Granulomatous lesions are distinctive confined cellular aggregates that encompass a variety of disorders of different nature. In granulomatous lesions, the imaging presentation needs to be differentiated from tumors. In our outpatient consultations, we have misdiagnosed nodular disease as lung cancer for radiotherapy or chemotherapy; we have misdiagnosed inflammatory granuloma as tumor for surgery;
There were cases where lymphoma-like granuloma was misdiagnosed as inflammation for 10 years because of multiple lesions in both lungs and failure to treat other lesions appropriately after surgery, which eventually proved (pathologically) to be lymphoma; there were also cases where Langerhans granuloma in both lungs was misdiagnosed as metastases. This section focuses on the imaging manifestations of sarcoidosis that are more difficult to distinguish from tumors from diagnostic imaging, and it is worth noting that these manifestations are not the only manifestations of sarcoidosis.
I. Pathology of granulomatous lesions
Granuloma lesions can be divided into granuloma with epithelioid cells and granuloma without epithelioid cells according to the presence or absence of epithelioid cells. Granulomas with epithelioid cells have necrotic epithelioid cells and are mostly primary infectious lesions, such as tuberculosis and fungal infections. Necrotizing nodular granuloma, central bronchial granuloma, Wegener’s granuloma and necrotizing epithelioid granuloma occurring in rheumatoid arthritis are all infectious granulomas.
Granulomas can also be formed without the occurrence of necrotizing epithelioid cells, such as nodular disease and allergic diseases. Inflammatory granulomas formed by bacterial infections are mostly granulomas without epithelioid cells. The differential diagnosis of pathological histology of epithelioid granulomatous lesions is sometimes not easy, and the diagnosis is even more difficult via chest wall lung puncture.
(i) Nodular disease
It is an epithelioid nodule without caseous necrosis and can occur in the lung. The early stage is a mononuclear cell infiltrate of the lung parenchyma, which is a nonspecific alveolitis and further develops into granulomas. Granulomas may be distributed in the lung parenchyma and in the peribronchial and perivascular interstitium. In advanced granulomas, a fibrous envelope is formed around the granuloma, and the peripheral part of the old granuloma produces fibrous tissue with hyaline degeneration, with a few giant cells remaining in the center, or it may be completely replaced by fibrous tissue. In nodal disease, involvement of hilar and mediastinal lymph nodes is more common than pulmonary involvement, and pathologic changes include cellular infiltration, granulomas, and fibrosis.
(B) Lymphoma-like granuloma
It is an angiocentric infiltrative granulomatous disease, also known as angiocentric lymphoma. The pathological changes are vascular-centered polymorphic cell infiltration and multifocal necrosis, and the infiltrating cells are mostly small lymphocytes, plasma cells, histiocytes and immune cells.
(C) Inflammatory granuloma
Inflammatory granulomas can be formed by bacterial and fungal infections, metaplasia, and other reactions. Granulomas are composed of inflammatory cells, macrophages, and in some cases, epithelioid cells. Exogenous alveolar inflammatory granuloma resembles nodular disease, but differs from nodular disease in that it does not usually involve the hilar and mediastinal lymph nodes.
(iv) Langerhans cell granuloma
Also known as eosinophilic granuloma. The early inflammatory lesions of Langerhans granuloma are eosinophilic, lymphocytic, and neutrophilic infiltrates centered on the fine bronchi, and Langerhans cells (Langerhans cells) and alveolar macrophages are seen in the alveolar lumen. The disease often involves small pulmonary arteries and veins. Interstitial fibrosis and small cysts occur in the late stages of the disease, which can involve the lungs and bones.
(E) Wegener’s granulomatosis (Wegener’s granulomatosis)
The basic lesion of Wegener’s granulomatosis is vasculitis and granuloma formation in small arteries and veins. The lesions often involve the bronchi and lungs and are necrotizing granulomas with polyangiitis. The granuloma is infiltrated by epithelioid cells, multinucleated giant cells, plasma cells, lymphocytes, and a few eosinophils. The central part of the granuloma may be necrotic and form a cavity. Bronchial granuloma may cause pulmonary atelectasis. The initial lesions may involve the upper respiratory tract, mainly in the nasal cavity, oral cavity and pharynx.
II. Imaging manifestations of granulomatous lesions
(A) Nodular disease
1. Overview Nodular disease lacks more characteristic clinical symptoms. Cough, shortness of breath, fever, and chest pain are the more common clinical symptoms, and many cases have no clinical symptoms and are found incidentally by chest examination. It is difficult to make a diagnosis of nodular disease based on clinical manifestations alone, and the finding of enlarged intrathoracic lymph nodes and intrapulmonary lesions by chest radiography and chest CT examination is the main basis to suggest the diagnosis of nodular disease.
For differential diagnosis, angiotensin-converting enzyme, blood calcium, urine calcium, serum ^y globulin, blood sedimentation, and alkaline phosphatase tests are sometimes required depending on the conditions. Patients with increased angiotensin-converting enzyme, high blood calcium and high urine calcium are mainly seen in active nodular disease. Increased serum Y-globulin, rapid sedimentation, and increased alkaline phosphatase are not specific for diagnosis, and these laboratory tests are often negative.
Bronchoscopy, supraclavicular lymph nodes, subcutaneous nodal biopsy and sometimes thoracoscopic biopsy are therefore the basis for confirming the diagnosis. In clinical practice, we have seen cases of bronchoscopy and thoracoscopy pathology reported as proliferative pulmonary tuberculosis, not excluding nodular disease, when diagnostic imaging and dynamic observation become an important basis for the diagnosis of nodular disease. Since there are certain limits to the imaging diagnosis of nodular disease, the diagnosis sometimes hovers between the diagnosis of lung cancer, lymphoma, metastases, tuberculosis and pneumonia.
The basic images of nodular disease are divided into intrathoracic lymph node enlargement, intrapulmonary lesions, pleural lesions and bronchial lesions.
(1) Enlarged intrathoracic lymph nodes: Enlarged intrathoracic lymph nodes are the most common imaging manifestation of nodular disease, and the literature reports that the number of cases of enlarged intrathoracic lymph nodes accounts for 77% of nodular cases. The author has reported that among 39 misdiagnosed cases of nodular disease, 23 cases had enlarged intrathoracic lymph nodes, accounting for 68.75% of the total number of cases. The most common sites of intrathoracic lymph node enlargement were the posterior superior vena cava lymph nodes, para-aortic lymph nodes, bronchial bifurcation and subbronchial bifurcation lymph nodes, with lymph node sizes ranging from 1.5 to 87.5 px.
Solitary anterior mediastinal lymph node enlargement was reported in the literature in only 10% of cases. Solitary posterior mediastinal lymph node enlargement is even rarer. Among the misdiagnosed cases of nodal disease reported by the author, there were no cases of solitary anterior and posterior mediastinal lymph node enlargement. Mediastinal lymph node enlargement combined with two hilar lymph node enlargement is a typical imaging manifestation of nodular disease, and the incidence has been reported in the literature to be 95%. Mediastinal multiple lymph node enlargement with hilar lymph node enlargement on one side accounted for 1.7%, and only mediastinal multiple lymph node enlargement without hilar lymph node enlargement was rare. The author reported 68.6% of the misdiagnosed cases with enlarged mediastinal lymph nodes combined with enlarged hilar lymph nodes.
(2) Intrapulmonary lesions: The intrapulmonary lesions of nodular disease are divided into alveolar nodular lesions, sarcoidosis and pulmonary fibrosis.
1, alveolar nodular lesions: alveolar nodular lesions become nonspecific alveolitis, manifesting as patchy lesions with blurred margins, in which air-containing bronchial images are seen. Lesions can occur in all lobes of both lungs, with more lesions in both upper lobes or limited to one upper lobe. The lesions may be diffuse and resemble pulmonary edema, sometimes located in the peri-pulmonary region and extending from the lung apex to the diaphragm. The lesions may be absorbed for a short time or may remain unchanged for several years.
2. Granuloma: If alveolitis develops, granuloma is formed. The lesions are nodular, scattered in all lobes of both lungs, ranging in size from corn to about 1 cm, with 5-6 mm being the most common. The nodules resemble metastases when they are 1 to 37.5 px and are common in multiple cases. Granulomas may be distributed within the lungs or in the bronchial and perivascular spaces. The distribution of granulomas along the bronchial vascular bundles may show thickening of the bronchial vascular bundles in a beaded shape. It is difficult to distinguish the large single mass formed from lung cancer, and this kind of manifestation is rare.
3. Pulmonary fibrosis: Fibrous envelope is formed around advanced granuloma, fibrosis occurs around old granuloma, and a few giant cells may remain in the center, which is more difficult to be detected by early fibrosis imaging. Progressive fibrocystic changes are difficult to differentiate from other causes of pulmonary fibrosis. Pulmonary fibrosis mostly occurs at the site of alveolar nodules.
The literature reports three main signs, bronchial distortion in 38.47%, peripheral foveal images in 23.29%, and diffuse linear images in 19.24%. The author reported one case of misdiagnosis in which pulmonary fibrosis occurred, in a case where the alveolar lesion was found untreated for 3 to 8 months. When the lesion was extensive it was in the periphery of both lungs, from the pulmonary apex to the diaphragm.
(3) Pleural lesions: pleural lesions due to nodal disease are less common than enlarged mediastinal hilar lymph nodes and intrapulmonary granulomatous nodules. The author reported 2 cases of small pleural effusions and 3 cases of pleural nodules among the misdiagnosed cases. Pleural multinodular nodules often coexist with intrapulmonary multinodular nodules.
(4) Bronchial lesions: The author saw only one case in which multiple small nodules in the bronchi were found by bronchoscopy and confirmed by pathology. In this case, the endobronchial lesions coexisted with alveolar nodular lesions. It has been reported in the literature that bronchial stenosis due to endobronchial nodular disease can lead to lobar atelectasis.
3, dynamic changes of nodular disease mediastinal multigroup lymph node enlargement and one side of the hilar lymph node enlargement is rare, the literature reports account for l-3%. The author misdiagnosed 5 cases of such manifestations accounting for 15.63% of the cases. In the author’s consultation, one case was initially diagnosed with unilateral hilar enlargement, and after 4 months, the hilar enlargement on the opposite side; some were initially diagnosed with hilar enlargement on both sides, and during the observation process, the enlarged lymph nodes on one side disappeared;
In some cases, only enlarged lymph nodes in the middle mediastinum without hilar lymph nodes were seen at the initial diagnosis, but during the observation process, alveolar nodules in both lungs and enlarged lymph nodes in both hilum appeared. It can be seen that the enlarged lymph nodes of the two hilar lymph nodes are not seen at the time of the patient’s visit, which may be because the lesion has not yet invaded the lymph nodes of the two hilar lymph nodes, or the enlarged lymph nodes of the two hilar lymph nodes have disappeared and only the enlarged mediastinal lymph nodes remain. In case of enlarged lymph nodes in nodular disease, oral prednisone 30mg/d once a day can significantly reduce the size of lymph nodes in about 2 weeks.
In some cases, there is no significant change after 3 months of treatment or longer, which may be related to granulomatous fibrosis in the lymph nodes. It is also thought that it may be related to vitreous degeneration due to ischemia and malnutrition of the lymph nodes. Intrathoracic lymph node enlargement is often seen at the onset of the disease, or it may develop outside the chest (skin, salivary glands, eyes, liver, etc.) and appear several years later.
The literature reports that the absorption of intrapulmonary lesions can suddenly present with intrathoracic lymph node enlargement. Intrapulmonary infiltrates preceding hilar and mediastinal lymph node enlargement are the exceptions, with alveolar infiltrative lesions resorbing faster than intrapulmonary granulomas after treatment. It is difficult to differentiate intrapulmonary fibrotic lesions from intrapulmonary interstitial infiltrative lesions. The manifestation of intrapulmonary interrogative lesions can be absorbed and reduced by treatment, and those without changes are mostly fibrosis.
4, the diagnosis and differential diagnosis of nodular disease nodular disease and other similar nodular disease manifestations of the disease is more difficult to distinguish. This is because the diagnosis of nodular disease requires a combination of clinical, imaging and pathological diagnosis. The single appearance of intrapulmonary lesions, enlarged hilar and mediastinal lymph nodes, pleural lesions and bronchial lesions in nodular disease is not specific. Differential diagnosis between nodular disease and proliferative tuberculosis is difficult in pathology.
Among the misdiagnosed cases encountered by the author, those showing enlarged mediastinal hilar lymph nodes were also seen with amyloidosis, which did not change with treatment and was diagnosed only after further examination. Tuberculosis, tumor metastasis (e.g., kidney cancer metastasis, lung cancer), and lymphoma are not excluded from nodal disease based on images alone, but all underwent thorough examination and dynamic observation before arriving at the correct diagnosis. However, the typical manifestations of nodular disease are much less common in amyloidosis, tuberculosis, tumor metastasis, lymphoma, and lung cancer than in nodular disease, and therefore the diagnosis of nodular disease is currently made based on the typical manifestations of nodular disease, combined with clinical exclusion of other diseases.
The diagnosis is more difficult when nodular disease is combined with tumor metastasis and tuberculosis. The author met a case of prostate cancer with lumbar metastasis, but the patient had enlarged lymph nodes in the hilum and mediastinum on one side, which was diagnosed as nodular disease after comprehensive examination. It should be emphasized that the diagnosis of atypical manifestations of nodular disease is difficult, without a definite diagnostic basis, and hormone therapy should not be used without basis.
(B) Exogenous allergic alveolitis
Exogenous metaplastic alveolitis is a non-caseating necrotizing granuloma, in which patients with mild clinical symptoms are more common and may have low fever, cough, and general malaise, similar to cold symptoms. Chest examination can be misdiagnosed as metastases if it shows multiple nodules or spherical lesions in both lungs, and when the lesions do not change significantly in the lungs with systematic anti-inflammatory therapy. We had one such case, for which comprehensive imaging examinations such as head CT and bone scan were done in order to find diagnostic evidence of tumor, and the diagnosis was finally confirmed by a puncture biopsy of the lesion in the chest wall and a pathology report of inflammation.
Therefore, patients with exogenous allergic alveolitis are often ineffective after a longer period of anti-inflammatory treatment, and the intrapulmonary lesions do not change or increase instead, which is more likely to lead to misdiagnosis as tumor. In these cases, after prednisone combined with anti-inflammatory treatment, the intrapulmonary lesions can shrink significantly or disappear in 1 to 2 weeks, and can be completely absorbed in 3 to 4 weeks. Without targeted treatment with hormones, the lesions may remain unchanged for several months.
1, pathological changes in the early stage, the infiltration of inflammatory cells is confined to the alveolar wall and around the respiratory fine bronchi, sometimes appearing in the alveolar cavity, dominated by neutrophil infiltration. As the lesion progresses, non-caseating necrotic granulomas are formed in the interstitial lung, with granuloma components of epithelioid cells, multinucleated giant cells and lymphocytes, mainly in the alveolar wall and peribronchial tissues, and vasculitic changes are rarely seen at the lesion site.
In the chronic course, the lesion is characterized by interstitial fibrosis of the lung and may be accompanied by interstitial pneumonia with a predominantly lymphocytic infiltrate, which may develop into a cellular lung in advanced stages. The allergens of exogenous allergic alveolitis can be inhaled fungi, plant pollen, animal feathers, proteins, etc.
2, clinical manifestations of the acute phase, in contact with the antigen 4 to 8 hours onset, patients appear breathing difficulties, dry cough, chest tightness, fever, general malaise and other symptoms. Sub-acute phase mostly developed from acute, but also can be no obvious acute phase, clinical symptoms are cough, shortness of breath and general discomfort. In the chronic stage, the symptoms are not obvious, and shortness of breath, cough, weakness and low fever are common clinical symptoms.
The acute phase is easily misdiagnosed as pneumonia or tuberculosis of other nature based on imaging. The subacute and chronic stages can be misdiagnosed as tuberculosis, tumor and other diseases according to different imaging manifestations. Skin antigen test and specific antibody test are sometimes not helpful for correct diagnosis.
3, imaging manifestations of exogenous allergic alveolitis manifestations are diverse, imaging diagnosis is more difficult, need to be differentiated from a variety of diseases.
(1) patchy, lamellar lesions: can be single, multiple, or diffuse, with blurred lesion margins. Solitary lesions may be patchy shadows of variable size to solid images occupying one lung segment. The lesions are of ground glass density or infiltrative lesion density, and bronchial gas images are sometimes seen in larger lesions above the lung segment, making differentiation from bacterial pneumonia and viral pneumonia difficult.
Diffuse distribution of large patchy lesions in both lungs, the manifestations of which are difficult to distinguish from SARS, respiratory distress syndrome, viral pneumonia, and pulmonary edema. Extensive and marked lesions with mild clinical symptoms in the patient and normal or slightly high total white blood cell count and neutrophils contribute to the diagnosis. Acute phase treatment can be absorbed in 1 to 2 weeks. Chronic lesions are absorbed slowly and can take up to a month or more.
(2) Corn-sized nodules: nodules of 2 to 3 mm in size, widespread and multiple in both lungs, uniformly distributed, with blurred lesion borders. Such manifestations of pigeon lung are common in the author’s consultation cases, and some of these cases are clinically significant reduction in clinical symptoms after leaving the pigeon raising environment. Generally prednisone treatment for 2 to 4 weeks can be completely absorbed.
(3) Multiple nodules and spherical lesions in both lungs: this presentation is more common than the previous two presentations and is often seen in consultation because it needs to be differentiated from a tumor. Patients may have no clinical symptoms or may have a mild cough, low fever, and general malaise. On CT of the chest, spherical or nodular lesions are seen scattered in both lungs with clear margins, and the lesions are mostly 1 to 50 px or larger. In some cases, metastases and alveolar carcinoma are diagnosed. In this kind of patients, the lesions show more uniform density and clearer margins on CT, so it is more difficult to exclude tumors. However, careful observation of chest radiographs showed lesions with blurred margins and different sizes and shapes on chest radiographs, which were inconsistent with the chest CT performance.
Therefore, chest radiographs are often an important supplement to chest CT for this type of lesion presentation. If the lesions still do not change after targeted treatment, they can also be biopsied by thoracic puncture, and the pathology report can be combined with anti-inflammatory treatment using prednisone if it is inflammation, and there are usually significant changes in 2-4 weeks, with smaller lesions disappearing and larger lesions becoming smaller, and some lesions may remain without absorption after treatment for a longer duration of the disease.
(4) allergic bronchopulmonary aspergillosis: allergic bronchopulmonary aspergillosis is a kind of allergic pulmonary disease of the body to parasitic bronchial mycobacteria. Bronchial injury centered on the bronchi, reactive eosinophil aggregation and interstitial fibrosis of the lung are the three pathological changes of this disease. Due to the recurrent disease can lead to lung segment and sub-segment bronchial dilatation, the dilated bronchus is filled with mucus fibrin, and fungal filaments are visible in the lumen, which can invade the airway wall and lung tissue.
A large number of eosinophils and monocytes can be seen infiltrating the bronchopulmonary tissues. Some advanced lesions may develop into interstitial lung fibrosis. The vast majority of patients have a history of asthma with recurrent lesions over days or months, with episodes of fever, cough, sputum, and intrapulmonary lesions that can be resolved with anti-inflammatory therapy. Clinically, allergic reactive bronchopulmonary aspergillosis is divided into 3 phases: phase I acute phase, with typical exacerbation symptoms; phase II remission phase, with symptoms relieved by bronchodilators and glucocorticoid therapy; and phase III relapsing exacerbation phase, with acute symptoms again.
Chest imaging of allergic reactive bronchopulmonary aspergillosis includes.
1, multiple patchy and solid images of pulmonary segments in the lungs, and increased lesions in the lungs during relapses or new lesions in other parts of the lungs.
2. Typical imaging presentation is a glove-like appearance in the lesion area due to the presence of mucus-filled dilated bronchi, with smooth lesion margins, increased density, and multiple columnar images of the lesion resembling a glove. Due to the presence of other lesions in the lung, the glove sign can sometimes be masked. After lesion resorption, the bronchial mucus empties and an inflated and dilated bronchial lumen is visible. Bronchiectasis is irreversible and can frequently become infected and does not disappear completely with treatment. Inflammatory lesions in the lungs may become chronic or undergo fibrosis and persist for a long time.
(C) Lymphomatoid granuloma
Lymphomatoid granulomatosis is a destructive infiltrative disease of the mid-cardiovascular system in which the infiltrating cells include atypical lymphocytes, plasma cells and histiocytes. Lymphomatoid granuloma can involve the skin, liver, kidney and peripheral nervous system, and is mostly a chronic progressive disease, sometimes developing rapidly.
1. Clinical symptoms Patients may have fever, cough, cough, hemoptysis, chest pain and shortness of breath, while fever and cough are the main symptoms. In the clinical often diagnosed pneumonia, after anti-inflammatory treatment, the symptoms can be relieved, but the basic changes of chest imaging is not obvious or enlarged, and new lesions may also appear.
The nodules are distributed along the bronchovascular bundles or lobular intervals, with irregular and blurred edges, and a few lesions with clear edges. The lesions in the lungs grow slowly, from 1m to 250px over several months to years. Bronchial air images or cavities are visible within the lesions. The cavities are caused by necrosis in the center of the lesion, and the cavity walls vary in thickness, forming either thick-walled or thin-walled cavities.
The growth of the mass into the vascular lumen may cause vascular obstruction or stenosis. Diagnosis by imaging is difficult and requires differentiation from inflammatory granuloma, lymphoma, lymphatic interstitial pneumonia, metastasis, Weyers granuloma, and mechanized pneumonia on imaging. Lymphoma-like granuloma requires pathologic examination to confirm the diagnosis, but puncture biopsy of the lesion in the lung via the chest wall is often not confirmed and an open chest biopsy is required.
(iv) Langerhans granuloma
Also known as eosinophilic granuloma. In the past, it was thought to be histiocytic hyperplasia, and some people think it belongs to a pre-cancerous lesion.
The early stage of Langerhans granuloma is an inflammatory lesion centered on fine bronchial tubes, which is a foci composed of various cells such as eosinophils, lymphocytes and neutrophils, and small pulmonary arteries and veins are often involved. Langerhans cells and macrophages are seen in the lung cell lumen. Alveolar cavity fibrosis and alveolar atrophy often lead to pulmonary fibrosis. Fibrosis and small cystic lesions are seen in the advanced stage of the lesion, the latter may be due to necrosis in the center of old nodular lesions.
2, clinical symptoms patients can be asymptomatic, but also dry cough, chest pain, dyspnea, fatigue and fever, occasionally hemoptysis, mostly with a history of rhinitis.
3, imaging manifestations of the two lungs multiple scattered nodules of different shapes and sizes, lesion size in 5-6mm or larger, lesion edge blurred, some lesions are seen in the cavity, cavity wall thickness varies, 1 to 2mm is common, or even thinner, this is the more characteristic imaging manifestations of the disease. In advanced stages, thin-walled honeycomb lung may be seen. To observe the cavities within the nodules, high-resolution CT is of great help. For hormonal therapy, the efficacy varies and some can be partially absorbed. Diagnostic imaging needs to be differentiated from tumors, tuberculosis, and inflammation. Pathological diagnosis is the basis for the final diagnosis.
(E) Wechsler’s granuloma
1. The pathological changes of granuloma of Wechsler are necrotizing granuloma and necrotizing vasculitis, both of which exist simultaneously. Necrotizing vasculitis, good occurrence in the lungs, kidneys and skin. Necrotizing vasculitis mainly involves small arteries and veins, and the main pathological changes are fibrinoid degeneration of the vessel wall, destruction of the muscular layer and elastic fibers, and visible pulmonary infarction, hemorrhage and small aneurysm formation.
Necrotizing granuloma can be divided into extensive (Weyers granuloma) and limited (Weyers granuloma), which are different stages in the development of the lesion and occur in the sinuses, nasopharynx, eccrine trachea and bronchi, lungs and kidneys, the latter without kidney damage. It can also involve the eyes, joints, skin, muscles, ears, pericardium and nervous system, as well as the liver, lymph nodes, large and small intestine, tongue, esophagus, bone marrow and adrenal glands. Necrotizing granuloma of lung lesions consists of neutrophils, lymphocytes, plasma cells, monocytes and a few eosinophils, fibroblasts, epithelioid cells, and multinucleated giant cells, and necrosis often occurs at the lesion.
2, clinical manifestations in the clinical performance of multi-system clinical symptoms, generally slow onset, but there are also acute onset of the disease. Nasal congestion and pus nasal discharge are often early symptoms, pharyngeal lesions, vocal cord ulcers or granulomas can cause sore throat and hoarseness, according to statistics, 85% of those with nasopharyngeal symptoms, easily misdiagnosed as paranasal sinusitis, rhinitis, nasopharyngeal cancer. Cough, bloody sputum, chest pain and shortness of breath are common symptoms of lung involvement, and fever is a systemic symptom. When the kidney is damaged, it starts with an insidious pattern and later develops renal failure. Skin damage occurs in the extremities and can be manifested as purple scarring blisters, nodules, ulcers and masses.
3.Imaging performance
(1) Cornules, nodules, spherical images and cavities: this is the typical imaging manifestation of sarcoidosis. The lesions can be single or multiple, small like corn, larger 2-150px or even up to 225px. 2/3 cases of spherical lesions appear as cavities with thick, irregular walls, in which fluid planes are visible. When the condition worsens, new lesions may appear.
(2) Patchy image: pulmonary hemorrhage and pulmonary infarction caused by pulmonary vasculitis. Patchy images may also appear in the presence of pneumonia. Larger lesions may occupy one lung segment. This manifestation is less common than cornu, nodule and spherical images. The lesion may shrink or disappear within 1 to 2 weeks, but a new lesion may appear.
(3) Tracheal stenosis: This is a manifestation of involvement of the upper airways, and tracheal stenosis may coexist with intrapulmonary lesions.
(4) Pleural effusion: the amount of pleural effusion can be large or small and can coexist with pulmonary lesions.
Understanding the clinical symptoms, the diagnosis of Wechsler’s granulomatosis is easier, and the diagnosis is difficult when I clinical manifestations are atypical, and needs to be differentiated from inflammation, tuberculosis, and tumor.
(F) Necrotizing nodular granulomatosis
Necrotizing nodular granulomatosis is pathologically a nodular granuloma with vasculitis of unknown etiology, probably exogenous allergic alveolitis. The lesion in the lung parenchyma is a non-caseating granuloma.
1. Clinical symptoms are common in young and middle-aged women. Clinical symptoms are nonspecific and may include fever, cough, hemoptysis, dyspnea, and pleural effusion. Pulmonary involvement is common.
2. Chest imaging shows single or multiple nodules in both lungs, with lesions ranging from corn-like to larger nodules, which may coexist with patchy lesions, some of which may appear as cavities, and there may also be pleural effusion. Enlarged hilar and mediastinal lymph nodes are rare.
III. Diagnostic imaging possibilities of granulomatous lesions
Granulomatous lesions in the lungs need to be differentiated from inflammation, lung cancer, and lymphoma. Differentiation based on imaging alone is difficult, if not impossible. Among these granulomatous lesions, those that may suggest a diagnosis based on the imaging presentation, combined with clinical information, are nodular disease, infectious granuloma, Weyers granuloma, and Langerhans granuloma.
Some of these diseases may present with characteristic manifestations.
1, nodular disease is more commonly manifested by enlargement of multiple groups of lymph nodes in both pulmonary hilum and mediastinum, with bead-like intrapulmonary lesions.
2. Granulomatous lesions of Weil’s granulomatosis coexist as nodules, masses, and patches, easily forming cavities, and the lesions are variable in size, shape, and location.
3, inflammatory granuloma in both lungs scattered corn nodules, patchy lesions, lesions with blurred edges and similar shape.
4. Langerhans granuloma presents with multiple nodules and cavities in the center of the nodules in the lungs with blurred lesion margins.
Granulomas that are difficult to diagnose differently from lung cancer include lymphoma-like granuloma (also known as atypical lymphoma), necrotizing nodular granulomatosis, and puncture biopsy helps to differentiate them from lung cancer. Lymphoma can be considered when enlarged lymph nodes in the hilum and mediastinum are found, but the diagnosis requires imaging combined with clinical and pathological findings.