What Is Nosocomial Pneumonia?

In 2005, the American Thoracic Society (ATS) guidelines expanded and refined the concept of HAP, and explicitly proposed ventilator-associated pneumoniae (VAP) and health care associated pneumonia (Health Care Associated Pneumonia, HCAP) and attribute it to HAP. VAP refers to pneumonia that occurs 48 to 72 hours after tracheal intubation or incision for mechanical ventilation. It is a common and special HAP for patients with mechanical ventilation. HCAP mainly includes the following patients with pneumonia: lived in an acute care hospital for 2-3 days in the last 90 days; lived in a nursing home or long-term care institution; received dialysis treatment in a hospital or clinic; 30 days before the infection People who have received intravenous antibiotics, chemotherapy or wound care.

Shi Yi (Chief physician) Department of Respiratory and Critical Care Medicine, Nanjing General Hospital of Nanjing Military Region
Yin Jie (Deputy Chief Physician) Department of Respiratory and Critical Care Medicine, Nanjing General Hospital of Nanjing Military Region
Hospital acquired pneumonia (HAP), also known as nosocomical pneumonia (NP), refers to the absence of a patient at the time of admission and the infection incubation period, which occurs 48 hours after admission. Types of pulmonary parenchymal inflammation caused by pathogens such as Mycoplasma, virus, or protozoa
Western Medicine Name
Hospital acquired pneumonia
English name
hospital acquired pneumonia, HAP
Affiliated Department
Internal Medicine-Respiratory Medicine
Main cause
Nosocomial infection

Introduction to Hospital Acquired Pneumonia

In 2005, the American Thoracic Society (ATS) guidelines expanded and refined the concept of HAP, and explicitly proposed ventilator-associated pneumoniae (VAP) and health care associated pneumonia (Health Care Associated Pneumonia, HCAP) and attribute it to HAP. VAP refers to pneumonia that occurs 48 to 72 hours after tracheal intubation or incision for mechanical ventilation. It is a common and special HAP in patients with mechanical ventilation, and has a higher morbidity and mortality. HCAP mainly includes the following patients with pneumonia: lived in an acute care hospital for 2 to 3 days in the last 90 days; lived in a nursing home or long-term care institution; received dialysis treatment in a hospital or outpatient department; 30 days before the infection People who have received intravenous antibiotics, chemotherapy or wound care.
According to the time when HAP occurs, it is divided into early-onset HAP and late-onset HAP. Early-onset HAP refers to pneumonia that occurs within 4 days of hospitalization, usually caused by sensitive bacteria, and has a good prognosis. Late-onset HAP refers to pneumonia that occurs 5 or 5 days after hospitalization. The pathogenic bacteria are often multidrug-resistant bacteria (MDR), and die The rate is high. [1]
HAP is currently the most common type of hospital-acquired infections, accounting for the second place in the United States, with an incidence rate of 5 to 10 cases per 1,000 hospitalized patients, accounting for 25% of all hospital-acquired infections in all ICUs, and accounting for patients treated with antibiotics More than 50% of the total. The incidence of HAP increases 6 to 20 times in patients with mechanical ventilation, that is, 9% to 27% of patients with tracheal intubation develop VAP, and almost 90% of HAP in the intensive care unit (ICU) occurs during mechanical ventilation. The risk of VAP occurring early in tracheal intubation is highest. The incidence of VAP increases by 3% per day for the first 5 days, and the incidence of VAP is 2% per day for 5-10 days. The risk is reduced to 1% per day after 10 days. This indicates that tracheal intubation itself is a high risk factor for HAP infection. HAP mortality is as high as 30% to 70%, but most HAP patients die from underlying disease rather than HAP itself. The attributable fatality rate of VAP is about 33% to 50%. The increased fatality rate is related to bacteremia, infection with drug-resistant bacteria (such as Pseudomonas aeruginosa, Acinetobacter), medical diseases rather than surgical diseases, inappropriate Antibiotic treatment and other factors are related. And because of the high rate of multidrug-resistant (MDR) infections, antibiotic treatment becomes more difficult.
The occurrence of HAP must be the development of a balance between the host and the microorganism in a direction that is conducive to bacterial colonization and lower respiratory tract invasion. [2]

Etiology and pathogenesis of hospital acquired pneumonia

1.Sources of pathogenic microorganisms
(1) Colonization and reproduction of oropharyngeal pathogenic bacteria: Inhalation of oropharyngeal colonized bacteria and inhalation of accumulated bacteria above the tracheal intubation balloon are considered to be the main ways for bacteria to enter the lower respiratory tract and cause HAP or VAP. There are two factors that cause colonization: under normal circumstances, there are normal flora in the oropharynx to maintain the dynamic balance of the oral flora. When improper use of antibiotics, tracheal intubation or nasal feeding occur, this balance is broken, and pathogenic bacteria can Oral and pharyngeal colonization is performed by eating and medical staff's hands. In general, the pH of gastric juice is 4, such as long-term nasal feeding, use of acid inhibitors, duodenal fluid reflux, and decreased gastric motility, etc. Pathogens can be retrograde from the small intestine to the gastroesophagus, and then colonize the oropharynx.
(2) Inhalation of contaminated aerosols and direct inoculation: In hospitals, especially ICU wards, the distribution of pathogenic microorganisms is extremely widespread, forming aerosols contaminated with pathogenic bacteria. Medical devices (such as oxygen flow meters, nebulizers, ventilator piping systems and humidifiers, etc.), the surrounding environment (water, ward) and the hands of medical staff can be contaminated by pathogenic bacteria, causing pathogenic microorganisms Spread between patients. But this is not the main route of HAP infection.
(3) Spread of blood-borne infections and bacterial translocation of the gastrointestinal tract: sepsis and sepsis caused by various infections such as bloating, endocarditis, venous catheter infection, and intestinal infection can form secondary pneumonia, but in HAP is rare. [3]
2. The patient's internal factors and the impact of treatment The severity of the patient's underlying disease, whether surgery, whether he has received antibiotics and other medications, and whether he had intubation were related to the onset of HAP or VAP.
3. Etiology The pathogenic spectrum of HAP and CAP are very different. Bacteria are the most common pathogens of HAP, accounting for about 90%, and one-third are mixed infections. There are significant differences in the spectrum of HAP pathogens at different onset times, basic conditions, severity of disease, and even in different regions, hospitals and departments.
(1) Patients without risk factors for MDR bacteria, early-onset HAP, VAP, and HCAP (group I): The common pathogens are Streptococcus pneumoniae, Haemophilus influenzae, methicillin-sensitive Staphylococcus aureus, and antibiotic-sensitive Enterobacteriaceae (such as Escherichia coli, Klebsiella pneumoniae, Proteus, Serratia etc.)
(2) Patients with HAP, VAP, and HCAP who are late and have risk factors for MDR bacteria (Group II): The common pathogens are Pseudomonas aeruginosa and Klebsiella pneumoniae producing extended-spectrum -lactamase (ESBL) Bacteria, Acinetobacter and other bacteria, or methicillin-resistant Staphylococcus aureus (MRSA) and Legionella pneumophila.
Risk factors for HAP, HCAP and VCA caused by MDR include:
1. Received antibacterial drugs in the previous 90 days;
2. Hospitalization 5 days;
3. High frequency antibiotic resistance in the ward of the local community or special hospital;
4. Risk factors for HCAP: 2 hospitalizations in the last 90 days; Living in a nursing home or expanded nursing facility; Intravenous infusion treatment (including antibacterial drugs); Long-term dialysis treatment within 30 days; Home wound care; Family members carry MDR pathogens;
5. Immunosuppressive diseases and / or treatments. [4]
Table 1 shows the main pathogens of HAP and their drug resistance.
Table 1 Introduction to the main pathogens and their resistance
Major pathogens
Drug resistance
Gram-negative bacilli
Multi-drug resistant non-fermentative bacteria
Pseudomonas aeruginosa
It has inherent resistance to many antimicrobials, and this resistance mechanism is mediated by a variety of efflux pumps. Data at home and abroad indicate that the resistance of P. aeruginosa to piperacillin, ceftazidime, cefepime, imipenem, meropenem, aminoglycosides or quinolones is increasing. Decreased expression of outer membrane porin (OprD) can cause resistance to meropenem but not to other -lactams. Currently, some MDR strains of Pseudomonas aeruginosa are only sensitive to polymyxin B
Acinetobacter (Acinetobacter baumannii, Acinetobacter lofi, etc.)
The incidence of HAP is getting higher and higher in recent years, and the situation of drug resistance is also very serious. At present, only carbapenems (imipenem and meropenem) have a sensitivity rate above 90%. For -lactam / -lactam enzyme inhibitor antibiotics, since sulbactam has a unique antibacterial activity against Acinetobacter, cefoperazone / Sulbactam has a good antibacterial activity against Acinetobacter. Its sensitivity can reach more than 70%. In addition to these two drugs, the sensitivity rate of other drugs including ceftazidime, piperacillin / tazobactam, cefepime, and ciprofloxacin did not exceed 60%.
Stenotrophomonas maltophilia
It exists widely in the natural environment and can often be isolated in the breathing and wounds of hospitalized patients, but it is mainly carried instead of infected pathogens. In recent years, the isolation rate of the bacteria has gradually increased, becoming one of the important pathogens of nosocomial infections, and can cause a variety of infectious diseases such as the respiratory tract and urinary tract. The bacteria mostly occur in immunocompromised, tumor patients and transplant patients. Among them, 87% of patients have various basic diseases, with chronic obstructive pulmonary disease (COPD) and respiratory failure being the most common. Unreasonable use of broad-spectrum antibiotics (especially carbapenems) and traumatic treatment are factors that increase the incidence of the infection. Stenotrophomonas maltophilia is naturally resistant to many antibiotics. The mechanism of resistance is mainly the low permeability of the outer membrane, and it can produce chromosome-mediated -lactam enzymes, which are a metal enzyme that directly hydrolyzes carbon. Penicnes. So no one drug is 100% sensitive and treatment is very difficult
Multidrug-resistant Enterobacteriaceae
Enterobacteriaceae producing extended-spectrum -lactamase (ESBL) (most common in Klebsiella pneumoniae and Escherichia coli)
Divided into several genotypes (CTX-M, TEM, SHV, etc.), not only resistant to all cephalosporins and aztreonam, but also resistant to quinolones and aminoglycosides. Can be inhibited by clavulanic acid, sulbactam and triazobactam, and sensitive to beta-lactam / beta-lactam enzyme inhibitors and carbapenems.
Enterobacteriaceae (mainly Enterobacter cloacae) producing chromosome-mediated type I B-lactamase (AmpC enzyme)
Since this enzyme is not inhibited by clavulanic acid, sulbactam, and triazobactam, these bacteria are also resistant to -lactam / -lactam enzyme inhibitors, cephalomycins, quinolones, aminoglycosides Resistant to imipenem, meropenem, and fourth-generation cephalosporins
Gram-positive cocci
Methicillin-resistant Staphylococcus aureus (MRSA)
It is a multi-resistant bacteria, but it has been sensitive to vancomycin for a long time. In 2002, the CDC in the United States reported the world's first case of vancomycin-resistant Staphylococcus aureus.
Methicillin-resistant coagulase-negative staphylococci (MRCON)
Because MRCON is a normal flora of human skin and has a high contamination rate, it is isolated in blood culture. The clinical significance needs to be carefully identified as a contamination or a pathogen. The resistance of this bacterium is also very common, especially Staphylococcus epidermidis and Staphylococcus hemolyticus, and there are also vancomycin-resistant strains, which should be taken seriously
Vancomycin-resistant Enterococcus (VRE)
Enterococci are inherently resistant to many antibiotics and sensitive to glycopeptides. In recent years, due to the unreasonable application of antibiotics, the drug resistance rate of the bacteria has increased. There are a large number of reports at home and abroad about the increased VRE separation rate

Diagnosis of hospital acquired pneumonia

History of hospital-acquired pneumonia

1. Clinical manifestations The clinical manifestations of HAP vary greatly, and the situation is complex. It is more common in elderly people who are weak, immune dysfunction, taking a lot of hormones or immunosuppressive agents, performing tracheal intubation, tracheotomy mechanical ventilation, chest and abdomen surgery, and coma And general anesthesia patients. Generally, the condition is severe and the disease progresses rapidly, and it will quickly turn into severe pneumonia. Clinical symptoms are not typical. When there is dementia, fever, unexplained dyspnea, and increased purulent secretions in the respiratory tract, the possibility of HAP should be considered and a chest X-ray examination should be performed as soon as possible. Typical symptoms of acute infections such as high fever, chills, and chest pain are uncommon. Auscultation of the lungs can smell scattered small and medium vesicles, which are more common at the base of the lungs. Dry rales and sputum can also be heard. It is generally difficult to see signs of consolidation of the lungs. Complicated atelectasis manifested as persistent dyspnea, increased breathing rate, inspiratory tricuspid sign, and hypoxemia. On examination, it was found that the trachea shifted to the affected side and the affected side's respiratory sounds disappeared. [5]
2. Complications Hospital-acquired pneumonia is mostly caused by Gram-negative bacilli, and some patients may be complicated by pulmonary suppuration, pleurisy, sepsis, and toxic shock of infection, or even respiratory cycle failure. In patients who have been bedridden for a long time, after thoracic and abdominal surgery, and tracheal intubation, due to bacterial infection, the sputum volume is large, the cough reflex is weakened, and sputum drainage is not easy to occur, with atelectasis on one side. Viral infection can cause complications such as myocarditis, encephalitis, radiculitis and Guillain-Barre syndrome. Legionella pneumoniae pneumonia is often accompanied by severe hyponatremia, and some patients are complicated by acute renal failure, shock, and DIC.

Hospital-acquired pneumonia

1. Generally, the peripheral blood white blood cell count of bacterial pneumonia is usually increased, and the neutrophils are mostly above 80%, with the left shift of the nucleus, and poisonous particles can be seen in the cells. In elderly people who are frail, alcoholic, and immunocompromised, the white blood cell count may not increase, but the percentage of neutrophils is still high. Mycoplasma pneumoniae or Chlamydia pneumoniae pneumonia is normal or slightly higher, the erythrocyte sedimentation rate is accelerated, and there may be a positive condensation test. Legionella pneumonia may have elevated liver enzymes and decreased blood sodium. In addition, arterial oxygen saturation, arterial blood gas analysis, liver and kidney function, and electrolytes are helpful for diagnosis.
2. Chest radiography or chest CT of chest radiography showed scattered spots, small pieces, and nodular infiltration shadows or interstitial changes in the two lungs, which are more common in the two lower lungs and may also be diffuse small pieces. Shape blur. As the disease progresses, the density of lesions can increase or merge, or form small voids. X-ray examination can be negative in patients with agranulocytosis and severe dehydration complicated by HAP, and 10% to 20% of patients with pneumocystis pneumonia are completely normal.
3. Etiological examination For the etiological examination, HAP requirements are stricter than CAP. The following principles should be followed: Routine blood culture and pleural effusion (when combined with pleural effusion) except for respiratory specimens. The culture of respiratory secretions must pay particular attention to quantitative or semi-quantitative culture. The problem with the pathogenic examination of sputum specimens (including lower respiratory tract specimens) of patients with HAP, especially mechanical ventilation, is not false negatives, but false positives. The significance of the culture results is determined by reference to the bacterial concentration. In addition, Staphylococcus epidermidis, Gram-positive bacteria other than Nocardia, Haemophilus bacteria other than Haemophilus influenzae, Micrococcus, Enterococcus, Candida and Anaerobic bacteria isolated from respiratory secretions The clinical significance is unclear. In immunocompromised hosts, attention should be paid to the inspection of special pathogens (fungi, Pneumocystis escherichia, mycobacteria, and viruses). In order to reduce the pollution of the upper respiratory tract flora, invasive lower respiratory tract pollution prevention sampling techniques should be used in selective cases. HAP patients in the ICU should be monitored for continuous etiology and drug resistance to guide clinical treatment. Acinetobacter, Staphylococcus aureus, Pseudomonas aeruginosa, Serratia, Enterobacteriaceae, Legionella, Fungi, Influenza virus, Respiratory syncytial virus and Mycobacterium tuberculosis can cause outbreaks of HAP, especially Pay attention to monitoring, tracing the source of infection and formulating effective control measures. [6]
(1) Specimen collection and microbiological examination
1) Sputum: It is the most convenient and non-invasive pathogenic diagnostic specimen, but sputum is easily contaminated by bacteria in the oropharynx. In turn, the quality of sputum specimens, whether they are submitted for inspection in a timely manner, and the quality control of the laboratory directly affect the bacterial isolation rate and interpretation of results, which must be standardized. Sputum specimens must be collected before antibiotic treatment. Instruct the patient to gargle first, and instruct or assist the patient in a deep cough, leaving the purulent sputum for examination. Mycobacteria and Pneumocystis edulis in sputum-free patients can be sputum guided by inhalation with hypertonic saline. Fungal and mycobacterial examinations should collect 3 early morning sputum specimens. Inspection should be submitted as soon as possible after collection, and it should not exceed 2 hours. Specimens that are delayed for submission or to be processed should be stored at 4 ° C (suspected Streptococcus pneumoniae infection is not included in this list), and the preserved specimens should be processed within 24 hours. For common bacteria, specimens should be cytologically screened first. Generally, sputum smear light microscopy is used to check 25 squamous epithelial cells per low magnification field, or squamous epithelial cells: leukocytes <1: 2.5 can be used as qualified specimens.
2) Fibrobronchoscope (fibrobroscopy) or artificial airway suction: The bronchoscope is inserted into the diseased site or the bronchus with more secretions attracts sputum. The specimen is inoculated in a petri dish and sent for examination. Those who have established an artificial airway can insert a fiberoptic bronchoscope through the artificial airway, or use a suction tube to insert the lower airway through the artificial airway and take a sputum specimen for examination. This method is less likely to be contaminated by oropharyngeal bacteria than sputum. If the concentration of attractant bacteria is 105 cfu / ml, it can be considered to be infected with pathogenic bacteria, and those below this concentration are mostly contaminated bacteria.
3) Protected specimen brush (PSB): The PSB is a nylon brush with a double-layer plastic tube and a polyethylene glycol seal at the distal end of the tube. The PSB is sampled through the bronchoscopy and can also be inserted through the artificial airway. After the bronchoscope reached the bronchial cavity where the pneumonia was drained, the PSB was inserted through the bronchoscope and beyond the front 1 to 2 cm, extended the top of the inner sleeve to seal the polyethylene glycol, and passed the outer tube about 2 cm, and then extended the brush The inner cannula is about 2 ~ 3cm to brush off the secretions. Then the brush and inner sleeve are retracted into the outer sleeve in order, and the entire PSB is finally pulled out. Sterilize the outer sleeve of the PSB with ethanol, cut off the top part of the inner and outer tube with sterile scissors, then extend the brush forward, cut it out and place it in a test tube filled with sterile physiological saline. . If the bacterial concentration is 103cfu / ml, it can be considered as the pathogen of infection. [7]
4) Bronchial alveolar lavage (BAL): When performing BAL, a bronchial bronchoscope is embedded in the bronchi of the corresponding segment or subsegment of the pneumonia, and 20 ml of physiological saline is injected. For those who have established artificial airways, anti-pollution catheters can be inserted directly into the lower respiratory tract for BAL. If the bacterial concentration is 104cfu / ml and the bacterial concentration of the anti-contamination BAL specimen is 103cfu / ml, it can be considered as a pathogen.
5) Percutaneous fine-needle aspiration (PFNA) and open chest lung biopsy: PFNA inserts a 22-gauge needle through the skin of the chest wall into negative lung tissue to attract the specimen for culture; open chest lung biopsy is Directly open the thorax to perform biopsy specimen culture and pathological examination of the infected tissue. The sensitivity and specificity of these two methods are very good, but because they are traumatic examinations, they can easily cause complications, such as pneumothorax, bleeding, etc. Clinically, they are generally used for those who do not respond to the empirical treatment of antibiotics or cannot determine other tests. Generally not required when not strictly necessary.
6) Blood and pleural effusion culture: Blood and pleural effusion culture is a simple and easy method for the diagnosis of the etiology of lung infections. Specimen collection is convenient, safe, has little chance of contamination, and high specificity, but the positive rate is relatively low, so it is often neglected clinically. The same bacteria were isolated from the blood and sputum cultures of patients with pneumonia and could be identified as the causative agent of pneumonia. If only blood culture is positive, but other reasons such as celiac infection and venous catheter-related infection cannot be used to explain bacteremia, blood cultured bacteria can also be regarded as the pathogen of pneumonia. Bacteria cultured from pleural effusion are basically considered pathogenic bacteria of pneumonia. Since blood or pleural effusion specimens are collected through the skin, the results must exclude skin bacterial contamination during the procedure. [8]
(2) Serological specimen collection and immunological diagnosis: Two serum specimens in the acute phase and the recovery phase were collected at intervals of 2 to 4 weeks, and are mainly used for the determination of specific antibody titers of atypical pathogens or respiratory viruses.
1) Serum Mycoplasma pneumoniae antibody detection: particle agglutination test, complement binding test (CF) and enzyme immunoassay (EIA);
2) Serum Chlamydia pneumoniae antibody detection: micro-immunofluorescence test (MIF), complement binding test (CF) and enzyme immunoassay (EIA);
3) Detection of Legionella pneumophila antibodies in serum: indirect fluorescent antibody method (IFA) and enzyme immunoassay (EIA);
4) Detection of Legionella pneumophila type I urine antigen: enzyme-linked immunoassay;
5) Serum influenza virus, respiratory syncytial virus and other antibody detection: complement binding test (CF), enzyme immunoassay (EIA), latex agglutination test (LA) and fluorescent antibody staining (FA);
6) Urine antigen detection of Streptococcus pneumoniae (immunochromatographic method);
7) The detection of Aspergillus galactomannan antigen (GM) and 1,3--D glucan antigen (G test) in fungal cell wall components in blood specimens is one of the basis of microbiological examination for the diagnosis of invasive fungal infections. , Its sensitivity and specificity have reached more than 80%. The GM test has clinical significance for the diagnosis of invasive Aspergillus infection, and it can be positive for several days before clinical symptoms and imaging have not appeared. It has early diagnostic value for continuous dynamic detection of high-risk patients (twice a week).
(3) Judgment of diagnostic significance of test results: see CAP section of the article.
4. Histological diagnosis is of diagnostic significance for mycobacteria, fungi, virus, pneumocystis and other infections. Lung tissue specimens can be obtained by percutaneous needle aspiration or lung biopsy with a biopsy gun, bronchoscopy lung biopsy, thoracotomy lung biopsy, and thoracoscopy lung biopsy. At least two specimens should be retained and sent to tissue disease Physical examination and cultivation. Histopathological examination is one of the main methods for the diagnosis of pulmonary mycosis. The basic pathological changes of pulmonary mycosis include purulent inflammation, non-purulent inflammation, granuloma formation (which may appear like tuberculous changes), coagulative necrosis, and vasculitis. Some fungal diseases have no inflammatory response, and these changes have no diagnostic value, and the diagnosis requires the discovery of fungi in the diseased tissue. Except for colored fungi with natural pigments, most fungi need to be stained in tissues before they can be seen under the microscope. Hematoxylin-eosin (HE) method, Gram staining method, Gridly staining method, Giemsa staining method, Grocott silver methylamine (GMS) method and Periodic acid tin (PAS) staining method can be used for fungal staining . For specimens suspected of fungal disease, a more specific staining method should be selected. The GMS method and the PAS method are more commonly used. Immunohistochemistry or fluorescent antibody staining can specifically identify various fungi and is mainly used to identify fungal species. [9]

Diagnosis and differential diagnosis of hospital acquired pneumonia

1. Diagnostic criteria The clinical diagnosis of HAP is the same as that of CAP, but the specificity of HAP diagnosis in clinical manifestations, laboratory and imaging findings is very low. The 2005 ATS clinical diagnosis of HAP included X-ray chest radiographs suggesting new or progressive exudative lesions, combined with 2 of 3 clinical manifestations (temperature> 38 ° C, increased or decreased WBC, and purulent sputum), which is the beginning Indications for empirical treatment of antimicrobials. X-ray examination can be negative in patients with granulocytic deficiency and severe dehydration complicated by HAP, and 10% to 20% of patients with Pneumocystis pneumoniae are completely normal. Reassessment is required after 2 to 3 days of clinical diagnosis to determine the use of antimicrobials.
The assessment of the severity of HAP can refer to the critical diagnosis criteria of CAP.
Mild and moderate: general condition is good, early onset (5 days after admission, mechanical ventilation <4 days), no high risk factors, stable vital signs, and no obvious abnormalities in organ function.
Severe: Same as CAP. Patients with late-onset disease (admission> 5 days, mechanical ventilation> 4 days) and high-risk factors are considered severe if they do not fully meet the criteria for severe pneumonia.
2. Differential diagnosis The diagnosis of HAP should be distinguished from other invasive diseases of the lungs, see Table 2.
Table 2 Main differential diagnosis of HAP
disease
Cause or underlying disease
Clinical manifestation
Film degree exam
other
Atelectasis
Tumor or sputum blockage or tumor or enlarged lymph node compression of the lumen
Pulmonary atelectasis occurs slowly or the symptoms are not obvious when the area is small. Sputum plugs are usually acute, with sudden chest tightness, shortness of breath, and difficulty breathing. Complicated infections may also include cough, sputum, fever, and hemoptysis, similar to pneumonia
The X-ray showed increased density, reduced volume, and the typical point of the lung pointed to the hilar sector and triangle, the size of the affected lung decreased, and the mediastinum shifted to the affected side.
Fiber bronchoscopy has greater diagnostic value for atelectasis
Heart failure and pulmonary edema
History of hypertension, coronary heart disease, rheumatic heart disease
Sudden severe shortness of breath, sitting up, cyanosis, sweating, coughing pink foamy sputum, both lungs and extensive wet rales and wheezing, enlarged left heart boundary, faster heart rate, apical scent and running horses law
X-ray examination showed enlarged heart boundary, hilum was butterfly-shaped, shadows of two lungs fused
Cardiac, diuretic, vasodilator and other active treatments can quickly relieve
Drug-induced lung injury
Have a history of using cytotoxic chemotherapy drugs (bleomycin), antiarrhythmic drugs (amiodarone), non-steroidal anti-inflammatory drugs, antibiotics (furantoin) and other drugs
Clinical manifestations vary widely and are not typical. Auscultation of the lungs The smell of the bottom of the lungs and the velcro rales are helpful for diagnosis
X-ray ground glass-like shadows, which gradually form diffuse nodular and reticular nodular shadows in both lungs
Pulmonary function showed restricted ventilation dysfunction and decreased diffuse function. Pathological examination of lung biopsy
Pulmonary thromboembolism
Has a history of thrombophlebitis, cardiopulmonary disease, trauma, abdominal or orthopedic surgery, long-term bed rest, and tumor history, with high risk factors for deep vein thrombosis
If the patient has severe chest pain, hemoptysis, dyspnea, and unconsciousness, pulmonary thromboembolism should be highly suspected
An X-ray chest radiograph shows a reduction in regional lung texture, with a typical change in a wedge-shaped shadow with the tip pointing toward the hilum
Arterial blood gas analysis see hypoxemia and hypocapnia. Examinations such as D-dimer, CT pulmonary angiography, radionuclide lung ventilation / perfusion scan, and MRI can help diagnose
Pulmonary hemorrhage-nephritis syndrome (Goodpasture syndrome)
Characterized by diffuse pulmonary hemorrhage, alveolar fibrosis, and glomerulonephritis
Cough, hemoptysis, and shortness of breath, often accompanied by anemia, hematuria, and proteinuria
X-ray shows diffuse point-like infiltrating shadows, scattered from the hilum to the periphery, and the apex of the lung is often clear
Serum anti-glomerular basement membrane (GBM) antibodies are often positive
Acute Respiratory Distress Syndrome (ARDS)
High risk factors for ARDS, including direct lung injury factors (severe infection, inhalation of stomach contents, lung contusion, inhalation of gas, drowning, oxygen poisoning, etc.) and indirect lung injury factors (infection poisoning, severe non-chest trauma, severe Pancreatitis, massive blood transfusion, extracorporeal circulation, disseminated intravascular coagulation, etc.)
Acute onset, frequency of breathing, and respiratory distress
X-ray examination reveals infiltrating shadows in both lungs
Hypoxemia (PaO2 / FiO2300 oxygenation index at ALI, PaO2 / FiO2 200 at ARDS). PAWP18mmHg or clinically can exclude cardiogenic pulmonary edema

Hospital-acquired pneumonia disease prevention

1. Avoid tracheal intubation and repeated intubation as much as possible. Mechanical ventilation must be used. Noninvasive methods should be used as much as possible. Oral intubation is better than nasal intubation.
2. The pressure of the water sac in the trachea cannula should be kept above 20cmH2O to prevent the pathogens around the waterproof sac from leaking into the lower respiratory tract. Sustained suction using subglottic secretions.
3. Remove condensing agents in the breath and circulation in time.
4. Paralyzing drugs should be avoided as much as possible, and the use of sedatives should be minimized in an effort to go offline as soon as possible.
5. The patient adopts a semi-recumbent position 30 to 45 °, avoiding the supine position, can reduce aspiration, especially for enteral nutrition patients.
6, enteral nutrition is superior to parenteral nutrition, because enteral nutrition can reduce complications related to central venous catheters, prevent small intestinal mucosal villous atrophy, and reduce bacterial colonization and transfer.
7. Oral antibacterials (selective digestive decontamination) can reduce the incidence of HAP in ICU patients and help suppress the outbreak of MDR pathogenic bacteria, but it is not recommended for routine use, especially for patients with MDR pathogenic bacteria colonization.
8. Prophylactic systemic use of antibacterials can reduce the incidence of HAP, but if antibacterials are used during the incubation period of pathogenic bacteria, the possibility of MDR pathogenic infection will increase. There is evidence that prophylactic systemic antimicrobials can prevent ICU-acquired HAP within 24 hours of acute tracheal intubation in patients with closed head injury. .
9. Try to avoid or reduce the use of H2-receptor blockers and antacids, or replace them with sucralfate. Sucralfate can reduce the incidence of HAP, but the incidence of major gastrointestinal bleeding is slightly higher.
10. Infusion of red blood cells and other people's blood products should strictly grasp the indications.
11. Intensive insulin therapy maintains blood glucose at 4.5 to 6 mmol / L, which can reduce the probability of nosocomial infections, the incidence of pneumonia, and the mortality rate in ICU patients, and shorten their ventilation treatment time and ICU stay time.
12. Beside bedside isolation for patients with MDR infection, avoid the spread of drug-resistant bacteria.
13. Diagnosis and treatment equipment, especially respiratory treatment equipment, is strictly disinfected and sterilized, and the aseptic operation system is effectively implemented. Hand washing is one of the easiest and most effective measures to reduce and prevent cross infection.
14. For patients with low immunity, such as those who need immunosuppressive therapy, granulocytopenia, diabetes, severe malnutrition, etc., they should focus on isolation, avoid cross infection, and stay in laminar flow ward when possible.
15, strengthen airway care, appropriate activities, do a good job to turn around and promote sputum. For tracheal intubation and tracheotomy patients, do airway humidification and enhance sputum suction.
16. Minimize the indwelling of various invasive ducts, such as deep vein catheters, nasogastric tubes, urinary catheters, arterial manometers, etc., while keeping the indwelling time as short as possible. [10]

Hospital-acquired pneumonia disease treatment

Choice of initial empirical antibiotics for hospital-acquired pneumonia

Table 3 Selection of initial empirical antimicrobials
patient
Probable pathogen
Drug choice
Patients without MDR bacterial risk factors, early-onset HAP, VAP, and HCAP (group I)
Streptococcus pneumoniae, Haemophilus influenzae, methicillin-sensitive Staphylococcus aureus, and antibiotic-sensitive Enterobacteriaceae bacteria (such as Escherichia coli, Klebsiella pneumoniae, Proteus, Serratia etc.)
Ceftriaxone, or levofloxacin, moxifloxacin, or ciprofloxacin, or ampicillin / sulbactam, or ertapenem
Patients with HAP, VAP, and HCAP who are late and have risk factors for MDR bacteria (group II)
Pseudomonas aeruginosa, Klebsiella pneumoniae, Acinetobacter, etc. producing extended-spectrum -lactamase (ESBL)
Anti-Pseudomonas cephalosporins (ceftazime, ceftazidime), carbapenems (imipenem, meropenem), or beta-lactam / beta-lactamase inhibitors (piracillin / tazolam) Batam), plus an anti-Pseudomonas quinolone (ciprofloxacin or levofloxacin), or an aminoglycoside (amikacin, gentamicin, or tobramycin)
Doubt MRSA
Plus linezolid or vancomycin
Legionella pneumophila
Add macrolides or fluoroquinolones
1.Precautions for initial antimicrobial selection
(1) A large amount of evidence-based medical evidence shows that inappropriate initial empirical treatment can increase antibiotic resistance, HAP mortality and medical costs, and prolong hospital stays. Moreover, even later adjustment of antibiotic treatment based on bacterial culture results will not reduce the high mortality associated with initial inappropriate antibiotic treatment.
(2) For MDR pathogens, initial combination therapy is required to ensure broad spectrum coverage and reduce the possibility of inappropriate initial empirical antibiotic treatment. However, it should be noted that if the patient has recently been treated with an antibiotic, empirical treatment should avoid using the same antibiotic, otherwise resistance to similar antibiotics is likely to occur.
(3) All treatments must select drugs according to the local antibiotic resistance and establish their own "best experience treatment plan" in order to truly achieve proper treatment.
2. Timing, dosage and duration of initial antibiotics The US ATS and IDSA guidelines require that patients begin correct empirical antibiotic treatment within 4 hours of admission or 4 hours after infection occurs. In order to achieve the goal of adequate treatment of HAP, not only need to use the correct antibiotics, but also need to use a reasonable dose, course of treatment and the correct route of administration. Patients with severe HAP or VAP must use adequate doses of antibiotics to ensure maximum efficacy.
(1) For adult patients with normal renal function, the doses of commonly used antibiotics are as follows: the full therapeutic dose of cefepime and ceftazidime is 2g, q8h; the therapeutic dose of meropenem (1g, q8h) is usually slightly greater than imipenem (0.5 g, q6h, or 1g, q8h); the dose of piperacillin-tazobactam not only requires at least 4.5g per dose, but also 4 times a day; among aminoglycosides, the amikacin The daily dose is 20 mg / kg; while the quinolone ciprofloxacin is 400 mg, q8h, levofloxacin is 750 mg, qd.
(2) If the patient has received the appropriate initial antibiotic regimen and the clinical response is good, efforts should be made to shorten the course of antibiotics from the traditional 14 to 21 days to 7 to 8 days to avoid causing new bacteria to colonize, but aeruginous fake orders The exceptions are non-fermentative bacterial infections such as bacillus and acinetobacter, which are prone to relapse if treatment is too short.
(3) If the aminoglycosides are included in the combined treatment plan adopted by the patient, as long as the patient has a response, the aminoglycosides can be discontinued after 5-7 days. [11]

Antibiotic treatment of hospital-acquired pneumonia specific pathogens

1. Combined therapy is recommended for Pseudomonas aeruginosa, mainly using -lactams in combination with aminoglycosides. The latter can be replaced by fluoroquinolones, mainly ciprofloxacin or levofloxacin.
2. The most effective drugs of the genus Acinetobacter are carbapenems, sulbactam, polymyxin E and polymyxin B, and tigecycline.
3. ESBLs-producing Enterobacteriaceae: Avoid using third-generation cephalosporin monotherapy, especially Enterobacter bacteria should avoid using third-generation cephalosporins. The most effective drug is carbapenems.
4. MRSA can choose vancomycin or norvancomycin. Linezolid is equivalent to vancomycin. Patients with renal insufficiency or are receiving other nephrotoxic drugs may be given priority for linezolid. [12]

Evaluation of hospital-acquired pneumonia in response to treatment

1. After the initial antibiotic treatment of HAP, the patient's response to the treatment should be closely observed. Once blood or respiratory secretion culture results are obtained, or the patient does not respond to the treatment, the empirical antibiotic treatment should be adjusted in a timely manner.
2. If no MDR pathogens (such as Pseudomonas aeruginosa or Acinetobacter) are found, or if the isolated pathogens are at least one kind of antibiotic that is less broad-spectrum than the drugs used in the initial protocol, step-down treatment should be used. .
3. The worsening or no improvement may be due to the following reasons: non-infectious diseases were misdiagnosed as HAP; or the first infection was drug-resistant bacteria, or other pathogens such as Mycobacterium tuberculosis, fungi, or respiratory viruses; and complications occurred .

Hospital-acquired pneumonia other treatments

HAP patients are generally older than CAP patients, with poor physiques and complex conditions, and often have organ dysfunction. Therefore, symptomatic and supportive treatment are particularly important, such as expectorant, asthma, maintaining water and electrolyte balance, correcting acid-base disorders, and protecting the viscera. Device functions. [13]

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