Clinical details about some syndromes and ailments of the Pulmonary system

When we talk about respiratory disorder, most of us tend to think of only Asthma, Pneumonia, Chronic Obstructive Pulmonary disease, Emphesyma, Chronic Bronchitis and respiratory failure. Yeah! We are all right and in fact, these are the commonest of all respiratory diseases, but there is more to respiratory diseases than just these afore-mentioned ailments. What are the other diseases or syndromes which constitute the respiratory diseases in general?

Essentials of Diagnosis

• Dyspnea if effusion is large; may be asymptomatic.

• Pain of pleurisy often precedes the pleural effusion.

• Decreased breath sounds, flatness to percussion, egophony.

• The underlying cardiac or pulmonary disease may be the major source of symptoms and signs.

• X-ray evidence of pleural fluid.

General Considerations

(A) Ultrasound (US) findings in a patient with pleuritic chest pain. The grayscale US reveals irregularity and interruption of the pleura. (B, C) Sonographic features in a patient with partial pneumothorax. Real-time US of the healthy side of the che

Source: Ultrasound findings in patients with pleuritic chest pain and partial pneumothorax

Note that the right lower lung field is clear and that the right diaphragm and lateral costophrenic angle seem sharp though it would seem peculiar that the right diaphragm should seem so high. Although pleural effusions are usually expected to blunt

Source: right upper lung field opacification which on later work-up was determined to be a primary cancer

(A) Transverse image through the intercostal space. The chest wall is visualized as multiple layers of echogenicity representing muscles and fascia. The visceral and parietal pleura appear as echogenic bright lines that glide during respiration (glid

Source: Sonographic images of normal pleura and chest wall using a 5- to 10-MHz linear scanner

(A) Pleural effusion is presented as an echo-free space between the visceral and parietal pleura. Compressive atelectasis of the lung may be seen in a huge effusion. (B-E) The effusion can be subclassified as anechoic (B), complex nonseptated (C), co

Source: Sonographic appearance of pleural effusion

(A) Ultrasound (US) shows a chest wall abscess in a patient with liver cirrhosis as an ill-defined lesion with soft-tissue echogenicity that extends to the pleura. Puslike material was obtained with transthoracic aspiration under US guidance, which y

Source: Extension of inflammatory diseases (A, B) or tumors (C, D) to the pleura

Any fluid collection (transudate or exudate) in the pleural space constitutes a pleural effusion. Numerous disease processes of inflammatory, circulatory, and neoplastic origin can cause pleural effusion. Every effort should be directed toward the diagnosis of the primary disease. "Idiopathic" pleural effusion often proves to be of tuberculous origin.

Clinical Findings

A. Symptoms and Signs: There may be no symptoms. Chest or shoulder pain may be present atonset, especially when fibrinous pleuritis precedes the effusion. Dyspnea may be mild or, with large or rap idly forming effusions, severe. Cardiac failure may be associated with effusion. Fever, sweats, cough, and expectoration may occur, depending upon the underlying cause.

Physical findings include decreased motion of the chest and decreased to absent vocal fremitus on the side of the fluid, flat percussion note and decreased to absent breath sounds over the fluid, and egophony (e-to-a sound) at the upper level of the fluid. With large effusions, the mediastinum shifts away from the fluid (as shown by displacement of the trachea and the cardiac apex), although underlying atelectasis may result in a shift toward the fluid. Signs resembling those of consolidation (dullness, bronchial breath sounds, bronchophony) are occasionally elicited over the fluid, presumably as a result of compression of the underlying lung by large, rapidly forming effusions.

B. X-Ray and Sonographic Findings (picture 1-6, figure 3-5) : Three hundred milliliters ormore must be present before fluid can be demonstrated by x-ray. Obliteration of the costophrenic angle is the earliest sign. Later, a homogeneous triangular density with a concave medial border extends upward to the axilla; other borders are formed by the lateral chest wall and the diaphragm. The mediastinum shifts away from the fluid (displaced heart and tracheal air shadow). The mobility of the fluid shadow, which ' 'pours'' into dependent areas of pleural space when the patient is placed on the involved side, may aid in the demonstration of small effusions. An atypical distribution of fluid along the interlobar fissures or in loculated areas may be noted.

C. Thoracentesis: This is the definitive diagnostic procedure. It demonstrates conclusively the presence of fluid and provides samples for study of physical characteristics, protein content, cells, and infectious agents. Thoracentesis should be done care fully to avoid introducing infection and puncturing the visceral pleura.

1. Removal of fluid for examination-Remove 50-1000 mL. Use a 3-way stopcock to avoid introduction of air. Care must be exercised to avoid contaminating the pleural space.

2. Pleural fluid examination-(Specimen must be fresh.) A specific gravity of more than 1.015 orprotein of more than 3 g/dL usually indicates an exudative fluid. More reliable indicators include a ratio of pleural fluid protein to serum protein greater than 0.5; a fluid LDH to serum LDH ratio of more than 0.6; or a pleural fluid LDH of more than 200IU, especially if all 3 conditions are present.

A stained smear should be examined for the detec tion of organisms and the nature of the cellular content. Collect a specimen in an anticoagulant tube for cell count. Cultures on appropriate media are indicated for all fluids from unexplained pleural effusions to demonstrate the presence of tubercle bacilli, other bacteria, or fungi. Cy tologic examination of the remaining fluid should be done if a neoplasm is suspected.

Lactic dehydrogenase (LDH) levels are frequently increased in effusions due to cancer. Chylous effusions usually signify interruption of the thoracic duct by cancer.

D. Pleural Biopsy: This procedure has become very simple and valuable as a result of the development of better biopsy needles (eg, Abrams' needle) that permit thoracentesis and removal of one or more tissue specimens with the same needle. Pleural biopsy is indicated whenever the diagnosis is in doubt. If the tissue is not diagnostic, several more specimens should be taken. If pleural fluid examination and needle biopsy do not yield a diagnosis, open pleural biopsy must be considered. A portion of the biopsy material should be cultured.

Treatment

A. Postpneumonic and Other Sterile Effusions: Remove readily obtainable fluid by multiplethoracentesis, at daily intervals if necessary. Removal of more than 1000 mL initially is not advisable.Reexamine subsequent fluid specimens to rule out empyema if the pleuritis does not respond to treatment.

B. Tuberculous Effusion: Uncomplicated pleural effusion due to tuberculosis is treated essen tially as minimal pulmonary tuberculosis. A course of isoniazid plus one of the other major antituberculosis drugs is recommended. Many patients with untreated tuberculous effusions develop pulmonary tuberculosis later, usually within 5 years.

Removal of all readily available fluid by thoracentesis is advisable to minimize later pleural fibrosis. When high fever persists for longer than 2 weeks, hematogenous dissemination should be suspected.

C. Effusions Due to Malignant Tumors: These tend to reaccumulate rapidly and require frequent removal. An attempt should be made to control the re-formation of fluid by irradiation of the hemithorax or by the use of intrapleural tetracycline or cytotoxic agents.

Prognosis

The prognosis is that of the underlying disease. 

Transudative pleural effusions are formed when normal hydrostatic and oncotic pressures are disrupted. Exudative pleural effusions occur when pleural membranes or vasculature are damaged or disrupted therefore leading to increased capillary permeabil

Lateral X-ray of chest with pleural effusion A-effusion B- pleural cavity

HEMOTHORAX

hemothorax I

hemothorax II

hemothorax III

Hemothorax (pooling of blood in a pleural space) is most commonly due to trauma but may also follow tumor, tuberculosis, and pulmonary infarction. The physical findings are the same as those of pleural effusion. Military experience has shown that early removal of all blood from the pleural space is desirable. If this cannot be accomplished by thoracentesis, an intercostal tube with water-seal drainage is indicated. If bleeding continues, thoracotomy is indicated. Great care must be taken during aspiration to avoid bacterial contamination of the pleural cavity. Surgical removal of residual blood clots may be necessary.

Published reports range of pulmonary artery rupture as a complication of the PA catheter range from 0.001% to 0.47%. Postulated mechanisms include distal tip migration penetrating the wall during balloon deflation, overdistention of the balloon with fluid and traction on an inflated, wedged balloon.

Proposed risk factors include age over 60 years, pulmonary hypertension, improper balloon inflation, improper catheter positioning, cardiopulmonary bypass and anticoagulation.

Thoracotomy appears to improve survival (50%) in patients who develop a hemothorax, whereas conservative treatment in these patients is not successful. Patients who do not develop a hemothorax have a 25% mortality rate.

Nonsurgical options include flexible bronchoscopy and Fogarty catheter tamponade, applying high PEEP  and conservative treatment, all of which are recommended in patients without a hemothorax. Double lumen intubation to protect the noninvolved lung has also been recommended. 

Surgical options require a thoracotomy with arterial repair,  pneumonectomy  or lobectomy.

PLEURAL EMPYEMA (Nontuberculous)

Acute infection of the pleural space may result from (1) direct spread from adjacent bacterialpneumonia, (2) postsurgical infection, (3) post-traumatic (including thoracentesis)infection. Underlying chronic obstructive pulmonary disease or broncho-genie carcinoma is frequently present. The availability of early and specific therapy for these conditions has made empyema an uncommon disease. However, the mortality rate remains high (50% in some series). The incidence of anaerobic infection appears to be increasing. Hospital-acquired infections have a more serious prognosis.

The clinical findings are often obscured by the primary underlying disease. Pleural pain, fever, and ' 'toxicity'' after clinical improvement of the primary disease, in association with physical and x-ray signs of pleural fluid, are characteristic. Thoracentesis reveals a frankly purulent exudate from which the causative organism may be cultured. Empyema, like lung ab scess, may become chronic, with a prolonged course and little tendency to spontaneous resorption (especially in bronchiectasis and tuberculosis).

The key to nonsurgical treatment of acute em pyema is early diagnosis. Any collection of fluid occurring in the course of pulmonary inflammatory disease should be removed at once. If pus is present, a specimen should be obtained for Gram staining and cultures, including cultures for anaerobic organisms. Specimens for anaerobic culture must be collected without exposure to air and must be placed into suitable transport media immediately. (Coagulase-positiveStaphylococcus aureusand gram-negative bacilli are the most common aerobic bacteria causing empyema; Bacteroides and peptostreptococci are the most frequently encountered anaerobic organisms.) The empyema should be aspirated as completely as possible. Some early localized empyemas can be treated by thoracentesis and antibiotic therapy alone. Any large or loculated empyema should be drained immediately via an intercostal tube. Open thoracotomy is sometimes required to ensure adequate drainage.

As soon as specimens have been obtained for culture, parenteral antibiotic treatment should be started with penicillin, 600,000 units intramuscularly every 6 hours, or, alternatively, cephalothin, 8 g intravenously daily. When the pus has a foul odor or the empyema is thought to be secondary to an intra-abdominal infection, chloramphenicol, 50 mg/kg daily orally, should be added to the initial treatment. The object is to obliterate the empyema space as soon as possible. Irrigations with saline through the catheter may be necessary. Chronic empyema usually results from inadequately treated acute empyema or from a bronchopleural fistula. Surgical drainage with or without decortication is usually necessary.

HYDROTHORAX

Acute hydrothorax

Massive hydrothorax

The term hydrothorax generally denotes the presence of a collection of serous fluid having a specific gravity of less than 1.015 or a protein content of less than 3 g/dL (transudate). The most common cause is congestive heart failure, but lymphatic obstruction and obstruction of the superior vena cava or vena azygos may also cause hydrothorax. The not unusual finding of hydrothorax in hepatic cirrhosis with ascites (6%) is explained by observations of ready transfer of radioiodine-labeled albumin from the peritoneal to the pleural spaces. The initial examination of the pleural fluid should be as described above.

The fluid should be removed by thoracentesis when it causes dyspnea.

The prognosis is that of the underlying disease.

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