Community-acquired pneumonia

　　1. Etiology

　　The pathogens mainly involved in community-acquired pneumonia include bacteria, mycoplasma, chlamydia, and viruses in four major categories. As for bacterial pathogens, community-acquired pneumonia, except for Mycobacterium tuberculosis and Legionella pneumophila, which can be directly inhaled into the lung substance through droplets, Pseudomonas aeruginosa can directly settle in the trachea, while the others are acquired through inhalation of infectious factors from the throat. The common bacterial pathogens of community-acquired pneumonia in clinical practice include Streptococcus pneumoniae, Mycobacterium tuberculosis, Haemophilus influenzae, Staphylococcus aureus, Legionella pneumophila, Klebsiella pneumoniae, and Moraxella catarrhalis, etc. The viral pathogens of community-acquired pneumonia include influenza A and B viruses, 1, 2, and 3 type influenza viruses, respiratory syncytial virus, and adenovirus, etc. Other microbial pathogens include Mycoplasma pneumoniae, Chlamydia pneumoniae, and Psittacosis chlamydia, etc.

　　2. Pathogenesis

　　There are three sources of pathogenic microorganisms that cause community-acquired pneumonia. The first is the direct inhalation of infectious particles from the surrounding air. The second is the accidental aspiration of microorganisms from the mouth, nose, pharynx, and larynx. The third is the pathogens from the infection foci in the adjacent areas penetrating or spreading to the lung tissue. The first situation mainly occurs when there is close contact with certain respiratory infection sources or in the epidemic areas of certain respiratory pathogens. The third situation is less common, such as the rupture of subphrenic abscess to the right lung or the hematogenous spread of staphylococcal sepsis in the lung. In clinical practice, the second situation is the most common. The normal flora of the upper respiratory tract is mainly a mixed parasitism of various aerobic bacteria, such as Streptococcus, Staphylococcus, Streptococcus pneumoniae, Neisseria (including Neisseria meningitidis), Corynebacterium diphtheriae, Haemophilus, etc. A few healthy individuals can also have Gram-negative bacilli, such as Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Lactobacillus, Bacteroides, and rare spirochetes and Candida albicans. In addition, a large number of anaerobic bacteria are parasitic in the spaces between the teeth and gums, and the concentration of bacteria in each milliliter of saliva can reach 10^8.

　　Some pathogenic microorganisms that cause community-acquired pneumonia are distributed in nature or on some animals. For example, legionella is a common environmental pollution bacterium, mainly transmitted through the aerosol of contaminated water. Fungi are widely distributed in the relatively humid natural world of tropical and subtropical regions, and their spores enter the respiratory tract with the dust. Mycoplasma is widely distributed in nature and can also寄生 in the human body, but it does not cause disease in normal circumstances. Acute patients are the source of infection, and others are infected by inhalation of droplets through the respiratory tract. There are two types of rickettsia that can cause pneumonia commonly seen in clinical practice: one is the Bejel rickettsia, and the other is the Prowazek rickettsia. The former causes Q fever pneumonia, with cattle and sheep as the main sources of infection. After the pathogen is excreted from the animal body, it presents in an aerosol state and mainly causes disease in humans through inhalation of the respiratory tract. The latter causes the rickettsial pneumonia of epidemic typhus, mainly through the skin lesions or skin破口 caused by human lice bites. In the genus Chlamydia, people knew in the past that psittacosis chlamydia could cause interstitial pneumonia in humans. In 1986, Grayston first discovered the pneumonia chlamydia, which is different from the chlamydia trachomatis and psittacosis chlamydia. The main difference is that the antigenic determinants on the outer membrane protein of the pneumonia chlamydia are fewer, and it is a non-immunogenic antigen during infection. Humans are the only known host, and the two peaks of infection are 8 to 9 years old and older than 70 years old. The clinical manifestations are the same as those of psittacosis pneumonia, but 70% to 90% are subclinical. In a detection of 2000 cases of pneumonia patients' serum samples, the infection rate of pneumonia chlamydia was 8%, the annual incidence rate was 1‰, and the incidence rate in people over 70 years old was 3‰.

　　Various pathogenic microorganisms may not necessarily cause disease even if they accidentally enter the lungs. Two conditions must be met to cause pneumonia. First, the pathogen itself must have sufficient survival numbers and virulence intensity, and second, the pathogen must overcome the body's defenses, especially the local immune defense mechanisms of the respiratory system, including the anatomical barriers and clearance functions of the nasopharynx and upper respiratory tract, and the immune clearance functions of local cells and humoral factors in the terminal gas exchange units. This defense mechanism can keep the first-level large bronchus below the normal lung sterile.

　　The upper respiratory tract and the airways can expel particulate matter through mechanical principles, including: ①Anatomical barrier function, such as the tight junctions between the epiglottis and mucosal surface cells; ②Reflexive closure of the glottis; ③Frequent branching of the bronchial tree, which can filter inhaled air through changes in gas dynamics; ④The mucociliary clearance system, which can remove particulate matter from the mucosa; ⑤Cough reflex. When the source of infection, especially bacteria, escapes the above defense mechanisms and enters the alveoli, another set of defense mechanisms is activated. The terminal units (alveolar ducts and alveoli) have non-ciliated epithelium and mucous secretion cells (goblet cells and mucous glands), at this time, coughing cannot effectively clear the pathogens that have entered the alveoli, and mainly relies on phagocytes and humoral factors for clearance.

　　Lysin: After bacteria or particulate matter reach the surface of the alveoli, most of them are rapidly digested by phagocytes. Although alveolar macrophages have a strong phagocytic effect on inert particles. However, the phagocytosis of live bacteria is slower, and the encapsulated or opsonized microorganisms can increase the phagocytic activity by 10 times. The surface liquid layer of the alveoli contains non-immunoglobulin opsonins (surface-active substances of lipoproteins secreted by type II alveolar epithelial cells and large molecular weight glycoproteins and cellulose produced locally by alveolar macrophages or angiogenic sources). Immunoglobulin opsonins include IgG antibodies and complement factor C3b, which can enhance the binding of specific membrane receptors. Opsonins can be produced locally or be part of the systemic humoral immune response.

　　IgG and its subtypes are present in bronchoalveolar lavage fluid, with a proportion similar to that in blood. The IgG subtypes include antibodies against capsular polysaccharides of respiratory pathogens (such as Streptococcus pneumoniae, Haemophilus influenzae), teichoic acid antibodies in Staphylococcus, and lipopolysaccharide antibodies in Gram-negative bacilli. The IgG1 and IgG4 subtypes, which are phagocytic or adhere to the plasma membrane surface of alveolar macrophages, are the most common. The FCgamma receptor of macrophages has the most IgG3, while IgG1, IgG2, and IgG4 receptors are less common and often covered.

　　In the airways, the complement system can be activated through the alternative pathway, leading to the lysis of susceptible microorganisms and the production of opsonin C3b. As soon as phagocytosis begins, intracellular killing processes also start, but the speed is usually slower than that of polymorphonuclear leukocytes. There may be mechanisms involved in both oxygen-dependent and oxygen-independent pathways. Macrophages, unlike polymorphonuclear leukocytes, usually lack myeloperoxidase, but can increase the production of superoxide anion and hydrogen peroxide (H202) after 'activation'.

　　Alveolar macrophages have the following characteristics in defense: ① Directly phagocytose pathogenic microorganism particles entering the alveoli. ② Further inhibit, destroy pathogens, and finally kill them. ③ Can survive for several days to several months and can cope with repeated infections by pathogenic microorganisms. ④ Have migratory properties, can quickly move from Kohn holes to other alveoli, or migrate to the distal airways. ⑤ Can guide the intracellular degradation of antigenic substances and present them to specific pulmonary lymphocytes, thus initiating specific immune responses. ⑥ Can enter the lymphatic tissue of respiratory bronchioles, by lymphocytes that produce humoral and cellular immunity. ⑦ Many active substances secreted by them participate in the immune effector system and are involved in the formation of chronic inflammation and fibrosis or granuloma.

　　Lymphocytes recovered from normal alveoli account for about 10% of the total airway cell population, of which 70% are T lymphocytes, and the proportion of the main lymphocyte subsets is similar to that in peripheral blood. Lymphocytes play an important regulatory role in the activation and inflammation of alveolar macrophages, and can also directly participate in the formation and regulation of antibody responses, activating dormant toxic lymphocytes. A small portion (7%) of helper T lymphocytes are HLA-DR positive lymphocytes, which are the main source of interleukin 2. Killer T cells may be dormant cells, but can be activated by gamma interferon. T cells secrete various cytokines, including gamma interferon and macrophage inhibitory factor, which can activate macrophages. Macrophages must have acquired cell-mediated immunity to inhibit or kill certain intracellular microorganisms. These microorganisms include Mycobacterium tuberculosis, Legionella, Pneumocystis carinii, Listeria monocytogenes, and cytomegalovirus.

　　Pneumonia caused by various pathogenic microorganisms exhibits roughly similar basic pathological changes, especially in the early stages of inflammation, where the progression and content of the pathological changes are essentially the same. These early basic pathological changes include: local tissue cell swelling,变性, and necrosis upon initial invasion by pathogenic microorganisms, congestion, expansion, and opening of adjacent microvessels, extravasation of cellular components and exudation of body fluid components, and the formation and participation of various inflammatory cells and mediators. In the later stages of the inflammatory process, the proliferation, repair, and healing of tissues and cells are also basically similar. In addition to the aforementioned basic similarities, different pathogenic microorganisms have their own characteristics in terms of the nature of inflammation, extent of injury, degree of damage, and healing outcomes. For example, bacterial pneumonia represented by Streptococcus pneumoniae is characterized by fibrous inflammation as the main pathological change, which can invade a lung segment or even the entire lung lobe. Although the main pathological changes occur in the alveoli, there is no destruction or necrosis of alveolar walls and other lung tissue structures throughout the process of the lesion, and the lung tissue can return to normal completely without leaving fibrotic scars after the inflammation subsides, and there is no emphysema. However, the same bacterial pathogens, when occurring in children, the elderly, and patients with weakened physical constitutions or those who have been bedridden for a long time due to various physiological defenses, are prone to form suppurative necrotic inflammation of the lung tissue centered on the bronchioles, which is commonly seen as bronchopneumonia or lobular pneumonia. Staphylococcus, Streptococcus, less pathogenic Streptococcus pneumoniae, and Haemophilus influenzae, Klebsiella pneumoniae, Pseudomonas aeruginosa, Escherichia coli, anaerobic bacteria are more common. The pathological changes of viral pneumonia are characterized by interstitial pneumonia as the main manifestation in early or mild viral pneumonia, while in late or severe viral pneumonia, it can further develop to involve the alveolar cavity, but it remains non-suppurative. Only certain severe viral pneumonia infections (mainly seen in adenovirus pneumonia and measles virus pneumonia) can exhibit suppurative necrotic pathological changes. The pathological changes of fungal pneumonia are characterized by coagulative necrosis, cell infiltration, and suppuration in the acute stage, and pulmonary fibrosis and granuloma formation in the chronic stage. Mycoplasma pneumonia is a non-suppurative interstitial inflammation of the lung, characterized by infiltration of inflammatory cells, mainly lymphocytes and monocytes, into the alveolar walls and other interstitial tissues of the lung, with the lesion scope often not exceeding a lung segment. The pathological changes of rickettsial pneumonia are mainly manifested in the swelling, proliferation, and necrosis of the interstitial vascular endothelial cells of the lung, with extensive perivascular inflammation and thrombotic vasculitis occurring, and nodular changes forming. The pathological changes of chlamydial pneumonia usually begin at the hilum and spread to the periphery, causing lobular and interstitial pneumonia. In the early stage, the alveoli are filled with neutrophils and edema exudate, which are soon replaced by monocytes.

　　Community-acquired pneumonia is caused by a variety of microorganisms such as bacteria, viruses, chlamydiae, and mycoplasma. Common complications include atelectasis, lung abscess or empyema, while less common complications include toxic myocarditis, toxic shock, pulmonary edema, respiratory failure, renal insufficiency, encephalitis, meningitis, drug fever, and secondary infections and dysbiosis caused by long-term use of large amounts of broad-spectrum high-efficiency antibiotics.

　　One, prodromal symptoms:The incidence of prodromal symptoms in community-acquired pneumonia is higher than that in hospital-acquired pneumonia, often appearing in the early stage of pneumonia. A considerable number of patients have clear causes of catching a cold or overexertion. The main prodromal symptoms include rhinitis-like symptoms or symptoms of upper respiratory tract infection, such as nasal congestion, clear nasal discharge, sneezing, dry throat, sore throat, sensation of foreign body in the throat, hoarseness, headache, dizziness, hot and swollen eyes, tears, and mild cough. Not every patient with community-acquired pneumonia will have prodromal symptoms, and the incidence varies with the pathogen, generally between 30% to 65%.

　　Two, systemic toxicosis manifestations:The vast majority of community-acquired pneumonia patients will present with systemic toxicosis symptoms to varying degrees, such as chills, shivering, fever, dizziness, headache, generalized muscle and joint pain, fatigue, poor appetite, nausea, and vomiting. Severe patients may also experience mental disturbances or psychiatric symptoms.

　　Three, respiratory system symptoms:That is, cough, sputum, hemoptysis, chest pain, and dyspnea, the five major symptoms. In different pathogens and different patients, the incidence and characteristics of the above five major symptoms are different, and not every patient or every pathogen-induced pneumonia will simultaneously present the above five major symptoms. For example, mycoplasma pneumonia often manifests as a dry, hacking cough, with severe cases accompanied by posterior sternal pain; viral and plasma cell pneumonia can gradually worsen cough, but chest pain and dyspnea are less common, and young people often present with typical acute symptoms during an attack. Elderly or severe patients may have less cough and sputum, or even no obvious respiratory symptoms. In the early stage of pneumonia in immunodeficient patients, it may only manifest as an increased respiratory rate, fever, restlessness, or no obvious respiratory symptoms. Typical pneumococcal pneumonia can produce rust-colored sputum, staphylococcal pneumonia can sometimes produce sputum with blood and pus, Klebsiella pneumoniae patients can produce sputum in brick red, Pseudomonas aeruginosa pneumonia sputum can be light green, and anaerobic bacteria pneumonia patients can produce purulent, malodorous sputum. Due to the widespread use of antibiotics in recent years, most of the community-acquired pneumonia patients observed in clinical practice currently have mild or atypical respiratory symptoms.

　　Four, extrapulmonary symptoms:Pneumonia, in addition to directly causing respiratory symptoms, can also lead to extrapulmonary symptoms, such as reflex shoulder and arm pain caused by pulmonary apex lesions, back pain due to posterior lesions stimulating the pleura, and upper abdominal pain and radiation to the shoulder caused by a few lower lobe lung infections stimulating the diaphragm. It can also be accompanied by belching and hiccups. Systemic toxicosis may be more prominent in one system, such as severe headache, nausea, frequent vomiting, and significant mental disturbances and psychiatric symptoms in severe patients. Although the incidence of these extrapulmonary symptoms is not high, they are easy to distract people's attention and lead to misdiagnosis. They should be given attention in diagnosis and differential diagnosis.

　　Five, Symptoms of Complications:Complications of community-acquired pneumonia are not common, especially in recent years, with the widespread use of potent broad-spectrum antibiotics, the frequency of complications continues to decline, but they have not completely disappeared. Clinically, pleurisy or empyema, meningitis, pericarditis, endocarditis, peritonitis, and early hematogenous dissemination can also cause arthritis, otitis media, otitis externa, sinusitis. Severe or septicemia patients may also develop shock and multiple organ failure. Clinical physicians cannot ignore this. On the other hand, due to the widespread use of broad-spectrum antibiotics, some previously rare complications have also emerged, such as secondary viral infection, infection by avirulent opportunistic pathogens, and secondary infections caused by dysbiosis and drug-resistant strain infections. These are the new problems we must face. Therefore, while paying attention to the symptoms of pneumonia itself, we should not overlook the existence of complications, especially after regular anti-infection treatment in accordance with the pathogen. If the body temperature does not decrease, or if the fever subsides and then recurs, or if symptoms worsen accompanied by an increase in white blood cell count, the possibility of complications should be considered.

　　Six, Pulmonary Signs:The clinical signs of community-acquired pneumonia vary with the location, size, and course of the lesion, as well as the presence or absence of complications. Common signs are manifested in the following four aspects:

　　1, General Signs:Such as high body temperature, acute febrile appearance, tachypnea or dyspnea, and in severe patients, there may be changes in consciousness.

　　2, Signs of Pulmonary Consolidation:Such as weakened respiratory movement on the affected side of the chest, increased vocal cord vibration, dullness on percussion, reduced respiratory sounds, enhanced phonation conduction, tubular respiratory sounds, and inspiratory wet rales at the focus site, etc.

　　3, Extra-pulmonary Signs:Such as cyanosis, mild jaundice, abdominal distension, epigastric tenderness, and simple herpes. Such signs are relatively rare in clinical practice.

　　4, Signs of Complications:Varies according to the specific type of complication.

　　Seven, Clinical Manifestations:The diagnosis of community-acquired pneumonia is not difficult. It is generally believed that it is similar to other pneumonias, with symptoms such as fever, recent onset of cough, purulent sputum, leukocytosis or leukopenia; chest X-ray findings show patchy, lobar, and alveolar high-density infiltrative lesions, etc. More than half of patients over 65 years of age have symptoms other than respiratory symptoms, and more than 1/3 of patients have no systemic signs of infection. During the course of the disease, most of them can be diagnosed initially from clinical symptoms and signs through the examination of body temperature, pulse, respiratory sounds, and rales. However, from clinical symptoms and signs, it is not possible to make a diagnosis of etiology. One of the etiological diagnoses is based on the relationship between the patient's illness background and microorganisms, that is, the epidemiological basis.

　　Eight, Laboratory Diagnosis:Obtain specimens as soon as possible after admission: commonly used sputum specimens, blood, urine, and lower respiratory tract secretions, etc. Detection methods include:

　　1. Sputum:Gram staining of deep sputum is performed. If relatively pure bacteria appear, such as all Gram-negative bacilli, it may be Haemophilus influenzae/Gram-negative aerobic bacteria. If Gram-positive bacteria are arranged in a diplococcal pattern, it may be the actual pathogen. At this time, the corresponding suspected bacteria's counterflow immunoelectrophoresis is a sensitive and specific detection method for sputum.

　　2. Blood specimens:Generally, early and late double blood specimens are taken. The early blood specimens are subjected to bacterial culture, isolation, and identification of pathogens, which is commonly determined by serum agglutination tests. For other pathogens such as mycoplasma, psittacosis chlamydia, viruses, and legionella, enzyme-linked immunosorbent assays (ELISA) can be used to detect corresponding antibodies in serum by fluorescent labeling antibody methods. A positive IgM or a fourfold increase in IgM double serum can make an etiological diagnosis. The polymerase chain reaction (PCR) established in recent years can directly and rapidly detect the specific nucleotide sequence of pathogens, making a rapid and accurate diagnosis.

　　3. Urine specimens:The latex agglutination test is commonly used to determine the antigen of pathogens (such as Streptococcus pneumoniae antigen and Haemophilus influenzae B antigen, etc.).

　　4. Lower respiratory tract secretions:The best method to obtain secretions is bronchoalveolar lavage (BAL), the technique of plug catheter (TPC), or percutaneous lung puncture aspiration. After obtaining specimens using one of these methods, pathogen isolation and culture can be performed, as well as rapid PCR in vitro amplification to make an etiological diagnosis in a short period of time.

　　For the experimental diagnosis of community-acquired pneumonia caused by Legionella, which has been widely valued by clinical doctors in recent years, various methods have been established. However, it is difficult to use each method individually for the diagnosis of Legionella infection. Therefore, it is usually emphasized to use a combination of multiple methods for the diagnosis of this bacterium. In China, the commonly used method is the direct fluorescent labeling antibody method, which requires multiple antibodies labeled with fluorescent substances to be completed in a shorter time. The DNA probe assay is a specific and sensitive method that can complete the detection of specimens within a few hours. Currently, there are commercialized reagents available, which is a good method for rapid detection of Legionella infection.

　　Nine, etiological diagnosis:The diagnosis of pathogens is of great significance for the treatment of pneumonia, the judgment of the condition, the prediction of the prognosis, and the summary of future experience. Clinical workers have been continuously seeking and exploring various methods to strive for the diagnosis of pathogens in pneumonia. However, to this day, this problem has not been solved ideally. The difficulties in the diagnosis and differential diagnosis of pneumonia pathogens include:

　　1. There are many types of pathogenic microorganisms that can cause pneumonia. There are no absolute characteristics in terms of clinical manifestations or X-ray images among various microorganisms or different species and subtypes of the same microorganism. Therefore, it is extremely difficult to make a definitive etiological diagnosis solely based on clinical manifestations and (or) X-ray images.

　　2. About 30% of pneumonia patients do not produce sputum.

　　3. Approximately 30% of pneumonia patients have already received antibiotic treatment before admission or during their visit.

　　4. Among the various pathogens causing pneumonia, about 25% of pathogens do not have a direct confirmation method in clinical laboratories to date, such as viruses, legionella, and Rickettsia burnetii, etc.

　　5. A considerable proportion of the results of many immunoserological methods are still false positives.

　　6. Even if a certain microorganism is isolated from sputum, it is difficult to be sure that it is the pathogenic microorganism when it cannot be excluded that it is contaminated from the upper respiratory tract. Due to the presence of these factors, the diagnostic rate of pathogens in clinical practice has always been very low, with general reports from foreign literature ranging from 10% to 36%, and even in large general hospitals in China, the diagnostic rate of pathogens in pneumonia has always been low. The work in this regard still needs to be continuously improved in the future. Currently, clinical doctors can only rely on the existing conditions, fully grasp the characteristics of the patient's medical history, clinical manifestations, and X-ray imaging features, and selectively choose relevant pathogenic tests to make as accurate a pathogenic diagnosis as possible.

　　It is very important to adopt comprehensive preventive measures for community-acquired pneumonia. For patients with chronic diseases, it is appropriate to pay attention to strengthening nutritional support therapy, improving the host defense mechanism, and enhancing the host's immune function, such as using influenza vaccine or pneumococcal vaccine every year. This vaccine is effective against 85% to 90% of bacterial infections. It induces the production of specific antibodies to increase opsonization, phagocytosis, and the killing of pneumococci by white blood cells and other phagocytes. The pneumonia vaccine is administered intramuscularly or subcutaneously, 0.5ml each time. For non-host factors, it is necessary to limit exposure to the population as much as possible during the influenza epidemic; in high-risk populations, the most effective antiviral drugs against influenza A virus, such as rimantadine, or drugs similar to rimantadine, should be used. Passive immunization therapy can also be adopted, such as intravenous injection of immunoglobulin, which can reduce the risk of bacterial infection; such as gamma globulin: 400mg per kilogram of body weight, intravenous injection, once every 3 weeks, or 500mg per kilogram of body weight, or 250mg. Once every 4 weeks, but there is no difference in efficacy, and low-dose prevention is appropriate. In summary, preventing community-acquired pneumonia is an important and effective method.

　　First, blood examination

　　1. Blood count changes:Most bacterial pneumonia cases exhibit a marked increase in peripheral blood leukocyte count, with an elevated proportion of neutrophils. In severe cases, there may also be left shift and toxic granulation. In a few cases of bacterial pneumonia caused by Escherichia coli and Pseudomonas aeruginosa, the total white blood cell count may be normal or slightly elevated, but the proportion of neutrophils usually increases. If bacterial pneumonia patients show a decrease in total white blood cell count, it often indicates a poor prognosis. White blood cell counts in viral pneumonia or pneumonia caused by other pathogens may not show significant changes, and the peripheral blood leukocyte count in viral pneumonia patients may even be lower than normal. If there is a concurrent bacterial infection, there may be an increase in white blood cell count. When judging the blood count changes in pneumonia patients, attention should be paid to the patient's bone marrow hematopoietic reserve function, the presence of alcohol intoxication and liver and kidney failure, as all these factors may affect the changes in white blood cell count during inflammation.

　　2. Changes in bone marrow imaging:Generally, in patients with mild pneumonia, the bone marrow image may show no obvious changes. In patients with moderate to severe pneumonia, the bone marrow image may show reactive hyperplastic changes due to the stimulatory effect of inflammation. In patients with severe pneumonia with obvious toxic symptoms or concurrent sepsis, the bone marrow image may show reduced or significantly suppressed hematopoietic function, but it is generally reversible and can return to normal with the improvement of the condition.

　　3. Blood gas analysis:Generally, due to excessive ventilation, arterial blood gas analysis often shows mild hypocapnia and respiratory alkalosis. Blood perfusion passes through the actual lung consolidation areas without ventilation function, and due to the imbalance of ventilation/perfusion ratio and physiological shunting, it can lead to hypoxemia. In patients with extensive severe pneumonia or concurrent severe bronchospasm, respiratory failure, and systemic sepsis, severe hypoxemia can occur, accompanied by respiratory and (or) metabolic acidosis.

　　4. Etiological examination:Bacterial, fungal, mycoplasma, rickettsia, and other pathogenic infectious pneumonia can be subjected to blood or bone marrow culture for pathogens. Positive results have a definite significance for clarifying the etiological diagnosis, guiding treatment, and judging the prognosis. However, the positive rate is generally not high, and it will only increase during the early stage of the disease, a short period of bacteremia or concurrent sepsis. If blood samples are taken after early application of antibiotics, the positive rate will be even lower. Therefore, blood samples should be taken and sent for bacterial culture as early as possible before the application of antibiotics.

　　5. Other hematology indicators examination:Generally, patients with mild to moderate pneumonia may have an increased erythrocyte sedimentation rate, mild elevation of transaminase or other enzymatic indicators. In severe pneumonia or patients with sepsis, the erythrocyte sedimentation rate can reach more than 100mm/h, and various enzymatic indicators change more明显ly, even with obvious changes in liver and kidney function indicators.

　　2. Sputum examination

　　Microscopic examination and etiological examination of respiratory secretions are crucial for rational treatment of pneumonia, but in actual clinical practice, there is often insufficient awareness of this. The main reasons are: first, there is doubt about the reliability of sputum specimen examination results; second, there is a lack of patience for the detection rate of positive sputum specimen results. In recent years, people have once again given full recognition to the importance of sputum examination in the diagnosis and treatment of pneumonia, and have made new explorations in theory, therapy, and quality control, such as improving the reliability of sputum specimens with strict quality control indicators. The United States stipulates that less than 1 to 2 oral squamous epithelial cells per high-power field are qualified sputum specimens. Some use direct collection of fresh sputum specimens from the patient's mouth under bedside supervision and immediate preparation or inoculation culture on the spot to minimize contamination and maintain the viability of pathogens in the sputum. For some critically ill, chronic, and refractory patients, as well as some long-suffering, physically weak, or immunosuppressed patients, reliable sputum specimens are needed to obtain reliable sputum specimens.

　　In recent years, it is more advocated to use protective sterile sputum brushes obtained directly from the lesion site through fiberoptic bronchoscopy, which may increase some pain for the patients, but compared with the reliability of pathogen diagnosis and the importance of guiding treatment and judging prognosis, it is still the most economical, simplest and most effective method. Fresh sputum specimens should be subjected to Gram staining and pathogen culture. Wet film microscopy to observe cell types helps to judge the reliability of the specimen. The method is to spread the mucus or purulent sputum specimen on a glass slide, emulsify it with a few drops of physiological saline, and observe it under 100x magnification. Sputum specimens from the lower respiratory tract can be seen to contain polymorphonuclear leukocytes and alveolar macrophages. The analysis accuracy of Streptococcus pneumoniae can be improved by treating the wet sputum specimen with a mixture of anti-capsular antibodies, which can cause capsule swelling or terminate the reaction. If the patient has little sputum, it can be stimulated to cough up sputum by ultrasonic atomization inhalation with distilled water or physiological saline. The diameter of the particles from the atomized inhalation should be between 0.8 to 10 μm, which can stimulate most patients to cough and produce sputum. Reports indicate that about 80% of AIDS patients with pneumonia and a few patients with non-human immunodeficiency virus infections can produce sputum using this method, and Pneumocystis carinii can be isolated.

　　Three, Serological examination

　　Immunoserological tests are not a routine method in the diagnosis of pneumonia, but they still have certain value for the etiological diagnosis of pneumonia. Foreign reports indicate that they can make etiological diagnoses of reference value for nearly 1/4 of pneumonia patients. Clinically, commonly used methods include the detection of specific polysaccharides for diagnosing Streptococcus pneumoniae by agglutination immunoelectrophoresis, the determination of muramic acid (muramic acid) antibodies for diagnosing Staphylococcus, cold agglutination tests for diagnosing Mycoplasma pneumoniae, the Weil-Felix reaction for diagnosing Rickettsial pneumonia, and immunofluorescence techniques for diagnosing Legionella, etc. The shortcomings of immunoserological test methods in diagnosing pneumonia pathogens are that the specificity and sensitivity are not very ideal, and most of them take too long, which is not of great guidance for early diagnosis and treatment, but has greater value for retrospective diagnosis. Generally, they require higher technical and equipment requirements, making it difficult to popularize and promote. Currently, the most successful application of immunofluorescence method in diagnosing Legionella is that its sensitivity can reach more than 75%, and its specificity is between 95% and 99%. Results can be obtained within 24 to 48 hours. Regarding the immunoserological tests for viruses, their reference value is even more limited, mainly because there are many types of viruses, they transform quickly, and the technical requirements are higher, taking longer. Therefore, their practical value in clinical application is not great, and they are mainly used for retrospective diagnostic investigations. It is worth mentioning that at the Third Asia-Pacific International Virology Conference held in Beijing in October 1994, a rapid diagnostic method for viruses using monoclonal antibody technology, developed and applied in clinical practice by Chinese scholar Duan Peiro, can accurately diagnose 8 respiratory viruses, including influenza virus, parainfluenza virus, adenovirus, and respiratory syncytial virus, within 2 to 3 hours, which is about 100 times faster than the classical virus isolation method, showing a good prospect for the rapid diagnosis of viral pneumonia pathogens.

　　Four. Polymerase Chain Reaction for Detecting Pathogens

　　Immunoserological methods confirm the presence of pathogens by detecting the antibody components of pathogens in the sample, while the polymerase chain reaction (PCR) detection method directly detects the antigen components of pathogens in the patient's sample. PCR is an in vitro DNA amplification technique designed based on the principle of DNA replication, which involves repeatedly performing the program of high temperature denaturation (90~95℃) - low temperature annealing (37~70℃) - appropriate temperature extension (70~75℃) for 25~35 cycles on the pathogen DNA fragments in the sample to be detected. In theory, it can increase the copy number of the original DNA fragments by more than 10^6, thereby detecting extremely small amounts of pathogen DNA in the sample. This technology has four significant characteristics:

　　1. High sensitivity:This is the most prominent feature of PCR. Literature reports that it can detect 1 to 100 fg of DNA in a sample, which is equivalent to 1 to 20 bacteria. After excluding various interfering factors in clinical specimens, the actual sensitivity of clinical detection is about the DNA amount of 1000 bacteria.

　　2. Strong specificity:The specificity of PCR mainly depends on whether the amplified fragment selected is a specific nucleic acid fragment of the cell (or pathogen), in addition, choosing a higher annealing temperature to ensure that the primers correctly bind to the template can also improve the specificity of PCR.

　　3. Simple:In addition to the complex and high requirements for the preparation of nucleic acids of some bacteria and clinical specimens, the operation process of PCR is relatively simple, especially with the application of thermostable DNA polymerase and the advent of DNA thermal cycling instruments, making PCR operation automated and time-saving.

　　4. Rapid:PCR detection of clinical specimens, from nucleic acid extraction to CR amplification, and electrophoresis detection to photography only takes 1-2 days.

　　PCR technology was first established by Mullis et al. in 1983, applied to clinical practice in the late 1980s, introduced to China in the early 1990s, and is not yet widely used in China. At present, it has been successfully applied in clinical tuberculosis and mycobacterial PCR detection technology, and is being applied in clinical practice, such as mycoplasma PCR detection technology, etc.

　　Fifth, chest X-ray examination

　　There are two main purposes in the diagnosis of pneumonia: one is to confirm whether pneumonia exists, and the other is to determine the location of the lesion. High-quality X-ray posterior-anterior chest films are helpful to show the lesions in the posterior area of the left heart, but even so, all patients with pneumonia should have lateral X-ray chest films taken to help localize the lesion. The X-ray manifestations of pneumonia depend on the location of the lesion (alveoli or interstitium), the extent of the lesion (alveoli, lobules, lung segments, or lobes), the nature of the lesion (suppurative or non-suppurative), and the route of infection (such as hemogenic or aerogenic). It is also closely related to the etiology and type of pathogen. Therefore, by analyzing the location, extent, morphology, and distribution characteristics of the lesion, it is sometimes helpful to speculate on the etiology and type of pathogen. The dynamic changes of the shadow of pneumonia are of great significance for the differential diagnosis of pneumonia and other shadows. Pneumonia can manifest in a variety of ways on X-ray. Based on their characteristics, combined with the pathological basis, the following is described:

　　1. Pulmonary vascular enhancement:This sign is common in bronchopneumonia. The pulmonary vascular enhancement caused by viral infection is often more obvious than that caused by bacterial infection. This is the X-ray manifestation caused by the pathogen being infected through the bronchi and spreading along the bronchi. Pathologically, there is exudative, proliferative, or necrotic inflammation in the mucosa from the trachea to the terminal bronchioles and respiratory bronchioles. The bronchial lesions below the 5th or 6th level are more severe, and the terminal bronchioles and respiratory bronchioles belonging to the lobules are more severe. Bronchial peripheral alveolitis is often present, so some people believe that pulmonary vascular enhancement is an early X-ray manifestation of pneumonia. The pulmonary vascular enhancement caused by pneumonia is often generalized, with blurred edge textures, which can be distinguished from vascular texture enhancement by this feature.

　　2. Small nodule shadows:This sign is often seen in adenovirus pneumonia, respiratory syncytial virus pneumonia, and measles virus pneumonia, and can also be seen in bacterial pneumonia and fungal pneumonia. The diameter of the lesions is mostly 1-6mm, with blurred edges, more common in the middle and lower lung fields. Pathologically, it is peripheral bronchiolitis or respiratory bronchiolitis around the terminal bronchioles, or alveolar inflammation within the alveolar ducts. The former is often accompanied by generalized pulmonary vascular enhancement and emphysema, more common in viral infections, and the latter often coexists with lobular fusion lesions, and can be seen in viral or bacterial infections.

　　3. Small patchy or patchy fusion shadows:This condition can be seen in bronchopneumonia caused by various reasons. On X-ray, it presents as patchy shadows with blurred edges, 1-2.5 cm in diameter, and the patchy shadows can merge. Pathologically, the patchy shadows are interlobular exudative or necrotic alveolitis, and the interlobular septa in the lesion area are clear, even after several foci merge. In terms of distribution, this type of focus is mostly distributed in both lungs, with the lower lobe being more than the upper lobe, the inner more than the outer, and the posterior more than the anterior.

　　4. Lobar and segmental shadows:This type of manifestation is often seen in Streptococcus pneumoniae pneumonia, Klebsiella pneumoniae pneumonia, Staphylococcus aureus pneumonia, Pneumocystis carinii pneumonia, and adenovirus pneumonia. Streptococcus pneumoniae pneumonia and Klebsiella pneumoniae pneumonia mostly occupy a lobe or segment of the lung. Pneumocystis carinii and adenovirus pneumonia can simultaneously affect several segments or lobes of the lung, and bronchial imaging can be seen in dense shadows. In macroscopic pathological specimens, the lesion appears as distinct, brown-red or gray-white consolidation areas, and the volume of the lesion does not usually decrease. Under the microscope, fibers, red blood cells, and white blood cells can be seen to exude in the alveolar spaces.

　　5. String-like and reticular shadows:This condition is seen in radiation pneumonia, chronic pneumonia, and interstitial pneumonia, with the lesion primarily being hyperplastic, mostly occurring in alveolar walls and interlobar septa, and can also coexist with parenchymatous alveolitis. This hyperplastic lesion can also coexist with partial lung atelectasis. Chronic pneumonia may be accompanied by bronchiectasis. On X-ray, it presents as patchy, irregular, string-like mixed shadows, with edges that can be clear or blurred. Generally speaking, this type of lesion absorbs more slowly than exudative alveolitis.

　　6. Spherical shadow:This condition is seen in Staphylococcus aureus pneumonia and fungal pneumonia, with the former being a abscess in pathology, with blurred or relatively clear boundaries. Blood源性 Staphylococcus aureus pneumonia is often multifocal. On X-ray, Staphylococcus aureus pneumonia can present as multiple or solitary spherical shadows, mostly 1-3 cm in diameter, with clear edges and relatively uniform density, but can form a cavity within a short period of time. The pathological basis of the spherical shadow formed by fungal pneumonia is an abscess or granuloma.

　　7. Cavity:It is mainly seen in suppurative pneumonia and fungal pneumonia, especially common in Staphylococcus aureus pneumonia. On X-ray, it presents as a ring-like lucency with clear or blurred edges, varying wall thickness, unclear boundary between the lesion and normal lung tissue, necrotic tissue in the cavity, and if the bronchus due to inflammation forms a flap, the cavity will increase in size and become thinner due to the continuous increase in gas content inside the cavity and the increased pressure, generally referred to as pulmonary bulla. This phenomenon is seen in Gram-positive cocci infections such as Staphylococcus aureus and Streptococcus hemolyticus type A, and on X-ray, it presents as a thin-walled cavity that can disappear shortly after the pneumonia is aspirated or may remain for several months. Pathologically, the wall is a thin layer of fibrous tissue.

　　8. Emphysema:This condition is often seen in children with bronchopneumonia, especially adenovirus pneumonia, measles pneumonia, and respiratory syncytial virus pneumonia. On X-ray, it presents as an enlarged chest, widened intercostal spaces, increased lung opacity, a flat diaphragm, and pathologically, it is characterized by panlobular emphysema, expansion of alveolar spaces, thinning of alveolar walls, and lesions commonly occur at the edges of various lung lobes, such as the anterior edges of the superior, middle, and inferior lobes.

　　9. Pleural Lesions:Pneumonia can be accompanied by pleural changes. When pleural effusion occurs, the nature of the effusion can vary, such as serous, serosanguinous, or purulent. Purulent pleural effusion often occurs with purulent pneumonia, serosanguinous effusion may be associated with viral pneumonia. On X-ray, fluid can be seen in the pleural cavity, and pleura can show congestion, edema, and inflammatory cell infiltration.

　　6. Fiberoptic Bronchoscopy

　　Fiberoptic bronchoscopy for pneumonia patients has become routine in some developed countries, but in most cases in China, it is still selective. The main purpose of fiberoptic bronchoscopy for pneumonia patients is: first, to directly observe the airway condition at the lesion site; second, to perform bronchoalveolar lavage and brush catheter sampling culture to clarify the etiological diagnosis; third, to directly clear secretions and mucus plugs in the airway, unblocking the airway; and fourth, to inject drugs into the lesion site. Therefore, fiberoptic bronchoscopy not only has a diagnostic role for pneumonia patients but also has direct therapeutic value. According to literature reports, the combined application of brush cytology and culture of bronchoalveolar lavage fluid based on the different pathogens can enable 50% to 90% of pneumonia patients to obtain an etiological diagnosis.

　　7. Invasive Examination

　　Lung function tests are generally only considered for those difficult cases that cannot be diagnosed or treated effectively through various routine examination methods, or for the necessity of differential diagnosis. For patients with pneumonia, the main purpose of invasive examinations is to obtain accurate and reliable diagnoses and differential diagnoses. Common techniques include: transtracheal needle aspiration of secretions, protected brush technique through bronchoscope, lung biopsy through bronchoscope, lung biopsy through chest wall needle aspiration, thoracentesis examination when there is pleural effusion or empyema, and open chest biopsy.

　　8. Lung Function Examination

　　The impact of pneumonia on lung function mainly depends on the size of the lesion range, the location of the lesion, the speed of disease progression, and the patient's original lung function baseline, among other factors. Generally, mild pneumonia with a small lesion range has little impact on lung function. The larger the lesion range, the more severe the condition, the faster the progression, the greater the impact on lung function. The location of the lesion also has the most significant difference in its impact on lung function. For example, pneumonia mainly affecting the alveolar substance can significantly affect tidal volume, residual volume, functional residual capacity, and lung total volume, among other lung volume indicators. It can also lead to restrictive ventilation dysfunction and a certain degree of diffusion dysfunction. Severe diffuse alveolitis patients may manifest severe gas exchange dysfunction. Interstitial pneumonia can cause restrictive ventilation dysfunction and gas diffusion dysfunction. Bronchopneumonia, which often occurs in elderly and weak patients or those who have been bedridden for a long time, primarily presents with diffusion dysfunction and ventilation/perfusion ratio imbalance in the early stage. In the later stage, due to the poor drainage of respiratory secretions, it can also be accompanied by severe obstructive ventilation dysfunction.

　　1. Food therapy: Mung bean Job's tears porridge

　　Main materials: 30g of Job's tears, 30g of mung beans

　　Auxiliary materials: 6g of mint

　　Seasoning: 15g of sugar

　　Preparation method:

　　1. Boil mint in water for about 30 minutes, strain the juice and set it aside for later use.

　　2. Soak mung beans in boiling water and cook them until half cooked.

　　3. Add Job's tears and cook until the beans are soft and the rice is broken.

　　4. Then add mint water and a little sugar to make it.

　　Effect: It has the effects of clearing heat and detoxifying, and is suitable for high fever or chest pain after fever subsides due to pneumonia.

　　2. Eat foods rich in high-quality protein.In a sense, protein is the material basis that determines the level of our body's immunity. If an adult lacks protein in the body, it can cause a decrease in physical strength, insufficient brainpower, overall weakness, premature aging, and easy to get sick, and the skin loses elasticity and luster; therefore, to prevent pneumonia, if we can pay attention to eating more high-quality protein foods in daily diet, such as lean meat, crabs, seafood, dairy products, soy products, eggs, etc., to enhance the body's immunity and avoid the invasion of external pathogens.

　　First, treatment

　　The treatment of community-acquired pneumonia cannot be delayed due to the numerous pathogens, and treatment should be given after obtaining the etiological results in clinical practice.

　　Antibiotics should be modified according to the results after the etiological diagnosis is established. Generally speaking, the pathogens of community-acquired pneumonia are mostly limited to a few main pathogenic bacteria, making it easier to select antibiotics. For those patients with community-acquired pneumonia without underlying risk factors and mild conditions, the pathogen has not been identified yet, so erythromycin is used, 0.3 to 0.5g each time, taken orally every 6 hours. Or 1.0 to 1.2g each time, intravenous infusion is sufficient for the most common pathogens such as Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella. Especially the latter three, as they reproduce intracellularly, only a few antibiotics are effective, and macrolides are the first choice; if it is confirmed that Streptococcus pneumoniae is the cause, then penicillin G should be首选, the usual dose is 800,000 to 1,600,000U, injected intramuscularly every 4 to 6 hours, for patients with toxic shock, the dose can be increased to 2 to 4 million U each time, 2 to 3 times a day, intravenous infusion, the course of treatment is 1 week, or stop the medicine after 72 hours when the body temperature returns to normal. Because although it has been reported abroad that there are resistant Streptococcus pneumoniae, but according to recent studies in China, penicillin G-resistant Streptococcus pneumoniae is still rare. For those allergic to penicillin, erythromycin can be used, 30 to 40mg per kilogram of body weight per day, the course of treatment is 7 to 10 days or stop the medicine after 72 hours after fever subsides. Chinese studies have shown that most of the bacteria are sensitive to cephalosporins, and the second and third generation cephalosporins have stronger activity and high stability to beta-lactamase, and high concentration in sputum. Therefore, for severe infections, it can be considered to be the first choice. For the treatment of Mycoplasma pneumoniae and Chlamydia pneumoniae pneumonia, macrolide antibiotics have significant efficacy, erythromycin is the first choice, or medecamycin, 0.2g each time, 3 to 4 times a day, taken orally. But both of them cannot be used for less than 10 days.

　　For the community-acquired pneumonia caused by Legionella, which has been discovered in recent years and gradually gaining attention from clinical physicians, the first-line drug is also erythromycin. Due to the intracellular growth of this bacterium, the study of effective antibiotic concentrations in recent years has found that erythromycin has a high concentration in polymorphonuclear leukocytes, which can kill the bacteria within it, making it the first choice. Since the lung lesions of this disease often take 1 to 2 months to disappear, early discontinuation of medication often leads to recurrence, so it is emphasized that the course of treatment should be at least 3 weeks or longer. The dose of erythromycin for adults is generally 2g per day, and for children, it is 50mg/(kg·d); taken orally or administered intravenously in divided doses. In severe cases, rifampin should be combined for treatment. The dose of rifampin for adults is generally 600mg per day [for children, 20mg/(kg·d)]. In recent years, studies on new macrolides such as clarithromycin (克拉红霉素) and azithromycin have found that they are more effective against Legionella infections than erythromycin, and have fewer gastrointestinal side effects. After oral absorption, 40% of clarithromycin is metabolized into 14-hydroxy derivative, which has the same antibacterial activity and has a synergistic effect with erythromycin, inhibiting bacterial growth and reproduction, especially against Haemophilus influenzae. It has a short half-life, and the blood concentration is 1.7mg/L 2 hours after oral administration, but the concentration in lung tissue can reach as high as 8.79?g/L. The dose of clarithromycin is 250-500mg per time, twice a day. Cefamet: 500mg per time, 4 times a day. The clinical effective rate of the former is 97%, and the bacterial clearance rate is 75%; the latter has an effective rate of 87%, but the bacterial clearance rate is only 25%. Reports indicate that in severe Legionella pneumonia cases, after ineffective treatment with erythromycin, ofloxacin, and rifampin, switching to clarithromycin (克拉红霉素) results in a clinical cure rate of 98%. Another drug, azithromycin, has higher concentrations and longer retention times in tissues and phagocytes. This drug is the only 15-ring macrolide antibiotic, and its application in China is still rare. Its characteristics include low blood concentration, with only 0.4mg/L 2 hours after taking 500mg orally. High tissue concentration, up to 3.94?g/L in the lung, higher than roxithromycin. It is currently the macrolide with the longest half-life, up to 41 hours. It can be administered once a day. The initial dose is 500mg, followed by 250mg once a day. Although the blood concentration of this drug is not high and the MIC is not ideal, the clinical efficacy has a

　　1. Treatment of Staphylococcus aureus pneumonia:It is best to select appropriate antimicrobial agents in a timely manner based on drug sensitivity tests. For sensitive strains, penicillin G is still the first choice. However, the number of drug-resistant strains outside of China is increasing, and it is generally easy to select penicillin preparations that are resistant to beta-lactamases, such as oxacillin (phenylisoxazole penicillin) 4 to 6g daily by intravenous infusion, or erythromycin and chloramphenicol 1.2 to 1.5g daily by intravenous infusion. Additionally, if amikacin 0.2g each time is added to the above antibiotics, given twice daily by intramuscular injection, or tobramycin 80 to 160mg each time, given twice daily by intramuscular injection, etc., synergistic effects can be produced, enhancing the antibacterial effect. If methicillin-resistant Staphylococcus aureus (MRSA) strains appear, which are resistant to various penicillins (including penicillinase-resistant and non-penicillinase-resistant strains) and cephalosporins, vancomycin, rifampicin, fusidic acid (Brown霉素), and fosfomycin can be selected. They will still be sensitive. The course of treatment should be maintained for 4 to 6 weeks.

　　2. Community-acquired pneumonia caused by Pseudomonas aeruginosa:Early combined use of sensitive antibiotics is the key to treatment. Generally, gentamicin or tobramycin combined with carbenicillin, furbenicillin, or piperacillin is administered intravenously. Third-generation cephalosporins such as cefoperazone and cefotaxime (cefotaxime carboxyhydrazone) can also be used, or fluoroquinolone drugs such as ofloxacin can be used. Good efficacy can be achieved for pseudomonas aeruginosa pneumonia.

　　3. Community-acquired pneumonia caused by Klebsiella pneumoniae:Although the proportion is not large, it should be given due attention. Effective antibiotics should be selected as soon as possible for the treatment of this bacterium, such as 20 to 40g of carbenicillin or 8 to 16g of piperacillin daily, administered intravenously in small quantities by adding to a small amount of liquid; or amikacin 0.2g each time, twice daily by intramuscular injection; or cefotaxime (cefotaxime carboxyhydrazone, Fudaxin) 2 to 4g daily, administered intravenously in small quantities by adding to a small amount of liquid. The dosage should be sufficient, and the course of treatment should be prolonged until the lesion is healed. Supportive therapy should be strengthened during administration.

　　4. Community-acquired pneumonia with significant underlying (or potential) diseases:Patients (such as those with chronic bronchitis, alcoholics, elderly and weak individuals, recent influenza patients, diabetics or individuals with mental disorders, and immunodeficient individuals, etc.) must first diagnose the cause and provide corresponding treatment, because all of the above factors are the most dangerous factors for infection by Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae, and Gram-negative bacteria. For such patients, the second-generation cephalosporin (cefuroxime) should be used at the beginning, 750mg to 1.5g each time, once every 8 hours; for immunodeficient individuals, those who have recently been hospitalized and received Gram-positive bacterial antibiotic treatment, and then developed community-acquired pneumonia, more broad-spectrum antibiotics can be used from the beginning. Such as third-generation cephalosporins, 1g each time, once every 8 to 12 hours. Cefoperazone, 1 to 2g each time, twice a day. Or use imipenem/cilastatin sodium (primaxin) 500 to 1000mg each time, 2000mg each time for severe cases, twice a day, or 500mg each time, administered intravenously in 3 to 4 divided doses, which can achieve better efficacy. The course of treatment is generally 5 to 7 days.

　　II. Prognosis

　　In the United States, the mortality rate of community-acquired pneumonia treated on an outpatient basis or at home is less than 1%; while the mortality rate of community-acquired pneumonia in hospitalization is 2% to 21%; the mortality rate of severe community-acquired pneumonia can be as high as 40%. China currently lacks statistical data on the mortality rate of community-acquired pneumonia. The risk factors for pneumonia death include: elderly age, absence of chest pain symptoms, rapid breathing, decreased diastolic pressure, confusion, increased blood urea nitrogen levels, increased or decreased white blood cell count, digitalis poisoning.

　　Many studies have found that plasma albumin levels