2. • Alveolar lung disease refers to filling of the airspaces with fluid or
other material (water, pus, blood, cells, or protein).
• The airspace filling can be partial, with some alveolar aeration
remaining, or complete, producing densely opacified, nonaerated
lung that obscures underlying bronchial and vascular markings.
• ALD producing dense airspace opacity is more easily distinguished
from interstitial lung disease (ILD) than lesser degrees of alveolar
filling.
3. • Different causes of ALD often cannot be distinguished based on the
radiographic distribution alone, but the clinical history, associated
radiographic findings, and chronicity of the process can help to
narrow the differential diagnosis.
• The processes to consider when an ALD pattern is seen are divided
into those that are acute and those that are chronic.
• All causes of acute ALD can resolve completely and subsequently
recur, and therefore they should also be considered in the
differential diagnosis of chronic ALD when serial chest radiographs
or patient history suggests a chronic process with exacerbations
and remissions
5. Pulmonary edema
Edema can be
(a) hydrostatic (from cardiac failure, renal failure, or
overhydration);
(b) nonhydrostatic, owing to increased capillary
permeability (in acute respiratory distress syndrome
[ARDS] and fat embolization syndrome); or
(c) inflammatory in etiology (as from chemical
pneumonitis or eosinophilic pneumonitis).
6. • Radiographic signs of cardiogenic pulmonary edema include
enlargement of the cardiac silhouette, pleural effusions, pulmonary
vascular congestion and redistribution, and interstitial and alveolar
opacities.
• Often, the chest radiograph shows evidence of interstitial and
airspace filling, although occasionally a predominantly interstitial
pattern may be seen.
• Interstitial edema can result in blurring of the margins of blood
vessels and hazy thickening of bronchial walls (peribronchial
cuffing), thickening of fissures (subpleural edema), and edematous
thickening of the interlobular septa (Kerley A and B lines).
• Subpleural pulmonary edema is seen radiographically as a
thickened fissure.
7. • Chest radiographs are highly sensitive for the diagnosis of
pulmonary edema and can show edema in patients who have not
yet developed symptoms; conversely, pulmonary edema may be
visible radiographically for hours or even days after the
hemodynamic factors have returned to normal.
• The distribution of airspace opacities in alveolar edema is usually
patchy, bilateral, and widespread, and the opacities tend to
coalesce.
• Air bronchograms may be evident, particularly when the edema is
confluent.
8. • Often, alveolar accumulation of fluid in pulmonary edema is most
pronounced centrally near the hila, resulting in a bat's wing• or
butterfly• configuration.
• A clue to the diagnosis of pulmonary edema, instead
of pneumonia, for example, is rapid change on radiographs taken
over short time intervals (several hours); rapid clearing is
particularly suggestive of the diagnosis.
• Edema fluid can also change distribution or shift from one lung to
the other as a result of the effect of gravity, as when a patient has
been lying on one side.
9. ARDS
• The radiographic features may be delayed by up to 12 hours or
more following the onset of clinical symptoms an important
difference from cardiogenic pulmonary edema, in which the chest
radiograph is frequently abnormal before or coincident with the
onset of symptoms.
• Findings on chest radiography include bilateral, widespread, patchy,
ill-defined opacities resembling cardiogenic pulmonary edema, but
without cardiomegaly, vascular redistribution, or pleural effusion .
• Although the lungs appear diffusely involved on chest radiographs,
computed tomographic (CT) scanning often shows a more patchy
distribution with preservation of normal lung regions.
• If an endotracheal tube is not present on the chest radiograph, the
diagnosis of ARDS is unlikely, except in the later stages of healing.
10. STAGES
• Stage 1 (first 24 hours): Capillary congestion and extensive
microatelectasis with minimal fluid leakage. The chest radiograph
may be normal, or it may show minimal interstitial edema or
decreased lung volume.
• Stage 2 (1 to 5 days): Fluid leakage and fibrin deposition and hyaline
membranes develop. Alveolar consolidation by hemorrhagic fluid
becomes extensive. The chest radiograph shows lung opacity
(usually bilateral and symmetric), similar in appearance to
cardiogenic pulmonary edema or pneumonia, which may start out
patchy but rapidly coalesces.
• Stage 3 (after 5 days): Alveolar cell proliferation, collagen
deposition, and microvascular destruction. The chest radiograph
shows a developing interstitial pattern that may result in
honeycomb lung.
11. • Patients with ARDS typically require mechanical ventilation,
sometimes with high positive end expiratory pressure because of
stiff, noncompliant lungs.
• This predisposes to barotrauma, with rupture of alveolar walls and
subsequent dissection of air into the perivascular bundle sheaths
and interlobular septa, resulting in pulmonary interstitial
emphysema.
• Discrete air-filled cysts, or pneumatoceles, may form in both central
and subpleural locations.
12. • These air collections can dissect into the mediastinum, causing
pneumomediastinum, and can rupture into the pleural space,
causing pneumothorax.
• The lung may be so stiff that it does not collapse easily, even when
a pneumothorax is present. Air may dissect from the mediastinum
into the neck and chest wall, retroperitoneum,peritoneal cavity.
•
The long-term outlook for survivors of ARDS is poorly documented.
Mortality is related mainly to multiple organ failure rather than
pulmonary dysfunction. Chest radiographs may return to normal or
show varying degrees of interstitial lung disease, including
pulmonary fibrosis
13. Pulmonary hemorrhage
• Bleeding into the lung parenchyma occurs as the result of a variety
of disorders. A triad of features suggesting pulmonary hemorrhage
is hemoptysis, anemia, and airspace opacities on chest radiography.
Bleeding into the lung, however, does not always lead to
hemoptysis.
• When bleeding into the lung is widespread, the pattern is referred
to as diffuse pulmonary hemorrhage (DPH). The pulmonary
features of all DPH syndromes are the same, and chest radiographs
are generally not helpful in distinguishing among them.
• Lung opacities range from patchy airspace opacities to widespread
confluent opacities with air bronchograms.
14. • The lung opacities show a perihilar or middle to lower lung
predominance, and they tend to be more pronounced centrally,
with sparing of the costophrenic angles and apices.
• In general, in cases of acute pulmonary hemorrhage (if there are no
complicating factors), rapid clearing in 2 to 3 days can be expected.
This can aid in narrowing the differential diagnosis when chest
radiography shows diffuse ALD.
• When the airspace disease clears, interstitial opacities are often
seen on chest radiography, as the result of by-products of blood
breakdown being taken up by the septal lymphatics.
15. •
Goodpasture syndrome, one of the pulmonary-renal syndromes and the most
common cause of DPH, is an anti-basement membrane antibody disease
manifesting as DPH and glomerulonephritis.
•
It is a disease of young white men and is only occasionally reported in children.
•
The presence of antiglomerular basement membrane antibodies in the serum is a
sensitive and specific indicator of the disease.
•
Renal biopsy shows evidence of subacute proliferative glomerulonephritis with
linear IgG deposition in the glomeruli.
•
The chest radiograph usually shows bilateral, relatively central, and symmetric
ALD, but this is a nonspecific pattern .
•
Many collagen vascular disorders and systemic vasculitides are associated with
DPH, with or without renal disease. The association is most commonly seen with
systemic lupus erythematosus and systemic necrotizing vasculitides of the
polyarteritis nodosa type.
16. • Wegener granulomatosis (WG) is characterized pathologically by
necrotizing granulomatous vasculitis of the upper and lower respiratory
tracts, a disseminated small-vessel vasculitis involving both arteries and
veins, and a focal, necrotizing glomerulonephritis.
• Mean age at presentation is 50, and there is a slight male predominance.
• Upper airway involvement with sinusitis, rhinitis, and otitis is the most
common clinical presentation.
• More than 90% of patients with active multiorgan WG have a positive test
for cytoplasmic antineutrophil cytoplasmic antibodies.
• There are two characteristic pulmonary radiologic findings:
– nodules, multiple or single, ranging from 3 mm to 10 cm in diameter, which
may cavitate;
– diffuse areas of lung opacity, representing pulmonary hemorrhage.
– Occasionally, ill-defined nodular opacities may be present, sometimes
appearing as areas of pleural-based, wedge-shaped consolidation, resembling
pulmonary infarcts.
17. • DPH can occur as a result of various coagulopathies, including
thrombocytopenia (such as in leukemia or after bone marrow
transplantation), anticoagulation, coronary thrombolysis, and
diffuse intravascular coagulation.
• Infectious hemorrhagic necrotizing pneumonias or hemorrhagic
neoplasms can result in diffuse, focal, or multifocal patchy areas of
pulmonary hemorrhage.
18. Alveolar proteinosis
• Alveolar proteinosis typically presents in a patient who feels
relatively well, in striking contrast to the markedly abnormal
radiograph, which shows bilateral diffuse or multifocal patchy
opacities.
• The opacities represent a phospholipoproteinaceous material that
fills the alveolar spaces and clears after bronchioalveolar lavage.
• Recurrence of disease can result in a chronic pattern of ALD, with
serial chest radiographs showing varying patterns of recurrent ALD
with interval clearing.
• Alveolar proteinosis is associated with an increased incidence of
lymphoma and infection with Nocardia.
19. Infectious pneumonia
• Infectious pneumonia is the most common cause of focal ALD, and
bacteria are the most common inciting agents.
• Fungal, mycobacterial, parasitic, and even viral pneumonias can all
produce focal or diffuse airspace opacities on chest radiography .
• Opacity of more than half a lobe with no loss of volume is virtually
diagnostic of pneumonia, and common causes are Streptococcus
pneumoniae or Mycoplasma pneumoniae.
• Lobar consolidation with expansion of the lobe, although
uncommon, strongly suggests bacterial pneumonia (particularly S.
pneumoniae, Klebsiella pneumoniae, Pseudomonas aeruginosa,
and Staphylococcus aureus pneumonias).
• A round consolidative process is likely to be caused by pneumonia.
20. • Organisms most likely to cause round pneumonia are S. pneumoniae, S.
aureus, K. pneumoniae, P. aeruginosa, Legionella pneumophila or L.
micdadei, Mycobacterium tuberculosis, and several fungi.
• The development of air-fluid levels within an area of consolidation that is
known or presumed to be pneumonia strongly suggests necrotizing
pneumonia with abscess formation, and likely pathogens include S.
aureus, Klebsiella sp, Proteus sp, and Pseudomonas sp, as well as mixed
infections.
• Multifocal pneumonia can be caused by numerous organisms, but the
bat's wing pattern• in the immunocompetent patient should suggest
aspiration pneumonia, Gram-negative bacterial pneumonia , and
nonbacterial pneumonias such as mycoplasma, viral, and rickettsial
pneumonia.
• Pneumonia in the immunocompromised host often results in the bat's
wing pattern from opportunistic organisms such as Pneumocystis jiroveci
and various fungi.
21. Aspiration pneumonia
• The radiologic manifestation of aspirated material into the lungs is
dependent on the type and volume of material aspirated, the immune
status of the patient, and the presence or absence of pre-existing lung
disease.
• Aspiration of bland substances such as blood or neutralized gastric
contents does not incite an inflammatory process, and associated lung
opacities clear rapidly with ventilation therapy or coughing.
•
Aspiration of acidic gastric contents and other irritating substances causes
inflammation of the lung.
• Within several hours of aspirating such substances, chest radiographs
usually show progressive airspace opacity in the gravitationally dependent
regions of the lungs.
• Radiologic improvement is generally seen within a few days unless the
patient develops superimposed infection or ARDS.
23. • Determining that the process is chronic requires serial chest radiographs
showing a static appearance or progression of ALD, typically over several
months.
• Two neoplastic processes should be considered in the differential
diagnosis of chronic ALD: lymphoma and bronchoalveolar cell carcinoma
(a type of primary bronchogenic adenocarcinoma).
• Alveolar proteinosis can also be recurrent.
• Sarcoidosis can result in myriad chest radiographic patterns, both typical
and atypical. Chronic ALD, although not a common pattern of sarcoidosis,
should be considered in a young, relatively asymptomatic patient.
Although the chest radiographic appearance mimics ALD, sarcoidosis
involves only the interstitial compartment of the lung. Areas of airspace
opacity, so-called alveolar sarcoidosis, represent a conglomeration of
interstitial granulomas.
24. Lipoid pneumonia
• Lipoid pneumonia results from aspiration of vegetable, animal, or mineral
oil, usually in elderly or debilitated patients, patients with neuromuscular
disease or swallowing abnormalities, or patients taking mineral oil as
therapy for chronic constipation.
• Most patients are relatively asymptomatic.
• Chest radiographs show homogeneous segmental areas of lung
opacification, or circumscribed masses (paraffinomas•) that remain stable
or slowly progress over a period of months and can be similar in
appearance to bronchogenic carcinoma.
• Because of the lipid content, these areas of opacification may be of
relatively low attenuation on CT scans of the chest, which may help
suggest the correct diagnosis.
• Dilated colon and chronic stool retention seen on chest or abdominal
radiographs may also provide clues to a patient who chronically aspirates
mineral oil.
