EMPYEMA THORACIS

Empyema thoracis (pyothorax) is the commonest pleural disease in Indian children, though tubercular pleural effusion is more common in older children gt;5 years of age.

Etiology: Empyema thoracis is mainly caused by Staph.

Most cases begin as parapeumonic effusions with under­lying lung pathology, followed by secondary bacterial infection. However, infection may also reach pleural space directly by: (a) rupture of the lung abscess, (b) external trauma or thoracocentesis, (c) extension from abdomen, e.g. amoebic abscess and (e) extension from mediastinum, e.g. mediastinitis.

Pathologically, empyema generally evolves through three phases, i.e. thin and sterile exudative phase (1-3 days), fibrinopurulent phase (4-14 days) and organization phase (gt;14 days) with development of adhesions and septations.

Clinically, empyema presents with high fever, cough, breathlessness, chest pain and following findings-(a) shift of mediastinum on opposite side, (b) restriction of movements on affected side, (c) stony dull percussion note, (d) diminished breath sounds and (e) decreased vocal resonance/vocal fremitus. Bronchial breathing with increased vocal resonance may be present at the upper level of effusion.

Diagnosis is established on:

• Chest skiagram showing dense homogenous opacity with—(i) shift of mediastinum on opposite side, and (ii) obliteration of costophrenic/cardiophrenic angles (Fig. 16.20). Upper border of fluid is usually curved due to surface tension, though typical findings may not be seen in loculated empyma.

• USG is the preferred investigations in all cases to confirm presence of fluid as well as for guided thoracocentesis/chest-tube insertion.

• CT scan is not routinely indicated, except to detect underlying abscess and before surgical interventions.

ICD: Intercostal drainage; VATS: Video-assisted thoracoscopic surger

• Pleural fluid examination, with smear and culture is necessary to identify causative pathogen, while antigen-based or PCR-based tests are useful in culture negative or pre-treated cases.

Clinical and radiological signs are generally similar in all pleural effusions and etiological differentiation is possible only on pleural fluid examination (Table 16.27). Complications: Untreated empyema may progress to cause: (a) pyopneumothorax, (b) bronchopleural fistula,

(c) empyema necessitans (rupture into thoracic wall) or

(d) thick pleural adhesions, leading to restrictive lung disease.

Management depends on the stage of disease, type of the fluid, presence of septations/membranes and response to therapy (Table 16.28) and includes:

• Removal of fluid by thoracocentesis or closed intercostals drainage (ICD). While maximum pleural fluid should be removed at the time of diagnostic tapping, ICD is necessary in almost all cases with significant empyema. Tube should be kept in situ until the drainage is lt;30-50 ml/day or cavity size is lt;50 ml. Deep breathing exercises and incentive spirometry help in better ICD drainage.

Some workers recommend intrapleural instillation of fibrinolytic agents, e.g. streptokinase (10,000­20,000 U/kg in 50 mlNormal saline) or Urokinase (10,000­40,000 IU in 10-40 ml of normal saline) every 12 hrs for 6 doses, in cases with multi-loculated empyema.

• Antibiotic therapy, based on in vitro sensitivity of cultured organism.

• Surgical decortication via video assisted thoracoscopic surgery (VATS) or open thoracotomy is needed in cases with no response after 72 hours of ICD and specific antibiotics.

Other important types of pleural effusions include: Dry (plastic) pleurisy, without significant effusion is usually seen in early empyema, viral infections, sub-pleural tubercular lesions and connective tissue disorders.

Clinically, these cases presents with characteristic chest pain due to friction between two inflamed layers of pleura, which aggravates on coughing or deep inspiration and pleural rub, without signs of significant pleural effusion.

Diagnosis d epends on chest skiagram, showing diffuse haziness or sharply demarcated homogenous opacity. Mediastinal shift is unlikely, considering small size of effusion.

Treatment is mainly directed towards the primary cause, though chest strapping may help to relieve the pain.

Exudative pleural effusion: Tuberculosis is the leading cause of non-purulent exudative pleural effusion (serofibrinous pleurisy), followed by pneumococcal or streptococcal pneumonia, collagen disorders, e.g. SLE, and intrathoracic malignancies.

Clinical presentation depends on the amount of fluid. Pleuritic pain and rub may be present in early stages but disappear soon after the collection is large enough to separate two layers of pleura. Apart from features of primary disease, signs of exudative pleural effusions are similar to empyema thoracis.

Diagnosis rests on—(a) chest skiagram, (b) USG, and (c) pleural fluid examination. Microbiological and serological studies in pleural aspirate, with special reference to tuberculosis and connective tissue disorders, are necessary to confirm etiology.

Management includes—(a) treatment of primary cause, and (b) therapeutic thoracocentesis, only in cases with large effusions causing respiratory distress. However, rapid removal of more than one litre of fluid may lead to re-expansion pulmonary edema and must be strictly avoided. Intercostal drainage may be needed if fluid refills rapidly or there is possibility of bacterial infections. However, it should be avoided in tubercular effusions, due to risk of fistula formation.

Hydrothorax, i.e. collection of non-inflammatory (transudative) fluid in pleural space, is caused by: (a) decreased oncotic pressure in hypoproteinemic states, e.g. nephritic syndrome, kwashiorkor; and (b) increased hydrostatic pressure in pleural vasculature, e.g. CCF, superior vena caval compression syndrome.

Clinical presentation depends on primary cause and lung signs are similar to other pleural effusions. Ascites and edema is common in hypoproteinemic states.

Diagnosis r ests on thoracocentesis to reveal transudative pleural fluid (Table 16.27).

Management is directed towards primary cause and therapeutic pleural tap is rarely indicated, except in cases with respiratory distress due to large fluid accumulation. Hemothorax, i.e. bleeding in pleural space, is rare in childhood, caused by—(a) thoracic trauma. (b) intrathoracic neoplasms, (c) systemic bleeding disorders, (d) post-thoracic surgery, and rarely, (e) congenital vascular anomalies of pleura/lung.

Diagnosis is established on thoracocentesis and hemorrhagic pleural fluid should always be examined for malignant cells.

Management includes treatment of primary cause, blood transfusions, intercostal drainage to prevent organization of blood and surgical intervention to treat the site of bleed, if identifiable.

Chylothorax, i.e. collection of lymph or chyle in pleural space, is caused by thoracic duct obstruction or injury due to—(a) cardiothoracic surgery, (b) thoracic trauma, (c) intrathoracic malignancy, and (d) congenital anomalies of thoracic duct (in newborns). Chylothorax is more common on left side, rarely being bilateral in severe cases.

Diagnosis rests on pleural tap that reveals a milky- white fluid due to high fat content, although it may be clear in newborns before feeds are given.

Presence of chyle may be confirmed by a simple bed­side test, i.e. mixing of pleural fluid with ether, formal­dehyde or any alkali, which clears the haziness of fluid. Triglyceride levels are high in chylous effusion.

Management: Spontaneous recovery occurs in gt;50% cases though repeated pleural aspirations may be needed to relieve intrathoracic pressure. Low-fat diet with medium chain triglycerides is advisable till spontaneous recovery. Total parenteral nutrition and surgical ligation of thoracic duct may be required in difficult cases.

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