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CHAPTER 236 Pleural Diseases

Carlos E. Kummerfeldt, MD

Nicholas J. Pastis, MD

John T. Huggins, MD

Key Clinical Questions

When does a pleural effusion require drainage? Why make the distinction between transudates and exudates? How does the pleural fluid analysis assist in guiding your differential diagnosis? When is a chest tube placement indicated? When should a pulmonary consultation be obtained?

EPIDEMIOLOGY

The seven leading causes of pleural effusions in the United States, in descending order include: (1) congestive heart failure; (2) bacterial pneumonia; (3) malignancy; (4) pulmonary embolism; (5) viral disease; (6) postcoronary artery bypass surgery; and (7)

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cirrhosis with ascites. Pneumothorax in the hospitalized patient is most commonly found in (1) blunt trauma (35%); (2) transthoracic needle aspiration biopsies (25%); (3) pleural biopsies (8%); (4) transbronchial lung biopsies (6%); (5) mechanically ventilated patients (4%); (6) thoracentesis (2%); and (7) central line insertions (1%-2%). Spontaneous pneumothorax occurs in about 15,000 cases per year in the United States: primary spontaneous pneumothorax occurs in adults with no underlying lung disease, whereas secondary spontaneous pneumothorax occurs in older adults with underlying lung disease, most commonly with chronic obstructive pulmonary disease.

PLEURAL EFFUSIONS A thoracentesis should be performed in most patients with a pleural effusion (Table 236- 1). Thoracentesis should be performed in patients with likely heart failure if the pleural effusion is unilateral, if one side is greater than the other, or if there is suspicion for a dual diagnosis. The major risks and complications of thoracentesis include the following: (1) pneumothorax; (2) bleeding; (3) infection; and (4) procedural related pain. There are no evidence based guidelines in patients with coagulopathies, and there are reports of thoracentesis being performed in patients with an elevated international normalized ratio, uremia, thrombocytopenia or on oral antiplatelet or anticoagulation therapies. The benefits of correcting coagulopathy with transfusions or by withholding antiplatelet or anticoagulation medications should be weighed against the risks in the individual patient and should always be discussed with the patient. Ultrasound should be performed in all patients undergoing thoracentesis to less the risk of complications associated with a blind tap. Ultrasound can identify the pleural fluid and other underlying anatomical structures, estimate the size of the effusion, and determine the presence of underlying septations or complexity that may indicate the presence of loculations (Figure 236-1) (see Chapter 124 [Thoracentesis]).

TABLE 236-1 Indications for Thoracentesis

1. Pleural effusion size ≥1 cm on chest radiography, ultrasound or computed tomography (CT)

2. Fever 3. Pleuritic chest pain 4. Dyspnea 5. Suspected hospital acquired infection 6. Evidence of loculation, complexity, or septations on imaging 7. Evidence of mediastinal shift, complete hemithorax opacification or large effusion on

imaging

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Figure 236-1 Ultrasound images show a large simple pleural effusion and a complex pleural effusion with septations. (A) Large simple anechoic pleural effusion causing atelectasis of the right lower lobe (arrow). The bright white line on the right (arrowheads) represents the diaphragm; the atelectatic lung is on the left and lower parts of the image. (B) Complex pleural effusion with septations demonstrating loculations and complexity (arrow). The small lines between the diaphragm and consolidated lung represent septations. (Images courtesy of John T Huggins, MD.)

PLEURAL FLUID ANALYSIS

Pleural fluid analysis is essential to determine the cause of the effusion. The hospitalist should familiarize themselves with the pleural fluid tests routinely ordered and the diagnostic clues they provide. The pleural fluid appearance, color, and even its smell may provide clues as to the diagnosis. Table 236-2 shows the differential diagnosis based on the appearance of the fluid. The following tests should always be obtained: protein, lactate dehydrogenase (LDH), pH, glucose, white cell count and differential, cytology and cultures. Other fluid tests that may assist in confirming a suspected diagnosis in selected patients include fluid amylase, triglyceride, cholesterol, adenosine deaminase (ADA), rheumatoid factor, and antinuclear antibody. Tables 236-3 through 236-5 summarize the use of these tests to narrow the differential diagnosis.

TABLE 236-2 Differential Diagnosis of Pleural Fluid Based on Appearance

Fluid Appearance Differential Diagnosis Light yellow Transudate

Urinothorax (smells like urine) Exudate

Dark yellow or serous Exudate Turbid Parapneumonic effusion, chylothorax, cholesterol effusion Purulent Empyema (putrid smell) Milky Chylothorax Bloody Parapneumonic, malignancy, hemothorax Clear or watery Cerebrospinal fluid leak, peritoneal dialysis, extravascular

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migration of central venous catheter Satin sheen Cholesterol effusion

TABLE 236-3 Routine Pleural Fluid Tests Used for Analyzing Pleural Fluid

Test Comment Protein Elevated in exudates; >5.0 g/dL associated with tuberculosis;

very low <0.5 g/dL seen in urinothorax, CSF leak, or extravascular migration of central venous catheter

Lactate dehydrogenase Elevated in exudates; if increasing with serial thoracentesis, indicates worsening degree of pleural space inflammation

pH* Low pH >7.2-7.3 associated with: (1) complicated parapneumonic effusion; (2) esophageal rupture; (3) rheumatoid and lupus pleuritis; (4) tuberculosis; (5) malignancy; (6) hemothorax; (7) urinothorax

Glucose Low glucose typically <60 mg/dL associated with: (1) parapneumonic effusion; (2) malignancy; (3) tuberculosis; (4) rheumatoid pleuritis (lupus has normal glucose); (5) hemothorax. When <40 mg/dL and presence of infection, chest tube insertion is indicated

Cytology Positive for malignancy in up to 60%; yield increases with repeat thoracentesis

Culture Yield increases when using blood culture bottles (aerobic and anaerobic); mycobacterial and fungal cultures useful when undiagnosed exudate present

*The pH should ideally be measured in a heparinized syringe, placed on ice if not immediately processed and analyzed in a blood gas machine.

LIGHT’S CRITERIA

Distinction between whether the effusion is an exudate or transudate these two categories may assist in determining the etiology of the effusion (Figure 236-2). Light’s criteria is a set of three characteristics that compare the following:

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Figure 236-2 Approach to the hospitalized patient with a pleural effusion. CABG, coronary artery bypass graft; CHF, congestive heart failure; CSF, cerebrospinal fluid; SF-A, serum to pleural fluid albumin gradient; SF-P, serum to pleural fluid protein gradient; smx, syndrome; TB, tuberculosis.

1. pleural fluid to serum protein ratio >0.5; 2. pleural fluid to serum lactate dehydrogenase >0.6; or 3. pleural fluid LDH > two-thirds of the upper normal limit for serum using an “or” rule.

The pleural fluid is classified as an exudate if one of the three criteria is met. The pleural fluid is a transudate if none of the three criteria are met.

Light’s criteria may misclassify some transudates as exudates. This commonly occurs in patients with pleural effusions due to congestive heart failure that have received diuretic therapy. In this setting, correct classification may be possible by applying the serum to pleural fluid protein and albumin gradients. If the difference between the serum to pleural fluid protein is >3.1 g/dL or the serum to pleural fluid albumin is >1.2 g/dL, then the effusion is reclassified as a transudate (see Figure 236-2).

Transudates occur as a consequence of changes in the hydrostatic or oncotic forces within the pleural space. The resulting pleural fluid is low in protein and LDH content. The two most commonly encountered transudates in the hospital are congestive heart failure and liver cirrhosis with ascites resulting in hepatic hydrothorax.

HEART FAILURE

Systolic and diastolic heart failure represents the most common cause of pleural effusion encountered in the hospital. Fluid accumulates in the pleural space by moving from the lung interstitium across leaky mesothelial cells. The triad of clinical signs and symptoms (dyspnea, orthopnea, lower-extremity edema), bilateral pleural effusions, and

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cardiomegaly on chest radiography establish the diagnosis. The majority of these effusions resolve with diuretic therapy and do not require thoracentesis for diagnosis (see Chapter 129 [Heart Failure]).

A thoracentesis is indicated if no cardiomegaly is appreciated on chest radiography, if the effusion is unilateral, or if the patient meets one of the criteria listed in Table 236-1. Thoracentesis may be indicated if dyspnea does not resolve with diuretic therapy after a few days or the effusion is large or does not appear to resolve. Thoracentesis should be performed if another concomitant cause for an effusion (dual diagnosis) is suspected or if one of the effusions is significantly greater than the other. The hospitalist should keep in mind that about 80% of patients have bilateral effusions, 15% to 20% a unilateral right side effusion, and only 5% to 10% have a unilateral left side effusion. Pulmonary consultation should be considered in the above settings or if a patient presents with refractory symptomatic pleural effusions despite optimal diuretic therapy. In such extreme cases, an indwelling pleural catheter or talc pleurodesis may be considered for palliative measures.

HEPATIC HYDROTHORAX

Hepatic hydrothorax is the second most commonly encountered cause of a transudate in the hospitalized patient. It is estimated that about 6% of patients with cirrhosis develop this complication. About 80% of the effusions develop on the right side, 17% on the left, and 3% occur bilaterally. Ascitic fluid moves via diaphragmatic pores and defects into the pleural space resulting in fluid accumulation. In addition, the negative pressure gradient between the pleural and peritoneal cavities favors movement of fluid into the pleural space. Hepatic hydrothorax may occur in patients without ascites if all the ascites has moved into the pleural cavity.

Thoracentesis should always be performed to exclude spontaneous bacterial pleuritis, defined as the presence of a positive bacterial culture, a pleural fluid neutrophil count >250 cells/μL, and absence of empyema or pneumonia with parapneumonic effusion. Culture negative spontaneous bacterial pleuritis occurs if pleural fluid cultures do not grow any microorganisms and the fluid neutrophil count is >500 cells/μL. A diagnostic thoracentesis should be performed in all cases of ascites and hepatic hydrothorax in patients presenting with fever, even when spontaneous bacterial peritonitis is excluded, due to the presence of hematogenous spread. Antibiotic therapy is the treatment of choice. Chest tube insertion or indwelling pleural catheters should be avoided as they result in persistent fluid drainage and protein loss that leads to malnourishment and higher rates of infection.

Definitive treatment of hepatic hydrothorax should target control of the ascites in consultation with both pulmonary and liver specialists (see Chapter 160 [Cirrhosis and Its Complications]).

OTHER TRANSUDATES

Less common transudates include nephrotic syndrome, urinothorax, peritoneal dialysis, trapped lung, myxedema, pericarditis, and cerebrospinal fluid leak (Table 236-6). Pulmonary consultation should be sought whenever the cause of a transudate remains unclear.

EXUDATES

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Exudates occur as a consequence of pleural membrane inflammation and disruption. The resulting pleural fluid is high in protein and LDH content. Exudates result from disruption of the pleural membranes due to inflammation (parapneumonic effusions), direct injury, or invasion as with malignancy (Table 236-7). Initial diagnosis will not establish a diagnosis in about 20% of exudates. When the exudate does not resolve spontaneously or if malignancy is being considered, pulmonary consultation should be obtained to assist with appropriate workup that may include pleural biopsy by either medical or surgical thoracoscopy.

PARAPNEUMONIC EFFUSIONS

About 40% of bacterial pneumonias are complicated by the development of a parapneumonic effusion. Three stages develop: (1) exudative; (2) fibrinopurulent; and (3) organized. During the first exudative stage, increased permeability in the visceral pleura results in pleural fluid formation characterized by high protein content but normal glucose, pH, and LDH. Bacterial invasion during the second fibrinopurulent stage results in leukocyte, bacteria and cell debris accumulation. Pleural fluid continues to accumulate, and fibrin deposits in the visceral and parietal pleura with resulting loculations. Anaerobic utilization of glucose results in a lower glucose and pH levels, and cell lysis results in increased LDH levels. During the third and final organized stage, pus formation occurs from cellular debris resulting in empyema formation and pleural thickening.

Unless the effusion is small in size (<1 cm when measured from the inner border of the chest wall), the majority of parapneumonic or suspected parapneumonic effusions require thoracentesis. Pleural fluid analysis will determine if chest tube drainage is required (see Figure 236-3). Complicated parapneumonic effusions and all empyemas require chest tube drainage. Pulmonary consultation is recommended when chest tube drainage is indicated for evaluation of intrapleural tissue plasminogen activator (t-PA) combined with DNase administration. Intrapleural t-PA with DNase has been shown to reduce hospital stay as well as surgical referrals. Surgical drainage via video-assisted thoracoscopic surgery (VATS) or open thoracotomy should be considered when there is ongoing sepsis, fever and infection despite appropriate antibiotics or chest tube drainage.

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Figure 236-3 Management of parapneumonic effusions.

MALIGNANT EFFUSIONS

Malignant effusions represent the second most common cause of exudates after parapneumonic effusions, affecting about 200,000 persons per year in the United States. Most patients present with dyspnea, cough and less often chest pain. In order of frequency, the most common causes of tumors leading to development of malignant pleural effusion include: (1) lung, most commonly adenocarcinoma (38%); (2) breast (17%); (3) lymphoma (12%); (4) genitourinary (9%); (5) gastrointestinal (7%); other (7%) and unknown cause (10%).

Malignant effusions develop as a consequence of both an increased amount of fluid entry and a decreased amount of fluid exit from the pleural cavity. Factors that lead to an increased amount of fluid entry include: (1) direct pleural and pulmonary vessel invasion with increased permeability; (2) increased hydrostatic pressures due to venous obstruction; (3) increased vascular endothelial growth factor (VEGF) formation by some tumors; and (4) in some occasions, disruption of lymphatic vessels leading to chyle accumulation. Factors that lead to a decreased amount of fluid exit include: (1) lymphatic obstruction in the parietal pleura or mediastinal lymph nodes; (2) decreased intrapleural pressure from atelectasis formation; and (3) increased central venous pressure if underlying thrombosis is present.

Pleural fluid may demonstrate a serous appearing or bloody effusion. Fluid analysis varies but typically shows an elevated LDH due to a high cell turnover with lysis, a differential showing lymphocyte predominance, and glucose and pH may be low. Fluid cytology may be positive in up to 60% of cases. If measured, amylase may be elevated in about 10% of the cases. A chylothorax may be present. If pleural fluid cytology is negative

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or indeterminate on initial thoracentesis and a malignant diagnosis is highly suspected, a repeat thoracentesis with cytology is recommended to increase the diagnostic yield. Pulmonary consultation should be sought at this time in order to assist with diagnosis.

Malignant effusions are the most common cause of near complete hemithorax opacification on chest imaging (see Figure 236-4). Contralateral shift of the mediastinum usually indicates a large effusion rather than a large mass. If a large effusion does not result in contralateral mediastinal shift, then the lung may be unable to expand. Unexpandable lung or the inability of the lung to fully expand to the chest wall results from the following: (1) trapped lung; (2) visceral pleural inflammation or invasion causing lung entrapment; (3) endobronchial obstruction; and/or (4) chronic atelectasis. Tumor causing endobronchial obstruction and atelectasis may require bronchoscopy; visceral pleural thickening from direct tumor invasion can be better visualized via a contrast chest CT (see Figure 236-5).

Figure 236-4 Postero-anterior chest imaging shows a large left-sided pleural effusion with mediastinal shift to the contralateral side. Note the right tracheal deviation, near-complete left hemithorax opacification. The patient had a malignant bloody effusion due to lung adenocarcinoma. (Image courtesy of Sharon Jessie, Radiology Department, TJ Samson Community Hospital.)

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Figure 236-5 Chest ultrasound shows a pleural opacity consistent with tumor invasion (arrow). (Image courtesy of Sharon Jessie, Radiology Department, TJ Samson Community Hospital.)

The goal of therapy of malignant pleural effusions is directed toward palliation of symptoms. Due to rapid reaccumulation and symptom recurrence, repeated thoracentesis is not recommended in the majority of cases. A chest physician should be consulted to recommend the most appropriate treatment, based on the individual circumstances:

1) Breast, small cell lung cancer and lymphoma are chemosensitive and respond well to chemotherapy.

2) Talc pleurodesis via chest tube or thoracoscopy may be considered if no evidence of unexpandable lung.

3) Indwelling pleural catheter insertion (such as PleurX® catheters) if unexpandable lung present; about 50% to 60% of effusions resolve after indwelling catheter has been inserted, with subsequent catheter removal and no evidence of recurrence.

4) Thoracic duct ligation or a pleuroperitoneal shunt with pump system is recommended in the presence of chylothorax; indwelling pleural catheters may result in protein and lymphocyte depletion with subsequent malnourishment and infections.

PULMONARY EMBOLISM

It is estimated that about 30% of patients with pulmonary embolism have an associated pleural effusion. The effusion may be unilateral or bilateral. Computed tomography imaging with contrast can identify segmental or subsegmental filling defects consistent with embolic disease. Treatment of the pulmonary embolism results in resolution of the associated effusion (see Chapter 115 [Advanced Cardiothoracic Imaging]).

POSTCORONARY ARTERY BYPASS SURGERY

About 10% of patients who undergo CABG develop a large pleural effusion within 1 month after the surgery most commonly in the left hemithorax, although it may be bilateral with

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the left effusion usually larger than the right. The effusion is typically bloody as the result of bleeding from the internal mammary harvest site. The cell count has a lymphocyte predominance. One or two therapeutic thoracentesis are required as treatment. Persistence of pleural effusion for greater than 6 months post-CABG is usually due to the presence of a trapped lung. Most often the effusions are transudative and are not associated with respiratory symptoms. However, surgical decortication should be considered if the trapped lung causes a large effusion.

POSTCARDIAC INJURY SYNDROME

Postcardiac injury syndrome (previously known as Dressler syndrome) occurs after myocardial infarction, cardiac surgery, pacemaker implantation or blunt chest trauma. It is characterized by the presence of fever, chest pain, a new pericardial friction rub and effusion, and in about 70% of cases small bilateral pleural effusions. Postcardiac injury syndrome may develop between 3 weeks and up to a year after cardiac injury. Postcardiac injury syndrome is usually treated with aspirin, colchicine, or indomethacin and in severe cases corticosteroids.

TUBERCULOSIS

Although uncommon in the United States, tuberculous pleuritis may result in serious health consequences both to the patient and from a public health perspective if not recognized. There is a 50% probability of developing active tuberculosis within 5 years if the patient does not receive antituberculous therapy. Tuberculous pleuritis may be a consequence of primary infection that occurred 3 to 6 months prior, or due to reactivation. Pleural fluid cultures are negative nearly 80% of the time, and a tuberculin skin test may be negative in up to one-third of patients.

About 67% of patients present with an acute clinical presentation that includes cough, dyspnea and chest pain; these symptoms may be confused with pneumonia and a parapneumonic effusion. Less commonly, patients may present with a chronic illness and a unilateral effusion. Pleural fluid analysis shows lymphocyte predominance. If thoracentesis is done in early stages, pleural fluid may show neutrophil predominance. A very high protein level of greater than 5.0 g/dL is highly suggestive of the diagnosis (Table 236-4). Pulmonary consultation may assist in recommending specific diagnostic pleural tests such as adenosine deaminase (see Table 236-6), polymerase chain reaction for mycobacterial DNA and pleural fluid interferon-γ. Induced sputum smear and culture will be positive in half of the patients. Pleural biopsy should be obtained if suspicion is high and exudative effusion has not resolved. Tuberculous pleuritis typically resolves in several months regardless if tuberculosis treatment is given; however, if tuberculosis treatment is not provided, these patients have a high risk for relapse (see Chapter 200 [Tuberculosis]).

TABLE 236-4 Differential Diagnosis Based on the Pleural Fluid Cell Count Differential

Neutrophil Predominance

Lymphocyte Predominance Eosinophil Predominance

Parapneumonic Tuberculosis Pulmonary embolism Empyema Malignancy Asbestos exposure Pulmonary embolism Lymphoma Hemothorax

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Acute pancreatitis Sarcoidosis Drug induced Intra-abdominal abscess Rheumatoid pleuritis Fungal infections Bilio-pleural fistula Postcoronary artery

bypass surgery Eosinophilic granulomatosis with polyangiitis (formerly Churg- Strauss)

Uremia Parasite infections Chylothorax

TABLE 236-5 Special Pleural Fluid Tests Used for Analyzing Pleural Fluid

Test Comment Albumin Useful when suspected transudate is misclassified as exudate

(see Figure 236-2); if SF-A gradient >1.2 g/dL, re-classify effusion as transudate

Amylase Elevated in: (1) esophageal perforation; (2) pancreatitis (3) pancreatico-pleural fistulas; (4) malignancy

Triglyceride Elevated to >110 mg/dL in chylothorax Cholesterol Elevated to >250 mg/dL in cholesterol effusion due to

tuberculosis, rheumatoid pleuritis, trauma, or parasitic infection

Hematocrit Hemothorax if fluid to peripheral blood hematocrit ratio >50% Adenosine deaminase Elevated in patients with tuberculosis; tuberculosis excluded if

<40 U/L Rheumatoid factor May be elevated to ≥1:320 in rheumatoid pleuritis Antinuclear antibody Elevated to >1:40 in lupus pleuritis Creatinine Elevated to higher level than serum in urinothorax

SF-A, serum to fluid albumin gradient.

TABLE 236-6 Other Less Common Causes of Transudates

Cause Characteristics Imaging Nephrotic syndrome Due to decreased oncotic pressure from

urine protein loss and increased intravascular hydrostatic pressure from salt retention

Usually bilateral effusions

Urinothorax Due to renal obstruction resulting in retroperitoneal urine collection and drainage across pressure gradient into pleural cavity; creatinine level in pleural fluid higher than serum

Effusion on same side as obstruction

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Peritoneal dialysis Leakage of dialysate rich in glucose from peritoneal cavity through diaphragmatic defects into pleural space; high glucose and low protein fluid

Usually right sided; may be bilateral

Trapped lung Old inflammation resulting in fibrous membrane with visceral pleural thickening that causes inability of lung to fully re- expand, increasing negative pressure within pleural space; pleural manometry recommended to establish diagnosis

Unilateral effusion; chest CT with air contrast shows visceral pleural thickening

Myxedema Forms from decreased lymphatic drainage Bilateral; concomitant pericardial effusion many times

Constrictive pericarditis

Increased pulmonary and systemic capillary pressures result in fluid formation

Bilateral; may be unilateral

Cerebrospinal fluid leak

Fistula formation between CSF and pleural cavity from surgery, trauma, or shunts; low protein and LDH in fluid; measurement of β2-transferrin virtually diagnostic

Unilateral

CT, computed tomography; LDH, lactate dehydrogenase.

TABLE 236-7 Causes of Pleural Effusions

Exudates Transudates Common Parapneumonic Malignancy

Common Congestive heart failure Liver cirrhosis

Less common Tuberculosis Pulmonary embolism Postcoronary artery bypass surgery Chylothorax Pseudo-chylothorax Hemothorax Uremia Rheumatoid pleuritis Lupus (drug induced or systemic)

Less common Nephrotic syndrome Urinothorax Peritoneal dialysis Trapped lung Atelectasis

Uncommon Asbestos exposure Drug induced

Uncommon Cerebrospinal fluid leak Constrictive pericarditis

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Yellow-nail syndrome Esophageal perforation Pancreatitis Postabdominal surgery Bilio-pleural fistula Sarcoidosis

Myxedema Pulmonary veno-occlusive disease Central venous occlusion Extravascular migration of central venous catheter Glycinothorax

HEMOTHORAX

Hemothorax or the presence of blood in the pleural cavity is defined as a pleural fluid hematocrit that is at least 50% that of blood. Table 236-8 summarizes the causes of hemothorax encountered in the hospital. Bleeding may be significant and lead to hemodynamic compromise and cardiovascular collapse if not recognized quickly. Clinicians should always consider hemothorax in the situations listed in Table 236-8. Management requires chest tube insertion in all cases in order to quantify the rate of bleeding and prevent any of the following complications: (1) retention of clot; (2) infection; and (3) fibrothorax. Thoracic surgical consultation is recommended if chest tube output is greater than 200 mL/h and there are no signs of slowing. Persistence of blood in the pleural space increases the risk for fibrothorax or trapped lung.

TABLE 236-8 Causes of Hemothorax

Traumatic Iatrogenic Nontraumatic Penetrating injury Thoracic surgery (heart or

lung) Malignant effusion

Nonpenetrating injury Central vein perforation after central line insertion

Anticoagulation therapy

Thoracentesis Ruptured aortic aneurysm Chest tube insertion Arterio-venous malformation Lung biopsy Hematological disorder (ie,

hemophilia, thrombocytopenia) Transbronchial biopsy Intrapleural fibrinolytics

Catamenial

CHYLOTHORAX AND CHOLESTEROL EFFUSIONS

Chylothorax is the accumulation of lipid from chyle in the pleural space due to disruption or obstruction of the thoracic duct. Chylothoraces may be unilateral or bilateral, depending on the level at which the thoracic duct disruption occurs: right sided if the disruption occurs below the fourth to sixth thoracic vertebrae, left sided or bilateral if the disruption occurs at this level or above. The pleural fluid has a characteristic milky appearance but may mimic that of empyema. Centrifugation of the fluid will result in layering and deposition of cellular debris at the bottom in empyema, whereas in chylothorax the

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appearance will remain the same. Pleural fluid analysis shows lymphocyte predominance, a relatively low LDH and high protein (protein discordance) level. Triglyceride levels are greater than 110 mg/dL (see Table 236-6). Chylomicrons should be measured if the triglyceride level falls between 50 and 110 mg/dL. Table 236-9 lists the causes of chylothorax encountered in the hospital.

TABLE 236-9 Causes of Chylothorax

Traumatic Nontraumatic Iatrogenic Surgery Radiotherapy Endoscopy

Tumors Lymphoma Metastatic pleural tumors

Noniatrogenic Chest wall trauma Childbirth

Lymphatic involvement Lymphangioleiomyomatosis Tuberous sclerosis Amyloidosis Yellow-nail syndrome Sarcoidosis Filariasis Dasatinib and tyrosine kinase inhibitors Gorham syndrome Venous pressure Mediastinal fibrosis Superior vena cava thrombosis Chylous ascites

A pulmonary consultation is recommended in all cases of chylothoraces to tailor …