- Lung abscess is classified as primary or secondary. Primary occurs without underlying lung disease, while secondary occurs in the context of structural or functional lung abnormalities. Clinical features include fever, cough, and dyspnea. Management involves appropriate
- Lung abscess is classified as primary or secondary. Primary occurs without underlying lung disease, while secondary occurs in the context of structural or functional lung abnormalities. Clinical features include fever, cough, and dyspnea. Management involves appropriate
- Lung abscess is classified as primary or secondary. Primary occurs without underlying lung disease, while secondary occurs in the context of structural or functional lung abnormalities. Clinical features include fever, cough, and dyspnea. Management involves appropriate
Causative organisms- most commonly by Streptococcus Pneumoniae , Staphylococcal aureus in developing nations, Asia and Post traumatic empyema. •Other causes- Rupture of lung absecess into pleural space, contamination introduced from trauma or thoracic surgery, mediastinitis or extension of intra-abdominal abscess. •Less common organisms- Group A Streptococcus, Gram-negative organisms, tuberculosis, fungi. Epidemiology Most commonly encountered in Infants and Preschool children. 5-10% children with bacterial pneumonia and 86% children with necrotizing pneumonia. Pathology
3 stages
Stage 1-Exudative stage- fibrinous
exudate forms on pleural surfaces. Stage 2- Fibrinopurulent stage- Fibrinous septa form, causing loculation of fluid and thickening of parietal pleura. If pus not drained – dissect through pleura into lung parenchyma producing bronchopleural fistulas and pyopneumothorax or into abdominal cavity. Rarely pus dissects through chest wall ( i.e. Empyema necessitans) Stage 3- Organizational stage- Fibroblast proliferation Pockets of loculated pus may develop into thick walled abscess cavities or the lung may collapse and become surrounded by a thick, inelastic envelope (peel) Clinical features Initial signs and symptoms those of bacterial pneumonia. Children treated with antibiotic agents may have an interval of few days between the clinical pneumonia phase and the evidence of empyema. Most patients are febrile, develop increased work of breathing or respiratory distress and often appear more ill. Physical findings similar to those for serofibrinous pleurisy and the 2 conditions are differentiated only by thoracocentesis which should always be performed when empyema is suspected. Lab findings
Radiographically all pleural effusions
appear similar , but absence of fluid shift indicates loculated empyema.
Septa confirmed by USG or CT.
Maximal amount of fluid obtainable should be withdrawn by thoracocentesis and analysed. Effusion is empyema if bacteria present on Gram staining, pH <7.20, >100,000 neutrophils/microliter. •Appearance of pus produced by different organisms is not distinctive. •Cultures of fluid must be performed. •Blood cultures have higher yield than cultures of pleural fluid. Leukocytosis and elevated ESR found. COMPLICATIONS
Staphylococcal infections- bronchopleural
fistulas and pyopneumothorax Others-Purulent Pericarditis Pulmonary abscess Peritonitis (extension through diaphragm) Osteomyelitis of ribs Septic complications- meningitis, arthritis, osteomyelitis Septicemia seen in H.Influenzae and Pneumococcal infections. Effusion organize into thick peel which may restrict lung expansion and may be associated with persistent fever and scoliosis. Treatment Aim- To sterilize pleural fluid and restore normal lung function. Systemic antibiotics Thoracocentesis and chest tube drainage initially with a fibrinolytic agent If no improvement VATS Open decortication if VATS and fibrinolysis fails If empyema diagnosed early- antibiotic therapy with thoracocentesis provides complete cure. Clinical response in empyema is slow, even with optimal treatment there may be little improvement for as long as 2 weeks. With staphylococcal infections resolution is very slow and systemic antibiotic therapy required for 3-4 weeks. When pus obtained by thoracocentesis, closed chest-tube drainage with fibrinolytics is initial procedure followed by VATS if there is no improvement. If pleural fluid septa are detected on USG, fibrinolysis is attempted followed by VATS if no improvement. Closed chest tube drainage is controlled by an underwater seal or continuous suction; sometimes more than one tube required to drain loculated areas. Closed drainage usually continued for 5-7 days. Chest tubes that are no longer draining are removed. Instillation of the fibrinolytic agents into the pleural cavity via chest tube may promote drainage, decrease fever, lessen need for surgical intervention, and shorten hospitalization; it does not shorten the course of disease when used after VATS. Streptokinase 15000 Units/ kg in 50 mL of 0.9% saline daily for 3-5 days and Urokinase 40000 units in 40ml saline every 12 hours for 6 doses . Alteplase has also been used.
There is risk of anaphylaxis with
streptokinase and all 3 drugs can be associated with hemorrhage and other complications. In the child who remains febrile and dyspnoeic for more than 72 hours after initiation of therapy with intravenous antibiotics and thoracostomy tube drainage, surgical decortication via VATS or, less often, open thoracotomy may speed recovery. If pneumatocoeles form, no attempt should be made to treat them surgically or by aspiration, unless they reach sufficient size to cause respiratory embarrassment or become secondarily infected.
Pneumatocoeles usually respond
spontaneously over time. LUNG ABSCESS
Lung abscess is a thick-walled cavity in the
pulmonary parenchyma that contains purulent material and is initiated or complicated by infectious organisms. Lung abscess is classified as primary or secondary depending on underlying conditions. Primary lung abscess occurs in the absence of a specific lung disease due to organisms causing underlying pneumonia eg: Streptococcus pneumonia, Staphylococcal aureus, Klebsiella pneumoniae Secondary lung abscess occurs in the presence of predisposing structural or functional lung diseases including congenital lung disorders, ciliary dyskinesia, and cystic fibrosis, systemic diseases such as neuro-developmental abnormalities and congenital immunodeficiencies that may lead to aspiration or infection. Clinical features Fever Cough Rhinorhoea Dyspnoea Chest pain Abdominal pain Lethargy Investigations
Chest Xray, USG and CT chest Management
Two basic principles are involved, namely
adequate appropriate antibiotic therapy and drainage of the abscess cavity Antibiotic therapy-
Primary- 3 rd gen Cephalosporin + Vancomycin + Aminoglycoside
Secondary- CP + Chloramphenicol Drainage
Endobronchial aspiration of the abscess
cavity by Bronchoscopy Postural drainage and chest physiotherapy
inhalation of an aerosol solution of 10%
propylene glycol, followed by percussion of the chest wall to implement coughing and drainage.