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Airspace Diseases
Introduction
Diseases of the air spaces are remarkably common, yet, the radiological approach to diagnosis is often considered challenging. In part, this is because a pattern of airspace opacification is non-specific ( Table 11.1 ). However, at its simplest, this radiological pattern simply indicates that air has been displaced, to a greater or lesser degree, from the lung. In clinical practice, airspace opacification is most commonly a manifestation of pulmonary oedema or infection. This chapter considers not only some of the common but also a few of the more unusual causes of airspace opacification in clinical practice. Airspace diseases caused by infection and cancer are considered in detail elsewhere.
TABLE 11.1
Causes of Airspace Opacification
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Suggested Approach to the Radiological Diagnosis of Airspace Diseases
The plain chest radiograph (CXR) is usually the first imaging test requested by clinicians. In patients with an abnormal CXR, radiologists should aim to formulate a sensible diagnosis or, at most, a short list of differential diagnoses. To this end, the radiologist must pay heed to the following: the clinical background, the distribution of radiographic abnormalities and serial changes (i.e. progression/resolution, time course etc.) on repeat studies where available. Clinical context is, of course, important when reporting imaging studies. For instance, the most likely cause of lobar consolidation in a patient with pyrexia and a productive cough is infection, whereas the same radiological pattern (only bilateral) in a critically ill patient is most likely to indicate non-cardiopulmonary oedema/acute respiratory distress syndrome (ARDS) ( Fig. 11.1 ). The distribution of airspace opacities on imaging studies can also provide important clues: in cryptogenic organising pneumonia (COP), for instance, areas of consolidation tend to be most obvious in the periphery and lower zones. By contrast, upper zone infiltrates parallel to the chest are typical in chronic eosinophilic pneumonia ( Fig. 11.2 ).
A review of serial radiographs should be considered de rigeur in the radiologist's routine. Rapid clearing—occurring over a period of hours or, at most, a few days—suggests oedema fluid ( Fig. 11.3 ) or pulmonary haemorrhage as the likely cause as opposed to, say, pneumonia. Opacities that are transient and migratory in a patient with constitutional symptoms should make the radiologist consider an eosinophilic pneumonia in the differential diagnosis.
Computed tomography (CT) is frequently requested in patients with airspace disease and, occasionally, the CT features will be helpful; the so-called ‘crazy-paving’ pattern is an example that immediately comes to mind, which, at least in its classical form, should be considered pathognomonic of pulmonary alveolar proteinosis (PAP). In other instances, the radiologist may only be able to limit the list of diagnostic possibilities despite the additional information from CT (e.g. cavitation that may not have been evident on plain radiographs). Therefore, except in certain circumstances, the advantages of CT over plain radiography in the diagnosis of airspace diseases are not clearly defined.
Anatomical Considerations
The air spaces are defined as the air-containing part of the lung, which includes the respiratory bronchioles but excludes the terminal bronchioles; the latter are the last purely conducting airways of the bronchial tree and the region of lung subtended by a terminal bronchiole is the acinus. Important pathways of collateral ventilation (the pores of Kohn) link different alveolar units and maintain lung inflation in the presence of proximal airway obstruction. These normal collateral pathways also facilitate the spread of certain diseases (most notably infections) into adjacent alveolar units.
An important unit of lung structure is the pulmonary lobule, defined as the smallest unit of lung bounded by connective tissue septa. Individual lobules are irregular polyhedrons, best seen in the subpleural lung and measuring between 5 and 30 mm in diameter, incorporating between 3 and 24 acini. The lobular bronchiole and accompanying artery form the core structures. Normal centrilobular arteries (with a maximum diameter of 0.2 mm) can be resolved on high-resolution computed tomography (HRCT), but the wall of the accompanying bronchiole is too thin to be seen ( Fig. 11.4 ). The implication is that when bronchioles are visible within 2 cm of the subpleural space (either because of wall thickening, dilatation and/or mucous plugging of the lumen) there is disease. Infiltration of the interlobular septa by oedema fluid or malignant cells, or thickening caused by fibrosis, will also render individual pulmonary lobules visible on HRCT ( Fig. 11.5 ).
Radiological Signs of Airspace Disease
One of the principal limitations of imaging airspace diseases is that a multitude of pathological processes manifest as a limited number of patterns; thus, for most airspace diseases, a nodular pattern, ground-glass opacification and consolidation represent the range of radiological abnormalities.
- 1.
A nodular pattern as a sole manifestation of airspace disease is relatively uncommon. The term ‘acinar nodules’ or ‘acinar rosettes’ has been used in the past to describe the appearance of poorly defined infiltrates on a CXR and HRCT. However, the diagnostic value of localising disease to the acinus is questionable; in pathological studies, the acinar pattern on plain radiographs, as described in radiology reports, does not generally correspond to the filling of acini as per strict anatomical definitions. This notwithstanding, the so-called acinar pattern is most frequently encountered in the context of bacterial infection or pulmonary haemorrhage ( Fig. 11.6 ).
- 2.
Ground-glass opacification is a relatively common sign that can reflect airspace disease. On plain radiography, ground-glass opacification is seen as hazy, increased lung opacity in which the margins of pulmonary vessels are obscured. Because of the greater contrast resolution, ground-glass opacification on CT appears as a hazy increase in lung attenuation but without obscuration of bronchial and vascular markings ( Fig. 11.7 ). It is important to remember that ground-glass opacification can be a manifestation of airspace and/or interstitial disease ( Fig. 11.8 ). Sometimes, particularly when there is diffuse disease, ground-glass opacification on CT may be subtle and barely perceptible. In such cases, a noticeable difference between the density of air in the lumen of an airway and that in the adjacent lung (the ‘black bronchus’ sign) ( Fig. 11.9 ) might be the clue needed to confirm the suspicion of lung infiltration: in the normal lung, the two densities will be roughly equal.
- 3.
Consolidation refers to the increase in lung density on a CXR or CT in which the margins of vessels and airways are obscured ( Fig. 11.10 ). An air bronchogram may or may not be seen. This radiological pattern indicates that air in the air spaces has been replaced (e.g. by inflammatory cells, blood or tumour). In some patients, the distribution of consolidation in relation to the pulmonary lobule is an important diagnostic pointer: a perilobular distribution in which there is dense opacification apparently ‘smeared’ around the lobule is a characteristic finding in organising pneumonia ( Fig. 11.11 ).
Pulmonary Oedema
Pulmonary oedema—defined as an excess of extravascular lung water—is caused either by an increase in hydrostatic pressure (sometimes termed ‘cardiogenic’ oedema) or increased vascular permeability (or ‘non-cardiogenic’ oedema) ( Table 11.2 ). However, despite the attraction of simplicity, the clinical utility of this dichotomous classification of pulmonary oedema is debatable. That said, hydrostatic oedema occurs when there is a shift of fluid out of the vascular compartment caused by an increase in venous/capillary pressure. Perhaps the commonest cause of increased hydrostatic pressure is left heart failure. A reduction in plasma osmotic pressure (as in hypoalbuminaemic patients) will have the same effect. Non-cardiogenic pulmonary oedema occurs in conditions where the permeability of the alveolar-capillary barrier is increased. The archetypal example of increased permeability oedema is ARDS.
TABLE 11.2
Computed Tomography Signs of Pulmonary Oedema
| Common Findings |
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| Ancillary Findings |
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Chest Radiography in Pulmonary Oedema
Plain CXR is undoubtedly more sensitive than clinical examination for the early detection of pulmonary oedema. At a pathological level, there is a roughly predictable sequence, with fluid first moving into the interstitium and then the alveoli. Accordingly, on CXRs, the signs of interstitial oedema generally precede frank airspace opacification. In the following sections, the radiographic features of pulmonary oedema are considered; for clarity, the vascular, interstitial and intra-alveolar changes are discussed separately.
Vascular Alterations
The signs of raised pulmonary venous pressure on a CXR are well documented, although the mechanisms causing blood flow ‘redistribution’ are not entirely clear. Signs of vascular redistribution (from bases to apex), namely balanced flow or inverted flow, often suggest elevation of the pulmonary venous pressure ( Fig. 11.12 ). Both vascular dilatation and redistribution are more appreciable in chronic or, at least, subacute left heart dysfunction. The ratio of the diameter of adjacent pulmonary arteries and bronchi seen end-on, particularly at the level of the upper lobes, is useful when judging whether vessels are abnormally enlarged.
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