Lung abscess is necrotic lesion and abscess formation of lung tissue caused by various pathogens. The clinical features are high fever, cough, and excessive purulent and foul-smelling expectoration. Chest x-ray or CT shows one or multiple cavities with air-fluid levels. If there are multiple cavities with a diameter less than 2 cm, the condition is also termed necrotizing pneumonia. Lung abscess can occur at any age, predominantly in young adults, and males are more affected than females. The pathogens are mainly anaerobic bacteria and facultative anaerobic bacteria. In recent years, the rate of aerobic infection has increased.
Etiology and pathogenesis
The pathogens of lung abscess are closely related to the route of infection. According to the route of infection, lung abscess can be divided into primary lung abscess, secondary lung abscess, and hematogenous lung abscess.
Primary lung abscess
Primary lung abscess, also known as aspiration lung abscess, is mainly caused by aspiration of pathogenic bacteria, mainly anaerobic bacteria, from the mouth, nose, and pharynx. Aspiration and the reduction of airway defense and clearance function are important causes for its occurrence. Common anaerobic bacteria include Peptostreptococcus, Prevotella, Fusobacterium, and Bacteroides fragilis; while aerobic bacteria and facultative anaerobic bacteria include mainly Streptococcus, Staphylococcus aureus, Pseudomonas aeruginosa, and Klebsiella pneumoniae. Lung abscess is often solitary, and the site is related to bronchial anatomy and anatomical position. Because the right main bronchus is steep and has a large diameter, aspirated substances are prone to entering the right lung. Abscess occurs mainly in the posterior segment of the upper lobe or the dorsal segment of the lower lobe, in the posterior basal segment of the lower lobe in sitting position, and in the anterior or posterior segment of the right upper lobe in right lateral recumbent position.
Secondary lung abscess
Lung abscess may be secondary to bacterial pneumonia caused by Staphylococcus aureus, Pseudomonas aeruginosa, and Klebsiella pneumoniae. Secondary infections of underlying lung diseases such as bronchial foreign body obstruction, bronchiectasis, bronchial cyst, bronchogenic carcinoma, and cavitary tuberculosis can also lead to secondary lung abscess. Suppurative lesions of adjacent organs, such as subphrenic abscess, perinephric abscess, spinal abscess, and esophageal perforation, can also cause lung abscess. Amebic liver abscess occurs mostly at the top of the right liver and can easily penetrate the diaphragm to the lower lobe of the right lung, forming amebic lung abscess.
Hematogenous lung abscess
In infectious toxicosis caused by skin and soft tissue infections, intravenous drug abuse, peripharyngeal space infections, or dissemination of liver abscess, bacterial emboli are disseminated to the lungs through the bloodstream, causing embolism, inflammation, and necrosis of small blood vessels, thereby forming hematogenous lung abscess. Staphylococcus aureus is the common pathogen of infectious toxicosis after skin and soft tissue infections or intravenous drug abuse. Hypervirulent Klebsiella pneumoniae often leads to multiple abscesses in the liver and lungs, and patients often have a history of diabetes or abnormal glucose tolerance. Streptococcus anginosus group, including Streptococcus intermedius, Streptococcus anginosus, and Streptococcus constellatus, often causes suppurative infections, particularly brain abscess and abdominal organ abscesses, as well as oral or respiratory tract infections, such as peripharyngeal space abscess, lung abscess, and empyema. The imaging manifestations of hematogenous lung abscess are multiple subpleural wedgy consolidations with abscess formation in both lungs.
Pathology
The infectious pathogen causes pneumonia and obstructs the bronchioles, and the reproduction of pathogenic bacteria causes inflammatory embolism of small blood vessels, resulting in necrosis of lung tissue and lung abscess formation. Subsequently, the necrotic tissue liquefies and ruptures into the bronchi, and the pus is partially discharged, forming an abscess cavity with air-liquid level. Residual necrotic tissue is often found on the surface of the cavity wall. The lesion tends to expand to the periphery, and even involves the interlobar fissures and visceral pleura. If the abscess is close to the pleura, localized fibrinous pleurisy and pleural adhesions may occur. If it is a tension abscess, it may rupture into the pleural cavity, forming empyema, pyopneumothorax, or bronchopleural fistula. Lung abscess can completely subside or only little fibrous scar remains.
Acute lung abscess cannot generally last for 4 - 6 weeks. Improper treatment or inadequate bronchial drainage can result in massive necrotic tissue remaining in the abscess cavity. If inflammation lasts for more than 3 months, it is termed chronic lung abscess. The fibroblasts in the abscess cavity wall proliferate, and the granulation tissue thickens the abscess cavity wall. The peripheral bronchioles may be involved, and deformation or dilation may occur.
Clinical manifestations
In the early stage, there are often pneumonia symptoms, and patients have chills, high fever (body temperature up to 39 - 40°C), cough, and mucus or mucopurulent expectoration. The involvement of the pleura can cause thoracodynia. There are also systemic symptoms such as listlessness, malaise, and anorexia. About 90% of patients with lung abscess have apparent risk factors of gingival diseases, oral uncleanliness, or aspiration, such as a history of surgery, alcohol intoxication, overexertion, cold exposure, and cerebrovascular diseases. Simple lung abscess caused by anaerobic bacteria can have an insidious onset. If the infection cannot be controlled quickly, cough intensifies in 1 - 2 weeks, and large amounts of purulent and foul-smelling sputum and necrotic tissue are coughed out, up to 300 - 500 ml every day, and can be separated into 3 layers after standing. About 1/3 of patients have little hemoptysis, and occasionally moderate or massive hemoptysis. Generally, after excessive purulent sputum is coughed out, the body temperature drops significantly, and the systemic symptoms are relieved. Lung abscess heals in several weeks. If the body's resistance decreases and the lesion progresses rapidly, the abscess can rupture into the pleural cavity, and symptoms of pyopneumothorax such as sudden thoracodynia and tachypnea occur. Hematogenous lung abscess has mostly a history of extrapulmonary infections, such as skin and soft tissue infections, peripharyngeal space infections, and liver abscess. Local symptoms caused by the primary lesion, as well as systemic symptoms of infectious toxicosis such as chills and high fever, are followed by pulmonary symptoms such as cough, little expectoration, and occasionally hemoptysis in several days to 2 weeks.
The signs are related to the size and location of the lung abscess. In the early stage of the disease, when the lesion is small or located deep in the lung, there may be no abnormal signs in the lungs. When the lesion is large, there may be inflammation around the abscess, signs of pneumonia consolidation may appear, and bronchial breath sounds can be heard. In case of large cavity, tympany and amphoric breath sound can be detected on percussion. If the lesion involves the pleura, pleural friction rub can be heard or signs of pleural effusion may appear. Patients with chronic lung abscess often present with symptoms of chronic wasting disease such as emaciation and anemia, and may have clubbed fingers (toes). Most hematogenous lung abscesses have no abnormal signs.
Laboratory and other examinations
Biochemical examination
The total white blood cell count in acute lung abscess reaches (20-30) x 109/L, neutrophils account for more than 90%, and there are significant left shift and toxic particles. The white blood cell count in chronic patients may be slightly elevated or normal, and red blood cells and hemoglobin are reduced.
Microbiological examination
Sputum smear Gram staining and sputum, pleural effusion, and blood cultures, including aerobic and anaerobic cultures, as well as antimicrobial susceptibility test, are helpful in determination of pathogens and selection of effective antibiotics. The ideal sampling method is bronchoscopic brushing or percutaneous fine-needle aspiration. In patients with pleural effusion, a positive culture of pleural effusion has great diagnostic value for the pathogen. Blood cultures in patients with hematogenous lung abscess can detect pathogenic bacteria.
Imaging examination
Frontal and lateral chest x-ray films are the most common means for diagnosis of lung abscess. The x-ray manifestations of lung abscess can vary depending on the type, stage of the disease, adequate or inadequate bronchial drainage, and presence or absence of pleural complications. In the early stage of primary lung abscess, chest x-ray shows patchy, dense, hazy infiltration with unclear edges or massive dense opacities in one or several lung segments. After lung abscess formation, pus is discharged through the bronchi, and peripheral circular lucent area and air-fluid level in the abscess cavity, surrounded by dense inflammatory infiltration, can be seen. The inner wall of the abscess cavity is smooth or slightly irregular. After drainage and antibiotic treatment, the inflammation around the lung abscess subsides, the abscess cavity shrinks or even disappears, and finally only irregular linear opacities can be seen. Chronic lung abscess is mainly characterized by thick-walled cavity, irregular inner wall, sometimes multilocular appearance, fibrous tissue hyperplasia and adjacent pleural thickening, lobar atrophy, and mediastinum shifting to the affected side. When complicated with empyema, the affected side of the chest shows massive dense opacity; if accompanied by pneumothorax, air-fluid level can be seen. Hematogenous lung abscess is manifested by multiple patchy, spherical, or oval, variously sized, dense opacities with regular edges on the periphery of one or both lungs, small abscess cavities and fluid levels can be seen. After the inflammation subsides, focal fibrosis or small air sacs can be seen. Chest CT examination can more accurately locate and detect small abscesses, and is of great significance for the diagnosis, differential diagnosis, and treatment.
Electronic bronchoscopy
Electronic bronchoscopy is helpful for clarification of the etiology, etiological diagnosis, and treatment. Sampling with bronchial needle aspiration and bronchial brushing through electronic bronchoscopy for aerobic and anaerobic bacteria cultures can clarify the pathogen. Pathological examination of tissue biopsy can be used to differentiate from tumors. With the help of electronic bronchoscopy, aspiration of pus and injection of antibiotics at the lesion site can promote bronchial drainage and abscess cavity healing.
Diagnosis
On the basis of risk factors for aspiration or history of aspiration, the clinical manifestations such as chills, high fever, cough, excessive purulent and foul-smelling expectoration, a significant increase in the total count of peripheral blood white blood cells and neutrophils, and abscess cavities and/or air-fluid levels in patchy dense inflammatory opacity in the lungs, a diagnosis can be established. Airway secretion and blood cultures, including aerobic and anaerobic cultures, and antimicrobial susceptibility test are of great value for determination of the pathogen and selection of antimicrobial drugs. In case of risk factors such as skin and soft tissue infections, intravenous drug abuse, peripharyngeal space infections, and dissemination of highly virulent Klebsiella pneumoniae infection; extrapulmonary infections; symptoms such as persistent fever, cough, and expectoration; and multiple subpleural wedgy consolidations with abscess formation in both lungs, hematogenous lung abscess can be diagnosed.
Differential diagnosis
Bacterial pneumonia
Early lung abscess resembles bacterial pneumonia in symptoms and x-ray manifestations. Streptococcal pneumonia is the most common bacterial pneumonia, often with oral blebs and rusty sputum, without excessive, foul-smelling, purulent sputum. Chest x-ray shows consolidation of the lung lobe or segment, or poorly marginated, hazy, patchy inflammatory opacity, without cavity formation.
Cavitary tuberculosis
Clinical manifestations include slow onset, long course, low-grade fever in the afternoon, malaise, diaphoresis, long-term cough, anorexia, and recurrent hemoptysis. Chest x-ray shows thick cavity wall, usually no fluid level, little inflammatory lesions, with or without irregular linear spots, nodules, calcified spots, and sometimes ipsilateral or contralateral dissemination lesions. Mycobacterium tuberculosis can be found in sputum.
Lung cancer
Tumors blocking the bronchi can cause distal obstructive pneumonia, and if infected with pyogenic pathogens, lung abscess can form. There are long course and little purulent sputum. Due to inadequate bronchial drainage, antibiotic treatment is poorly effective. Squamous cell carcinoma of the lung itself can also undergo necrosis and liquefaction to form cavity, termed cancerous cavity, but generally there are no acute infection symptoms. Chest imaging shows thick-wall cavity, mostly eccentric, rough inner wall of the cavity caused by the remaining tumor tissue, little inflammatory infiltration around the cavity, and hilar lymph node enlargement. Therefore, it is not difficult to differentiate from lung abscess. If cancer cells are found through electronic bronchoscopy or in sputum, the diagnosis can be confirmed.
Secondary infection of pulmonary bullae or cysts
In case of infections secondary to pulmonary bullae or lung cysts, there are air-fluid levels in the pulmonary bullae or cysts, with mild peripheral inflammatory reaction, and inapparent symptoms and purulent sputum. It is easier to differentiate if there are previous imaging results for comparison.
Treatment
The treatment principles of acute lung abscess include effective antiinfection treatment and adequate drainage.
General measures
Patients with lung abscess generally have manifestations of wasting disease, particularly in patients with weak constitution, nutritional treatment should be strengthened. Oxygen therapy can be given in case of hypoxia.
Antibiotic treatment
Primary lung abscess is a mixed infection mainly caused by anaerobic bacteria. Most anaerobic bacteria are sensitive to penicillin. Penicillin can be empirically selected at a daily dose of 1.2 million to 10 million units intravenously in 3 - 4 divided doses. If the efficacy of penicillin is not good, clindamycin 0.6 - 1.8 g/d or metronidazole 1.0 - 1.5 g/d intravenously in 2 - 3 divided doses can be used. If the efficacy is still not good, attention should be paid to selection of appropriate antibiotics according to antibiotic sensitivity test in bacterial culture. Other antibiotics such as carbapenems and β-lactam/β-lactamase inhibitors can also be selected.
The pathogens of hematogenous lung abscess are mostly Staphylococcus aureus, Klebsiella pneumoniae, and Streptococcus anginosus group. For Staphylococcus aureus infection, penicillinase-resistant semi-synthetic penicillin such as oxacillin sodium 6 - 12 g/d intravenously in divided doses can be selected; For methicillin-resistant Staphylococcus aureus (MRSA), vancomycin, teicoplanin, or linezolid should be preferred. When infected with Gram-negative bacilli such as Klebsiella pneumoniae, the second and third generation cephalosporins or carbapenems in combination with aminoglycosides or ciprofloxacin can be administered for anti-infection treatment. Streptococcus anginosus group infections can be treated with penicillin, and vancomycin can be selected in case of resistance to penicillin. Hematogenous lung abscess should be treated using antibacterial drugs with high local concentration, the primary infection should be properly treated, and incision and drainage should be performed for skin and soft tissue abscesses, peripharyngeal space abscesses, and liver abscesses.
The course of antibiotic treatment is generally 6 - 8 weeks until the clinical symptoms completely subside, and chest imaging shows that the abscess cavity and inflammatory lesions completely subside, leaving only irregular linear opacities. With effective antibiotic treatment, the body temperature can decrease in about 3 - 7 days and return to normal in 7 - 14 days, and the foul smell of sputum disappears within 3 - 10 days. After clinical symptoms improve, intravenous infusion of antibiotics can be replaced by intramuscular injection or oral administration.
Purulent drainage
Purulent drainage can shorten the course and improve the efficacy. In patients with thick expectoration, expectorants such as ambroxol and acetylcysteine and inhalation of nebulized saline or bronchodilators can be used to facilitate sputum drainage. In patients in good physical condition, postural drainage can be used to drain sputum. The drainage posture should remain the abscess at the highest position, the affected area can be gently tapped, each drainage lasts for 10 - 15 minutes, and 2 - 3 drainages a day should be performed. Flushing and aspiration in electronic bronchoscopy are also very effective.
Surgery
The indications for surgical treatment include chronic lung abscess without reduction of abscess cavity after more than 3 months of medical treatment, uncontrolled or recurrent infections, or large abscess cavity (more than 5cm); concurrent bronchopleural fistula or empyema with ineffective or poor treatment of aspiration and rinse; massive or life-threatening hemoptysis with ineffective medical treatment; and bronchial obstruction caused by inadequate drainage in lung abscess with suspected lung cancer.
Prevention
Attention should be paid to the treatment of chronic infection lesions in the oral cavity and upper respiratory tract. Before oral, thoracic, or abdominal surgery, oral hygiene should be maintained. During surgery, blood clots and secretions from the oral cavity and upper respiratory tract should be removed. Patients should be encouraged to cough, foreign bodies in the respiratory tract should be removed, and respiratory drainage should be adequate. In comatose patients, more attention should be paid to oral hygiene.