Diagnosis and differential diagnosis of pulmonary infiltrative shadow
Department of Respiratory Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China Xin Jianbao
Pulmonary infiltrates can be seen in infectious diseases as well as non-infectious diseases. Without any clinical information or detailed history and physical examination, please do not make any conclusion about a patient with fever and pulmonary infiltrative shadow. For example, in a patient with a right lower lung inflammatory infiltrative shadow accompanied by fever, the clinical diagnosis is often right lower pneumonia, mostly considered as a bacterial infection. If we ignore the fact that the patient has a history of contact with patients with respiratory tract infection and has signs of an aggregated case, there is a risk of epidemic and spread of the disease due to failure to take appropriate measures. Xin Jianbao, Department of Respiratory Medicine, Wuhan Union Medical College Hospital
I. Common causes of pulmonary infiltrative shadow
Lung tissue infiltrated with abnormal cells or the presence of tissue, cells or other substances that should not be present under normal circumstances or excessive accumulation of certain pre-existing substances can be called pulmonary infiltrate. On imaging, this often appears as a shadow in the lung. In general, pulmonary infiltrates are often pathologic and suggest abnormalities in the lung tissue. There are numerous causes of pulmonary infiltrative shadows, which can be broadly classified into two categories: infectious and non-infectious causes (Table 1).
Table 1 Common causes of infiltrative lung shadow
Infectious factors
Bacteria (Pseudomonas aerugenosa, Staphylococcus aureus)
Fungi (Aspergillus, Mucormycosis, Candida)
Viruses (CMV, VZV, HSV, RSV, parainfluenza, influenza)
Bifidobacteria (Mycobacterium tuberculosis and nontuberculous mycobacteria)
Others (e.g. PCP)
Non-infectious factors
Progression of pre-existing lung disease
Pneumoconiosis
Pulmonary changes in connective tissue disease
Pulmonary vasculitis
Eosinophilic pneumonia
Lipid pneumonia
Diffuse lung injury
Radiation lung injury
Drug-related lung disease
Alveolar microlithiasis
Diffuse alveolar hemorrhage (DAH)
Cryptogenic mechanized pneumonia (COP)
Tumors (bronchoalveolar carcinoma, carcinomatous lymphangitis, lymphoma, multiple myeloma, hematogenous metastatic carcinoma)
Alveolar protein deposition disease
Transfusion-associated lung injury
Others (such as pulmonary edema,,)
Second, the diagnosis of pulmonary infiltrative shadowing should pay attention to a number of issues
(i) History questioning and physical examination are important clues to obtain an accurate diagnosis
Infiltrative shadow of the lung basically covers all aspects of lung diseases such as inflammation, tumor, immunity, etc., and the imaging features of different diseases with the same image and different images of the same disease are especially prominent in the infiltrative shadow of the lung. If we leave the meticulous and reliable clinical data, it is difficult to obtain an accurate judgment of the infiltrative shadow of the lung simply from imaging to imaging analysis.
1. Medical history inquiry
(1) Epidemiological history
Careful inquiry of epidemiological history can often obtain important clues to the diagnosis of certain diseases. Such as contact with highly pathogenic avian influenza A (H5N1) infection of sick/dead birds or exposure to A (H5N1) contaminated environment after the occurrence of lung infection, is an important basis for considering human avian influenza; during the influenza A (H1N1) epidemic lung infiltrates should pay attention to whether the influenza A (H1N1) related, raw food crab or| history of mayfly, especially in areas where lung schistosomiasis is endemic, is to consider the presence of pulmonary schistosomiasis important clues.
(2) Occupational history
Based on the occupational history of exposure to a large number of chemicals in a short period of time, with clinical manifestations of acute respiratory damage, combined with blood gas analysis and other examination findings, with reference to on-site occupational health survey data, comprehensive analysis, on the basis of excluding other diseases can be considered the diagnosis of occupational acute chemical toxic respiratory disease. Since the disease often has the characteristics of a cluster and a clear occupational history, the diagnosis is generally not difficult. In particular, exposure to water-soluble irritant gases (such as ammonia, chlorine, hydrogen chloride, sulfur dioxide, sulfur trioxide, etc.) has no incubation period, and irritant symptoms, such as tearing, photophobia, conjunctival congestion, runny nose, sneezing, sore throat, choking and coughing, will appear once exposed to such gases. Sudden inhalation of high concentrations of gas can cause laryngospasm, edema, tracheitis and bronchitis, and even pneumonia and pulmonary edema, which can be life-threatening. However, in exposure to gases with small water solubility (such as nitrogen oxides, phosgene, etc.), because there is an incubation period after exposure to such gases, no symptoms or very mild symptoms in the early stage after inhalation do not attract the attention of the person concerned, especially in single-onset cases, which are easily misdiagnosed if a detailed medical history is not taken.
The diagnosis of pneumoconiosis can be made based on a reliable history of productive dust exposure, based on the performance of anterior chest radiographs after high kV X-rays, with reference to on-site occupational hygiene, pneumoconiosis epidemiological survey data and health surveillance data and clinical manifestations and laboratory tests, and after excluding other similar diseases of the lungs. It is worth noting that the diagnosis of occupational diseases has rather strong regulatory requirements and must be made by an occupational disease diagnostic institution approved by the relevant health administrative department before it has the authority to diagnose occupational diseases. Do not blindly operate on pneumoconiosis by misdiagnosing it as a neoplastic disease without careful questioning of the dust work history.
(3) Past history
History of blood transfusion or multiple sexual partners should be checked for HIV to rule out Pneumocystis carinii pneumonia (PCP); history of intravenous drug use or drug abuse should be considered for positive coccus (especially MRSA) infection; contact with birds should be considered for Chlamydia psittaci or novel cryptococcal infection; medication history is an objective basis for considering the presence of drug-related lung injury, and certain drugs (e.g., amiodarone, bleomycin Certain drugs (e.g., amiodarone, bleomycin, azathioprine, mitomycin, azathioprine benzoate, leucovorin, gemcitabine, etc.) can cause lung injury; history of radiation exposure or treatment is a direct cause of radiological lung injury; long-term application of adrenal glucocorticosteroids is often prone to pulmonary fungal, positive cocci (MRS), Pseudomonas aeruginosa, Pneumocystis carinii or mixed infections.
Systemic diseases such as rheumatoid arthritis, systemic lupus erythematosus, polymyositis-dermatomyositis, systemic sclerosis, mixed connective tissue disease, nodular disease, and pulmonary vasculitis (Wegener’s granulomatosis, Churg-Strauss syndrome) often also involve lung tissue and should be of concern to clinical workers. Even if there is no clear previous history of systemic disease, the presence of a pulmonary infiltrative shadow along with damage to organs such as the kidney or skin should be noted to rule out the presence of systemic disease or that the pulmonary infiltrative shadow is a pulmonary manifestation of systemic disease.
(4) Host immune status
The presence of immune compromise is crucial to the etiologic diagnosis of pulmonary infiltrates, and differentiating between immunocompetent and immunocompromised hosts is a key step in the diagnosis and differential diagnosis of pulmonary infiltrates. The etiology and clinical manifestations of pulmonary infiltrates in immunocompromised hosts differ significantly from those in immunocompetent hosts, even for the same disease. In particular, in patients with diffuse pulmonary infiltrates with fever, shortness of breath, and hypoxemia, it is difficult to determine whether the infiltrate is a tumor, a pulmonary manifestation of connective tissue disease or vasculitis, a cardiogenic pulmonary edema or heart failure, a drug-related lung injury, or an opportunistic infection. The clinical differentiation is often quite difficult between drug-induced lung injury or opportunistic infection.
However, some diseases can be rapidly progressive and aggressive, such as human avian influenza, severe pneumonia, diffuse alveolar hemorrhage, or bronchoalveolar carcinoma presenting as pneumonia.
Table 2 Pulmonary infiltrative shadow features and possible causes in immune-compromised hosts
Imaging features
Possible causes
Infection
Non-infected
Local infiltrate
Any pathogen
Progression of pre-existing disease
Diffuse alveolar hemorrhage (DAH)a
Cryptogenic mechanized pneumonia (COP)
Drug-induced lung injury
Graft-versus-host disease (GVHD)
Pulmonary alveolar protein deposition disorder (PAP)
PTLD
Radiation lung injury
Diffuse infiltrates
Legionella
Mycobacterium bifidum (tuberculosis and nontuberculous branching bacilli)
Pneumocystis carinii
Viruses
Diffuse alveolar hemorrhage (DAH)
Progression of pre-existing disease (especially leukemic cell infiltration, lymphatic spread of tumors)
Drug-induced lung injury
Implantation syndrome
GVHD
Idiopathic pneumonia syndrome (IPS)
Pulmonary alveolar protein deposition disorder (PAP)
PTLD
Radiation lung injury
Cavitary lesions or nodular changes
Bacteria
Fungi
Bifidobacterium
Pneumocystis carinii
Viruses (small nodules)
Progression of pre-existing disease
Drug-related lung injury
(5) Time to organ transplantation
Ninety-five percent of pulmonary infections after solid organ transplantation occur within one month postoperatively, and the causative agents are similar to those of general thoracic or laparotomy, with S. pneumoniae and E. coli being more common, or due to sepsis caused by indwelling intravenous catheters. The infectious or non-infectious etiology of pulmonary infiltrative shadowing varies considerably with the different times after organ transplantation and should be carefully identified, please refer to Table 3.
Table 3 Etiology of pulmonary infiltrative shadow at different times after solid organ or bone marrow transplantation
Time
Infectious
Non-infectious
>1 month
Bacteria
Invasive fungus
Acute lung injury
cardiogenic pulmonary edema
diffuse alveolar hemorrhage
Thrombocytopenia-induced pulmonary hemorrhage
Transfusion-associated lung injury
1-3 months
Cytomegalovirus infection
Opportunistic infection
Drug-related lung injury
Idiopathic pneumonia syndrome
>3 months
Delayed cytomegalovirus pneumonia
Mycobacterium bifidum infection
Cryptogenic mechanized pneumonia (COP) Graft-versus-host disease
2. Physical examination
Physical examination reveals pestle finger and bilateral inspiratory phase burst sounds at the base of the lungs (especially the latter) to help the diagnosis of interstitial lung disease; systemic lymph node palpation is a direct basis for obtaining a cytologic or pathologic diagnosis of lung cancer or lymphoma with pneumonia as the main manifestation; nasal examination is an important clue to detect granulomatous disease; spinal pressure pain is an important sign to consider vertebral tuberculosis; abdominal mass often suggests tuberculosis or Lymphoma; skin damage is an important clue to consider systemic diseases.
(ii) Evaluation of laboratory tests and imaging tests for the diagnosis of pulmonary infiltrative shadow
1.Laboratory tests
White blood cell count or classification, C-reactive protein (CRP), calcitoninogen (PCT), etc. help to determine the infectious disease and monitor the response to treatment. Routine tests such as liver and kidney function and serum electrolytes are helpful in determining the severity of the disease and monitoring the dysfunction of extra-pulmonary tissues and organs. Significant abnormalities in enzymes such as serum glutamic aminotransferase, glutamic oxalacetic aminotransferase, phosphocreatine kinase, and lactate dehydrogenase suggest the possibility of serious immune abnormalities or systemic immune responses due to infectious agents, such as human infection with highly pathogenic avian influenza, AIDS, and other viral infections. Arterial blood gas analysis or pulse oximetry can be used to determine the need for oxygen and to identify the presence of respiratory failure.
Tests related to connective tissue diseases such as rheumatoid factor, ANA, dsDNA, ENA, and anti-neutrophil antibodies or tumor markers may be considered when necessary. In particular, pulmonary infiltrates combined with other organ damage such as kidney or skin or suspected systemic disease are strong indications for these tests.
2.Chest radiography
Routine radiological examinations are of limited value to clarify the etiology of pulmonary infiltrates, but they are useful to detect emerging pulmonary lesions and to monitor the response to treatment. Although an emerging pulmonary infiltrate is the primary indicator for the diagnosis of community-acquired pneumonia (CAP), the need to combine 2 of the secondary criteria and exclude tuberculosis, pulmonary neoplasm, noninfectious interstitial lung disease, pulmonary edema, pulmonary atelectasis, pulmonary infarction or embolism, foreign bodies, pulmonary eosinophilic infiltrates, and pulmonary vasculitis and others is emphasized without exception in the diagnosis of pneumonia before a clinical diagnosis of CAP can be established (Table 4: Diagnostic criteria for CAP).
Table 4: Diagnostic criteria for CAP
Primary criteria
Secondary criteria
New infiltrative shadow on chest radiograph
T>38.5 or T<36.5
WBC>10×109/L or <4×109/L
Pus sputum
Typical signs of pneumonia
Basis for pathogenetic diagnosis
3.CT examination
CT scans can reveal microscopic or occult infiltrative shadows in the lungs that appear normal on chest radiographs, facilitating early detection of intrapulmonary lesions and helping to guide the localization of bronchoscopy or percutaneous fine-needle aspiration biopsy for histopathological or microbiological pathogenic diagnosis. In immunocompromised hosts, CT scans not only provide timely detection of lesions, but also assist clinicians as a basis for changing treatment regimens. For example, CT examinations can reveal dynamic changes in the typical “halo sign” (early signs) and “crescent sign” (late signs) on CT to facilitate the diagnosis of invasive Aspergillosis and the appropriate treatment. It is worth noting that if the dynamic change from halo sign to crescent sign is not seen, the diagnosis of Aspergillosis based on crescent sign alone may lead to misdiagnosis due to neglecting the diagnosis of the primary disease (e.g. tumor). High-resolution CT scan (HRCT) shows a fine morphology of lesions, which can be observed in many lesions that cannot be shown by 10mm layer thickness, and has a good reference significance for the differentiation of benign and malignant lesions, and improves the diagnostic efficiency of pulmonary infiltrative shadowing, but it should be noted that the application of HRCT also has its limitations, such as showing exudative inflammation as mass-like changes. Therefore, the diagnosis suggested by HRCT should be closely combined with clinical data, and invasive examination means can be taken to clarify the diagnosis when necessary.
(iii) The diagnosis of infectious diseases should be based on definite evidence
The initial diagnosis of pulmonary infiltrative shadow is often clinically considered as infectious disease, and it is worrying that clinicians would rather try a variety of antibiotics and ignore the identification of non-infectious disease. The diagnosis of infectious disease should be based on definitive evidence. Culture of pharyngeal swabs or sputum specimens has limited value in clarifying the etiologic diagnosis of pulmonary infiltrative shadow, but sputum specimens (including induced sputum specimens) have good diagnostic value for Pneumocystis carinii pneumonia or tuberculosis. Microscopic examination after staining of lung tissue specimens, alveolar lavage fluid, or sputum specimens is often an important basis for obtaining bacterial or fungal infections.
Certain tests are of greater reference significance for the etiological diagnosis of infectious diseases. For example, blood, pleural fluid, ascites or bone marrow specimens obtained at different times or from different sites cultured for the same pathogen, as well as pleural fluid (ascites or bone marrow specimens) and blood cultured for the same pathogen then combined with clinical response to treatment are of confirmatory value for the etiologic diagnosis of pulmonary infections; collection of double serum specimens at 2-4 week intervals in the acute and recovery phases to detect atypical pathogens or Certain antigen tests such as Legionella or Streptococcus pneumoniae urinary antigen, blood or cerebrospinal fluid Cryptococcus podococcal antigen, blood galactomannan or β-glucan have a greater reference value for pathogenic diagnosis.
(iv) Bronchoscopy or lung biopsy is necessary to obtain the correct diagnosis for the decision
Not all pulmonary infiltrates require invasive testing, and invasive testing strategies should only be considered when non-invasive testing is unsuccessful, empirical therapy is ineffective, specimens such as lung tissue or bronchoalveolar lavage fluid need to be obtained to clarify the diagnosis of pulmonary infiltrates, or fiberoptic bronchoscopy is required to rule out other diseases. Especially in immunocompromised hosts, invasive screening strategies are sometimes particularly important to identify the cause of the disease to facilitate targeted therapeutic measures. However, there are no feasible options for when to perform invasive testing and how to weigh the pros and cons to minimize patient suffering while facilitating the diagnosis of the etiology of the pulmonary infiltrative shadow as much as possible.
In a study of pulmonary infiltrates in non-AIDS immune-compromised hosts, this technique was used to make a definitive etiologic diagnosis in 80% (162/200) of cases, 77% of which were infections and 23% of which were non-infectious diseases (e.g., pulmonary edema, diffuse alveolar hemorrhage, etc.). Among the non-infectious diseases, serological tests, blood cultures, antigen testing, nasal rinse fluid, sputum and tracheobronchial aspirates led to a diagnosis in 40% of cases. Bronchoalveolar lavage provided a higher positive diagnosis of approximately 51% (68/135), and its value was particularly evident in the etiological diagnosis of infectious disease, approximately 69% (56/81). Bronchoalveolar lavage (BAL) is useful for the etiologic diagnosis of ground glass or alveolar shadows in immunocompromised hosts as revealed by high-resolution CT scan (HRCT), which helps to identify infections, tumor cell infiltration, or drug-induced lung injury. A variety of etiologic diagnoses of diffuse pulmonary infiltrative shadows in immunocompromised hosts or immunocompetent hosts are facilitated by BAL (Tables 5-6 ).
Table 5. Diagnostic value of bronchoalveolar lavage for diffuse pulmonary infiltrative shadowing in immunocompromised hosts
Pneumocystis carinii pneumonia (P. carinii pneumonia)
Branched bacteriosis (Mycobacteriosis)
Legionellosis (Legionellosis)
Viral pneumonia (Inclusion bodies in the nucleus and cytoplasm)
Diffuse lung injury (pulmonary type II cellular reaction and extracellular plasma structureless material)
Alveolar proteinosis (Alveolar proteinosis)
Eosinophilic pneumonia (Eosinophilic pneumonia)
Alveolar hemorrhage (Alveolar hemorrhage)
Epithelial carcinoma cells (Epithelial neoplastic cells)
Lymphoma cells
Multiple myeloma cells
Table 6. Diagnostic value of bronchoalveolar lavage for diffuse infiltrative lung shadowing in immunocompetent hosts
Pneumoconiosis (asbestos vesicles, silica)
Alveolar proteinosis (Alveolar proteinosis)
Lipoid pneumonia (Lipoid pneumonia)
Chronic eosinophilic pneumonia (Chronic eosinophilic pneumonia)
Acute eosinophilic pneumonia (Acute eosinophilic pneumonia)
Diffuse lung injury (Diffuse alveolar damage)
Alveolar hemorrhage (Alveolar hemorrhage)
Langerhans cell histiocytosis (Langerhans cell histiocytosis)
Bronchoalveolar cell carcinoma (Bronchoalveolar cell carcinoma)
Carcinomatous lymphangitis (Carcinoma)
Hematogenous metastases (Hematogenous metastases)
Low-grade B cell lymphoma (MALT type)
Alveolar microlithiasis (Microlithiasis)
Gaucher and Niemann-Pick cells
Intracytoplasmic inclusions in Hermansky-Pudlak disease
Lower airway specimens can be collected via the artificial airway for tracheal intubation or tracheotomy. Lower airway secretions can be collected via fiberoptic bronchoscopy if necessary. Anti-contamination specimen brush sampling via fiberoptic bronchoscopy is a better way to obtain lower respiratory specimens. Transbronchoscopic lung biopsy or percutaneous lung aspiration lung biopsy techniques may also be used when indicated to clarify the etiologic or etiologic diagnosis. The following are indications for the use of these diagnostic techniques: (1) when empirical treatment has failed or the disease continues to progress, especially if antimicrobial drugs have been changed more than once; (2) when a specific pathogen is suspected and the causative agent cannot be identified with respiratory specimens obtained by conventional methods; (3) when the immunosuppressed host has CAP and antimicrobial therapy has failed; and (4) when differentiation from non-infectious pulmonary infiltrative lesions is required. (iv) when the diagnosis needs to be made with non-infectious pulmonary infiltrates. Close cooperation between clinical staff and related departments such as microbiology and pathology is required to make the test effective, and prompt advice from clinicians is sometimes essential.
Open-chest lung biopsy is an important tool to clarify the diagnosis of pulmonary infiltrates of unknown etiology, but it is not yet commonly performed clinically because of its invasive nature. Open lung biopsy has been reported to obtain a clinicopathologic diagnosis in 86% (31/36) of patients, even under mechanical ventilation, and in 64% of patients the treatment plan was modified, suggesting that open lung biopsy may be a trade-off for obtaining a diagnosis when the cause of the infiltrative lung image is not clear despite multiple measures. The procedures for the treatment of pulmonary infiltrates in immunocompromised and immunocompetent hosts can be found in Figure 1-2.
Regular evaluation is the basic strategy for the diagnosis and differential diagnosis of pulmonary infiltrates.
Since most of the causes of pulmonary infiltrates are infectious lesions, in clinical practice, for new pulmonary infiltrates suspected to be pulmonary infections, empirical antimicrobial therapy is often given based on clinical features after appropriate history taking and laboratory and pathogenic investigations. 48-72 hours is an important time window for empirical antimicrobial therapy, and the initial treatment can be modified or maintained through a thorough evaluation. The need for step-down therapy can be considered based on clinical response in those with significant effects, and in those who are ineffective, maintenance of the original treatment regimen or a change in regimen, with invasive testing measures to obtain lung tissue specimens to facilitate clarification of the etiology of the pulmonary infiltrative shadow if necessary.
(i) Assessment of host immune function status
There are significant differences in the etiology of pulmonary infiltrates in immunocompromised or immunocompetent hosts, and the clinical presentation varies more markedly. The immune function status of the patient should be evaluated if the initial treatment is not significant, and if necessary, certain diseases causing immune impairment (e.g., AIDS) should be tested. The relationship between the type of immune impairment and the possible susceptible causative agent can be found in Table 7.
Table 7 Type of immune impairment and susceptible pathogens and common diseases
Type of immune impairment
Common diseases
Susceptible pathogen
Phagocytic system impairment
Granulocytopenia
Streptococcal shade, gram-negative bacteria, Candida, Aspergillus
Humoral immunodeficiency
Myeloma, CLL
Enveloped bacteria (Pneumococcus, H. influenzae, S. aureus, P. aeruginosa)
Complement system deficiency disease
Complement c3, c5 deficiency
Envelope bacteria
Cellular immunodeficiency
Lymphoma
Intracellular pathogens (viruses, tuberculosis, Legionella)
Splenectomy or splenic hypofunction
Splenectomy
Envelope bacilli
Note: CLL: chronic lymphocytic leukemia
(ii) Evaluation of empirical treatment
Whether an etiologic diagnosis has been obtained for those suspected of having CAP, and whether the corresponding treatment has been given based on the possible etiology when an etiologic diagnosis has not been obtained. In clinical work, the clinical characteristics, risk factors that increase the risk of specific bacterial infections (Table 8), pathogens that predispose patients with CAP in certain specific states (Table 9), X-ray imaging characteristics (Table 10), and epidemiological characteristics of pathogenic microorganisms (especially the pathogenic characteristics of CAP in the region) can be used to synthesize the information and infer the possible pathogenic microbiology of CAP to give the corresponding drug treatment or give modified starting treatment regimen.
Table 8 Risk factors that increase the risk of specific bacterial infections
Specific bacteria
Risk factors
Drug-resistant Streptococcus pneumoniae
Age <65 years; treatment with beta-lactam antibiotics within the last 3 months; alcohol abuse; multiple clinical comorbidities; immunosuppressive diseases (including glucocorticoid therapy); exposure to children in day care centers
Legionella spp.
Smoking; cellular immunodeficiency: e.g., organ transplant patients; renal failure or hepatic failure; diabetes mellitus; malignancy
Enteric gram-negative bacilli
Residence in nursing homes; underlying cardiac or pulmonary disease; multiple clinical comorbidities; recent antibiotic therapy
Pseudomonas aeruginosa
Structural lung disease (e.g., bronchiectasis, pulmonary cysts, diffuse panbronchiolitis, etc.); application of glucocorticoids (prednisone >10 mg/d); broad-spectrum antibiotic application >7 d in the past 1 month; malnutrition; peripheral blood neutrophil count <1×109/L
Table 9 Pathogens that predispose CAP patients to infection in some specific states
Status or comorbidity
Specific pathogens susceptible to infection
Alcoholism
Streptococcus pneumoniae (including drug-resistant Streptococcus pneumoniae), anaerobic bacteria, enteric gram-negative bacilli, Legionella spp.
COPD/smokers
Streptococcus pneumoniae, Haemophilus influenzae, Cataplasma spp.
Residing in nursing homes
Streptococcus pneumoniae, enteric gram-negative bacilli, Haemophilus influenzae, Staphylococcus aureus, anaerobic bacteria, Chlamydia pneumoniae
Influenza
Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae
Exposure to birds
Chlamydia psittaci, Cryptococcus novelis
Suspected inhalation factor
Anaerobic bacteria
Structural lung disease (bronchiectasis, pulmonary cysts, diffuse panbronchiolitis, etc.)
Pseudomonas aeruginosa, Burkholderia cepacia, Staphylococcus aureus
Recently applied antibiotics
Drug-resistant Streptococcus pneumoniae, intestinal gram-negative bacilli, Pseudomonas aeruginosa
Table 10 X-ray imaging features and CAP pathogenesis
X-ray features
Possible aetiology
Localized exudate with massive pleural fluid
Bacteria,,.
cavitary lesions
pulmonary abscess, tuberculosis, fungus, Nocardia (spp.),,.
Cornual lesions
tuberculosis, fungal,,
Rapidly progressive or multilobar changes
Legionella, pneumococcus, aureus, human avian influenza,,
Interstitial changes
Virus, Mycoplasma, Chlamydia, Pneumocystis
For those suspected of HAP, are there any risk factors for causing multi-drug resistant (MDR) pathogens, such as ① previous application of anti-infective drugs, e.g. antibiotics within 90 d before onset; ② late onset VAP; ③ admission to ICU or prolonged hospitalization (e.g. hospitalization > 5 d); ④ high frequency of drug-resistant bacteria in the community or ward; ⑤ immunosuppressed patients or application of immunosuppressive drugs, etc. Whether the coverage of anti-infective drugs is adequate and whether anti-infective drugs need to be changed in a timely manner; whether the treatment of the underlying disease is appropriate and effective, and whether it is associated with pulmonary infection, etc., need to be given adequate attention. Whether the etiology is influenced by humoral or cellular immunity, as in the case of neutropenic pulmonary infiltrative shadows, may require antifungal therapy early on and, if necessary, as one of the first options. Appropriate pharmacologic intervention strategies for most possible aetiologies (e.g., positive, negative, invasive Aspergillosis) can significantly reduce the rate of infection and morbidity and mortality in immunocompromised hosts.
For those with suspected non-infectious disease, whether the relative management has been given, such as anticoagulation or thrombolytic therapy for pulmonary embolism, cardiac and diuretic therapy for cardiogenic pulmonary edema, and appropriate hormonal therapy for diffuse alveolar hemorrhage.
When the initial treatment is ineffective, based on the clinical characteristics of the patient, should we consider the selection of drugs that the starting treatment fails to cover certain pathogenic bacteria, such as cephalosporins or penicillins for the initial treatment and drugs that take into account the ability to treat atypical pathogenic infections (such as fluoroquinolones or macrolides anti-infectives) when changing drugs. If a pathogenic diagnosis is available, the appropriate drug should also be selected in conjunction with its results. In addition, the reasonableness of the usage, dosage, and dosing interval of the selected drug should be evaluated, whether the selected drug has a more desirable local concentration, and whether there are factors such as poor drainage that affect the effect of anti-infective drugs.
In cases of cool pneumonia, where the effect of anti-infective drugs is not obvious and there is no basis for non-infectious disease through multiple examinations, is it necessary to consider diagnostic anti-tuberculosis treatment when tuberculosis is suspected and lung tissue specimens are not available?
(iii) Evaluation of etiologic diagnosis
After the initial treatment is given, is a comprehensive analysis performed to evaluate all clinical data, such as whether the pulmonary infiltrative shadow is combined with a nasal lesion, which is an important clue for the suspicion of Wegener’s granulomatosis; combined proteinuria is an important basis for considering systemic diseases such as systemic vasculitis or SLE; in cases of bleeding tendency, care should be taken to exclude pulmonary hemorrhagic diseases (e.g. pulmonary-renal syndrome).
When the etiologic diagnosis is not obtained by conventional examination, patients should be evaluated for invasive examinations, such as fiberoptic bronchoscopy, percutaneous lung aspiration, or even open lung biopsy, to obtain material for the diagnosis of pulmonary infiltrative shadowing. When invasive testing is limited, serology, microbiology, biomarkers or even PTET-CT testing are indicated or necessary for review.
Even if the basis for an etiologic diagnosis is obtained by laboratory tests or invasive tests, it is still important to assess whether it fits with the clinical data, whether it fully explains all the clinical signs of the case, and whether the etiologic diagnosis obtained is consistent with the pathophysiologic changes or pathophysiologic processes of the disease. The diagnosis of any disease should be considered for its consistency with the pathophysiologic process of the development of that disease. If the “infection” that resembles pneumonia persists for a considerable period of time? The diagnosis of pulmonary embolism should be evaluated after the diagnosis of pulmonary embolism has been confirmed by various tests, and whether pulmonary embolism is only a symptom of the disease and the tumor is the exact cause of the changes. If the cerebrospinal fluid examination is consistent with tuberculous changes, it is still necessary to observe the effect of anti-tuberculosis treatment and pay attention to the presence of other lesions such as fungi.
In conclusion, timely assessment of diagnosis and treatment during the treatment of pulmonary infiltrates is a basic measure to avoid misdiagnosis or underdiagnosis and should be carefully implemented in clinical practice.
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