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Diffuse Air Space Opacities
Questions
- 1.
The images in Fig. 15.1, A and B , were of a patient who presented in the emergency department with a known diagnosis of granulomatosis with polyangiitis. Which one of the following complications is most likely?
- a.
Pneumonia.
- b.
Hemorrhage.
- c.
Diffuse alveolar damage (DAD).
- d.
Pulmonary edema.
- e.
Acute interstitial pneumonia (AIP).
- a.
- 2.
Which one of the following is not a sign of air space disease?
- a.
Diffuse coalescent opacities.
- b.
Air bronchograms.
- c.
Acinar nodules.
- d.
Fine reticular opacities.
- e.
Air alveolograms.
- a.
- 3.
The asymmetric distribution of the diffuse coalescent opacities in Fig. 15.2 is suggestive of which diagnosis?
- a.
Pneumonia.
- b.
Goodpasture syndrome.
- c.
Chronic renal failure.
- d.
Alveolar proteinosis.
- e.
Congestive heart failure.
- a.
- 4.
A 24- to 48-hour delay in the development of pulmonary edema is commonly observed in which of the following conditions?
- a.
Congestive heart failure.
- b.
Pulmonary emboli.
- c.
Smoke inhalation.
- d.
Heroin reaction.
- e.
High-altitude pulmonary edema.
- a.
Discussion
The diffuse air space consolidation 22, 601 shown in Fig. 15.1, A and B , is a classic appearance and consists of the following: coalescent or confluent opacities with ill-defined borders; butterfly-shaped perihilar distribution; ill-defined nodular opacities around the periphery of the process (“acinar pattern”) 601, 666 ; and interspersed small lucencies. 457, 460 Air-filled bronchi surrounded by the confluent opacities are seen as dark branching shadows. These were described by Fleischner 162 as the “visible bronchial tree” and are commonly referred to as air bronchograms 150 (see Fig 15.2 ). The small, interspersed lucent spaces represent groups of air-filled alveoli surrounded by airless consolidated lung. The term air alveologram was applied to these lucent spaces by Felson 150 ; they are the alveolar equivalent of the air bronchogram. The distribution of opacities caused by air space consolidation may be diffuse, lobar, or segmental (see Chapter 14 ). There is a tendency for air space opacities to be labile—that is, changing in severity over a short period of time on serial examinations.
Diffuse ground-glass opacity is occasionally used to describe less opaque, diffuse, confluent opacities seen on chest radiographs, but is more commonly used in reporting high-resolution computed tomography (HRCT). This differs from consolidation in degree of opacity and implies minimal disease. Ground-glass opacities appear on HRCT as gray areas of confluent attenuation that fail to obliterate normal vascular shadows. Ground-glass opacity demonstrated by HRCT results from minimal filling of the alveolar spaces or from thickening of the alveolar walls and septal interstitium. 133 Reticular opacities, whether or not they are demonstrated on a chest radiograph or computed tomography (CT) scan, are not a finding of air space disease. (Answer to question 2 is d .)
Cardiac Pulmonary Edema
Pulmonary alveolar edema ( Fig 15.3 ) is a classic example of a diffuse air space filling process ( Chart 15.1 ). The presence of alveolar edema, however, does not imply the absence of interstitial edema. Cardiac pulmonary alveolar edema is always preceded by interstitial edema, but the extensive alveolar consolidation obscures the fine reticular opacities of the interstitial process. Radiologic documentation of the underlying interstitial process entails examination of areas not significantly involved by the alveolar filling process. When alveolar pulmonary edema is secondary to congestive heart failure, the alveolar edema often has a perihilar distribution, and Kerley B lines may be present in the costophrenic angles.
Chart 15.1
Diffuse Air Space Opacities
- I.
Edema
- A.
Cardiac failure
- B.
Noncardiac (see Chart 15.2 )
- A.
- II.
Exudate (pneumonias)
- III.
Hemorrhage
- IV.
Other
The latter sign confirms the underlying interstitial process. Other radiologic signs that may be associated with cardiopulmonary edema and can be helpful in suggesting the diagnosis include: (1) prominence of the upper lobe vessels 454 ; (2) indistinctness of vessels 291 ; (3) peribronchial cuffing 390 ; (4) increased width of the vascular pedicle 390 ; (5) pleural effusion, frequently with fluid in the fissures; and (6) cardiac enlargement with a left ventricular prominence. Correlation of the radiologic findings with clinical findings usually confirms the diagnosis. An electrocardiogram indicating cardiac enlargement or an old or acute myocardial infarction is also supportive evidence, whereas an S3 heart sound, neck vein distention, hepatomegaly, or peripheral edema usually confirm the diagnosis of congestive failure. Also, auscultation over the lungs usually reveals characteristic basilar rales.
Occasionally, alveolar edema is not distributed uniformly. As a result of gravity, when the patient is upright, the edema fluid has a predominantly lower lobe distribution, but when the patient is supine, the fluid tends to have a more posterior distribution. When the patient favors one side, the fluid tends to gravitate to the dependent side. The resolution of pulmonary edema is often not uniform, so that serial chest radiographs reveal a change in the distribution from diffuse perihilar opacities to a pattern of more uneven multifocal opacities. Other causes for atypical or nonuniform distribution of pulmonary edema are usually of pulmonary origin. The best known of these is severe emphysema, which results in a patchy distribution of the alveolar edema. Presumably, loss of vasculature in the emphysematous areas of the lung results in the development of edema in the more normal areas. Pulmonary embolism is a complication of pulmonary edema that may result in a nonuniform or patchy distribution of the alveolar edema. Two factors may determine the distribution of the air space edema following pulmonary embolism: (1) abrupt interruption of perfusion to an area of lung may prevent the development of typical pulmonary edema; and (2) severe ischemia of the lung may give rise to pulmonary hemorrhage. Clinical suspicion of pulmonary embolism in a patient with congestive heart failure will usually require computed tomography angiography (CTA).
Concomitant infection is another cause of uneven distribution of pulmonary edema. Like the diagnosis of pulmonary embolism, this requires correlation with the clinical history. An elevated temperature, leukocytosis, or purulent sputum should prompt a bacteriologic study to rule out superimposed pneumonia.
Cardiac enlargement in combination with diffuse alveolar opacities that are otherwise characteristic of pulmonary edema is not always a reliable indicator that the patient’s primary problem is a cardiac disorder. For instance, chronic renal failure with uremia can cause pulmonary edema (uremic pneumonitis) as well as hypertension and associated heart disease, with the result of cardiac enlargement. Not only does uremia cause true cardiomegaly, which is probably related to chronic hypertension, but it also may cause pericardial effusion. Thus, the pulmonary edema that results from chronic renal failure and uremia is typically associated with enlargement of the cardiac silhouette. Correlation with the clinical history should readily identify uremic pneumonitis.
In contrast to pulmonary alveolar edema and cardiac enlargement, the presence of a normal-sized heart might suggest a noncardiac form of pulmonary edema, but there are situations in which such patients may actually have cardiac pulmonary edema. These include acute cardiac arrhythmias and acute myocardial infarction, which result in pulmonary edema before dilation of the heart. Thus, there are at least two mechanisms for cardiac pulmonary edema with a normal-sized heart.
Noncardiac Pulmonary Edema
The preceding discussion suggests that the radiologic appearance of noncardiac pulmonary edema is similar to that of cardiac pulmonary edema. 546 In general, the most helpful radiologic feature for distinguishing the two is the presence or absence of cardiac enlargement. Accurate assessment of heart size is often difficult. Technical factors—including supine and anteroposterior positioning, especially when done with portable units—may all contribute to cardiac magnification. Patient condition may also lead to inaccurate cardiac size estimation. Patients with emphysema often have cardiac enlargement, although the chest radiograph is suggestive of a normal or even small heart size. Aggressive intravenous (IV) fluid resuscitation may actually enlarge the heart and cause pulmonary edema. The evaluation of serial radiographs is especially useful for distinguishing a number of the causes of noncardiac edema because the evolution of the edema may be strikingly different. Many of the entities listed in Chart 15.2 may result in acute alveolar edema in the absence of the pulmonary vascular and interstitial changes that precede the edema because of either renal failure or cardiac failure. These entities tend to occur in very acute cases of pulmonary edema and are often best diagnosed by clinical correlation, 5 as is shown in the following discussions of acute toxic inhalations, near-drowning, acute airway obstruction, drug reactions, and ARDS.
Chart 15.2
Noncardiac Pulmonary Edema
- I.
Chronic renal failure
- II.
Toxic inhalations
- III.
Anaphylaxis (e.g., penicillin, transfusion, 62 radiologic contrast medium 205 )
- IV.
Narcotics (e.g., morphine, methadone, cocaine, heroin) 201 , 473 , 671
- V.
Drug reaction (e.g., interleukin-2 therapy, 90 , 518 β-adrenergic drugs 391 )
- VI.
Acute airway obstruction 422 (e.g., foreign body)
- VII.
Near-drowning 448
- VIII.
High altitude 254
- IX.
Fluid overload
- X.
Cerebral (trauma, stroke, tumor) 467
- XI.
Hypoproteinemia
- XII.
- XIII.
Pancreatitis 494
- XIV.
Amniotic fluid embolism 537
- XV.
Fat embolism
- XVI.
Re-expansion following treatment of pneumothorax or large pleural effusion
- XVII.
Organophosphate insecticide ingestion 339
- XVIII.
Hanta virus pulmonary syndrome 291
Acute Toxic Inhalations
Nitrogen dioxide inhalation (silo filler’s disease) is an excellent model for acute toxic pulmonary edema. In the first few days after a grain storage silo is filled, nitrogen dioxide forms. The gas reacts with water in the respiratory tract to produce an irritation of the tracheobronchial tree and alveoli. In the acute phase, this disease has the radiologic appearance of bilateral diffuse alveolar edema. This phase is usually followed within a few days or weeks by complete resolution, although bronchiolitis obliterans may develop weeks to months later as a result of the small airway injury. Chest radiographs of patients with bronchiolitis obliterans often show a fine nodular or reticular pattern. The other chemicals listed in Chart 15.2 produce a similar reaction.
Smoke inhalation is the most common cause of death due to fires. Fire victims may have thermal injuries to the airways and are exposed to toxic gases, soot, and carbon monoxide. Inhalation of these substances may cause airway and alveolar injury with alveolar leak as the cause of pulmonary edema ( Fig 15.4 ). Patients with smoke inhalation must be carefully monitored because the radiologic appearance of pulmonary edema may be delayed by as much as 24 to 48 hours (answer to question 3 is c). The risk of a delayed onset of edema is greatest in patients with low oxygen saturation and elevated carboxyhemoglobin, which reflects carbon monoxide poisoning with potential concomitant lung damage. 445 Early onset of pulmonary edema indicates severe alveolar injury with increased risk of diffuse alveolar damage and ARDS.
Near-Drowning
Near-drowning 448 is another important cause of noncardiac pulmonary edema. The history should confirm the diagnosis; however, aspiration of water provides only a partial explanation for the diffuse alveolar opacities that may develop in near-drowning victims. Again, there may be a delay of 24 to 48 hours before edema develops. Other mechanisms that may contribute to the development of this type of edema include prolonged hypoxia, respiratory obstruction, and fibrin degradation. Fibrin degradation raises the possibility of a subclinical consumptive coagulopathy with microembolization, which may lead to a diffuse pulmonary capillary leak and thus to pulmonary edema. Severe hypoxia may occur in a near-fatal–drowning victim, even when the initial chest radiograph is normal. Patients should therefore be followed for 24 to 48 hours to exclude a significant pulmonary injury.
Acute Airway Obstruction
The diagnosis of acute airway obstruction is usually made on the basis of the clinical history. The obstruction is frequently an aspirated object, such as a large bolus of food or a surgical sponge. The resultant pulmonary edema is usually related to severe hypoxia. This mechanism may be nearly identical to that described for near-drowning. The collection of alveolar fluid is most likely due to a diffuse alveolar leak caused by severe injury to the alveolar capillary membrane. 422
Drug Reactions
Adverse reactions to a variety of drugs ( Chart 15.3 ) may cause acute and chronic pulmonary responses. 18, 52 These reactions have been described as chemotherapy lung, 551 but a large variety of drugs have pulmonary complications. These include antibiotics, narcotics, heart medications, arthritis drugs, radiographic contrast, and a number of chemotherapeutic agents. Acute drug reactions may cause the rapid development of diffuse, confluent air space opacities or patchy, multifocal, confluent opacities (as seen in Chapter 16 ). These acute reactions are the result of edema, hemorrhage, or DAD, which may resemble ARDS. Subacute and chronic reactions include eosinophilic pneumonia, COP, and NSIP. The more chronic reactions cause air space opacities in the early stages but later progress to cause reticular opacities, indicating a fibrotic reaction. Pleural effusions (see Chart 4.1 ) may also be associated with some of these reactions. This is especially true of drugs that are known to cause a lupus-like reaction. 489
Chart 15.3
Pulmonary Drug Reactions
Modified from Rossi SE, Erasmus JJ, McAdams HP, et al. Pulmonary drug toxicity: radiologic and pathologic manifestations. Radiographics. 2000;20:1245-59. Used with permission.
- I.
Edema
- II.
Hemorrhage 489
- A.
Anticoagulants
- B.
Amphotericin B
- C.
Cytarabine
- D.
Cyclophosphamide
- E.
Penicillamine
- A.
- III.
Diffuse alveolar damage (DAD) 489
- A.
Bleomycin
- B.
Busulfan
- C.
Carmustine
- D.
Cyclophosphamide
- E.
Gold
- F.
Melphalan
- G.
Mitomycin
- A.
- IV.
Eosinophilic pneumonia 489
- A.
Nitrofurantoin
- B.
Nonsteroidal antiinflammatory drugs
- C.
Para-aminosalicylic acid
- D.
Penicillamine
- E.
Sulfasalazine
- A.
- V.
Cryptogenic organizing pneumonia (COP) 489
- VI.
Nonspecific interstitial pneumonitis (NSIP) 489
- A.
Amiodarone
- B.
Carmustine
- C.
Chlorambucil
- D.
Methotrexate
- A.
Anaphylaxis is an acute response to a variety of substances and is a cause of edema. Acute alveolar edema may occur following administration of IV radiologic contrast, morphine, heroin, and other opiates. Cocaine has been reported as a cause of both cardiac and noncardiac pulmonary edema. 201, 473 Although the mechanism for the noncardiac pulmonary edema is unknown, it is generally believed to represent an idiosyncratic reaction with an alveolar capillary injury. Since the opiates cause central nervous system depression, there may also be a relationship to neurogenic edema. Methadone, a slow-acting narcotic, may cause a slower onset of edema than heroin or morphine, and may also resolve more slowly. 201, 671 The typical radiographic pattern for narcotic-induced edema is diffuse, bilateral, confluent air space opacification without cardiomegaly and without pleural effusion. In contrast to narcotics, the allergic edema of interleukin-2 commonly causes interstitial edema (as seen in Chapter 18 ) with septal lines and peribronchial edema. 90, 518 This so-called allergic edema infrequently becomes more severe with the development of alveolar edema. 291
Acute DAD causes permeability edema with the radiologic appearance of diffuse confluent opacities that may sometimes appear multifocal. Therefore, in its early stages, DAD may be indistinguishable from hydrostatic pulmonary edema. The acute edema is rapidly followed by cellular necrosis, inflammation, and later fibrosis. Bleomycin, busulfan, and cyclophosphamide are all possible causes of DAD, and the resulting ARDS is the most severe life-threatening drug reaction.
Eosinophilic pneumonia is a true allergic reaction. Diffuse confluent air space opacities with a peripheral distribution are typical. Histologic changes include infiltration of alveolar walls with eosinophils and other inflammatory cells. Peripheral eosinophilia is also a common finding. Eosinophilic pneumonia responds well to withdrawal of the medication but sometimes requires steroid therapy for complete resolution. Nitrofurantoin is a urinary antibiotic that may cause eosinophilic pneumonia.
COP, previously known as BOOP ( b ronchiolitis o bliterans o rganizing p neumonia), is more likely to produce multiple areas of diffuse confluent opacity. Like eosinophilic pneumonia, the opacities tend to be in the periphery of the lung. CT often shows the areas of consolidation to be more nodular than expected from the radiograph. Even though there is histologic evidence of fibrosis, this reaction usually responds well to withdrawal of the drug and steroid therapy. 489 Amiodarone, bleomycin, methotrexate, and nitrofurantoin are all possible causes of COP.
NSIP is more likely to present with minimal patchy or multifocal basilar opacities that may appear confluent on the chest radiograph. HRCT shows mainly ground-glass opacity with some reticular opacities. This reaction is more likely to progress to interstitial fibrosis with reticular opacities, honeycombing, and traction bronchiectasis. 489 Amiodarone and methotrexate are also causes of NSIP.
The diagnosis of drug reaction is best suggested by a history of medication with any of the drugs known to produce pulmonary reactions. In patients who are undergoing chemotherapy for cancer, the differential includes the following: (1) opportunistic infection; (2) diffuse hemorrhage; (3) drug reaction; and (4) spread of the primary tumor. 94
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