On physical exam the patient was in moderate respiratory distress. Vital signs revealed a respiratory rate of 40, BP 126/60, temp 38.5o C, and HR 127. HEENT exam revealed no lymphadenopathy. Lung exam revealed dullness and decreased tactile fremitus 1/2 to 2/3 up the left lung. The upper half of the left lung revealed crackles and egophony. The right lung also had some crackles. Cardiac exam revealed a rapid but regular rate without murmurs. Extremities were without clubbing, cyanosis, or edema.
Laboratory studies revealed a Na 136, K 4.6, Cl 103, Bicarb 20, WBC 15500 with left shift, and an arterial blood gas with 7.40 pH, 36 pCO2, and 68 pO2 on 40% FiO2 by face mask. A chest x-ray and a chest CT scan were performed.
Chest CT Scan
The patient was admitted to the University of Iowa MICU and a thoracentesis was performed which revealed gross pus. A chest tube was placed and drained 2 liters of pus over the next 12 hours.
The first is the exudative stage which results from a focus of parenchymal infection leading to increased pulmonary interstitial fluid. Some of this fluid crosses the visceral pleura and accumulates as a small sterile pleural effusion. The pleural fluid is an exudate with primarily PMNs, a normal glucose level, and a normal pH level. Antibiotics begun in this stage will affect resolution of both the pneumonic and pleural process.
The initial sterile free flowing exudative parapneumonic effusions may rapidly progress (within a day) to the second stage. This is the fibropurulent stage characterized by infection of sterile pleural fluid. Pleural fluid further accumulates and contains many PMNs, bacteria, and cellular debris. Fibrin deposits cover both the visceral and parietal pleura. Fibrin membrane partitions result in loculated effusion. This loculation makes complete pleural space drainage difficult. During this stage, the pleural fluid pH and glucose levels become low, LDH levels increase, and bacterial organisms or frank pus may be present.
The third stage is the organization stage. Fibroblasts grow into the exudate from both the visceral and parietal pleural surface to produce an inelastic membrane called the pleural peel. These untreated effusions may also drain spontaneously through the chest wall (empyema necessitans) or into the lung to produce a bronchopleural fistula.
Also the incidence of infected pleural fluid depends on the organism causing the pneumonia. Approximately 35% of patients with anaerobic pneumonia will have a culture-positive pleural effusion, whereas fewer than 5% of patients with parapneumonic effusions secondary to pneumococcal pneumonia will have culture-positive pleural effusions (Light et al. Am. J. Med. 69:507-511, 1980).
If a pneumonia is suspected and the chest x-ray reveals blunted costophrenic angles or a non-visible diaphragm, bilateral decubitus chest radiographs should be obtained. With the involved side dependent, if the thickness exceeds 10 mm, a diagnostic thoracentesis should be performed immediately. An empyema or complicated pleural effusion can be identified only by examination of the pleural fluid. Clinical evaluation is inadequate to predict simple sympathetic effusion from complicated effusion.
Pleural fluid should be examined grossly for color, turbidity, and odor. If pus is present, the pleural space should be drained via tube thoracostomy. In the absence of gross pus, pleural fluid is sent for other studies to assist in determining if immediate chest tube placement is required. These pleural fluid studies should include glucose, LDH, amylase, protein, pH, WBC count plus differential, Gram stain, aerobic and anaerobic bacterial cultures. Depending on the clinical setting, fungal and mycobacterial smears and cultures and cytological studies should be done. Accurate pH measurements requires that the pleural fluid be collected anaerobically in a heparinized syringe (0.2 ml of 1:1000 heparin is drawn up into the syringe and then flushed to eliminate any artifact due to low pH of heparin). The syringe is then placed on ice, and the pH should be measured expeditiously.
The treatment of the parapneumonic pleural effusions has been largely determined by the characteristics of the pleural fluid. Since Hippocrates, physicians have recognized the need to immediately drain grossly purulent pleural fluid (i.e. empyema). If this is not drained, the empyema may progress to the organizing stage and form a pleural peel rendering the lung nearly functionless.
If the pleural fluid is not grossly purulent, implications of other pleural fluid characteristics need to be interpreted by the physician to determine if immediate chest tube drainage should occur. In the Textbook of Respiratory Medicine by Murray and Nadel (2nd edition), Richard Light offers the following recommendations for implementing chest tube drainage: 1) purulent pleural fluid, 2) positive pleural fluid Gram stain, 3) pleural fluid glucose less than 50 mg/dl, 4) pleural fluid pH below 7.00 and 0.15 units lower than arterial pH. If these four criteria are not met, a chest tube should still be considered if pleural fluid pH is below 7.20 or if pleural fluid LDH is above 1000 IU/L.
Although these guidelines should be followed, physicians should know that the recommendations for immediate chest tube drainage of nonpurulent complicated parapneumonic effusions are based on retrospective studies of very few patients with no control patients treated with antibiotics alone (Light et al. Chest 64: 591-96, 1973; Potts et al. Chest 70: 328-31, 1976; Light et al. Am J Med 69: 507-12, 1980). Furthermore, contained within these and other studies are mention of patients who met the above recommendations but improved on antibiotics alone. For example, there has been some suggestion that non-purulent complicated parapneumonic effusions secondary to Strep pneumonia have a more benign clinical course. Taryle et al. (Chest 74: 170-73, 1974) reported three cases with Strep pneumonia positive pleural fluid cultures who improved on antibiotics. Berger et al. (Chest 97: 731-35, 1990) reported on two patients with a pleural fluid pH less than 7.00 and a pneumococcal pneumonia; neither required chest tube drainage. Also in this report, one patient with a pleural fluid pH of 6.81 (negative pleural fluid culture and Gram stain) and five patients with pleural fluid pH ranging from 7.00 to 7.20 improved with antibiotic therapy alone. In another example, Light et al. (Am J Med 69: 507-12, 1980) described four patients with a pleural fluid pH between 7.10 and 7.20 (negative Gram stain and culture) who improved with antibiotic therapy alone. Light also described another patient who had a positive pleural fluid culture for Strep pyogenes and a pH of 7.20 whose pneumonitis and pleural disease "resolved without undue delay" with antibiotic therapy alone. Undoubtedly, a prospective randomized study will be required to determine the superiority of immediate chest tube drainage vs antibiotics alone in the treatment of nonpurulent complicated effusions.
Nonetheless, with the guidelines, if the pleural fluid characteristics are borderline for chest tube placement, repeating a thoracentesis at 12- to 24- hours may be helpful. If the pleural fluid LDH decreases and the pH and glucose increases, the patient is likely improving. But if the LDH is increasing and the pH and glucose are decreasing a chest tube should be placed.
If the decision is made to use fibrinolytics, the usual dose of streptokinase is 250,000 U, in 30 to 60 ml normal saline given intrapleurally via chest tube. The usual dose of urokinase is 100,000 U diluted in the same manner. It appears that streptokinase and urokinase are equally effective. The chest tube is clamped for 1 to 2 hours. This treatment can be repeated for up to 14 days. The decision regarding fibrinolytics versus surgery should be made in consultation with a thoracic surgeon.
2. Berger HA, Morganroth ML: Immediate drainage is not required for all patients with complicated parapneumonic effusions. Chest 97: 731-35, 1990.
3. Heffner JE, Brown LK, Barbieri C, DeLeo JM: Pleural Fluid Chemical Analysis in Parapneumonic Effusions. Am J Respir Crit Care Med 151, 1700-1708, 1995.
4. Light RW, Girard WM, Jenkinson SG, George RB: Parapneumonic effusions. Am. J. Med. 69: 507-512, 1980.
5. Light RW, MacGregor MI, Ball WC Jr, Luchsinger PC: Diagnostic significance of pleural fluid pH and PCO2. Chest 64: 591-96, 1973.
6. Light RW. Pleural Effusions. In: Textbook of Respiratory Medicine. J. F. Murray and J. A. Nadel (Ed.), W.B. Saunders Company, pp. 2164-2192, 1994.
7. Poe RH, Marin MG, Israel RH, Kallay MC: Utility of pleural fluid analysis in predicting tube thoracostomy/decortication in parapneumonic effusions. Chest 100, 963-67, 1991.
8. Potts DE, Levin DC, Sahn SA: Pleural fluid pH in parapneumonic effusions. Chest 70: 328-31, 1976.
9. Sahn SA: Management of complicated parapneumonic effusions. Am Rev Respir Dis 148: 813-817, 1993.
10. Taryle DA, Potts DE, Sahn SA: The incidence and clinical correlates of parapneumonic effusions in pneumococcal pneumonia. Chest 74: 170-73, 1978.
Media for Pleural Disease: Parapneumonic Effusions
Test for Pleural Disease: Parapneumonic
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