eMedicine Specialties > Radiology > Chest
Aspergillosis, Thoracic
Updated: May 1, 2008
Introduction
Background
Pulmonary aspergillosis is a spectrum of mycotic diseases caused by the Aspergillus species, usually Aspergillus fumigatus.1,2 This intensely antigenic and ubiquitous soil fungus is commonly found in the sputum of healthy individuals. However, in susceptible hosts, its ability to invade the arteries and veins facilitates its hematogenous spread.
The development of disease and its histologic, clinical, and radiologic manifestations depend on the virulence and number of spores inhaled and, more importantly, on the patient's immune status.
Pulmonary aspergillosis may take any of 4 forms1,2 :
- Allergic bronchopulmonary aspergillosis (ABPA) is caused by a hypersensitivity reaction to the fungus and most commonly occurs in those with asthma.
- Saprophytic aspergillosis, or aspergilloma, is the most common form, which is noninvasive and involves colonization of preexisting cavities.
- Chronic necrotizing aspergillosis, also called airway-invasive or semi-invasive aspergillosis, is a chronic cavitary pneumonic illness that often affects patients with preexisting chronic lung disease.
- Angioinvasive aspergillosis affects immunocompromised patients and is often fatal.
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Asthma
Chronic Granulomatous Disease
Lung, Primary Tuberculosis
Pneumonia, Fungal
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CME Highlights of the United States and Canadian Academy of Pathology 2007 Annual Meeting: Pulmonary Pathology of Transplantation
Pathophysiology
A fumigatus exists in 2 forms: (1) conidiophores, the reproductive forms that produce and release thousands of spores, and (2) hyphae, which represent mature spores that are characterized by a 45º dichotomous branching pattern (see Images 1 and 2). The fungus grows widely in soil, water, and decaying vegetable or animal material. The spores are readily inhaled, and the fungus is a common commensal organism in the upper respiratory tract.
Most patients with pulmonary aspergillosis have either an underlying preexisting chronic lung disease or impaired immunity. Examples of preexisting chronic lung disease include bronchiectasis, chronic obstructive lung disease (COPD), and tuberculosis. Impaired immunity secondary to alcoholism, advanced age, poorly controlled diabetes mellitus, underlying malignancy, cirrhosis, malnutrition, sepsis, organ transplantation, or acquired immunodeficiency syndrome (AIDS), for example.3,4,5,6,7,8
ABPA represents a hypersensitivity reaction to A fumigatus in patients with long-standing asthma or cystic fibrosis. Excessive mucus production in association with impaired ciliary function leads to mucoid impaction of the airways. The plugs of inspissated mucus contain A fumigatus and eosinophils, but the organisms remain within the bronchial lumen; this feature differentiates ABPA from invasive aspergillosis.
Precipitating antibodies incite a type I acute hypersensitivity reaction with the subsequent release of immunoglobulin E (IgE) and immunoglobulin G (IgG). Immune complexes and inflammatory cells are then deposited within the bronchial mucosa. This deposition produces tissue necrosis and eosinophilic infiltrate, a type III reaction, and results in damage to the bronchial wall with the subsequent development of bronchiectasis. Patients may cough up mucus plugs, from which hyphal elements can be cultured or observed at microscopy.
The primary diagnostic criteria for ABPA include the following:
- Asthma, 84-96%
- Blood eosinophilia, 8-40%
- Elevated serum IgE levels
- Positive skin test results for A fumigatus
- Elevated serum levels of IgE and IgG specific for A fumigatus
- Presence of precipitating antibodies to A fumigatus
The primary radiologic criteria include fixed or transitory pulmonary infiltrates and central bronchiectasis as a late manifestation.9,10 A set of secondary criteria can sometimes be applied; these include the presence of A fumigatus mycelia in the sputum, the expectoration of brown sputum plugs, and a delayed cutaneous reaction to A fumigatus antigen.
ABPA can be staged by using the following clinical and radiologic criteria:
- Stage I – Acute presentation with 6 of the 8 primary diagnostic criteria listed above
- Stage II – Resolving pulmonary infiltrates with decreasing IgE levels leading to remission
- Stage III – Recurrence of acute symptoms after a period of remission
- Stage IV – Steroid dependency
- Stage V – Irreversible lung damage leading to fibrosis
In the saprophytic form (ie, aspergilloma), noninvasive colonization of a preexisting cavity, cyst, bulla, or ectatic bronchus occurs. The most common underlying conditions are tuberculosis, sarcoidosis, and bronchiectasis. Others include cystic fibrosis, ankylosing spondylitis, bronchogenic cysts, pneumoconiosis, pulmonary sequestration, cavitating malignancy, and pneumatoceles secondary to Pneumocystis carinii pneumonia.
Histologically, the aspergilloma represents a fungal ball, or mycetoma, which consists of a masslike conglomerate of intertwined hyphae intermingled with fibrin, cellular debris, mucus, and other blood products. This mycetoma may calcify in an amorphous or ringlike fashion. Elevated serum precipitin levels are present in approximately 50% of the patients.
Chronic necrotizing aspergillosis, or semi-invasive aspergillosis, is an indolent disease that affects patients with mild immunosuppression due to chronic debilitating illness, particularly those with COPD. Other recognized predisposing illnesses include alcoholism, advanced age, and prolonged steroid administration. Bronchiolitis and bronchopneumonia develop, with slowly progressive cavitating consolidation predominating in the upper lobes (see Images 7 and 8). This consolidation may be indistinguishable from tuberculosis. Histologically, a proliferation of organisms within the alveolar spaces, intra-alveolar hemorrhage, and bronchial wall invasion that leads to tissue necrosis with microabscess formation are present, but no angioinvasion is observed.
Invasive aspergillosis is the most common fungal pulmonary infection in severely immunocompromised patients, particularly those with reticuloses. Transplant recipients are also at particular risk.6,7 The spores proliferate in the airways; this proliferation leads to transbronchial angioinvasion that causes hemorrhagic infarction. These areas may become cavitated and contain a devitalized sequestrum of infected lung; moreover, these areas can mimic a mycetoma. Also, the fungus can disseminate systemically in approximately 33% of cases and affect the heart, brain, kidneys, liver, spleen, thyroid, and gastrointestinal tract.
A fumigatus may also infect the pleura, causing an empyema in patients with pulmonary tuberculosis or bronchopleural fistulae. Occasionally, A fumigatus may secondarily infect an existing bacterial empyema.
Frequency
United States
Approximately 1-2% of asthmatic patients and 10% of patients with cystic fibrosis have ABPA. Aspergillomas are reported to account for 0.02% of hospital admissions. The precise incidence of chronic necrotizing aspergillosis is unknown, but it is thought to be increasing.
The number of patients with invasive aspergillosis has substantially increased. One of the reasons for this increasing incidence is the development of new intensive chemotherapy for leukemia, lymphoma, and myeloma, as well as the increasing numbers of solid organ transplantations. Invasive pulmonary aspergillosis (IPA) is reported in 5% of bone marrow transplant recipients, 3-9% of renal transplant recipients, and 1-5% of heart and/or lung or liver transplant recipients.
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International
Aspergillomas are complications in 15-20% of patients with lung cavities 2 cm or larger. The incidence of invasive aspergillosis in AIDS patients is 1-12% worldwide. In the United Kingdom, the incidence is estimated to be 4-5%.
Mortality/Morbidity
The mortality and morbidity rates with pulmonary aspergillosis depend on the type of disease.1,2,11
- In most patients, ABPA responds to steroids, but a small proportion of cases are refractory to treatment and progress to stage V disease.
- Approximately 10% of mycetomas resolve spontaneously. Massive hemoptysis, defined as the expectoration of more than 600 mL of blood in 48 hours, is a well-recognized complication.12,13 Most patients are not candidates for surgery and are treated conservatively. However, the mortality rate in these patients can be as high as 50-55%, compared with a 1-23% surgical mortality rate.
- Chronic necrotizing aspergillosis has a significant morbidity rate, and, if left untreated, this condition has a significant mortality rate. However, the precise incidences are unknown. The slow progression of clinical and radiologic findings may contribute to a delay in diagnosis.
- The prognosis in invasive aspergillosis is uniformly poor, and the mortality rate is high. Early diagnosis and prompt treatment are essential in determining survival.
Sex
The male-to-female incidence is 3:1.
Age
Pulmonary aspergillosis mostly affects adults aged 20-90 years.
Anatomy
Most mycetomas derive their blood supply from the bronchial arteries. The bronchial arteries not only perfuse the bronchi but also contribute blood supply to the mid esophagus, diaphragm, mediastinal visceral pleura, and vasa vasorum of the aorta and pulmonary arteries. In addition, an occasional contribution to the thoracic spinal cord and the myocardium may be present. Knowledge of the bronchial arterial supply is important to prevent potentially catastrophic complications from arterial embolization of mycetomas.
Presentation
Acute clinical symptoms in ABPA include a low-grade fever, wheezing, productive cough, weight loss, malaise, headaches, and chest pain. Patients with ABPA also have a history of recurrent pneumonia. However, patients with aspergillomas are frequently asymptomatic. The most common clinical manifestation is hemoptysis, which may be life threatening.
Symptoms of chronic necrotizing aspergillosis are often insidious at onset and nonspecific. These symptoms include a productive cough, fever, and constitutional upset, and they represent acute tracheobronchitis, bronchiolitis, or bronchopneumonia. Hemoptysis occurs in only 15% of patients.
The angioinvasive form often causes nonspecific constitutional symptoms that make clinical diagnosis difficult. Patients often have an unremitting fever and pleuritic chest pain, which may mimic the findings of pulmonary embolism.
Aspergillus spp cultured in the aspirates/sputum of patients with COPD are generally considered contaminants.3 However, despite poor documentation of the IPA incidence in this population, patients with severe COPD may be at higher risk of developing IPA. There are some data to suggest that COPD is the underlying disease in 1% of patients with IPA. Because the clinical diagnosis of IPA in patients with COPD is often difficult to ascertain, it is based on a combination of clinical findings, high-resolution computed tomography (HRCT) findings, microbiologic results, and, occasionally, serologic tests.1,2
Bulpa and associates analyzed the literature reports of 56 patients with IPA and COPD and found that 77% were receiving corticosteroids on hospital admission.3 Breathlessness with wheezing was present in 79% of patients, whereas fever occurred in 38.5%, and chest pain and hemoptysis were unusual. In this group, the median delay between symptoms and diagnosis was 8.5 days. The prognosis in the group was extremely poor, with a mortality of 95% despite invasive ventilation and antifungal treatment. The authors suggested that the outcome in these patients could perhaps have been improved by more rapid diagnosis and prompt therapy.
Preferred Examination
Chest radiography is an initial examination of choice in patients with respiratory symptoms or suspected pulmonary disease.9,10 However, many different causes of bronchiectasis, including ABPA, cannot be accurately diagnosed on chest radiographs. Also, radiographic features of pulmonary aspergillosis are generally nonspecific.
Although the CT scan features of ABPA are not specific, the demonstration of bronchial dilatation, wall thickening, and centrilobular nodules in an asthmatic patient should suggest the diagnosis.14 The demonstration of a mobile mass within a cavity on supine and prone scans is virtually diagnostic of a mycetoma. The CT scan appearances of chronic necrotizing aspergillosis are also nonspecific, but CT does provide useful information regarding the extent of pulmonary disease and any associated pleural thickening. CT scan findings in angioinvasive aspergillosis are more specific, and the presence of nodules with a halo of ground-glass attenuation in the appropriate clinical setting allows confident diagnosis.
Limitations of Techniques
The appearances of the different types of thoracic aspergillosis are nonspecific, and a wide variety of lesions can mimic an aspergilloma. Examples of these include chronic necrotizing aspergillosis, angioinvasive aspergillosis, a tuberculous cavity with a Rasmussen aneurysm, cavitating bronchogenic carcinoma, lung abscess, hematoma, and P carinii pneumonia. Similarly, bronchial dilatation has a variety of causes.
Differential Diagnoses
Asthma
Bronchiectasis
Bronchogenic Cyst
Pneumonia, Pneumocystis Carinii
Wegener Granulomatosis, Thoracic
Other Problems to Be Considered
Differential diagnosis of cavitating upper lobe consolidation
Amyloidosis
Chronic necrotizing aspergillosis
Mucormycosis
Mycobacterium avium-intracellulare complex (MAIC) infection
Sarcoidosis
Tuberculosis
Viral and mycoplasmal pneumonia
Differential diagnosis of multiple pulmonary nodules
Angioinvasive aspergillosis
Hemorrhagic metastases
Infection with Mucorales fungi, Candida spp, herpes simplex virus, or cytomegalovirus
Wegener granulomatosis
Kaposi sarcoma
Differential diagnosis of tree-in-bud appearance
Okada and associates analyzed the clinical/pathologic findings in 553 patients undergoing HRCT with 2 patterns of centrilobular opacities with a tree-in-bud appearance.14 Their findings revealed that centrilobular nodules with a tree-in-bud appearance and bronchial wall thickening were observed in patients who were carriers of human T-lymphotropic virus type 1, Mycoplasma pneumoniae, Mycobacterium tuberculosis, MAIC, M kansasii, allergic bronchopulmonary aspergillosis, diffuse panbronchiolitis, and diffuse aspiration bronchiolitis.
The authors also noted that ill-defined centrilobular nodules of ground-glass attenuation were frequently seen in patients with conditions such as subacute hypersensitivity pneumonitis, metastatic calcification, Churg-Strauss syndrome, microscopic polyangiitis, systemic lupus erythematosus, and respiratory bronchiolitis-associated interstitial lung disease.14 Okada et al concluded that knowledge of the 2 centrilobular patterns is of proven benefit in the differential diagnosis when a tree-in-bud appearance is encountered.
Radiography
Findings
In ABPA, chest radiographic appearances include the following: (1) fleeting alveolar subsegmental or lobar infiltrates, which are usually bilateral (65%) and predominant in the upper lobes (50%); (2) central 1-2-cm ring shadows that represent varicose or cystic bronchiectasis; and (3) tram-link bronchial walls due to edema.1,9,10 The second-order bronchi may become plugged with mucus, and they may be visible as 2.5- to 6-cm long V- or Y-shaped branching tubular opacities that may grow over time and persist for months; this is the so-called finger-in-glove sign (see Image 3).
Other features include lobar consolidation, atelectasis, postobstructive pneumonia, cavitation, air trapping, and parenchymal scarring or fibrosis, all of which are more pronounced in the upper lobes. Focal pleural thickening is also reported. Occasionally, mycetomas develop in ectatic bronchi.
The characteristic chest radiographic appearance of an aspergilloma is that of a round or oval mass with the opacity of that of a soft-tissue mass. Often, an adjacent crescent-shaped air space (ie, the air-crescent sign) separates the fungal ball from the cavity wall (see Image 6). The mycetoma may rarely contain amorphous or rimlike calcification. The fungal ball is usually mobile and moves when the patient changes position. Often, extensive adjacent apical pleural thickening may be present; this finding may herald the development of the mycetoma.
The radiologic manifestations of chronic necrotizing aspergillosis include unilateral or bilateral segmental areas of consolidation that are predominant in the upper lobes; frequently, these progress to cavitation. Pleural thickening is also a recognized feature.
The most common chest radiographic appearance of invasive aspergillosis is that of patchy areas of consolidation, which progress despite the use of broad-spectrum antibiotics. Multiple nodules and peripheral wedged-shaped lesions due to hemorrhagic infarcts are also observed as the disease progresses. These frequently become cavitated, and an air-crescent sign that mimics mycetoma may also be observed.
Degree of Confidence
The many different causes of bronchiectasis, including ABPA, cannot be accurately diagnosed with radiographs (see Differentials and Other Problems to Be Considered). Also, the radiographic features of pulmonary aspergillosis are generally nonspecific.
Cortese et al were able to show the limited usefulness of conventional chest radiographs in the diagnosis of ABPA in patients with cystic fibrosis.9 The authors found the most significant abnormalities were nonspecific, and they were commonly seen in cystic fibrosis without ABPA that persisted after treatment in most cases.
False Positives/Negatives
An air-crescent sign may occur in the following: aspergilloma, chronic necrotizing aspergillosis, angioinvasive aspergillosis, tuberculous cavity with a Rasmussen aneurysm, cavitating bronchogenic carcinoma, lung abscess, hematoma, and P carinii pneumonia.
Computed Tomography
Findings
Bronchiectasis and peribronchial thickening are the most common CT findings in ABPA.15,16 Appearances tend to be more severe than in those of chronic uncomplicated asthma. ABPA typically involves the segmental and subsegmental bronchi, particularly those in the upper lobes. However, studies have shown that central bronchiectasis simply indicates long-standing severe inflammation; as a marker, it is not as specific for ABPA as was once thought.
High-attenuating mucoid impaction, present in as many as 30% of patients, is a characteristic finding. Occasionally, lobar or segmental atelectasis may be a feature. Mucus plugging of the small airways can be observed on high-resolution CT scans, with resultant centrilobular nodularity and the tree-in-bud sign.14 Abnormalities of lung attenuation due to either mosaic perfusion or air trapping may also be identified. Scans obtained during expiration are useful in differentiating the findings in this instance.
The CT scan and chest radiographic appearances of an aspergilloma are similar. The fungal ball is seen as a mass of soft-tissue attenuation within a pulmonary cavity. An anterior air crescent is visible if the patient is supine (see Images 6 and 8). The mobile nature of the mass can be demonstrated by scanning the patient in the prone position; the fungal ball falls to the dependent portion of the cavity. The cavity wall and adjacent pleura are frequently thickened, although these findings have been shown to resolve with successful treatment or with the spontaneous resolution of the infection.
CT scan findings in chronic necrotizing aspergillosis include areas of chronic progressive peripheral consolidation, multiple nodular opacities, and low-attenuating masslike lesions. Abnormalities may be unilateral or bilateral, with an upper-lobe predilection. Cavitation is a common feature, and this often leads to the development of an intracavitary segment of sequestrated lung, which may mimic a mycetoma. Extension into the chest wall and mediastinum are also described.
CT scan findings of angioinvasive aspergillosis include multiple nodules associated with a halo of ground-glass attenuation, which represents adjacent hemorrhage, and pleural-based wedge-shaped areas of consolidation, which correspond to hemorrhagic infarcts. The air-crescent sign may be observed in the recovery phase.
Degree of Confidence
Although the CT scan features of ABPA are not specific, the demonstration of bronchial dilatation, wall thickening, and centrilobular nodules in an asthmatic patient should suggest the diagnosis. The presence of ABPA is even more likely if bronchiectasis is severe, affects 3 or more lobes, and has a central distribution. Many pulmonary lesions become cavitated; however, the demonstration of a mobile mass within a cavity on supine and prone scans is virtually diagnostic of a mycetoma.
CT scan appearances of chronic necrotizing aspergillosis are nonspecific, although CT scanning does provide accurate information regarding the distribution and extent of pulmonary disease and any associated pleural thickening. CT scan findings in angioinvasive aspergillosis are more specific, and the presence of nodules with a halo of ground-glass attenuation in the appropriate clinical setting allows confident diagnosis.
False Positives/Negatives
The causes of false-positive and false-negative results are the same as those with chest radiography, as discussed in Radiograph, False Positives/Negatives.
Angiography
Findings
See Intervention, below.
Intervention
Massive hemoptysis may complicate a mycetoma. Surgical resection of the cavity is the treatment of choice. Contraindications to surgery include bilateral advanced lung disease, large transpleural blood vessels, failure to identify the bleeding site, and continued hemoptysis after previous surgery. Bronchial artery embolization is a valuable technique in patients with persistent hemoptysis who are not surgical candidates.
Before bronchial artery embolization is attempted, angiography is performed to assess the bronchial arterial anatomy, nonbronchial systemic blood supply to the mycetoma, and presence and extent of any contribution of blood supply from the pulmonary artery (see Images 11 and 12). The technique involves selective bronchial artery catheterization with a femorovisceral 5-French end-hole catheter. After a preliminary bronchial angiogram study is performed, the catheter is securely inserted into the bronchial artery to be embolized. A coaxial catheter may be required for more selective and more distal placement.
Various embolic agents can be used; the simplest material is polyvinyl alcohol (PVA), a particulate agent that is available in a variety of sizes. Because mycetomas can derive their blood supply from the intercostal arteries, the thyrocervical trunks and pulmonary arteries may also need to be selectively embolized (see Images 13-18).
Percutaneous CT- or fluoroscopically guided intracavitary injection of a paste containing glycerin and amphotericin B or other fungal agents has been successful in the treatment of aspergillomas and chronic necrotizing aspergillosis. The fungal ball partially or completely resolved in 75% of patients. The intracavitary instillation of sodium or potassium iodide has also been used successfully in the treatment of hemoptysis in patients who are not surgical candidates.13
Medicolegal Pitfalls
- Chest pain may occur, particularly after embolization of an intercostal artery.
- Rarely, mild dysphagia may occur as a result of an interruption of blood supply to the mid esophagus. This dysphagia is self-limiting and resolves spontaneously.
- Transverse myelitis and bronchial necrosis are the most serious complications; fortunately, these are rare.
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Special Concerns
- Most case reports of transverse myelitis are historical and were most probably related to contrast agent toxicity.
- Bronchial necrosis is more frequently encountered when absolute alcohol is used for embolization.
- Nontarget embolization leading to infarction is also reported. This complication is less likely to occur when a superselective approach with an end-hole catheter is used.
Multimedia
Media file 1: Microscopic slide of lung tissue. This image shows broad hyphae, which branch at acute angles.
Media file 2: Section of a blood vessel. This image shows branching fungal hyphae that invade the vessel wall.
Media file 3: Posteroanterior chest radiograph in a patient with allergic bronchopulmonary aspergillosis. This image shows branching finger-in-glove tubular opacities in the left lower lobe (ie, retrocardiac location) due to mucus plugging of ectatic bronchi.
Media file 4: High-resolution computed tomography scan (same patient as in Image 3). This image shows peribronchial thickening and apparent nodular opacities in the lower lobes due to bronchiectasis with mucoid impaction.
Media file 5: High-resolution computed tomography scan shows central bronchiectasis in a patient with allergic bronchopulmonary aspergillosis. The patient had previously undergone left upper lobectomy for severe bronchiectasis.
Media file 6: Posteroanterior chest radiograph shows multiple aspergillomas in a patient with tuberculosis. Note the numerous air crescents.
Media file 7: Posteroanterior chest radiograph shows chronic, cavitating, upper lobe consolidation in a patient with long-standing fibrosing alveolitis; this finding is consistent with chronic necrotizing aspergillosis. Aspergillus fumigatus was cultured from the sputum and percutaneous aspiration samples.
Media file 8: Axial computed tomography scan obtained at the level of the aortic arch (same patient as in Image 7). This image shows a masslike consolidation, with a developing air crescent adjacent to the central sequestrated lung, which mimics a mycetoma.
Media file 9: Axial nonenhanced computed tomography scan obtained through the lower thorax. This image shows a subtle left lower lobe nodule due to invasive aspergillosis in a renal transplant recipient. The patient had multiple other nodules, one of which was examined at biopsy to confirm the diagnosis. Note the esophagus has thickened walls secondary to concurrent cytomegaloviral infection.
Media file 10: Posteroanterior chest radiograph shows a left upper lobe mycetoma with an indwelling catheter for drug delivery.
Media file 11: Flush thoracic aortogram obtained in a patient with a mycetoma and hemoptysis. This image shows anastomosis involving the bronchial artery, intercostal arteries, and pulmonary artery. Note also the anastomosis with blood vessels from the lateral thoracic wall.
Media file 12: Right bronchial angiogram in a 40-year old man with a known right lung mycetoma (arrow). This image shows extensive anastomosis between the right bronchial artery and the intercostal arteries.
Media file 13: This posteroanterior chest radiograph was obtained in a 36-year-old woman who was previously treated for pulmonary tuberculosis (same patient in Images 13-18). The patient had a left upper lobe mycetoma and presented with recurrent life-threatening hemoptysis. The disease failed to respond to systemic and local antifungal therapy.
Media file 14: Angiogram of the left thyrocervical trunk in a 36-year-old woman with a left upper lobe mycetoma and a past history of being treated for pulmonary tuberculosis (same patient in Images 13-18). This image shows that the blood supply to the mycetoma is derived from the thyrocervical trunk.
Media file 15: Delayed-phase angiogram in a 36-year-old woman with a left upper lobe mycetoma and a past history of being treated for pulmonary tuberculosis (same patient in Images 13-18). This image shows anastomosis of the branches of the thyrocervical trunk with the left pulmonary artery at the site of the mycetoma.
Media file 16: Angiographic series of the thyrocervical trunk in a 36-year-old woman with a left upper lobe mycetoma and a past history of being treated for pulmonary tuberculosis (same patient in Images 13-18). This image was obtained after embolization and shows a pruned-tree appearance of the arterial trunks. Note that the left internal mammary artery had to be sacrificed.
Media file 17: Angiogram of the right fifth intercostal artery in a 36-year-old woman with a left upper lobe mycetoma and a past history of being treated for pulmonary tuberculosis (same patient in Images 13-18). This image shows that the artery meanders around to the left hemithorax and supplies the left-sided mycetoma.
Media file 18: Angiogram of the right 5th intercostal artery in a 36-year-old woman with a left upper lobe mycetoma and a past history of being treated for pulmonary tuberculosis (same patient in Images 13-18). This image shows the blind stump of the artery after embolization. When this article was written, the patient was alive and well and had had no further episodes of hemoptysis for more than 3 years.
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Keywords
pulmonary aspergillosis, Aspergillus fumigatus, A fumigatus, allergic bronchopulmonary aspergillosis, ABPA, saprophytic aspergillosis, aspergilloma, chronic necrotizing aspergillosis, airway-invasive aspergillosis, semi-invasive aspergillosis, angioinvasive aspergillosis, finger-in-glove sign, tree-in-bud sign, air-crescent sign
Contributor Information and Disclosures
Author
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.
Coauthor(s)
Sarah Al Ghanem, MBBS, Consulting Staff, Department of Medical Imaging, King Fahad National Guard Hospital, Riyadh, Saudi Arabia
Disclosure: Nothing to disclose.
Klaus L Irion, MD, PhD, Consulting Staff, The Cardiothoracic Centre Liverpool NHS Trust, The Royal Liverpool University Hospital, UK
Klaus L Irion, MD, PhD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR is a member of the following medical societies: British Medical Association, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.
Carolyn M Allen, MB, BCh, MRCP, FRCR, CCST, Consultant Radiologist, Department of Clinical Radiology, North Manchester General Hospital, UK
Carolyn M Allen, MB, BCh, MRCP, FRCR, CCST is a member of the following medical societies: Society of Thoracic Radiology
Disclosure: Nothing to disclose.
Medical Editor
Satinder P Singh, MD, Associate Professor of Radiology, Chief of Cardiopulmonary Radiology, Director of Cardiac CT, Director of Combined Cardiopulmonary and Abdominal Radiology, Department of Radiology, University of Alabama at Birmingham
Disclosure: Nothing to disclose.
Pharmacy Editor
Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
Managing Editor
Eric J Stern, MD, Professor of Radiology, Adjunct Professor of Medicine, Adjunct Professor of Medical Education and Biomedical Informatics, University of Washington School of Medicine; Director of Thoracic Imaging, Harborview Medical Center; Associate Medical Staff, Seattle Cancer Care Alliance
Eric J Stern, MD is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, European Society of Radiology, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.
CME Editor
Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.
Chief Editor
Barry H Gross, MD, Professor, Department of Radiology, University of Michigan Medical School; Professor, University of Michigan Cancer Center
Barry H Gross, MD is a member of the following medical societies: American College of Chest Physicians, American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Michigan State Medical Society, Physicians for Social Responsibility, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.