The radiological diagnosis of pneumonia in the adult: A commentary

The Radiological

Diagnosis of Pneumonia in the Adult: A Commentary By E. Robert Heitzman

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ESPITE THE FREQUENCY and significance of pneumonia, relatively few articles in the recent radiologic literature have covered this important subject. Furthermore, most contemporary reports on the subject have concerned themselves only with a small portion of the problem. Almost ten years ago, an issue of Seminars in Roentgenology (Vol 15, NO 1) reviewed the radiological aspectsof the pneumonias in depth. This article is an effort to update that material and to provide some personal opinions and prejudices. The broad topic of opportunistic lung infection will not be discussed. TERMINOLOGY

Pneumonitis is a word often used instead of pneumonia, possibly because some radiologists believe it to be lessspecific than the termpneumonia and, therefore, feel that a lesser degree of diagnostic commitment is implied. However, Spencer’ usespneumonia and pneumonitis interchangeably. It is thought here that, for reasonsof clarity and consistency,pneumonia is the preferable designation. The use of the word consolidation is discouraged since it carries no specific pathologic connotation. Opacity or density are preferred to consolidation as a radiologic descriptor. If it is not possible to determine the cause of an opacity on a radiograph, the use of consolidation cannot be justified as being an easy way out. The film reader should admit his dilemma; “an opacity consistent with pneumonia or infarction” is appropriate phrasing. PATHOLOGY

Traditionally, the classification of pneumonia has been based on the morphological changes it produces in the lung. Lobar, lobular or bronchopneumonic, and acute interstitial types form a standard classification, Such a subdivision has From the Department of Radiology. SUNY Health Science Center at Syracuse, Syracuse, NY. Address reprint requests to E. Robert Heitzman, MD, Department of Radiology, SUNY Health Science Center at Syracuse, 750 E Adams St, Syracuse, NY 13210. o I989 by W.B. Saunders Company. 0037-l 98X/89/2404-0003$5.00/0 212

limited usefulness to the clinician; therefore, it has been largely replaced by a classification based on the causal organism. Nevertheless, the radiologic diagnosis of pneumonia must be dependent on the gross morphologic changes depicted on the radiographs. For this reason, a basic understanding of the gross pathology of pneumonia is important for the radiologist. Lobar Pneumonia

The organisms that produce lobar pneumonia reach the terminal air spacethrough the airway. The initial reaction is an outpouring of edema fluid into the alveolae followed by a multiplication of microorganisms in the fluid and an invasion of the fluid by polymorphonuclear leukocytes. The mechanism of alveolar wall injury and the factors that influence white cell migration into the alveolae are not completely understood.2 Thus, lobar pneumonia is an infected pulmonary edema. Although complete lobar involvement wascommon before 1950, it is rare today.3 It is still identified, at times, under circumstances that delay diagnosis.’ Nevertheless, lobes that appear to be involved in a relatively uniform manner are not uncommonly seenon radiographs; such cases are almost always due to confluent lobular or bronchopneumonia. A radiographic distinction between lobar pneumonia and confluent bronchopneumonia cannot be made. Since the most common community-acquired pneumonia that requires hospitalization is caused by Streptococcus pneumoniae4*’ and becauseit is responsible for 25% of nosocomial pneumonia6 somecurrent facets of the radiologic diagnosis of pneumococcaepneumonia will be reviewed. As one would exPneumococcal pneumonia. pect from an understanding of the underlying pathology, a common radiographic appearance of pneumococcal pneumonia is that of diffuse air space opacification, often with an air bronchogram. This pattern was identified in 86 out of 104 patients with pneumonia and pneumococcal septicemia studied by Ziskind in 1970.’ In 1981, Kantor’s study’ emphasized the variability in the radiographic appearanceof pneumo-

Seminars in Roentgenology, Vol XXIV, No 4 (October). 1989: pp 2 12-2 17

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nia caused by Streptococcus pneumoniae. In his series, the patterns of disease were: diffuse opacification in 12 patients, patchy densities in 12, an interstitial pattern in nine, and mixed patterns in seven patients. This variability in radiographic appearance is greater than previously reported but is supported by the later studies of Ort.9 Of Ort’s group of patients, 61% presented with a patchy, bronchopneumonic pattern and 39% presented with a diffuse segmental or lobar one. The two groups did not appear to be different clinically, but 54% of the group that had a lobar pattern also had an associated bacteremia, whereas only 9% of the bronchopneumonic group had positive blood cultures. Providing that the radiologic criteria used by Kantor and Ort were not different from those used by Ziskind, one is permitted to conjecture that the radiographic appearance of pneumococcal pneumonia, at least in hospitalized patients, is changing. This has been our experience at Syracuse. Certainly, a patchy or bronchopneumonic pattern on a radiograph should not be considered inconsistent with the diagnosis. Rose and Ward lo reported 2 1 cases of pneumonia in which the inflammatory process adopted a spherical shape. The appearance is sometimes referred to as “round” pneumonia. In nine out of 17 patients who had cultures taken, Streptococcus pneumoniae was isolated; no growth was obtained from the remaining patients. Whereas round pneumonia suggests a pneumococcal origin, it is far from pathogonomic. Round pneumonia can simulate a mass. The study by Rose and Ward showed a change on the first follow-up radiograph made between two and seven days, a helpful point in differential diagnosis. Bronchopneumonia

or Lobular Pneumonia

Bronchopneumonia is referred to by pathologists as lobular pneumonia because the process respects septal boundaries, involving some pulmonary lobules while sparing others. Bacteria initially damage the walls of the terminal and respiratory bronchioles rather than the terminal air space.’ A peribronchiolar focus of infection develops; subsequently, it spreads along the intralobular airway to the alveolus and from alveolus to alveolus until the pulmonary lobule is partially or totally involved. As a result the lung surface has an appearance resembling a patchwork quilt.

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On gross pathological examination some involved lobules stand out in relief against adjacent uninvolved lobules. The radiographic appearance of bronchopneumonia is one of patchy, poorly defined opacities. Since several foci of disease are often seeded at the same time the process is diffuse; frequently both lungs are involved. If one or more lobes are extensively involved, pathologists will diagnose confluent bronchopneumonia. Although bronchopneumonia is most commonly the result of infection by the Staphylococcus or gram negative organisms, anaerobic organisms may also be the infecting agents. Some unique features of anaerobic lung infection will now be discussed. Anaerobic pneumonia. A wide variety of anaerobic organisms can cause bronchopneumonia. In the study by Bartlett and Finegold” 15 different organisms were responsible, the most common being Fusobacterium nucleatum and Bacteroides melaninogenicus. Multiple isolates are the rule. The incidence of anaerobic lung infection has not been established because anaerobic cultures are often not performed or are performed improperly in many cases of thoracic infection. The incidence is no doubt considerably higher than is generally appreciated.” Anaerobic infection is highly necrotizing; necrosis was present in 50% of the cases in Ianday’s study12 and abscess formation was present in 50% of the cases in Bartlett and Finegold’s study.” The pathogenesis of most cases of anaerobic lung infection implicates the aspiration of infective material from the gingiva or teeth. In a study of anaerobic lung infection carried out by Bartlett and Finegold,” conditions predisposing to aspiration were found in 104 of 143 patients. In 60% of the patients who had a lung infection periodontal disease was found during a dental evaluation.” In this group of 143 patients there were 12 who had associated carcinoma. In 131 patients who did not have carcinoma. 9 were edentulous and out of the 12 who had carcinoma, 7 were edentulous. On the basis of these figures, Bartlett and Finegold” report that finding an anaerobic lung infection in an edentulous patient requires a diligent search for underlying carcinoma.

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Acute Interstitial Pneumonia The cause of acute interstitial pneumonia is almost always a virus or a mycoplasma. The pathology of viral pneumonia has beenstudied by several investigators;1,13*‘4 mycoplasma pneumonia produces identical changes in the lung.‘5-19 The evolution of viral pneumonia begins with the deposition of the inhaled viral agent on the bronchiolar walls and the subsequentdestruction of mucosal cells. Airway walls become edematous and infiltrated with mononuclear cells; these changes extend from peribronchial tissues into the interlobular septa. In some instances the focal inflammatory reaction is characterized by leukocytic infiltration and necrosis involves the terminal air passagesand alveoli. Whole lobules may be involved, but sometimesthe focal inflammatory response may affect only the peribronchial portions of lobules. Either interstitial viral pneumonia or focal alveolar inflammatory changes may result in localized or generalized hemorrhagic pulmonary edema. In this stage of the disease,the alveoli are filled with edema fluid and show marked hemorrhage and infiltration of polymorphonuclear leukocytes; often they are lined by a hyaline membrane. Sometimes frank interstitial fibrosis is the end result. It is possible that many instances of so-called idiopathic chronic interstitial fibrosis are caused by a viral infection. The radiographic abnormalities that result from viral pneumonia are many and varied but can be explained in terms of the underlying pathology. It is clear that viral pneumonias, although commonly considered to be interstitial processes,often have a significant alveolar component. Lobular, segmental, and lobar opacifications occur commonly as the result of bacterial pneumonia but may be caused by a viral infection as we11.20-22 A radiographic distinction between bacterial and viral causes is not possible when these patterns are presented.‘6’21’23-25 A nodular pattern due to peribronchiolar inflammatory foci is probably encountered more frequently in the viral pneumonias than in the bacterial pneumonias.20*22 It is important to recognize that in some casesviral pneumonia can produce a pattern simulating an extensive perihilar pulmonary edema, which may rapidly worsen.2o721 In pa-

E. ROBERT HEITZMAN

tients who present with diffuse alveolar diseaseparticularly those who first appear with marked air hunger, toxemia, and a rapidly progressive clinical course-viral pneumonia should be considered as a possible origin.*‘*** Pleural effusion in viral pneumonia is not uncommon. DIFFERENTIAL DIAGNOSTIC CONSIDERATIONS IN PNEUMONIA

It is our belief that, with few exceptions, the identification of the organism causing pneumonia should (and must) be left to the microbiologist. What then are the basic objectives of a study of the radiograph of a patient who has pneumonia or suspect pneumonia? These objectives have been concisely reported by Genereux and Stilwe1126 as follows, “to identify the location and extent of the consolidation, to decide whether the findings are consistent with a pneumonic process, to assessthe evolution as seenon sequential films and to identify any complicating features.” However, what the clinician most often wants to know is whether the patient has pneumonia or some other noninfectious process. Unfortunately, this determination is often not easy. The radiologist should initially approach the differential diagnosis by determining if the processinvolves the air space, using the traditional roentgen criteria for alveolar disease. Following this, an attempt should be made to establish, on the basis of serial films or a clinical history, whether the processis acute or chronic in character. If it can be determined that the processis an acute air space disease, one can confidently predict in an adult that the differential diagnosis will lie between pneumonia, pulmonary edema, or pulmonary hemorrhage. In this context it is important to keep in mind that the most common causeof pulmonary bleeding is pulmonary thromboembolism. It is, of course, not possible for the radiographic method to differentiate fluid containing white blood cells from fluid containing red cells or from edema fluid with a high protein content. Clinical correlations with radiographs are helpful and should be used. The patient with an acute air space process, who on clinical examination has chills, fever, and purulent sputum, very likely has pneumonia. However, the clinical data are often less specific and their correlation with

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radiographs often fails to lead to a definitive diagnosis. The correlation between radiographic appearances and physical signs is even less helpful.27 Laboratory data are often of little value when attempting to distinguish pneumonia from pulmonary hemorrhage or an infarction resulting from embolism.‘s From a radiographic point of view it is helpful to divide the differential diagnostic considerations into two groups, localized disease and diffuse disease. Localized Pulmonary Disease

Localized parenchymal opacifications of a lobar or segmental type can be caused by pulmonary edema or pulmonary hemorrhage, as well as by pneumonia. In the former category, it should be recognized that localized edemacan be caused by the aspiration of acid gastric content; this may result in an appearance identical to pneumonia. A history of aspiration, an appropriate clinical setting for aspiration, and a change in the appearance of the radiograph after a few hours or one to two days supports a diagnosis of aspiration. The distinction of localized pneumonia from the effects of thromboembolism is a common and more difficult problem. Both conditions may produce single or multiple areas of air spaceabnormality. Patients who present with a classical appearance of Hampton’s hump29are likely to have a pulmonary infarction; however, this is far from a pathognomonic sign and is not frequently encountered. The ultimate examination to clarify this differential diagnosis is, of course, isotopic scanning. The presenceof multiple perfusion defects when there is only one area of parenchymal abnormality indicated on the radiograph strongly favors a pulmonary embolism, as doesthe demonstration of a perfusion defect that is much greater in size than the radiographic abnormality. It is important to recognize that many casesof pneumonia that cause a localized pulmonary abnormality cannot be diagnosed on radiologic grounds. Temporal considerations. Doesthe length of time required for the development of a radiographic abnormality, following the onset of clinical symptomatology, help to distinguish pneumonia from pulmonary infarction? There are no well-constructed studies that answer this ques-

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tion with certainty. However, it is thought that the average appearance time from the onset of symptoms is about 12 hours for each condition; there is considerable variation in this interval. The “melting sign,“30 although useful for distinguishing pneumonia from an infarction in retrospect, is of no value in determining the acute problem. Therefore, temporal criteria are usually of little help for differential diagnosis. State of hydration. Another frequently discussed issue relating to the time of development of pneumonic opacities on radiographs concerns whether hydration accelerates the development of the radiographic abnormality, a possibility raised by Scanlon3’ It is suggested that many dehydrated patients are admitted because of chest symptoms before any radiographic abnormalities have developed and that the development of pneumonia a few hours later following fluid administration is a radiologic “lag phenomenon” unrelated to hydration. This may well be the case in many instances. Caldwell suggestedthat dehydration did not have an effect on the development of pneumonia. In this study 20 patients that were admitted for dehydration and pneumonia had a radiographic abnormality on their initial radiographs. Other experimental work performed by Caldwell led to the conclusion that hydration did not alter the development of pneumonia in dogs. However, more recently it has been shown that, in dogs with pneumococcal pneumonia, hydration does actually produce a heavier pneumonic lobe than develops in control dogs who are not hydrated.33Recently, Hall and Simon34reported a clinical casethat supports the contention that hydration influences the radiographic picture. However, they emphasized that the issue remains unsettled. Chronic pneumonia behind endobronchial tumor. Another problem in the differential diag-

nosis of a localized pulmonary opacity is the differentiation of pneumonia from an endobronchial neoplasm that is producing chronic inflammation behind it. Not infrequently, an acute flare-up of the chronic processwill produce fever and leukocytosis, simulating an uncomplicated acute pneumonia. Bronchoscopy is commonly used to resolve this dilemma; however, how long should the opacity be observed before bronchoscopy is suggested?

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Israe13’ studied 139 patients who had bacterial pneumonia and found that resolution was usually complete in one month. However, 13%of pneumonias were not resolved at four weeks;the majority of these had disappeared by 8 weeks. Israel and his colleagues found that delayed resolution was more often related to factors such as diabetes or old age than to a localized structural abnormality. Israel suggested that operative intervention in debilitated patients should not be undertaken before eight weeks.The decision is clearly dependent on the clinical setting. Pneumonia versus atelectasis. Patchy shadows of increased density are often seenunilaterally or bilaterally, usually in the basal portions of the lung. Theseshadowsusually represent subsegmental pneumonia or subsegmental atelectasis. Since these diagnoses cannot be distinguished and often occur together it is our preference to report the presenceof subsegmental pneumonia and/or atelectasis. Since infarction may look similar, should this possibility be mentioned also? This decision is a matter of philosophy but ordinarily we do not mention infarction unless the clinical setting or the presenceof Hampton’s hump makes it a good possibility. Di$%se Pulmonary Disease

Differential diagnosis is equally difficult when pneumonia appears as a generalized pulmonary abnormality. Pulmonary edema and adult respiratory distress syndrome are the most common conditions to be distinguished when a diffuse air space process is encountered. Occasionally, the rapidity of resolution of the process is helpful. Adequately managed, uncomplicated pulmonary edema will usually clear within a day or two, whereas the significant clearing of pneumonia generally takes longer26*35even in previously healthy patients. Zimmerman36 has recently advocated that patients who have air spacedisease be placed in a decubitus position for a few hours and have a subsequent frontal radiograph com-

pared with an earlier one. A shift or change in the radiographic pattern of disease suggestspulmonary edema. The correlation of radiographs with the state of hydration of the patient as judged clinically to include or exclude edema can lead to diagnostic errors. Correlations with pulmonary wedge pressure measurementsmade from Swan-Ganz measurements may fail to reflect left atria1 pressure in patients who receive assisted ventilation with high positive end-expiratory pressures.37Butler3’ reported that this will be the case if the alveolar pressure exceedsthe left atria1 pressure. Another philosophical yet practical concern for the radiologist who is faced with a diffuse pulmonary abnormality concerns when to diagnose the adult respiratory distress syndrome (ARDS). This condition is clearly a syndrome that is rigidly defined by someinvestigators38and more loosely defined by others.3gThe radiologist usually does not know whether the patient meets the diagnostic criteria being used by the patient’s physician. It is our feeling that if a diffuse pulmonary abnormality remains unchanged or progressesover a period of more than three days, the phrase “findings are consistent with ARDS” may be included in the report. Obviously, ARDS can improve, but if this is the case it cannot be distinguished from slowly resolving pneumonia or pulmonary edema. Radiographs should always be interpreted with a knowledge of the magnitude of the positive end expiratory pressure (PEEP) being used. An apparent radiological improvement with higher PEEP may reflect only that more alveolae are being recruited, whereas the absolute degree of lung diseaseis the sameor worse. The differentiation of the causes of diffuse pulmonary disease often cannot be achieved on clinical or radiographic grounds. Under the appropriate circumstances a lung biopsy may be required.

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217 23. George R, Weill H, Rosch JJ, et al: Roentgenographic appearance of viral and mycoplasmal pneumonias. Am Rev Respir Dis 96: 1144- 1150, 1967 24. Janower ML, Weiss EB: Mycoplasmal, viral and rickettsial pneumonias. Semin Radio1 15:25-34, 1980 25. Tew J, Calenoff L, Berlin BS: Bacterial or nonbacterial pneumonia: Accuracy of radiographic diagnosis. Radiology 124:607-612, 1977 26. Genereux BP, Stilwell GA: The acute bacterial pneumonias. Semin Roentgen01 15:9- 16, 1980 27. Osmer JC, Cole BK: The stethoscope and roentgenogram in acute pneumonia. South Med J 59:75-77, 1966 28. Moser KM: Pulmonary embolism. Am Rev Respir Dis 115:829-852, 1977 29. Hampton CA, Castleman B: Correlation of postmortem chest teleroentgenograms with autopsy findings with special reference to pulmonary embolism and infarction. Am J Roentgen01 43:305-326, 1940 30. Woesner ME, Sanders I, White GW: The melting sign in resolving transient pulmonary infarction. Am J Reontgenol 111:782-790, 1971 3 1. Scanlon CT, Unger JD: The radiology of bacterial and viral pneumonias. Radio1 Clin North Am 11:317-338, 1973 32. Caldwell A, Glauser FL, Smith WR: The effect of hydration on the radiologic and pathologic appearance of experimental canine segmental pneumonia. Am Rev Respir Dis 112:651-656, 1975 33. Cooligan TG, Light R, Duke K, et al: The effect of volume infusion in canine lobar pneumonia. Am Rev Respir Dis 121:122, 1980 34. Hall FM, Simon M: Occult pneumonia associated with dehydration: myth or reality. Am J Roentgen01 148:853854.1987 35. Israel HL, Weiss W, Eisenberg GM, et al: Delayed resolution of pneumonias. Med Clin North Am 40: 12911303, 1956 36. Zimmerman JE, Goodman LR, St Andre AC, et al: Radiographic detection of mobilizable lung water: the gravitational shift test. Am J Roentgen01 13859-64, 1982 37. Butler J, Culver BH, Huseby J, et al: The hemodynamits of pulmonary edema. Am Rev Respir Dis I 15: 173-l 80, 1977 (suppl) 38. Moore FD: Post-traumatic pulmonary insufficiency. Philadelphia, PA, Saunders, 1969 39. Murray JF: Mechanisms of acute respiratory failure. AmRevRespDis 115:1071-1078. 1977