Diagnostic Radiology
Air Crescent Sign of Invasive Aspergillosis 1 Anne MeS. Curtis, M.D., G. J. Walker Smith, M.D., and Carl E. Ravin, M.D.2
Pulmonary infection in Immunocompromised patients Is frequently difficult to diagnose. Therapy for the more common pathogens differs greatly from that for infection with unusual opportunistic organisms. However, neither of these Infectious agents offers specific radiographic signs. The authors report on 4 patients with acute leukemia and Invasive aspergillosis whose radiographs demonstrated a distinctive feature of one or more air crescents within an area of pulmonary infiltrate. Autopsy studies correlated the radiographic changes with an infection due to Aspergillus species fungi. While the sign is not pathognomonic for Aspergillus infection, seen in a suitable host, it would suggest the possibility of invasive aspergillosis. INDEX TERMS: Aspergillosis. Immunity. Leukemia. complications and sequelae. Lungs. infection. (Lungs. fungus infection. 6[01.205). (Lungs. Aspergillus infection, 6[01.2056). (Lungs. immune deficiency with pneumonia.
6[0].251) Radiology 133:17-21. October 1979
HE immunologically compromised patient with Aspergillus infection. especially in the presence of hematologic malignancy, continues to pose a significant problem associated with hig, morbidity and mortality (1-6). Recent evidence suggests that early treatment with amphotericin B may lead to increased survival in this patient poputation (1-8). Unfortunately, this drug has significant side effects. Therefore the diagnosis should be definite or strongly suspected prior to initiation of therapy. Establishing the diagnosis of invasive aspergillosis frequently requires aggressive evaluation, including lung biopsy using transbronchial. percutaneous, or open thoracotomy techniques. While specific opportunistic infections may offer relatively characteristic radiographic findings (9), often the various bacterial, fungal, viral, and protozoan pathogens manifest overlapping and therefore nonspecific clinical and radiographic appearances (6. 10). Any radiographic feature which would suggest Aspergillus infection as opposed to any other infectious agent would be helpful in supporting aggressive diagnostic and therapeutic measures in these critically ill patients. We recently observed 3 cases of invasive aspergillosis complicating leukemia in which the radiographic sign of single or multiple air crescents was noted to develop within patchy or nodular chest infiltrates. A fourth patient with aspergillosis had an anatomical lesion which correlates well with radiographic air crescents. Although the sign is not entirely specific for Aspergillus, it is sufficient to strongly suggest the diagnosis.
T
disease or following chemotherapy. All had received chemotherapy during or prior to the onset of infection. Steroid therapy had been given to 1 patient intermittently and to another continuously. All had persistent spiking fevers in spite of broad spectrum antibiotic coverage for both gram-negative and qrarn-positive bacterial organisms. In 2 patients, rib and/or pleuritic pain developed antecedent to the pulmonary infiltrates (TABLE I). The diagnosis of invasive pulmonary aspergillosis was not established premortem in any patient. In only 1 patient was premortem sputum positive for Aspergillus. Two patients had negative transbronchial biopsies and brushings on both smears and subsequent cultures. No patient had blood cultures positive for Aspergillus. The precipitin titers to Aspergillus rose appropriately, i.e., by a fourfold increase in 2 of the patients tested. In spite of the difficulty in establishing the diagnosis of Aspergillus infection, it was strongly suspected in 3 of 4 patients, and 2 of these 3 received appropriate antifungal therapy with at least amphotericin B. Two patients died as a direct result of Aspergillus infection with massive hemoptysis, one despite 10 days of therapy with amphotericin Band 5-fluorocytosine. A third patient died of respiratory failure, probably due primarily to Aspergillus pneumonia. A fourth patient survived the acute pulmonary infection and received amphotericin B for approximately two months. In this case, the lesions stabilized or regressed somewhat, but the chest radiograph never reverted to normal (Fig. 1).
MATERIALS AND METHODS
Radiological Features
All 4 patients had acute leukemia, and all were leukopenic at the time of infection either as a direct result of
Two of the 4 patients initially presented either with single
1 From the Departments of Diagnostic Radiology (AMcBC. C.ER) and Pathology (GJW.S.), Yale University School of Medicine. New Haven. Conn. Received Sept. 25. 1978; accepted and revision requested Nov. 24; revision received Apr. 25. 1979. 2 Present address: Department of Radiology. Duke University Medical Center. Durham, N. C. 27710. as
17
18
ANNE
MeS.
TABLE
CASE
I II III
IV • ALL + AML
CURTIS AND OTHERS
October 1979
I: CLINICAL SUMMARY
Diagnosis
Pleuritic Pain
Hemoptysis
ALL·. relapse AML +• relapse AML. initial AML. initial
Present Present Absent Absent
Present Absent Present Absent
Precipitin Titres
1:32 1:32 Not done Not done
Sputum or Biopsy
Antifungal Therapy
o o
10 days 45 days
+ o
= acute lymphocytic leukemia = acute myelogenous leukemia
or multiple nodules in both lungs. A predilection for the upper lobes was not noted. A third patient presented with bilateral patchy pneumonic infiltrates and the fourth initially had an interstitial pattern progressing to consolidation. Three patients were seen with crescent shaped radiolucencies surrounding or within the preexisting parenchymal densities from one day to three weeks following the development of the initial abnormality (Fig. 2). There were no radiographs obtained in the fourth patient during the three days prior to death, but necrotic lesions with peripheral circumferential cavitation were evident at autopsy. The development of air crescents was not associated either with recovery from the leukopenic state or improved survival. None of the patients were examined in the supine or decubitus positions to see if the lucencies changed shape or location with a corresponding change in position. Postmortem Features
At autopsy, all 4 patients demonstrated multiple focal lesions characterized by central necrosis and peripheral crescentic or circumferential cavitation. In 2 patients the lesions grossly resembled white infarcts. Large areas of hemorrhage surrounded these lesions in 3 of the 4 cases and were almost certainly a direct complication of the fungal infection. Microscopically in all 4, the solid material within the cavities contained necrotic tissue and fungal elements. Masses of mycelia as seen in aspergilloma were not noted. In each case fungal invasion of the vessels within these necrotic lesions was demonstrated, a finding not observed with mycetoma. Special histochemical techniques were useful in demonstrating a residual vascular and airway framework within the necrotic sequestrum. This was particularly true in the patient who died four months following Aspergillus infection. In the patient who underwent open lung biopsy, the necrotic foci were present at the center of a much more extensive zone of pneumonic consolidation, the periphery of which contained no fungi. In retrospect, wedge biopsy from this peripheral zone of induration accounted for the false-negative study. No patient demonstrated evidence of Aspergillus infection outside of the lung. DISCUSSION
To produce an air crescent, all that is required is that air be sandwiched between a radiodense parenchymal lesion
and the surrounding lung structures. as with an intracavitary fungus ball, intralesional air in a cavitating carcinoma, or an abscess cavity. Thus, many entities having little in common have been reported to produce air crescents: echinococcal cyst, tuberculosis. Rasmussen aneurysm in a tuberculous cavity, other lung abscesses, malignancies such as carcinoma, bronchial adenoma and sarcoma, hematoma, hamartoma, mycetoma, and most recently, sclerosing hemangioma (11-18). A review of the literature suggests that the mycetoma of Aspergillus is the most common cause of the air crescent sign (14, 19-21). While other authors have described the air crescent sign in association with Aspergillus infections in patients with leukemia, they have unfortunately referred to these lesions as mycetomas (5, 21, 22). In the vasoinvasive form of pulmonary aspergillosis, as seen in all 4 of our patients, thrombosis of vessels and infarction of the central portion of the inflammatory focus occur. With retraction of the infarcted center or resorption of necrotic tissue at the periphery, a sequestrum of devitalized lung tissue infiltrated with fungi is formed. A subsequent filling lucency by air of the space between the sequestrum and peripheral lung tissue results in the air crescent seen radiographically. The morphologic differentiation between a fungus ball and necrotic tissue invadedby fungi may be made using elastic and/or reticulin fiber stains. These techniques allow visualization of vascular and airway structures within the area of necrosis. Earlier reports of air crescents in patients with leukemia and pulmonary aspergillosis probably represent cases similar to ours with sequestra rather than mycetoma as the anatomical basis of formation. The incidence of air crescent formation is not known. During the 20-month period when our 4 patients were observed, there were 25 cases of proved or strongly suspected pulmonary aspergillosis in immunocompromised hosts at our institution. This suggests that, with increasing survivals of immunocompromised patients, the air crescent sign may emerge as an important tool in the diagnosis of pulmonary aspergillosis. FlJ1her observation and study are necessary to establish the specificity of the air crescent sign for vasoinvasive pulmonary aspergillosis in immunocompromised hosts. If the development of the air crescent sign depends on vascular invasion with lung infarction, then Candida and the phycomycetes including Mucor, Absidia, and Rhisopus might be expected to produce air crescents as well. The radiographic presentation of opportunistic Asper-
AIR CRESCENT SIGN OF INVASIVE ASPERGillOSIS
Vol 133
19
Diagnostic Radiology
1a-c
d,e Fig. 1. CASE II. a. PA chest radiograph showing bilateral upper lobe densities that developed one month after relapse. band c. Air crescents. demonstrated on tomography, were evident on the plain radiograph as well. These appeared after two weeks of antiflllgal therapy. d. Residual cavity in the left upper lobe. radiographically stable after 45 days of antifungal therapy. e. This cavity persisted for four months. The irregular piece of necrotic tissue seen in the cavity contained lung structures, identifying it as a sequestrum of lung tissue.
gil/us infection may be highly variable and nonspecific (23). However, similar experience with 4 patients with leukemia who had air crescents seen radiographically and were SUbsequently proved to have vasoinvasive Aspergillus indicates the air crescent sign in the immunocompromised host to be consistent with the diagnosis of pulmonary aspergillosis. When the air crescent sign is seen, aggressive measures should be undertaken to establish the diagnosis and appropriate antifungal therapy initiated. REFERENCES 1.
Hutter RVP. Collins HS:
The occurrence of opportunistic
fungus infections in a cancer hospital. Part II. Lab Invest 11:1035-1045. Nov 1962 2. Bodey GP: Fungal infections complicating acute leukemia. J Chronic Dis 19:667--687, Jun 1966 3. Young RC. Bennett JE, Vogel Cl, et al: Aspergillosis. The spectrum of the disease in 98 patients. Medicine 49: 147 -173. Mar
1970 4. Mirsky HS. Cuttner J: Fungal infection in acute leukemia. Cancer 30:348-352, Aug 1972 5. Meyer RD. Young LS. Armstrong 0, et al: Aspergillosis complicating neoplastic disease. Am J Med 54:6-15. Jan 1973 6. Williams OM, Krick JA. Remington JS: Pulmonary infection in the compromised host. Part I. Am Rev Respir Dis 114:359-394, Aug 1976 7. Pennington JE: Successful treatment of aspergillus pneumonia in hematologic neoplasia. N Eng J Med 295:426-427, 19 Aug 1976
:20
ANNE
McB. CURTIS AND OTHERS
October 1979
2a,b
c,d
FIG. 2. CASE III. a. Perihilar infiltrates with a single. faint air crescent on the left that developed 12 days after the onset of intermittent hemoptysis. b. Faint air crescent in the left midlung zone. c. Radiograph obtained 24 hours later demonstrates multiple air crescents on the left as well as increasing nodular infiltrates on the right. d. Multiple air crescents 24 hours later. (Part e is on facing page.)
8. Aisner J. Schimpff SC. Wiernik PH: Treatment of invasive aspergillosis: relation of early diagnosis and treatment to response. Ann Intern Med 86:539-543. 1977 9. Bragg DG. Janis B: The radiographic presentation of pulmonary opportunistic inflammatory disease. Radiol Clin North Am 11: 357-369. Aug 1973 10. Williams DM. Krick JA. Remington JS: Pulmonary infection in the compromised host. Part II. Am Rev Respir Dis 114:593-627. Sep 1976
11. Evans WA Jr: Echinococcus cyst of the lung. Radiology 40: 362-366. Apr 1943 12. Stivelman BP. Malev M: Rasmussen aneurysm: its roentgen appearance; report of a case with necropsy. JAMA 110:1829 1831. 28 May 1938 13. Weens HS. Thompson EA: The pulmonary air meniscus. Radiology 54:700-705. May 1950 14. Felson B: Chest roentgenology. Philadelphia. Saunders. 1973. p 327
Vol 133
AIR CRESCENT SIGN OF INVASIVE ASPERGILLOSIS
21
Diagnostic Radiology
2e
Fig. 2. e. Two lesions which had crescentic cavitation at the periphery are seen in this gross specimen. Note the vascular thrombosis (arrow). The rule is 1 cm in length.
15. Cubillo-Herguera E, McAlister WH: The pulmonary meniscus sign in a case of bronchogenic carcinoma. Radiology 92: 1299-1300, May 1969 16. Bobrowitz 10: Round densities within cavities. Lung lesions simulating the pathognomonic roentgen sign of echinococcus cyst. Am Rev Tuberc 50:305-312, Oct 1944 17. Bard R, Hassani N: Crescent sign in pulmonary hematoma. Respiration 32:247-251, 1975 18. Bahk YW, Shinn KS, Byung SC: The air meniscus sign in sclerosing hemangioma of the lung. Radiology 128:27-29, Jul 1978 19. Goldberg B: Radiological appearances in pulmonary aspergillosis. Clin Radiol (Lond) 13:106-114. Apr 1962 20. Landrigan PL, Wasty G, Nigam S: Pulmonary aspergillosis: report of seven cases. Canad Med Ass J 98:642-645. 30 Mar 1968
21. Aslam PA, Eastridge CEo Hughes FA Jr: Aspergillosis of the lung-an eighteen-year experience. Chest 59:28-32, Jan 1971 22. Burke PS, Coltman CA Jr: Multiple pulmonary aspergillomas in acute leukemia. Cancer 28:1289- 1292, Nov 1971 23. Orr DP, Myerowitz RL. Dubois PJ: Patho-radiologic correlation of invasive pulmonary aspergillosis in the compromised host. Cancer 41:2028-2039, May 1978
G. J. W. Smith. M.D. Department of Pathology Yale University School of Medicine New Haven, Conn. 06510
Air Crescent Sign of Invasive Aspergillosis 1 Anne MeS. Curtis, M.D., G. J. Walker Smith, M.D., and Carl E. Ravin, M.D.2
Pulmonary infection in Immunocompromised patients Is frequently difficult to diagnose. Therapy for the more common pathogens differs greatly from that for infection with unusual opportunistic organisms. However, neither of these Infectious agents offers specific radiographic signs. The authors report on 4 patients with acute leukemia and Invasive aspergillosis whose radiographs demonstrated a distinctive feature of one or more air crescents within an area of pulmonary infiltrate. Autopsy studies correlated the radiographic changes with an infection due to Aspergillus species fungi. While the sign is not pathognomonic for Aspergillus infection, seen in a suitable host, it would suggest the possibility of invasive aspergillosis. INDEX TERMS: Aspergillosis. Immunity. Leukemia. complications and sequelae. Lungs. infection. (Lungs. fungus infection. 6[01.205). (Lungs. Aspergillus infection, 6[01.2056). (Lungs. immune deficiency with pneumonia.
6[0].251) Radiology 133:17-21. October 1979
HE immunologically compromised patient with Aspergillus infection. especially in the presence of hematologic malignancy, continues to pose a significant problem associated with hig, morbidity and mortality (1-6). Recent evidence suggests that early treatment with amphotericin B may lead to increased survival in this patient poputation (1-8). Unfortunately, this drug has significant side effects. Therefore the diagnosis should be definite or strongly suspected prior to initiation of therapy. Establishing the diagnosis of invasive aspergillosis frequently requires aggressive evaluation, including lung biopsy using transbronchial. percutaneous, or open thoracotomy techniques. While specific opportunistic infections may offer relatively characteristic radiographic findings (9), often the various bacterial, fungal, viral, and protozoan pathogens manifest overlapping and therefore nonspecific clinical and radiographic appearances (6. 10). Any radiographic feature which would suggest Aspergillus infection as opposed to any other infectious agent would be helpful in supporting aggressive diagnostic and therapeutic measures in these critically ill patients. We recently observed 3 cases of invasive aspergillosis complicating leukemia in which the radiographic sign of single or multiple air crescents was noted to develop within patchy or nodular chest infiltrates. A fourth patient with aspergillosis had an anatomical lesion which correlates well with radiographic air crescents. Although the sign is not entirely specific for Aspergillus, it is sufficient to strongly suggest the diagnosis.
T
disease or following chemotherapy. All had received chemotherapy during or prior to the onset of infection. Steroid therapy had been given to 1 patient intermittently and to another continuously. All had persistent spiking fevers in spite of broad spectrum antibiotic coverage for both gram-negative and qrarn-positive bacterial organisms. In 2 patients, rib and/or pleuritic pain developed antecedent to the pulmonary infiltrates (TABLE I). The diagnosis of invasive pulmonary aspergillosis was not established premortem in any patient. In only 1 patient was premortem sputum positive for Aspergillus. Two patients had negative transbronchial biopsies and brushings on both smears and subsequent cultures. No patient had blood cultures positive for Aspergillus. The precipitin titers to Aspergillus rose appropriately, i.e., by a fourfold increase in 2 of the patients tested. In spite of the difficulty in establishing the diagnosis of Aspergillus infection, it was strongly suspected in 3 of 4 patients, and 2 of these 3 received appropriate antifungal therapy with at least amphotericin B. Two patients died as a direct result of Aspergillus infection with massive hemoptysis, one despite 10 days of therapy with amphotericin Band 5-fluorocytosine. A third patient died of respiratory failure, probably due primarily to Aspergillus pneumonia. A fourth patient survived the acute pulmonary infection and received amphotericin B for approximately two months. In this case, the lesions stabilized or regressed somewhat, but the chest radiograph never reverted to normal (Fig. 1).
MATERIALS AND METHODS
Radiological Features
All 4 patients had acute leukemia, and all were leukopenic at the time of infection either as a direct result of
Two of the 4 patients initially presented either with single
1 From the Departments of Diagnostic Radiology (AMcBC. C.ER) and Pathology (GJW.S.), Yale University School of Medicine. New Haven. Conn. Received Sept. 25. 1978; accepted and revision requested Nov. 24; revision received Apr. 25. 1979. 2 Present address: Department of Radiology. Duke University Medical Center. Durham, N. C. 27710. as
17
18
ANNE
MeS.
TABLE
CASE
I II III
IV • ALL + AML
CURTIS AND OTHERS
October 1979
I: CLINICAL SUMMARY
Diagnosis
Pleuritic Pain
Hemoptysis
ALL·. relapse AML +• relapse AML. initial AML. initial
Present Present Absent Absent
Present Absent Present Absent
Precipitin Titres
1:32 1:32 Not done Not done
Sputum or Biopsy
Antifungal Therapy
o o
10 days 45 days
+ o
= acute lymphocytic leukemia = acute myelogenous leukemia
or multiple nodules in both lungs. A predilection for the upper lobes was not noted. A third patient presented with bilateral patchy pneumonic infiltrates and the fourth initially had an interstitial pattern progressing to consolidation. Three patients were seen with crescent shaped radiolucencies surrounding or within the preexisting parenchymal densities from one day to three weeks following the development of the initial abnormality (Fig. 2). There were no radiographs obtained in the fourth patient during the three days prior to death, but necrotic lesions with peripheral circumferential cavitation were evident at autopsy. The development of air crescents was not associated either with recovery from the leukopenic state or improved survival. None of the patients were examined in the supine or decubitus positions to see if the lucencies changed shape or location with a corresponding change in position. Postmortem Features
At autopsy, all 4 patients demonstrated multiple focal lesions characterized by central necrosis and peripheral crescentic or circumferential cavitation. In 2 patients the lesions grossly resembled white infarcts. Large areas of hemorrhage surrounded these lesions in 3 of the 4 cases and were almost certainly a direct complication of the fungal infection. Microscopically in all 4, the solid material within the cavities contained necrotic tissue and fungal elements. Masses of mycelia as seen in aspergilloma were not noted. In each case fungal invasion of the vessels within these necrotic lesions was demonstrated, a finding not observed with mycetoma. Special histochemical techniques were useful in demonstrating a residual vascular and airway framework within the necrotic sequestrum. This was particularly true in the patient who died four months following Aspergillus infection. In the patient who underwent open lung biopsy, the necrotic foci were present at the center of a much more extensive zone of pneumonic consolidation, the periphery of which contained no fungi. In retrospect, wedge biopsy from this peripheral zone of induration accounted for the false-negative study. No patient demonstrated evidence of Aspergillus infection outside of the lung. DISCUSSION
To produce an air crescent, all that is required is that air be sandwiched between a radiodense parenchymal lesion
and the surrounding lung structures. as with an intracavitary fungus ball, intralesional air in a cavitating carcinoma, or an abscess cavity. Thus, many entities having little in common have been reported to produce air crescents: echinococcal cyst, tuberculosis. Rasmussen aneurysm in a tuberculous cavity, other lung abscesses, malignancies such as carcinoma, bronchial adenoma and sarcoma, hematoma, hamartoma, mycetoma, and most recently, sclerosing hemangioma (11-18). A review of the literature suggests that the mycetoma of Aspergillus is the most common cause of the air crescent sign (14, 19-21). While other authors have described the air crescent sign in association with Aspergillus infections in patients with leukemia, they have unfortunately referred to these lesions as mycetomas (5, 21, 22). In the vasoinvasive form of pulmonary aspergillosis, as seen in all 4 of our patients, thrombosis of vessels and infarction of the central portion of the inflammatory focus occur. With retraction of the infarcted center or resorption of necrotic tissue at the periphery, a sequestrum of devitalized lung tissue infiltrated with fungi is formed. A subsequent filling lucency by air of the space between the sequestrum and peripheral lung tissue results in the air crescent seen radiographically. The morphologic differentiation between a fungus ball and necrotic tissue invadedby fungi may be made using elastic and/or reticulin fiber stains. These techniques allow visualization of vascular and airway structures within the area of necrosis. Earlier reports of air crescents in patients with leukemia and pulmonary aspergillosis probably represent cases similar to ours with sequestra rather than mycetoma as the anatomical basis of formation. The incidence of air crescent formation is not known. During the 20-month period when our 4 patients were observed, there were 25 cases of proved or strongly suspected pulmonary aspergillosis in immunocompromised hosts at our institution. This suggests that, with increasing survivals of immunocompromised patients, the air crescent sign may emerge as an important tool in the diagnosis of pulmonary aspergillosis. FlJ1her observation and study are necessary to establish the specificity of the air crescent sign for vasoinvasive pulmonary aspergillosis in immunocompromised hosts. If the development of the air crescent sign depends on vascular invasion with lung infarction, then Candida and the phycomycetes including Mucor, Absidia, and Rhisopus might be expected to produce air crescents as well. The radiographic presentation of opportunistic Asper-
AIR CRESCENT SIGN OF INVASIVE ASPERGillOSIS
Vol 133
19
Diagnostic Radiology
1a-c
d,e Fig. 1. CASE II. a. PA chest radiograph showing bilateral upper lobe densities that developed one month after relapse. band c. Air crescents. demonstrated on tomography, were evident on the plain radiograph as well. These appeared after two weeks of antiflllgal therapy. d. Residual cavity in the left upper lobe. radiographically stable after 45 days of antifungal therapy. e. This cavity persisted for four months. The irregular piece of necrotic tissue seen in the cavity contained lung structures, identifying it as a sequestrum of lung tissue.
gil/us infection may be highly variable and nonspecific (23). However, similar experience with 4 patients with leukemia who had air crescents seen radiographically and were SUbsequently proved to have vasoinvasive Aspergillus indicates the air crescent sign in the immunocompromised host to be consistent with the diagnosis of pulmonary aspergillosis. When the air crescent sign is seen, aggressive measures should be undertaken to establish the diagnosis and appropriate antifungal therapy initiated. REFERENCES 1.
Hutter RVP. Collins HS:
The occurrence of opportunistic
fungus infections in a cancer hospital. Part II. Lab Invest 11:1035-1045. Nov 1962 2. Bodey GP: Fungal infections complicating acute leukemia. J Chronic Dis 19:667--687, Jun 1966 3. Young RC. Bennett JE, Vogel Cl, et al: Aspergillosis. The spectrum of the disease in 98 patients. Medicine 49: 147 -173. Mar
1970 4. Mirsky HS. Cuttner J: Fungal infection in acute leukemia. Cancer 30:348-352, Aug 1972 5. Meyer RD. Young LS. Armstrong 0, et al: Aspergillosis complicating neoplastic disease. Am J Med 54:6-15. Jan 1973 6. Williams OM, Krick JA. Remington JS: Pulmonary infection in the compromised host. Part I. Am Rev Respir Dis 114:359-394, Aug 1976 7. Pennington JE: Successful treatment of aspergillus pneumonia in hematologic neoplasia. N Eng J Med 295:426-427, 19 Aug 1976
:20
ANNE
McB. CURTIS AND OTHERS
October 1979
2a,b
c,d
FIG. 2. CASE III. a. Perihilar infiltrates with a single. faint air crescent on the left that developed 12 days after the onset of intermittent hemoptysis. b. Faint air crescent in the left midlung zone. c. Radiograph obtained 24 hours later demonstrates multiple air crescents on the left as well as increasing nodular infiltrates on the right. d. Multiple air crescents 24 hours later. (Part e is on facing page.)
8. Aisner J. Schimpff SC. Wiernik PH: Treatment of invasive aspergillosis: relation of early diagnosis and treatment to response. Ann Intern Med 86:539-543. 1977 9. Bragg DG. Janis B: The radiographic presentation of pulmonary opportunistic inflammatory disease. Radiol Clin North Am 11: 357-369. Aug 1973 10. Williams DM. Krick JA. Remington JS: Pulmonary infection in the compromised host. Part II. Am Rev Respir Dis 114:593-627. Sep 1976
11. Evans WA Jr: Echinococcus cyst of the lung. Radiology 40: 362-366. Apr 1943 12. Stivelman BP. Malev M: Rasmussen aneurysm: its roentgen appearance; report of a case with necropsy. JAMA 110:1829 1831. 28 May 1938 13. Weens HS. Thompson EA: The pulmonary air meniscus. Radiology 54:700-705. May 1950 14. Felson B: Chest roentgenology. Philadelphia. Saunders. 1973. p 327
Vol 133
AIR CRESCENT SIGN OF INVASIVE ASPERGILLOSIS
21
Diagnostic Radiology
2e
Fig. 2. e. Two lesions which had crescentic cavitation at the periphery are seen in this gross specimen. Note the vascular thrombosis (arrow). The rule is 1 cm in length.
15. Cubillo-Herguera E, McAlister WH: The pulmonary meniscus sign in a case of bronchogenic carcinoma. Radiology 92: 1299-1300, May 1969 16. Bobrowitz 10: Round densities within cavities. Lung lesions simulating the pathognomonic roentgen sign of echinococcus cyst. Am Rev Tuberc 50:305-312, Oct 1944 17. Bard R, Hassani N: Crescent sign in pulmonary hematoma. Respiration 32:247-251, 1975 18. Bahk YW, Shinn KS, Byung SC: The air meniscus sign in sclerosing hemangioma of the lung. Radiology 128:27-29, Jul 1978 19. Goldberg B: Radiological appearances in pulmonary aspergillosis. Clin Radiol (Lond) 13:106-114. Apr 1962 20. Landrigan PL, Wasty G, Nigam S: Pulmonary aspergillosis: report of seven cases. Canad Med Ass J 98:642-645. 30 Mar 1968
21. Aslam PA, Eastridge CEo Hughes FA Jr: Aspergillosis of the lung-an eighteen-year experience. Chest 59:28-32, Jan 1971 22. Burke PS, Coltman CA Jr: Multiple pulmonary aspergillomas in acute leukemia. Cancer 28:1289- 1292, Nov 1971 23. Orr DP, Myerowitz RL. Dubois PJ: Patho-radiologic correlation of invasive pulmonary aspergillosis in the compromised host. Cancer 41:2028-2039, May 1978
G. J. W. Smith. M.D. Department of Pathology Yale University School of Medicine New Haven, Conn. 06510
