Consolidation is the most common cause of pulmonary opacities in the acute airway obstruction population. In contrast to ground-glass opacities (GGO), consolidation obscures underlying vascular structures and frequently is associated with absence of volume loss and air bronchograms by opacification of lung acini with little or no involvement of conducting airways. By definition, diseases that produce consolidation are characterized by a replacement of alveolar air by fluid, cells, tissue, or some other substances (Hansell et al. 2008). If acute, consolidation is most commonly caused by pulmonary edema (of both cardiogenic and noncardiogenic causes), pulmonary hemorrhage, acute eosinophilic pneumonia, acute extrinsic allergic alveolitis, radiation pneumonitis, pulmonary infarction, or infectious pneumonia (Table 3).

Oncologic patients often experience emergent complications that are either direct result of the underlying malignancy or an indirect result related to the therapy (Table 4).

Airway obstruction complicates approximately 20–30 % of patients with lung cancer, and large masses that compress the central airways may result in postobstructive atelectasis or pneumonia and airway compromise. Rapidly growing tracheal, mediastinal, and hilar masses are most common causes (Fig. 3) (Quint 2009; Guimaraes et al. 2014). Knowledge of airway narrowing is important before attempting percutaneous and surgical biopsy because it may lead to collapse of residual normal lung and sudden respiratory decompensation (McCurdy and Shanholtz 2012). Muscle relaxant drugs used during anesthesia may precipitate dangerous respiratory compromise in patients with pre-existing airway compression by tumor owing to loss of chest wall tone.

Lung edema includes (1) hydrostatic edema caused by increased capillary pressure or decreased oncotic pressure, (2) ARDS (permeability edema caused by DAD resulting in interstitial and alveolar fluid accumulation), (3) permeability edema without alveolar damage (such as heroin-induced edema, edema following cytokine administration, and high-altitude edema) primarily resulting in interstitial fluid accumulation, and (4) mixed forms of hydrostatic and permeability edema (such as neurogenic edema, reperfusion and re-expansion edema, edema following lung transplantation, etc.)

High-altitude illness includes the cerebral syndromes of acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and the pulmonary syndrome of high-altitude pulmonary edema (HAPE), recognized as an alveolar fluid accumulation in unacclimatized individuals by Houston in 1960 and attributed solely to high-altitude exposure (Houston 1960); it is mainly seen in children or young adults who rapidly ascend to heights of 2000–3500 m or greater and typically occurs 3–48 h after ascent, with the hallmark symptom being dyspnea at rest, often associated to dry or with frothy pink sputum production cough and restlessness. Approximately 50 % of patients with HAPE also show symptoms of AMS/HACE, but these two forms of altitude illness can exist independently of each other (Bartsch et al. 2005). The mechanism remains unclear: HAPE is believed to be a form of noncardiogenic pulmonary edema without alveolar damage caused by exposure to the low pO2 found at high altitudes. Hypoxia leads to uneven areas of vasoconstriction within the pulmonary vascular bed, resulting in a pattern of patchy overperfusion (Swenson et al. 2002); these foci of high vascular pressure lead to localized violation of the capillary endothelium, causing fluid extravasation. When available, CXR features initially are heterogeneous peripheral alveolar patchy, fluffy infiltrates progressing eventually to widespread, confluent airspace involvement more severe in lung bases, but the pattern of distribution is usually unpredictable. Portable lung ultrasonography provides a more feasible imaging option in remote locations and shows progressively larger numbers of extravascular fluid comet tails in patients ascending to altitude and suffering from HAPE (Fagenholz et al. 2007; Pratali et al. 2010). The most modifiable risk factor for the development of HAPE is the rate of ascent to high altitude; the mainstay of therapy increases alveolar and arterial oxygen by descent or with supplemental oxygen. HAPE is a potentially life-threatening illness that is completely preventable; as the popularity of trekking and climbing grows among the general population, physicians will be increasingly relied on as a source of education, prophylaxis, and treatment, making a working familiarity with altitude-induced illnesses such as HAPE an indispensable tool for emergency physicians.

A number of intracranial conditions, including head trauma, hemorrhage (usually subarachnoid), tumors, and encephalitis, can be associated with acute pulmonary edema. It can occur within a minute to hours following a neurologic insult and usually resolves within 72 h. Patients may present with varying degrees of dyspnea, tachypnea, and cyanosis shortly after suffering the brain insult. The onset of symptoms occurs in <4 h in the majority and death in 10 %. The mechanism is unclear: it has been suggested that a sudden burst of neural activity stimulates the sympathetic nervous system and an adrenergic response leading to increased extravascular lung water, increased pulmonary hydrostatic pressure, and increased lung capillary permeability (Tan and Lai 2007). The CXR picture is indistinguishable from that of cardiogenic PE (nonspecific, bilateral, rather homogeneous airspace consolidative appearances with an apical predominance are present in about half of cases) except that the heart is not enlarged and it can take up to 24 h to be apparent on imaging (Fig. 4). Radiologic findings in neurogenic pulmonary edema also disappear within 1–2 days, thereby confirming the absence of any associated DAD (Gluecker et al. 1999).

The condition occurs often in young patients in the setting of rapid expansion of a collapsed lung, with acute-onset shortness of breath usually occurring within hours of re-expansion. The onset of pulmonary edema can be delayed by up to 24 h in some cases (Echevarria et al. 2008). It occurs following approximately 1 % of pneumothorax re-expansions or thoracentesis procedures (mostly if large-volume drainage >3 l). Although the exact mechanism of REPE has not been identified, it appears to be caused by multiple mechanisms. Increased capillary permeability due to hypoxic injury, reperfusion injury with release of toxic oxygen free radicals, and surfactant depletion are all thought to play a major role. Furthermore, a delay in lymphatic return by stasis during prolonged collapse and bronchial occlusion may also partly account for the development of REPE. It can progress for 24–48 h and usually shows slow resolution over 5–7 days. REPE may lead to severe hypoxemia, which will increase lung damage and may result in extensive adult respiratory distress syndrome (ARDS) and multiorgan failure. CXR findings are alveolar opacities usually unilateral in those portions of the lung that were previously collapsed; rarely edema can develop in the contralateral lung (Baik et al. 2010). Thin-section MDCT findings of REPE are peripheral patchy areas of GGO frequently combined with consolidation as well as interlobular septal and intralobular interstitial thickening (Fig. 5). The British Thoracic Society guidelines suggest that less than 1.5 l of pleural fluid be drained at a time (BTS Pleural Disease Guideline 2010). Drainage catheters can be intermittently plugged to prevent rapid lung re-expansion. Rapid re-expansion of pneumothoraces is less easily controlled and caution should be taken to avoid high negative intrapleural pressures.

Atelectasis or collapse (Hansell et al. 2008), a decrease in lung volume accompanied by increased opacity (CXR) or attenuation (CT scan) in the affected part of the lung, is a common cause of pulmonary opacities in the acute airway obstruction population. One of the commonest mechanisms is resorption of air distal to airway obstruction (e.g., an acutely complicated endobronchial neoplasm or foreign body). Atelectasis can mimic pneumonia, particularly when signs of volume loss, such as crowding of air bronchograms, fissural deviation, mediastinal shift, and diaphragmatic elevation, are absent. Flat, platelike opacities are characteristic of discoid atelectasis. Complete lung collapse, lobar collapse, or segmental collapse can also be seen. The characteristic LUS finding is a homogenous, well-demarcated hyperechoic lung consolidation. In comparison with pneumonia, no air bronchograms are usually visible. The size of the lung consolidation may vary during the breathing cycle due to ventilation. Atelectasis is categorized according to mechanism as obstructive, compressive, cicatricial, and adhesive.

Aspirated foreign bodies are by far the most common cause of intraluminal airway abnormalities in childhood, unusual in adults, and often overlooked as a cause of airway obstruction (Yadav et al. 2007). Up until age 15, both right and left main bronchi arise at about the same angle from the trachea so that objects may be aspirated into either side; afterward, the right main bronchus arises in a less acute, more straight path than the left (Kosucu et al. 2004). The most frequently aspirated foreign bodies are food (especially nuts), teeth, dental devices, and medical instruments, and 70 % will be nonopaque on conventional radiography (Fig. 7).

Some nuts, such as peanuts, have an oil that leads to inflammation and edema making them more difficult to expel. When a foreign body enters the lung parenchyma, prolonged irritation with intermittent infections may cause massive hemoptysis. At radiology, an aspirated foreign body may cause one lung or lobar/segmental overinflation or atelectasis (obstructive emphysema) with chronic volume loss in the affected lobe, mediastinal shift, pneumomediastinum, recurrent pneumonias, and bronchiectasis; it can occasionally mimic a congenital malformation or neoplasm (Fig. 8).

If the patient is clinically able, an expiratory CXR may demonstrate air trapping on the affected side by lack of collapse of the lung and shift of the mediastinum away from the side with the foreign body. If the patient is a child or otherwise not able to cooperate for an expiratory study, a decubitus view of the chest, with the suspected side down, may show a lack of collapse of the air-trapped lung. CT may demonstrate the foreign body and is far more sensitive than CXR in demonstrating subtle low-attenuation intrabronchial material (Fig. 9) (Zissin et al. 2001).

Drowning is a process resulting in primary respiratory impairment from submersion in a liquid medium (Idris et al. 2003) and may be either a fatal or nonfatal event (Szpilman et al, 2012). Deaths because of drowning have estimated approximately 305,000 deaths in 2008 (WHO 2011). Young children are at particularly high risk of drowning, and males in general face a significantly greater risk than females. Drowning may be further classified as cold-water (<20 °C) or warm-water injury (>20 °C). The most important contributory factors to morbidity and mortality from drowning are hypoxemia and acidosis and the multiorgan effects of these processes. Central nervous system (CNS) damage may occur because of hypoxemia sustained during the drowning episode (primary injury) or may result from arrhythmias, ongoing pulmonary injury, reperfusion injury, or multiorgan dysfunction (secondary injury), particularly with prolonged tissue hypoxia. After initial breath holding, when the victim’s airway lies below the liquid’s surface, an involuntary period of laryngospasm is triggered by the presence of liquid in the oropharynx or larynx (stage 1, “dry drowning”). At this time, the victim is unable to breathe in air, causing oxygen depletion and carbon dioxide retention. In stage 2, the victim still usually presents with laryngospasm but may begin to swallow water into the stomach. As the oxygen tension in blood drops further, laryngospasm releases, and the victim gasps and hyperventilates, possibly aspirating variable amounts of liquid. This leads to further hypoxemia (stage 3). Ultimately, if the process of drowning is not interrupted, hypoxia progresses to the point of complete circulatory collapse and cardiac arrest (Tourigny and Hall 2012). Pulmonary infections may occur in a delayed fashion from aspirated material, some of which may result from rare or atypical pathogens such as fungi. Patients in cardiac arrest are more likely to display a nonshockable cardiac rhythm (i.e., asystole or pulseless electrical activity). Those who survive the initial resuscitation phase are at significant risk for developing serious delayed sequelae, such as ARDS, pancreatitis, disseminated intravascular coagulation, or rhabdomyolysis during their subsequent hospital stay. The acute aspiration of massive amounts of water produces a pulmonary edema that is radiographically indistinguishable from pulmonary edema from other causes (Hunter and Whitehouse 1974; Causey et al. 2000). The clinical significance of near drowning depends more on the volume of water aspirated than on whether the aspirate is freshwater or saltwater. Classic CXR findings in severe near drowning consist of alveolar edema with extensive “fluffy” areas of increased opacity that tend to coalesce throughout both lungs (Fig. 10). In mild near drowning, findings range from normal to confluent irregular peripheral areas of increased opacity in a subsegmental or segmental distribution with peripheral sparing. Pneumonia may be a complication of the aspiration of either fresh- or saltwater and, depending on the water source, may be caused by a variety of microorganisms including bacteria, fungi, and mycobacteria (Tourigny and Hall 2012).

Vomiting with massive aspiration of gastric contents is a very frequent phenomenon; gastric acid with a pH <2.5 can cause pathologic reactions varying from mild bronchiolitis to hemorrhagic pulmonary edema. The posterior segments of the upper lobes and the superior segments of the lower lobes are the most frequently involved lung sites when the patient is recumbent. Acid liquid introduced into the airways is rapidly disseminated throughout the bronchial tree and lung parenchyma, producing a chemical pneumonitis within minutes. The magnitude of injury is directly related to the pH and volume of the aspirated material. The overall mortality rate associated with massive aspiration of gastric acid is approximately 30 % and is greater than 50 % in patients with initial shock or apnea, secondary pneumonia, or adult respiratory distress syndrome (Bynum and Pierce 1976). Classic CXR findings in acute gastric acid aspiration include bilateral perihilar, ill-defined, alveolar consolidations, multifocal patchy infiltrates, and segmental or lobar consolidation, which are usually localized to one or both lung bases (Fig. 6a).

Exogenous lipoid pneumonia is a rare condition caused by inhalation or aspiration of plant, animal, or mineral fats and may take an acute or chronic form. Acute form is usually associated with accidental poisoning in children; in an adult population, it typically occurs in fire-eaters, who use oily substances in their shows (Betancourt et al. 2010). Clinically, acute lipoid pneumonia presents most often with cough, dyspnea, and fever. CXR pictures show consolidation, reticular and mixed alveolar-interstitial changes, as well as nodular lesions. Other rarer abnormalities, which may be noted on radiograms, are pneumatocele, pneumothorax, pneumomediastinum, and pleural effusion (Franquet et al. 2000). Most commonly, CT shows areas of a negative attenuation coefficient (between −150 and −30 HU) consolidation and ground-glass opacities as well as interstitial changes such as interlobular septal thickening and intralobular lines; fine, poorly demarcated centrilobular nodules and nodular lesions; pneumatocele; pneumothorax; pneumomediastinum; and pleural effusion (Brander et al. 1992; Laurent et al. 1999). Changes involve one or both lungs and are usually located in lower lobes or in the right middle lobe and may be multifocal or bilateral (Fig. 11).

The term bronchiectasis is derived from the Greek term bronkia (bronchial tubes), ek (out), and tasis (stretching), which together literally mean “the outstretching of the bronchi” (Feldman 2011). First described by Laennec in 1819, later detailed by Sir William Osler in the late 1800s, and further defined by Reid in the 1950s, this condition is generally defined as an abnormal and permanent focal or diffuse dilatation of the cartilage-containing airways (bronchi) caused by weakening or destruction of the muscular and elastic components of the bronchial walls (Hansell et al. 2008). Care must be taken to distinguish this large airway dilatation from dilatation of the small airways (bronchioles) that do not contain cartilage (Javidan-Nejad and Bhalla 2010). In contrast to established bronchiectasis occurring in adults, some children with bronchiectasis have been shown to have resolution or considerable improvement of the changes seen on CT scanning, suggesting the possibility that the condition may be reversible in some cases (Al Subie and Fitzgerald 2010).

Bronchiectasis results from the occurrence of one of the three main pathogenic mechanisms: bronchial wall injury, bronchial lumen obstruction, and traction from adjacent fibrosis (Shoemark et al. 2007). The latter two mechanisms are usually apparent on imaging and are suggested by an endobronchial filling defect or adjacent interstitial lung disease, while when it is met the first mechanism the radiologist is faced with a more difficult differential diagnosis (Javidan-Nejad and Bhalla 2009). The dominant feature of bronchiectasis is clearly the presence of airway inflammation, in association with bacterial infection and, in particular, nonclearing infection. An initial airway insult, such as an infection, often on the background of genetic susceptibility, compromised host clearance mechanisms and, in particular, the mucociliary escalator mechanism, which facilitated persistent bacterial colonization and infection. This damages the airway further, both directly and indirectly, as a consequence of the initiation of a secondary host inflammatory response. The three pathogenic elements in bronchiectasis—namely, airway infection, inflammation, and enzymatic activities—interact to result in progressive airway damage. Many patients eventually harbor Pseudomonas aeruginosa (PA) in their airway, which is associated with significant morbidity (Pappalettera et al. 2009).

The Reid morphological classification, derived from bronchographic and autopsy studies, specifies three patterns (Reid 1950):

Oftentimes, more than one type of bronchiectasis can be seen in the same patient. As the airway dilatation increases, there may be progressive collapse and fibrosis of the distal lung parenchyma. Bronchiectasis can frequently occur in parallel with more common forms of chronic lung disease including COPD (up to 50 % of patients) and asthma (overlap syndromes) (Patel et al. 2004). There are many medical conditions that may lead to the development of bronchiectasis and these are detailed in Table 6.