A parapneumonic pleural effusion is a pleural effusion secondary to pneumonia (bacterial or viral) or lung abscess. An abscess is the presence of pus in the chest cavity, which is a thick, viscous, thick fluid. If the culture of pleural effusion is positive, there is an indication for invasive operation.
1.Pathophysiology
The development of pleural effusion and pus in the pleural cavity next to pneumonia can usually be divided into the following stages.
(1) Dry pleuritis stage
Inflammation of the lung parenchyma spreads to the dirty pleura, causing a confined pleural inflammatory response, which can lead to a pleural rubbing sensation (sound) and characteristic chest pain caused by both layers of the pleura during respiration. The chest pain is caused by the more sensitive nerves in the wall pleura. Most patients with pneumonia have only chest pain and do not progress to the pleural effusion stage, meaning that most patients with pneumonia involve the pleura only to this stage.
(2) Exudative stage
As inflammation continues to develop, inflammatory mediators can lead to increased permeability of local tissues and capillaries. The increase in fluid accumulation in the pleural cavity may be the result of a combination of inflow of intertissue fluid from the lung and local microvascular exudation. This effusion is usually clear and sterile, with a particularly neutrophilic cellular classification, normal ph, and ldh activity of 1000 iu/L.
(3) Fibro-purulent stage
Those patients who are untreated or ineffective with antibiotics will quickly (about hours) progress to this stage. It is characterized by protein deposits in the pleural cavity and the formation of a fibrous membrane, which can cause the pleural cavity to become compartmentalized and is often accompanied by bacterial invasion of the lung parenchyma. This fluid is often cloudy or purulent. Cytologic examination is dominated by neutrophils, most of which are degenerated and necrotic, and Gram stain as well as bacterial cultures are often positive. This exudate has a high metabolic and cytolytic activity, so it tends to have a low ph (7.2) and high ldh activity (often greater than 1000 iu).
(4) Mechanized stage
The final stage is characterized by the formation of fibroblasts, which causes the interpleural fibrous membrane to turn into a thick and inelastic pleura. The gas exchange function of an already mechanized septic chest will be severely impaired (lung collapse). If it develops further, the outcome varies from self-resolving but with permanent impairment of lung function to chronic pustulothorax with the possibility of complications such as bronchopleural fistula, lung abscess, open pustulothorax, etc.
2.Bacteriology
Unless the amount of pleural effusion is very small, thoracentesis should be performed in all patients with suspected parapneumonic pleural effusion (e.g., Figure 15-1). Bacteriologic examination should include Gram staining, as well as aerobic and anaerobic bacterial cultures. Many different species of bacteria have been identified that can cause parapneumonic pleural effusions or abscess chests. In recent decades, the previously common bacterial spectrum has changed, in part due to the constantly updated application of antibiotics. In addition, the differences in the reported bacterial spectrum are also related to the different subjects chosen by the investigators conducting the studies. According to recent series from the United States and Europe, the majority of positive bacteriological cultures of pleural effusions are due to aerobic infections, however, up to 15％ are due to anaerobic infections alone, and the rest are due to multiple factors, often a mixture of aerobic and anaerobic bacteria. Aerobic gram-positive bacteria are more common as streptococci (mostly Streptococcus pneumoniae) and staphylococci (mostly Staphylococcus aureus). The most common aerobic gram-negative bacteria include Escherichia coli, Klebsiella, and Pseudomonas. Escherichia coli and anaerobes are often mixed with other bacteria. The most common anaerobic bacteria are Bacillus spp. and Streptococcus pepticus. Sometimes, Actinomyces spp., Nocardia spp. and fungi are also the causes of pustulosis.
3.Clinical manifestations
The clinical manifestations of patients with pneumonia are similar regardless of the presence or absence of parapneumonic pleural effusion, and there is no significant difference in either the white blood cell count or chest pain manifestations in the two cases.
Pneumonia due to aerobic bacterial infection tends to show acute fever, while anaerobic bacterial infection is more likely to show a subacute or chronic course, with symptoms often lasting longer and accompanied by significant weight loss. Pneumonia due to anaerobic bacteria is often due to aspiration of oral or gastric contents by mistake. These patients have poor oral hygiene with oral colonization by anaerobic bacteria and also have high risk factors for misaspiration, such as seizures, syncope from other causes, and alcohol abuse, which is associated with alcohol abuse in as many as 29% to 40% of patients.
Those patients whose symptoms persist for a longer period of time before receiving medication or who have an inadequate course of treatment are at high risk of developing complex pneumonia parietal pleural effusion or abscess thorax.
Septic pleurisy without pneumonia can be seen as a post-pneumonic pustulothorax in patients whose lung inflammation has resolved. An abscess is not necessarily caused by pneumonia; most non-pneumonia abscesses are of medical origin, most commonly as a complication of pneumonectomy or other open-heart surgery. Open-heart surgery results in about 20% of abscess thoraxes, chest trauma in about 5%, and esophageal perforation in 5% (often of medical origin). Those caused by thoracentesis and spontaneous pneumothorax each account for 2%, and those caused by abdominal infection account for about 1%, mainly originating from the subdiaphragmatic region and occurring mostly after surgical procedures, especially cholecystectomy or splenectomy.
4.Diagnosis and differential diagnosis
Fever, pulmonary inflammatory infiltrate and pleural effusion are not always caused by pneumonia or complications of surgical procedures, and the possibility of pulmonary embolism must be considered. Pulmonary embolism is a common disease and the incidence of pleural effusion is about 25% to 50%. Pleural effusion may be secondary to infection, and the treatment plan in this case is the same as for pleural effusion next to complicated pneumonia. There are other diseases that should be differentiated, such as tuberculosis, lupus erythematosus and other autoimmune diseases, acute pancreatitis and other gastrointestinal diseases, and drug-induced pulmonary pleural disease. A pustule with cloudy or milky pus is sometimes misdiagnosed as celiac disease or pseudo-celiac disease.
(1) Imaging examination
When pneumonia is accompanied by ipsilateral pleural effusion, routine chest X-ray is able to detect it. Lateral chest radiographs are particularly significant for the detection of posterior rib septal angle effusion. A bilateral prone chest radiograph can identify whether the fluid is a free-flowing pleural effusion or a dense inflammatory shadow in the lung. The most typical imaging sign of a septic chest is an encapsulated effusion.
Ultrasonography can be used to guide thoracentesis or chest tube placement. Ultrasound diagnosis is more important for small amounts of pleural effusion and for pleural effusions that require accurate localization (e.g., effusions with compartmentalization).
CT signs include pleural thickening, echogenic enhancement, and increased density of adjacent subcostal tissue. Nonetheless, CT imaging changes cannot help in the clinical staging of a pus-filled chest.
MRI sagittal view provides detailed information on the layers of the chest wall and the presence of inflammatory infiltration or malignant metastases. Simple parapneumonic pleural effusions usually do not cause significant changes in the chest wall, whereas malignant pleural effusions are usually seen with changes in the peripleural fat layer and the inner intercostal muscles, and these findings help to differentiate benign from malignant pleural effusions. However, the chest wall infiltrates of complex pleural effusions and pustules are likely to have similarities with malignant disease.
New imaging techniques can provide more detailed morphologic information and can provide a basis for determining the nature of pleural effusions and the cause of pleural effusion formation. However, they cannot replace thoracentesis and other invasive examinations.
(2) Biochemical analysis of pleural effusion
Pleural effusion next to pneumonia is usually exudate, if it is leaking fluid, it can be ruled out as a pleural effusion next to pneumonia, and there is a high possibility of other disease conditions such as heart failure, liver cirrhosis, hypoproteinemia, etc.
(3) Cytological examination
Pleural effusion next to pneumonia and abscess pleural effusion is predominantly neutrophilic. If other cells are detected as predominant, other diseases should be considered, such as lymphocyte-dominated exudate, which is likely to be tuberculosis or malignant tumor.
5.Treatment
(1) Antibiotic treatment
The most important of the various treatments for parapneumonic pleural effusion and abscess chest is systematic antibiotic therapy. Antibiotic therapy should be started as soon as the bacteriological basis is obtained from pleural fluid samples, sputum, and blood samples. Empiric antibiotic therapy involves the selection of those antibiotics that are sensitive to the common pathogens of parapneumonic pleural effusions, and the odor of the pleural fluid (malodor due to anaerobic infection) as well as other clinical manifestations can influence the initial antibiotic regimen. In patients with community-acquired pneumonia, antibiotic choices should include a 2nd or 3rd generation cephalosporin, or a beta-lactam/beta-lactamase inhibitor combination, with concomitant metronidazole or clindamycin if co-infection with anaerobic bacteria is suspected. For suspected Legionella infections (which can cause parapneumonic pleural effusions, although they rarely have a tendency to complicate), macrolide antibiotics such as erythromycin and clarithromycin may be used. For severe nosocomial pneumonia, a third-generation cephalosporin or imipenem should be preferred. In patients infected by Gram-staining negative bacteria, due to purulent, acidic pleural fluid and low local oxygen partial pressure, aminoglycosides may be ineffective at this time and a combination of aminotransomide should be considered. Further antibiotic therapy should be adjusted according to the results of Gram stain and bacterial culture.
(2) Thoracic drainage
All patients with complex pleural effusions should have chest tube drainage, preferably under ultrasound or CT guidance, to ensure optimal localization. For pleural effusions with internal compartments, a second tube may be placed into the small cavity of the compartment to facilitate treatment. Conventional wisdom recommends the use of a large tube (26 C 32F) for drainage, but evidence suggests that at least for small tubes of pleural fluid without viscous pus is sufficient. For viscous pus, a double-lumen catheter can be placed for drainage and the pleural cavity can be flushed with saline. The use of topical antibiotics via catheter is not yet recommended.
The effectiveness of chest tube drainage should be verified within 24 hours (including imaging suggestive of decreased pleural fluid and improvement in clinical symptoms), and prolonged or ineffective chest tube drainage will increase the incidence of infection and mortality. Therefore, if chest tube drainage is ineffective, other more effective treatment methods should be used immediately.
(3) Intra-thoracic injection of fibrinolytic agent
Intrathoracic injection of streptokinase and streptokinase was reported more than 50 years ago to promote chest drainage in patients with septic chest. The use of intrathoracic injection of streptokinase and streptokinase was later abandoned due to the high number of systemic side effects associated with intrathoracic injection, including fever, general malaise, and neutrophilia.
The results of a recently published study on thoracic injection of fibrinolytic agents for the treatment of pleural effusions adjacent to complicated pneumonia were disappointing. In this multicenter, randomized, double-blind study, 427 patients received intrathoracic injection of streptokinase or placebo, and it was found that there was no significant difference in mortality or the proportion of patients requiring surgery between the two groups. In addition, no benefit was shown for the use of streptokinase based on mortality, surgical rates, x-ray findings, or comparison of hospital days.
Studies on enzyme debridement for the treatment of pleural effusions adjacent to multifocal pneumonia have used a double chain of enzymes including streptokinase and streptokinase, but it is less clear how much streptokinase is needed to be effective. simpson et al. also recently demonstrated that recombinant human streptokinase is very effective for purulent pleural effusion mucosity, and the treatment of complex pleural effusions or abscesses with or without streptokinase is currently being explored.
(4) Thoracoscopic release of pleural adhesions
Another option for patients with parapneumonic pleural effusion without complete drainage is to perform thoracoscopy, which should be preceded by a CT scan of the chest to obtain anatomical information on the size and severity of the abscess cavity. When thoracoscopy is performed, multiple small cavities in the pleural cavity are opened up so that the pleural cavity can be completely drained and the chest tube can be placed in the optimal position. In addition, the pleural surface can be examined to determine if pleurodesis intervention is warranted. If thoracoscopy reveals a large amount of pleural hypertrophy that cannot be treated and pleurodesis is considered necessary, the hypertrophic pleura can be removed by enlarging the thoracotomy incision.
(5) Pleurodesis
Pleurodesis involves removal of all fibrous tissue from the dirty and mural pleura, evacuation of all pus or debris from the pleural cavity, and elimination of pleural sepsis, resulting in lung expansion. Pleurodesis is a highly invasive thoracic surgery procedure that usually requires a complete thoracotomy and therefore cannot be performed in patients with significant failure.
In patients with acute stage thoracic infection, pleurodesis is considered for infection control only. After 6 months, if the pleura is still hypertrophic and the patient’s lung function is significantly reduced to the point of limiting activity, then debridement should be considered, as lung function increases significantly in patients who undergo debridement.
(6) Open drainage
Chronic drainage of the chest cavity can be accomplished with open drainage. There are two different ways to do this, the simplest of which is to insert a short, large, perforated tube into the abscess cavity, followed by daily flushing of the catheter with a mild antiseptic solution and collection of the catheter drainage in a colostomy bag placed over the catheter. Another operation is to fill the pus cavity with gauze, an operation that allows the patient to avoid the use of suction devices and provides more complete drainage.
It is also important that open drainage is not performed too early in complex parapneumonic pleural effusions. If the dirty, mural pleura adjacent to a pus-filled chest has not yet fused due to the inflammatory process, the pleural cavity is open to the outside atmosphere leading to a pneumothorax. The above possibilities are evaluated before performing open drainage. A chest tube is placed for a short period of time and allowed to communicate with the outside atmosphere, followed by radiological examination to determine whether the lung is atrophied.