferior vena cava. Similar to its use in the thorax, ultrasound can be used for identification and qualitative assessment of intraperitoneal fluid, as well as a guide for paracentesis.

In addition to its use in pleural and peritoneal fluid aspiration, ultrasound can be used as a tool in a multitude of bedside procedures such as central line placement, pulmonary artery catheterization, biopsies, and drainage of fluid collections. Its use in cardiac and hemodynamic assessment is becoming increasingly important in critical care.

Computed Tomography

By virtue of multiplanar imaging capabilities and improved contrast resolution, multidetector CT (MDCT) has been shown to be very valuable in increasing diagnostic accuracy and guiding therapeutic procedures for critically ill patients. MDCT allows for more rapid scanning of patients, with imaging of the entire chest, abdomen, and pelvis with thin sections during a single breath-hold. Such short acquisition times have facilitated the use of CT for evaluation of vascular disorders such as aortic dissection and pulmonary embolism. CT is a critical diagnostic tool for the evaluation of an acute abdomen and also allows for improved characterization of pulmonary diseases.

Transportation of the ICU patient to the CT scanner poses significant risks and requires a coordinated effort from hospital personnel, including ICU physicians and nurses, respiratory therapists, radiology technologists, and radiologists. Careful monitoring during transport and throughout the procedure is essential and should be performed by a dedicated team skilled in airway management and resuscitation.

Nuclear Scintigraphy

Nuclear scintigraphy has a number of applications in the critically ill patient. Myocardial perfusion and infarct scanning in cardiac disease, ventilation-perfusion scanning in patients with suspected pulmonary embolism, evaluation of gastrointestinal hemorrhage and acute cholecystitis, and localization of occult infection are among the most common indications for radionuclide imaging in the ICU patient.

Magnetic Resonance Imaging

MRI provides excellent differentiation of vascular and nonvascular structures without the use of intravenous contrast material or ionizing radiation and provides cross-sectional images in multiple planes. It is generally considered the single best imaging method for evaluation of the central nervous system (CNS), head and neck, liver, and musculoskeletal system. However, in many cases, MRI is not feasible in the evaluation of the critically ill patient because of interference caused by ferromagnetic monitoring devices, the difficulty of adequately ventilating and monitoring patients within the narrow MRI gantry, and long scan times. MRI may be appropriate in selected diagnostic dilemmas if MR-compatible equipment and coordinated effort among caregivers can be arranged.

Peripheral venous access, particularly in an antecubital or large forearm vein is the preferred route of contrast agent administration in imaging. The flow rate should be appropriate for the gauge of the catheter used; a 20-gauge or larger catheter is preferable for flow rates of 3 mL/s or higher. When peripheral access is difficult, existing central venous catheters (CVCs) may be considered, provided that certain precautions are followed. First, catheter placement should be confirmed prior to its use, and its integrity and patency should be checked before and after injection. Additionally, flow rates greater than 2.5 mL/s should be avoided in order to keep intraluminal pressures below most manufacturers' specified limits; this flow rate limitation may in turn produce a suboptimal study. Finally, contrast media should not be administered by a power injector unless permitted by the manufacturer's specifications because of the risk of catheter breakage. Hospital personnel should be knowledgeable about the specific catheters used at their institution and adapt their practice accordingly.

Adverse reactions to iodinated contrast agents occur at low rates but are encountered not infrequently given their widespread use. Idiosyncratic reactions range from benign urticaria to, very rarely, life-threatening hypotension, laryngeal edema, and bronchospasm. These events are not considered truly allergic in nature because they are not antibody mediated and are inconsistently reproducible with subsequent administrations. Prior allergy-like reaction to contrast media is associated with an up to 5-fold increased likelihood of the patient experiencing a subsequent reaction. A history of asthma or other allergic diatheses may also predispose individuals to reactions. The predictive value of allergy to shellfish, previously thought to be helpful, is now recognized to be unreliable.

In high-risk patients, pretreatment with steroids should be given beginning at least 6 hours prior to the injection of contrast media whenever possible. Supplemental administration of an H₁ antihistamine (eg, diphenhydramine) may reduce the frequency of urticaria, angioedema, and respiratory symptoms. Although pretreatment with corticosteroids appears to be effective for mild events, no randomized controlled clinical trials have demonstrated premedication protection against severe life-threatening adverse reactions. In the latter situation, an alternative imaging modality such as MRI should be considered.

Contrast-induced nephropathy (CIN) is another important complication of intravascular iodinated contrast use. The most important risk factor for CIN is preexisting renal insufficiency. Multiple other predisposing factors have been proposed, including diabetes mellitus, dehydration, cardiovascular disease, advanced age, and exposure to multiple doses of iodinated contrast in a short time interval (< 24 hours), but these have not been rigorously confirmed as independent risk factors. There is no specific creatinine or estimated glomerular filtration rate (eGFR) level that absolutely precludes the use of contrast agents; the decision to use contrast must be made on a case-by-case basis, carefully weighing the need for the study in high-risk patients. The major preventive action against CIN is to ensure adequate hydration with isotonic fluid. Substitution of sodium bicarbonate for 0.9% saline or addition of N-acetylcysteine to intravenous hydration is controversial. Multiple studies and a number of meta-analyses have had disparate results and neither strategy can be definitively recommended.

If CIN does develop, its clinical course depends on a number of variables, including baseline renal function, coexisting risk factors, and degree of hydration. Serum creatinine usually begins to rise within 24 hours of intravascular iodinated contrast medium administration, peaks within 4 days, and often returns to baseline within 7 to 10 days. Progression to end-stage renal disease is exceptionally rare and usually develops in the setting of multiple risk factors.

Endotracheal and Tracheostomy Tubes

Both endotracheal intubation and tracheostomy may cause potentially serious complications. Malpositioning of the endotracheal tube (ETT) occurs in approximately 15% of endotracheal intubations. The clinical assessment of tube location is frequently inaccurate, and a chest radiograph should be obtained immediately following intubation. With the neck in neutral position, the ideal position of the tube tip is 5 to 7 cm above the carina; flexion of the head and neck causes a 2-cm descent of the tip of the tube, whereas extension of the head and neck causes a 2-cm ascent of the tip. In 90% of patients, the carina projects between the fifth and seventh thoracic vertebrae on the portable radiograph; when the carina cannot be clearly seen, the ideal positioning of the ETT is at the T2-T4 level. The aortic arch also may be used to estimate tube location because the carina is typically at the level of the undersurface of the aortic arch. If the ETT is too high, there is a risk of either inadvertent extubation or hypopharyngeal intubation, which can cause ineffective ventilation, gastric distention, or vocal cord injury. If the ETT is too low, selective intubation of the right mainstem bronchus may occur, resulting in segmental or complete collapse of the left lung, hyperinflation of the right lung, and possible pneumothorax (Figure 11–1). The balloon cuff should fill but not dilate the trachea. Cuff overinflation can cause tracheal injury, including tracheomalacia, tracheal stenosis, or acute tracheal rupture.

Inadvertent placement of the ETT into the esophagus is uncommon but may be catastrophic when it does occur. Esophageal intubation may be difficult to diagnose on the portable chest film because the esophagus frequently projects over the tracheal air column. Gastric or distal esophageal distention, location of the tube lateral to the tracheal air column, and deviation of the trachea secondary to an overinflated intraesophageal balloon cuff are radiographic signs of esophageal intubation. The right posterior oblique view with the patient's head turned to the right allows ease of separation of the esophagus and trachea and can be obtained in equivocal cases.

Tracheostomy is typically performed in the patient who requires relatively long-term ventilatory support. The tip of the tracheostomy tube should be located at approximately one-half to two-thirds of the distance from the stoma to the carina, and unlike the ETT's position, the tracheostomy tube's position is not changed by extension or flexion of the patient's head. Although small amounts of subcutaneous emphysema and pneumomediastinum may be seen after an uncomplicated tracheostomy tube placement, significant emphysema may be a sign of tracheal perforation. Pneumothorax can occur after tracheostomy tube placement and may also be a sign of tracheal perforation. Late complications include tracheal stenosis, stomal infection, aspiration, tube occlusion, and development of a fistula between the trachea and esophagus, pleura, or mediastinum. The fistula is caused by erosion through the posterior tracheal membrane and usually occurs at the level of the tracheal cuff. If the fistula develops below the level of the cuff, gastric contents may be aspirated into the lungs. If the fistula develops above the level of the cuff, gastric contents may collect in the upper trachea.

Central Venous Catheters

CVCs are used frequently in the ICU patient for venous access, monitoring central venous pressure, and hemodialysis. The subclavian, internal jugular, and femoral veins are the sites of venous access used most commonly; smaller-caliber central catheters can also be peripherally inserted via antecubital veins. CVCs inserted via a thoracic vein are visible on the chest radiograph, and knowledge of normal thoracic venous anatomy is required to assess catheter location. The subclavian vein originates by the lateral aspect of the first rib and courses posterior to the clavicle, and anterior to the first rib. The internal jugular vein courses vertically in the neck; its convergence with the subclavian vein to form the brachiocephalic vein usually occurs behind the sternal end of the corresponding clavicle. Whereas the right brachiocephalic vein has a vertical course as it forms the superior vena cava, the left brachiocephalic vein crosses the mediastinum from left to right in a retrosternal position to enter the superior vena cava. The superior vena cava is formed by the junction of the right and left brachiocephalic veins at the level of the first anterior intercostal space, with its upper border usually just superior to the angle of the right mainstem bronchus and the trachea. On a chest radiograph, the junction of the superior vena cava and right atrium lies approximately 4 cm below the carina, or 1 to 2 cm below the superior right heart border. CVCs are optimally positioned when the tip within the superior vena cava, ideally slightly above the right atrium.

Appropriate catheter position must be verified radiographically, as malposition has been described in up to 40% of CVCs. Positioning of the catheter tip within the right atrium is common and may result in cardiac perforation and tamponade. Placement into the right ventricle may result in arrhythmias secondary to irritation of the endocardium or interventricular septum. A misplaced CVC may have its tip terminating in central systemic veins, which can result in inaccurate venous pressure readings as well as venous thrombosis or venous wall perforation. The most common location for a misplaced catheter entering the subclavian vein is the ipsilateral internal jugular vein. Less frequently, thoracic CVCs may enter the azygous, internal mammary, superior intercostal (Figure 11–2), thymic, left pericardiophrenic, or inferior thyroid veins. Looping, knotting, and kinking of the catheter may also occur (Figure 11–3), which can place mechanical stress on the vein and occasionally require removal by surgical or interventional radiology techniques.

Other complications of central venous catheterization include pneumothorax, hemothorax, and perforation, which may result in pericardial effusion, hydrothorax, mediastinal hemorrhage, or ectopic infusion of intravenous solutions (Figure 11–4). Less common complications include air embolism and catheter fracture or embolism. Pneumothorax occurs in up to 5% of CVC insertions; the incidence of is higher with a subclavian approach than with an internal jugular approach. Pneumothorax may be clinically occult, and a chest radiograph should be obtained to exclude a pneumothorax following line placement. A radiograph should be obtained even following an unsuccessful attempted line placement.

Venous air embolism is an uncommon complication of central venous catheterization. Radiographically, air in the main pulmonary artery is diagnostic, but other features include focal oligemia, pulmonary edema, and atelectasis. Intracardiac air or air within the pulmonary artery is seen easily on CT.

Long-term complications of venous access devices include delayed perforation, pinch-off syndrome, thrombosis, catheter knotting, and catheter fragmentation. Left-sided catheters have a greater risk for perforation, with increased risk in catheters abutting the right lateral wall of the superior vena cava. In pinch-off syndrome, the catheter lumen is compromised by compression between the clavicle and the first rib, leading to catheter malfunction and possible catheter fracture. This is frequently first observed as subtle focal narrowing of the catheter as it crosses the intersection of clavicle and rib.

Pulmonary Artery Catheters

The pulmonary artery catheter (PAC) plays an important role in the hemodynamic monitoring of the critically ill patient. The catheter is inserted via the subclavian or internal jugular vein and its tip should lie within the right or left main pulmonary artery. The catheter tip should remain within 2 cm of the hilum so that it does not extend beyond the proximal interlobar arteries. Complications related to CVC insertion, such as pneumothorax, vascular injury, infection, and knotting, kinking, or coiling of the catheter may also occur with PAC insertion. Ventricular arrhythmias are also common during PAC insertion, though usually self-limited. Another major complication is pulmonary infarction (Figure 11–5), usually caused by peripheral migration and occlusion of the vascular lumen by the catheter, or by continuous wedging of the inflated balloon in a central pulmonary artery. The radiographic appearance of pulmonary infarction secondary to a PAC is similar to that of infarction from other causes and consists of a wedge-shaped parenchymal opacity seen in the distribution of the vessel distal to the catheter. Management consists of removal of the catheter. Anticoagulation is generally not required, and resolution of consolidation usually occurs in 2 to 4 weeks.

Pulmonary artery rupture is a catastrophic complication of pulmonary artery catheterization, with a reported mortality rate of 46%. The incidence is low—no more than 0.2% of catheter placements. Risk factors include pulmonary hypertension, advanced age, and improper balloon location or inflation. The mortality rate increases in anticoagulated patients. Pseudoaneurysm formation has been reported secondary to rupture or dissection by the balloon catheter tip. This appears radiographically as a well-defined nodule at the site of the aneurysm, but it may be obscured initially by extravasation of blood into the adjacent air spaces. Chest radiographic findings often precede clinical manifestations, and death due to rupture of pseudoaneurysm may occur weeks following catheterization. The CT appearance of a pulmonary artery pseudoaneurysm has been described as a sharply defined nodule with a surrounding halo of faint parenchymal density. Pulmonary artery pseudoaneurysm now may be treated in some patients with transcatheter embolization rather than surgical resection.

Intra-Aortic Balloon Counterpulsation

Intra-aortic balloon counterpulsation is used to improve cardiac function in patients with cardiogenic shock and in the perioperative period in cardiac surgery patients. The device consists of a fusiform inflatable balloon surrounding the distal portion of a catheter that is placed percutaneously from a femoral artery into the proximal descending thoracic aorta. The balloon is inflated during diastole, thereby increasing diastolic pressure in the proximal aorta and increasing coronary artery perfusion. During systole, the balloon is forcibly deflated, allowing aortic blood to move distally and decreasing the afterload against which the left ventricle must contract, thus decreasing left ventricular workload. The tip of the balloon ideally should be positioned just distal to the origin of the left subclavian artery at the level of the aortic knob (Figure 11–6). Complications occur in 8% to 36% of intra-aortic balloon pump (IABP) placements and are most often secondary to malpositioning of the catheter. Overadvancement of the catheter may cause occlusion of the left subclavian artery, resulting in arm ischemia, or obstruction of the left common carotid or left vertebral arteries, causing cerebral ischemia. Caudal placement of the catheter can obstruct renal or mesenteric arterial flow. Aortic dissection has been reported in 1% to 4% of IABP catheter insertions, and an indistinct aorta on chest radiographs has been suggested as an early clue to intramural location, requiring confirmation by angiography. Balloon leak or rupture with gas embolization has also been described as an extremely rare but potentially fatal complication.

Cardiac Pacemakers and Automatic Implantable Cardioverter-Defibrillators

Cardiac pacemakers can be inserted by 3 approaches: transvenous, epicardial, and subxiphoid. Most often the transvenous approach is used, whereby an introducer sheath is used to establish central venous access and allow for insertion of the pacing wire, which is then guided into the right ventricle under electrocardiogram (ECG), ultrasound, or fluoroscopic guidance. The right internal jugular and the left subclavian veins are often preferred, as these routes take advantage of the natural curve of the pacing catheter, allowing for smoother, more direct placement of the wire.

When viewed on a chest radiograph, the pacemaker lead should terminate in the right ventricular apex, slightly to the left of the thoracic spine and at the anterior-inferior aspect of the cardiac shadow. A lateral view can be obtained to confirm that the catheter courses anteriorly to the right ventricle if proper placement is in question. The pacemaker lead should curve gently throughout its course, as regions of sharp angulation will have increased mechanical stress and enhance the likelihood of lead fracture. Excessive lead length can result in myocardial perforation, causing hemopericardium and cardiac tamponade. Shorter leads can become dislodged and enter the right atrium. Leads also may become displaced and enter the pulmonary artery, coronary sinus, or inferior vena cava. Other complications include venous thrombosis or infection, either at the pulse generator pocket or within the vein.

Nasogastric Tubes

Nasogastric tubes are used frequently to provide nutrition and administer oral medications as well as for suctioning gastric contents. Ideally, the tip of the tube should be positioned at least 10 cm beyond the gastroesophageal junction. This ensures that all side holes are located within the stomach and decreases the risk of aspiration.

Small-bore flexible feeding tubes have been developed to facilitate insertion and improve patient comfort. However, inadvertent passage of the nasogastric tube into the tracheobronchial tree is not uncommon, most often occurring in the sedated or neurologically impaired patient. In patients with endotracheal tubes in place, low-pressure, high-volume balloon cuffs do not prevent passage of a feeding tube into the lower airway. If sufficient feeding tube length is inserted, the tube actually may traverse the lung and penetrate the visceral pleura (Figure 11–7). Removal of the tube from an intrapleural location may result in tension pneumothorax, and preparations should be made for potential emergent thoracostomy tube placement at the time of removal. Other complications of nasogastric intubation include esophagitis, stricture, and, rarely, rupture of the pharynx, esophagus, or stomach.

In addition to feeding tubes, balloon tamponade tubes occasionally are used for nasogastric intubation in the treatment of bleeding esophageal and gastric varices. The balloon can be easily recognized when distended, and correct positioning can be evaluated radiographically (Figure 11–8). Esophageal rupture complicates approximately 5% of cases in which balloon tamponade tubes are used.

Thoracostomy Tubes

Thoracostomy tubes (“chest tubes”) are used for the evacuation of air or fluid from the pleural space. When chest tubes are used for relief of pneumothorax (Figure 11–9), apical location of the tip of the tube is most effective, whereas a tube inserted to drain free-flowing effusions should be placed in the dependent portion of the thorax. Chest radiographs, ultrasound, or CT should be used to guide correct placement of the tube for adequate drainage of a loculated effusion. Failure of the chest tube to decrease the pneumothorax or the effusion within several hours should arouse suspicion of a malpositioned tube. Tubes located within the pleural fissures are usually less effective in evacuating air or fluid collections. An interfissural location is suggested by orientation of the tube along the plane of the fissure on frontal radiographs and by lack of a gentle curvature near the site of penetration of the pleura, indicating failure of the tube to be deflected anteriorly or posteriorly in the pleural space. The lateral view may be confirmatory. Uncommonly, thoracostomy tubes may penetrate the lung, resulting in pulmonary laceration and bronchopleural fistula. Unilateral pulmonary edema may occur following rapid evacuation of a pneumothorax or pleural effusion that is of long standing or has produced significant compression atelectasis of lung.

Portable chest radiographs are frequently obtained in ICU patients. Almost all portable chest radiographs are taken with the patient supine and with the film placed behind the back of the patient (anteroposterior) rather than in the conventional upright, posteroanterior position used in the radiology department. Supine chest radiographs result in decreases in lung volume and can alter the size and appearance of the lungs, the pulmonary vasculature, and the mediastinum. Anteroposterior chest radiographs cause cardiac magnification, making evaluation of true cardiac size more difficult. Inspiratory films may be difficult to obtain because of respiratory distress, pain, sedation, or alterations in mental status. These technical limitations complicate diagnostic interpretation. Nonetheless, portable radiography continues to be a primary method of imaging critically ill patients.

Traditionally, routine daily chest radiographs have been performed on ICU patients, particularly those requiring mechanical ventilation. However, the benefit of this practice has recently been questioned. Multiple recent studies have found a low incidence of significant findings in routine radiographs, and no significant difference in mortality, length of stay, or ventilator days in patients receiving chest radiographs on a daily basis compared with those receiving chest radiographs for specific clinical indications. The American College of Radiology Thoracic Expert Panel concluded that chest radiographs should be obtained if there is a change in the clinical condition of the patient, or after placement of an ETT, central venous pressure or pulmonary artery catheter, chest tube, or nasogastric tube. Routine daily chest radiographs are not indicated.

Atelectasis is one of the most common pulmonary parenchymal abnormalities seen in the ICU. It refers to collapse of previously inflated lung and results in diminished lung volume. The spectrum can be subtle, with only segmental or subsegmental involvement and minimal clinical significance, or extensive, with lobar involvement and ventilation-perfusion defects. Distinguishing atelectasis from pneumonia can be a challenge as the signs and symptoms often coexist. Atelectasis has a basilar predominance, particularly in the left lower lobe, and can be influenced by gravity. It also has a more rapid resolution than pneumonia.

Multiple factors contribute to the development of atelectasis. Hypoventilation results in atelectasis of the dependent lung in the bedridden patient. Bronchial obstruction from retained secretions cause mucous plugging and may result in postobstructive collapse of the distal lung. A right mainstem bronchial intubation can cause atelectasis of the nonventilated left lung (see Figure 11–1). In postcardiac surgery patients, left lower lobe collapse occurs frequently due in part to the weight of the heart unsupported by pericardium, which compresses the left lower lobe bronchus. Central neurogenic depression, anesthesia, or splinting may decrease alveolar volume, reducing surfactant and promoting diffuse microatelectasis. Pleural processes, including pneumothorax and pleural effusion, may also result in compressive atelectasis.

Radiographic Features

The radiographic appearance of atelectasis depends largely on the degree and cause of lung collapse. Dependent (gravity-related) atelectasis occurring in supine patients may be demonstrated on thoracic CT even in healthy individuals but is usually not appreciated on plain chest radiography. Linear bands of opacity may be seen in “discoid” or “plate-like” atelectasis on a subsegmental level. Focal patchy opacities can be seen with atelectasis of lung subtended by a segmental bronchus. Lobar or lung collapse (Figure 11–10) results in a dense homogenous opacity of the involved lobes and radiologic signs of volume loss. These signs include displacement of fissures and the hila, mediastinal shift, deviation of the trachea, elevation of hemidiaphragm, and sometimes hyperexpansion of the uninvolved lung.

The left lower lobe is the most frequent location of lobar atelectasis, followed by the right lower lobe and right upper lobe. The radiographic features of left and right lower lobe collapse are similar and involve triangular opacities and silhouetting of the corresponding hemidiaphragm (Figure 11–10A). The right upper lobe also collapses into a triangular density, with superior and medial migration of the horizontal fissure, anterior migration of the oblique fissure, and silhouetting of the right superior mediastinum. Due to the lack of a horizontal fissure in the left lung, the left upper lobe collapses anteriorly; atelectasis in this region presents as a hazy opacification in the left upper lung zone that gradually fades inferiorly. Collapse of the lingula or right middle lobe usually results in obscuring of the corresponding heart border but causes minimal signs of volume loss.

Patients with severe pneumonia complicated by sepsis, respiratory failure, hypotension, or shock are seen frequently in the ICU. While many patients will have acquired pneumonia outside of the hospital, a substantial number will have nosocomial pneumonia, defined as lower respiratory tract infection occurring more than 48 hours after admission. Nosocomial pneumonia is the second most common nosocomial infection in the United States and is associated with high morbidity and mortality. Factors contributing to the high incidence of nosocomial pneumonias include endotracheal intubation or tracheostomy, prolonged mechanical ventilation, aspiration, and impaired host defenses. Inappropriate use of antimicrobials and emerging patterns of resistance has created additional treatment challenges.

Most radiologists sort the radiographic appearance of pneumonia into 3 categories that may aid in differentiation: lobar (alveolar or air space) pneumonia, lobular pneumonia (bronchopneumonia), and interstitial pneumonia. Lobar pneumonia is characterized on x-ray by relatively homogeneous regions of increased lung opacity and air bronchograms. The entire lobe does not need to be involved, and since the airways are not primarily involved, volume loss is not a frequent finding. Streptococcus pneumonia is the classic lobar pneumonia, although other organisms produce a similar pattern. Lobular pneumonia (bronchopneumonia) results from inflammation involving the terminal and respiratory bronchioles. The distribution is more segmental and patchy-appearing, affecting some lobules while sparing others. Mild volume loss may also be present. The most common organisms producing typical bronchopneumonia are Staphylococcus aureus and Pseudomonas species. Interstitial pneumonia is typically caused by viruses, Mycoplasma pneumoniae or, in immunocompromised patients, Pneumocystis jiroveci. Chest radiographs demonstrate an increase in linear or reticular markings in the lung parenchyma with peribronchial thickening.

Radiographic Features

Plain Films

The chest radiograph assesses for the presence and extent of pneumonia, as well as the existence of associated complications such as parapneumonic effusions, pneumatoceles, cavitation, and abscess formation. It also helps to gauge response to antibiotic therapy. A persistent pneumonia on the radiograph despite adequate therapy may raise suspicion for mimics of infectious pneumonia, including cryptogenic organizing pneumonia or bronchioalveolar carcinoma, or the presence of an obstructing mass.

The silhouette sign on the chest radiograph is useful for determining the site of pneumonia. When consolidation is adjacent to a structure of soft tissue density (eg, the heart or the diaphragm), the margin of the soft tissue structure will be obscured by the opaque lung. Thus, a right middle lobe consolidation may cause loss of the margin of the right heart border, lingular consolidation may cause loss of the left heart border, and lower lobe pneumonia may obliterate the diaphragmatic contour.

Cavitation and abscess formation are also important complications of pneumonia caused by necrosis of the pulmonary parenchyma. Typical causative agents include anaerobes and gram-negative organisms, but cavitation can also be caused by staphylococci, Mycobacterium tuberculosis, atypical mycobacteria, and fungi. Lung abscesses may also be polymicrobial. Complications of lung abscess include sepsis, cerebral abscess, hemorrhage, and spillage of contents of the cavity into uninfected lung or pleural space. A lung abscess usually appears as a rounded, focal mass with a thickened (5-15 mm), irregular wall and an air-fluid level. An air crescent sign (crescentic radiolucency around lung parenchyma) or a halo sign (pulmonary opacity surrounded by a zone of ground-glass attenuation) may also be present (Figure 11–11). Abscesses may be surrounded by adjacent parenchymal consolidation (Figure 11–12) or appear as areas of lucency within an area of consolidation.

Pneumatoceles (Figure 11–13) are associated with pneumonia and are caused by alveolar rupture and resulting formation of subpleural air collections. Radiographically, they appear as single or multiple cysts with thin, smooth walls that often change in size and location on serial imaging. The most common causative agent is S aureus. Complications include pneumothorax and secondary infection.

Computed Tomography

The cross-sectional imaging plane and superior contrast resolution make CT useful in the evaluation of complicated inflammatory diseases. Cavitation, which may be obscured on plain films, is easily identified on CT.

Localization of parenchymal diseases facilitates the direction of invasive studies such as bronchoscopy or open lung biopsy. Superimposed pleural and parenchymal processes are more easily differentiated on CT than on plain films (Figure 11–14). The administration of intravenous contrast material can further facilitate the differentiation of pleural and parenchymal disease; pleural lesions will exhibit little to no enhancement with contrast, whereas parenchyma will demonstrate enhancement as well as the presence of blood vessels.

Aspiration results from inhalation of oropharyngeal or gastric secretions into the larynx or lower respiratory tract. Aspiration can result in multiple pulmonary syndromes, including aspiration pneumonitis, a chemical injury caused by the inhalation of gastric contents, or aspiration pneumonia, an infectious process in which oropharyngeal secretions colonized by pathogenic bacteria are inhaled, resulting in lower respiratory tract infection. Several clinical conditions predispose patients to aspiration. Depressed levels of consciousness secondary to medications, seizures, drug overdose, anesthesia, or neurologic disease result in impaired upper airway reflexes (Figure 11–15). Mechanical factors predisposing patients to aspiration include endotracheal intubation, enteral feeding tubes, gastric distention, vomiting, gastroesophageal reflux, and decreased esophageal and gastrointestinal motility. Pneumonia can develop when oral or gastric secretions contaminated with bacteria are aspirated. Poor oral care may result in bacterial colonization of oropharyngeal secretions. Although gastric acidity maintains sterility of stomach contents in normal circumstances, antacid therapy for stress ulcers prophylaxis increases gastric pH, which may result in gastric colonization with pathogenic bacteria. Enteral feedings, small bowel obstruction, and gastroparesis may also result in bacterial colonization of gastric contents.

Radiographic Features

The radiographic pattern seen in aspiration depends on the position of the patient, as well as the volume and the nature of aspirated contents. In a supine patient, the posterior segments of the upper lobes and superior segments of the lower lobes are typically affected. In a semirecumbent or upright patient, the basilar segments of the lower lobes are usually involved. The right lung is more frequently involved than the left due to the larger caliber and straighter course of the right mainstem bronchus.

Aspiration of small amounts of water or neutralized gastric content may produce minimal airspace opacities that rapidly resolve. If acidic gastric contents are aspirated (Mendelson syndrome), airspace disease rapidly develops, and can resemble pulmonary edema if the amount of aspirate is massive. Aspiration of bacteria resulting in pneumonia will produce infiltrates in characteristic bronchopulmonary segments; bilateral and multilobar consolidation may occur. Complications result from parenchymal necrosis and include the development of cavitary disease, empyema, or lung abscess.

Pulmonary embolism (PE) is a common, life-threatening disorder that results from venous thrombosis, usually arising in the deep veins of the lower extremities. The signs and symptoms of pulmonary embolism are nonspecific, and can be seen in a variety of pulmonary and cardiovascular diseases. The clinician must stay alert to the possibility of pulmonary embolism in any patient at risk for Virchow triad of venous stasis, intimal injury, and hypercoagulable state. A variety of imaging resources, including chest radiography, ventilation-perfusion scans, pulmonary angiography, and spiral or helical CT, play a role in the diagnosis of pulmonary embolism.

Radiographic Features

Chest Radiograph

The chest radiograph is often abnormal but rarely, if ever, diagnostic of PE. Common findings can include cardiomegaly, pulmonary artery enlargement, atelectasis, and pleural effusion. Less frequently, Westermark sign (focal oligemia distal to the site of PE), or Hampton hump (wedge-shaped peripheral consolidation resulting from infarction, Figure 11–16A) may be seen, but these are also poor predictors of PE. Consequently, the role of the chest radiograph in PE is mainly limited to ruling out other diagnoses and aiding in the interpretation of the ventilation-perfusion radionuclide scan.

Ventilation-Perfusion Lung Scan

Ventilation-perfusion scans are based on the premise that pulmonary thromboembolism results in a region of lung that is ventilated but not perfused. The study consists of two scans—the perfusion scan and the ventilation scan—that are compared for interpretation. The perfusion scan involves injection of technetium-99m-labeled macroaggregated albumin. This agent is trapped via the precapillary arterioles and identifies areas of normal lung perfusion; regions of the lung with absent perfusion will appear photon deficient. The ventilation scan is performed by obtaining images after having the patient inhale a radioactive gas (xenon) or radioaerosol (technetium-99m diethylenetriamine penta-acetic acid). Perfusion and ventilation images are compared; perfusion defects in areas of normal ventilation are suggestive of pulmonary embolism.

Although the concept behind V/Q scanning is simple, image interpretation is complex and has several limitations in ICU patients. V/Q scanning must be done in conjunction with a chest radiograph, as perfusion abnormalities may have many etiologies other than PE, including chronic obstructive pulmonary diseae (COPD), pulmonary edema, lung mass, pneumonia, and atelectasis, all frequently seen in ICU patients. Additionally, the reliability of radionuclide inhalation in intubated patients is unclear. Finally, while normal and high-probability V/Q scans have high negative and positive predictive values for PE, respectively, many V/Q scans are interpreted as intermediate- or low-probability and require further diagnostic testing.

CT Pulmonary Angiography

Ventilation-perfusion imaging has been largely replaced by multidetector computed tomography pulmonary angiography (CTPA), which is the current standard of care for detecting PE. Based on data obtained from the prospective investigation of pulmonary embolism diagnosis (PIOPED) II study, CTPA has a sensitivity of 83% and specificity of 96% in the diagnosis of pulmonary embolism. When CTPA was combined with CT venography (CTV), the sensitivity increased to 90% without significant changes in specificity. Data from PIOPED II also demonstrated high concordance between lower limb compression ultrasonography (CUS) and CTV in the detection of lower extremity deep venous thrombosis (DVT); use of CUS obviates the additional radiation exposure associated with CTV.

CT findings of pulmonary embolism (Figure 11–16B) include the following:

• Intraluminal filling defects that sharply interface with intravascular contrast material.

• Complete arterial occlusion resulting in dilation of the artery in comparison with the adjacent bronchus.

• Partial filling defects surrounded by contrast. These may manifest as the “rim sign” in the axial plane or the “railway track sign” in the long axis of a vessel.

• Partial eccentric intraluminal filling defects making an acute angle with the arterial wall.

Of note, small subsegmental filling defects must be seen definitively in more than one axial image in order to be considered consistent with PE. Other nonspecific CT findings include ground-glass opacities consistent with pulmonary hemorrhage, wedge-shaped consolidations resulting from pulmonary infarction and pleural effusions. Oligemia of lung parenchyma distal to the occluded vessel may be present. Signs of right ventricular dysfunction, such as right ventricular dilatation or leftward deviation of the interventricular septum, may also be present.

Pitfalls in the interpretation of CTPA include breathing artifact, inadequate contrast opacification of the pulmonary arteries, and suboptimal visualization of obliquely oriented vessels (eg, segmental branches of the right middle lobe and lingula). Partially opacified veins may be confused with thrombosed arteries; hilar lymph nodes and mucus-filled bronchi may be misinterpreted as thrombi. Flow- and motion-related artifacts can also result in false-positive findings.

Pulmonary Angiography

Pulmonary angiography is an invasive test and is considered the gold standard for the diagnosis of pulmonary embolism. Angiography is indicated when the pretest probability for PE is high and the results of CT angiography and V/Q show conflicting or indeterminate results. It also may be useful when therapy involves more complicated treatment such as an inferior vena cava filter, surgical embolectomy, or thrombolytic therapy.

Pulmonary angiography requires the percutaneous placement of an intravascular catheter through the femoral vein, past the right ventricle and into the pulmonary artery. Contrast is then injected at a rapid rate and images are acquired. A filling defect or abrupt cutoff of a small vessel is indicative of an embolus in this study. Other nonspecific findings may include decreased perfusion, delayed venous return, abnormal parenchymal stain, and crowded vessels. Complications of pulmonary angiography are frequently related to catheter insertion and manipulation and include arrhythmias, heart block, cardiac perforation, right-sided heart failure, and cardiac arrest.

Magnetic Resonance Angiography

The PIOPED III study investigated the diagnostic accuracy of gadolinium-enhanced magnetic resonance angiography (MRA) alone or in combination with venous phase magnetic resonance venogram (MRV) for the diagnosis of PE. The sensitivity and specificity of MRA was 78% and 99%, respectively; combined MRA/MRV had a sensitivity of 92% and specificity of 96%. However, due to an unacceptably high percentage of patients with technically inadequate examinations, the investigators recommended that MRA only be performed in centers with significant pulmonary MRA experience and in patients with contraindications to all other standard tests.

General Considerations

Septic pulmonary emboli occur as a result of infections of the right side of the heart or of the peripheral veins. Major risk factors include intravenous drug use, indwelling catheters, and skin and soft tissue infections. Oropharyngeal infections can result in infectious thrombophlebitis of the internal jugular vein (Lemierres syndrome), a rare but significant cause of septic pulmonary emboli. Most patients with septic pulmonary emboli have positive blood cultures at the time of imaging, with S aureus being the most commonly isolated organism.

Radiographic Features

The radiographic features of septic pulmonary emboli include multiple wedge-shaped or rounded peripheral opacities of varying size and lower lobe predominance, reflecting increased blood flow to dependent portions of lung. Cavitation is common, with necrotic debris often present within cavities. Hilar and mediastinal lymphadenopathy can occur, as can empyema.

CT imaging may detect disease earlier than the plain radiograph and better characterize its extent. In addition to the above findings, CT may also reveal peripheral nodules with feeding vessels and contrast enhancement of wedge-shaped lesions (Figure 11–17).

General Considerations

Pulmonary edema—an excess of water in the extravascular lung space—is a frequent cause of respiratory distress in the critically ill patient. According to Starling law, fluid accumulates in the extravascular space in one of two ways:

• Increased hydrostatic pressure within the lung capillaries (cardiogenic pulmonary edema), resulting from fluid overload or cardiac dysfunction.

• Increased capillary membrane permeability (noncardiogenic pulmonary edema), which can be caused by a variety of insults to the microvasculature of the lung.

In the ICU patient, more than one mechanism may contribute to the formation of edema, increasing the difficulty of diagnostic interpretation on radiographs.

Radiographic Features

The earliest sign of cardiogenic pulmonary edema is vascular redistribution, manifested as hyperperfusion of the upper lobes, or cephalization. This finding is best seen in an upright film and may be difficult to see in the supine or semiupright films obtained in critically ill patients. As hydrostatic pressure increases, fluid accumulates in the interstitium; corresponding radiographic signs may be present prior to the onset of symptoms and include Kerley lines, peribronchial cuffing, loss of vascular definition, thickening of the fissures, and pleural effusions (Figure 11–18). Kerley A lines represent distension of anastomotic channels between lymphatics and appear as long, irregular linear opacities extending from the hila to the periphery. Kerley B lines are caused by edematous interlobular septa and are short, horizontal lines found predominantly at the lung bases. Kerley C lines are reticular opacities primarily seen at the lung bases and signify thickened interlobular septa in transverse orientation. Kerley B lines are seen more frequently than Kerley A or C lines. Peribronchial cuffing results when fluid-thickened bronchial walls become visible producing rounded, “doughnut-like” densities in the lung parenchyma.

As extravascular fluid continues to accumulate, alveolar edema develops. Clinical signs and symptoms of heart failure are generally apparent at this point, and the chest radiograph will reveal airspace opacities that can coalesce into diffuse consolidations, frequently with a perihilar or basilar distribution. Air bronchograms are usually absent, and the lung periphery is often spared, sometimes resulting in a “batwing” appearance. In general, cardiogenic pulmonary edema is bilateral and symmetric, but atypical edema patterns may be seen in patients with underlying lung disease or as a consequence of gravitational forces related to patient positioning. Destruction of the lung due to emphysema may cause a patchy, asymmetric distribution of edema that spares regions of bullous disease.

Widening of the vascular pedicle is also seen in cardiogenic pulmonary edema. The vascular pedicle width extends from the superior vena cava on the right side of the mediastinum to the proximal descending aorta on the left. Vascular pedicle width greater than 7 cm is consistent with volume overload.

Distinguishing cardiogenic from noncardiogenic pulmonary edema is not always possible radiographically, and the 2 processes may be seen concurrently in ICU patients. In noncardiogenic pulmonary edema (Figure 11–19), the vascular pedicle width tends to be normal, and pleural effusions, septal thickening, and peribronchial cuffing are absent. Edema is more likely to be patchy and peripheral in distribution, in contrast to the central or basilar distribution seen in cardiogenic pulmonary edema.

General Considerations

ARDS is a diffuse, acute, inflammatory lung injury manifested by severe hypoxia and bilateral radiographic infiltrates of noncardiogenic etiology. It can result from either direct pulmonary injury or in response to a systemic insult. Imaging plays an important role in the diagnosis of ARDS and may help determine its underlying etiology.

Radiographic Features

The radiographic manifestations correlate with the pathologic changes seen in the lung parenchyma and vary with the stage of lung injury. There are 3 phases of ARDS as described below:

• Exudative phase (days 1-7): This phase is characterized by endothelial and epithelial injury and an influx of protein-rich fluid, first into the interstitium and subsequently into the alveoli. Alveolar atelectasis and hyaline membrane formation are seen. Radiographically, interstitial edema is initially seen, followed by alveolar consolidation; both patterns may be present concurrently (Figure 11–20A). Additionally, if a direct lung injury such as pneumonia was the trigger for ARDS, its presence may be evident.

• Proliferative phase (days 8-14): Infiltration with fibroblasts and type II pneumocytes occurs in this phase as a response to injury and coarse reticular opacities may develop on the chest radiograph. Imaging will otherwise remain relatively static, as alveolar and interstitial edema will persist. The development of additional airspace opacities should generate concern for new infection or other complications.

• Fibrotic phase (day 15 onward): This late phase of ARDS may overlap with the proliferative phase and is characterized by collagen deposition and fibrosis. The degree of fibrosis is variable and the radiographic findings can range from complete resolution to the development of widespread reticular markings, cysts, airway distortion, and persistent ground-glass opacities (Figure 11–20B).

General Considerations

Pleural fluid is primarily formed on the parietal pleural surface and absorbed on the visceral pleural surface. Approximately 25 mL of fluid is normally present in the pleural space. When there is an imbalance between production and absorption of pleural fluid, excess intrapleural fluid accumulates and pleural effusions form. While the plain chest radiograph can be useful for detecting and estimating the amount of pleural effusion, pleural fluid is more easily visualized and distinguished from lung parenchyma with CT or bedside ultrasound. The role of ultrasound in visualizing pleural effusions is detailed in Chapter 12.

Radiographic Features

The appearance and distribution of fluid within the pleural space is greatly affected by lung elastic recoil and gravity. On erect frontal and lateral radiographs, free pleural effusions typically have a concave, upward-sloping interface with the lung (the meniscus sign) and result in blunting of the costophrenic angle (Figure 11–21A). Blunting of the costophrenic angle may occur with as little as 175 mL of fluid on an erect frontal radiograph; smaller amounts of fluid can be detected on a lateral upright or lateral decubitus view but these views are logistically difficult to obtain in the ICU patient. A massive pleural effusion can produce near-complete opacification of the involved hemithorax, accompanied by contralateral mediastinal shift (Figure 11–21B).

Multiple diagnostic challenges exist when visualizing pleural effusions with a chest radiograph. Atelectasis and lung consolidation may be difficult to distinguish from pleural effusion because they too may obscure the hemidiaphragm. Pleural fluid can accumulate along the pleural fissures and result in a mass-like appearance, or pseudotumor. However, unlike a true mass, a pseudotumor will change in shape and size as the patient is repositioned. Pleural effusions may also be found in a subpulmonary location between the lung base and diaphragm without causing blunting of the lateral costophrenic sulcus. The chest radiograph will reveal what appears to be an elevated hemidiaphragm, which is actually the displaced pleural-visceral interface simulating a “pseudodiaphragm.” Signs that can help distinguish subpulmonic effusion from diaphragmatic elevation include the flatter shape of the pseudodiaphragm in comparison with a true hemidiaphragm, and increased distance between the gastric bubble and the pseudodiaphragm (Figure 11–22).

An additional challenge specific to ICU patients is that many radiographs are performed with the patient in the supine position, making the diagnosis of pleural effusion more difficult, particularly with smaller effusions. When a patient is supine, the most dependent regions of the pleural space are the posterior aspects of the bases and the lung apex. Free pleural effusions layer posteriorly, resulting in a homogeneous increased density of the lower involved hemithorax. Fluid also may accumulate at the apex of the thorax, resulting in apical capping.

Given the limitations of chest radiography in visualizing pleural effusions, ultrasound and CT are frequently utilized. Ultrasound imaging is detailed in Chapter 12. Pleural effusions on CT typically appear as sickle-shaped, posterior opacities (Figure 11–23). CT is extremely sensitive in the detection of small effusions, demonstrating loculations, and distinguishing pleural and parenchymal processes. In complicated cases, intravenous contrast administration can help differentiate parenchyma from pleura, as consolidated lung will enhanced, whereas pleural processes will not. While the attenuation of the effusion cannot help distinguish all transudates from exudates, very high attenuation may suggest the presence of a hemorrhagic or proteinaceous collection.

One typically high-attenuation collection is an empyema. Empyema is defined as pus in the pleural space and warrants additional radiographic considerations. While empyemas may initially appear as free-flowing pleural effusions, they often subsequently develop loculations as they pass through their fibrinopurulent and organizing phases. Loculations appear lenticular in shape with obtuse angles to the chest wall. If a concurrent bronchopleural fistula is present, an air-fluid level can be identified in the pleural space. Air-fluid levels can also be seen in lung abscesses, making the 2 difficult to distinguish on a frontal chest radiograph; CT imaging can better distinguish the 2 given its cross-sectional nature. The visceral and parietal pleura frequently enhance due to increased blood supply to the inflamed pleural surfaces during the organizing phase with resultant uptake of intravenous contrast. The “split pleura” sign results from this enhancement as well as separation of the visceral and parietal pleura. Surrounding edema and a local increase in extrapleural fat are also often seen, suggesting the chronic nature of the empyema (Figure 11–24).

General Considerations

Pneumothorax is a frequent and serious complication in the ICU. Iatrogenic pneumothorax frequently develops as a sequela of invasive diagnostic or therapeutic procedures, or barotrauma from mechanical ventilation. Other etiologies of pneumothorax include chest trauma and complications of pulmonary diseases such as COPD, asthma, interstitial lung disease, and cavitary pneumonia. Recognition of even small pneumothoraces is crucial for the prevention of progressive accumulation of pleural air collections, particularly in patients being maintained on mechanical ventilation.

Radiographic Features

As with fluid in the pleural space, the distribution of a pneumothorax is influenced by gravity, lung elastic recoil, potential adhesions in the pleural space, and the anatomy of the pleural recesses. Radiographically, a pneumothorax is identified by separation of the visceral pleural surface from the chest wall and the absence of pulmonary vessels peripheral to the pleural line. A pneumothorax is typically better seen on expiratory images because of a relative decrease in lung volumes compared with the air in the pleural space. In the upright patient, air accumulates in the nondependent region of the pleural space, the apex.

Expiratory, upright radiographs are generally unattainable in ICU patients; images are usually obtained in the supine position, altering the radiographic appearance of pneumothorax. In this position, the least dependent regions of the pleural space are the anteromedial and subpulmonary regions. Pleural air in the anteromedial space results in sharp delineation of mediastinal contours, including the superior vena cava, the azygos vein, the heart border, the inferior vena cava, and the left subclavian artery. The accumulation of air in the subpulmonary region results in a hyperlucent upper quadrant of the abdomen, a deep, hyperlucent lateral costophrenic sulcus (“deep sulcus sign”), sharp delineation of the ipsilateral diaphragm, and visualization of the inferior surface of the lung (Figure 11–25). Air can accumulate in the apicolateral pleural space in the supine patient just as in the erect patient, especially when a large pneumothorax is present. In the presence of lower lobe pneumothorax, air can accumulate in the posteromedial pleural recess, resulting in sharp delineation of the posterior mediastinal structures, including the descending aorta and the costovertebral sulcus.

Tension pneumothorax occurs when the pressure of air in the pleural space exceeds ambient pressure during the respiratory cycle. With this pressure gradient, air enters the pleural space on inspiration but is prevented from exiting the pleural space during expiration. A tension pneumothorax may result in acute respiratory distress and, if untreated, cardiopulmonary arrest. Radiographic signs include displacement of the mediastinum toward the contralateral thorax, inferior displacement or inversion of the diaphragm, and total lung collapse. Adhesions may prevent mediastinal shift, and lung collapse may not occur in patients with stiff lungs such as those with ARDS.

Bedside ultrasound is a reliable tool for the diagnosis of pneumothorax and is further described in Chapter 12. CT may be particularly useful in the diagnosis of loculated pneumothorax and in guiding appropriate chest tube placement.

Several conditions may be confused with a pneumothorax. Pneumoperitoneum may result in a hyperlucent upper abdomen, mimicking pneumothorax. Skin folds can be confused with apicolateral pneumothorax but should be recognized when they extend outside the bony thorax or are traced bilaterally. Pneumomediastinum may simulate medial pneumothorax; however, pneumomediastinum will often cross the midline and extend into the retroperitoneum.