Pleural Effusions
Brenda K. Shelton
Beth Kozak Onners
I. Definition
A. Excess fluid accumulation in the pleural space (Antunes et al., 2003)
1. Large effusion is defined as more than two thirds of the hemithorax involved.
2. Massive effusion is defined as complete or almost complete opacification of the hemothorax.
B. The pathophysiologic effects are:
1. Collapse of alveoli and impaired oxygenation.
2. Increased work of breathing due to changes in the intrapleural pressures.
C. Incidence
1. Affects about 15% of patients with cancer sometime during the course of their disease (American Thoracic Society, 2000).
2. Significant association with metastatic disease
a. Over 50% with metastatic disease develop pleural effusion (Pollack et al, 2001).
b. Average life expectancy of a patient with cancer after diagnosis of pleural effusion is 3 to 12 months (Antunes & Neville, 2000; Shoji, Tanaka, Yanagihara, Inui & Wada, 2002).
3. Dyspnea, often from pleural effusions, is described as one of top three distressing symptoms in patients with advanced cancer (Campbell, Draper, Reid & Robinson, 2001; Sahn, 2001)
II. Etiology
A. Normal pleural mechanics (Antony, 2003)
1. Pleura cover the lungs and adhere to the inner chest wall, serving as a protective barrier for the lungs.
2. The potential “space” between the visceral and parietal pleura contains 5 to 30 mL of fluid at any given time, but circulates 1 to 2 L of fluid a day through a pumping action produced when the lungs expand and relax.
3. The pressure in the pleural space is normally negative, allowing for easy inflow of air when the diaphragm and intercostal muscles are contracted and pull the pleura against the chest wall.
4. Passive exhalation occurs with relaxation of the chest muscles.
5. Increased pleural fluid increases the pressure within the pleural space, increasing the work of breathing.
6. Symptoms of pleural effusion usually begin with increased work of breathing to maintain the same “oxygenation standard,” but, as
pleural fluid becomes excessive, alveoli are unable to fully expand, and oxygenation is impaired.
pleural fluid becomes excessive, alveoli are unable to fully expand, and oxygenation is impaired.
B. Both malignant and nonmalignant etiologies of pleural effusions exist, but more than 50% of all symptomatic pleural effusions presenting for treatment are related to malignancy (Antunes & Neville, 2000).
1. Etiologies can be listed by pathophysiologic triggers.
a. Excess pleural fluid production—Most pleural fluid production occurs in the apex, and abnormalities in this area may increase the risk of effusion (Antunes et al., 2003).
(1) Inflammation—Infection, malignant infiltration of the pleura
(2) Fluid overload
b. Inadequate pleural fluid drainage—Pleural fluid is drained by way of parietal cells located in the mediastinum and diaphragm, so diseases causing injury or pressure in these areas may obstruct pleural fluid drainage (Antunes et al., 2003).
(1) Lymphatic obstruction
(2) Altered pleural dynamics due to masses
(3) Diaphragmatic irritation (eg, hepatomegaly, pancreatitis)
2. Most common malignant associations.
a. Most common cancers—Lung, mesothelioma, breast, lymphoma.
b. Any cancer with enlarged mediastinal lymph nodes may obstruct lymph drainage from thoracic duct.
c. Other commonly noted malignant etiologies:
(1) Ovarian cancer
(2) Sarcoma
d. Certain chemo/biotherapy agents (Micromedex, 2003).
(1) Aldesleukin (interleukin-2)
(2) Cytosine arabinoside
(3) Docetaxel—Decreased incidence if treated before or after therapy with dexamethasone (Markman, 2003)
(4) Gemtuzumab (Mylotarg)
(5) Interferon
(6) Oprelvekin (Neumega)
(7) Trastuzumab (Herceptin)
(8) Vinca agents: Vinblastine, Vincristine, Vindesine
3. Nonmalignant conditions that may cause pleural effusion
a. Amyloidosis
b. Cirrhosis—Called hepatic hydrothorax; more common if ascites is also present (Hayes, 2001)
c. Congestive heart failure—Presents as unilateral right-sided, or bilateral with equal fluid distribution, usually associated with left ventricular failure, not right ventricular failure (Mitrouska, 2002)
d. Hypothyroidism
e. Human immunodeficiency virus (HIV) disease (Miller, Howling, Reid & Shaw, 2000)
(1) Anthrax
(2) Cryptococcus
(3) Legionella
(4) Nocardia
(5) Pneumococcus
(6) Pneumocystis carinii
(7) Tuberculosis
g. Nephrotic syndrome
h. Pancreatitis (usually left-sided)
III. Patient Management
A. Assessment
1. Patient history for risk factors
a. Concomitant diseases associated with pleural effusion
b. Malignant disease of the chest or one of high-risk malignancies
c. Exposure to medications that enhance capillary permeability (eg, biologic therapies, cytosine arabinoside)
d. Hypoalbuminemia
2. Physical complaints
a. Severity of symptoms relate to how fast fluid has accumulated and the severity of compromise to lung expansion.
b. Related to fluid collection in the pleural space.
(1) Increased effort to breathe, use of accessory muscles.
(2) Dyspnea.
(a) Most common and distressing symptom
(b) Not present in 15% to 25% of patients (Antunes et al., 2003)
(c) Positioning for best breathing is sitting up and leaning forward
(3) Pleuritic chest pain.
(4) Cough is stimulated as the brain detects atelectasis and attempts to stimulate alveolar expansion.
c. Related to increased work of breathing
(1) Fatigue and weight loss are common due to the energy expenditure used for breathing.
(2) Difficulty focusing or concentrating.
d. Related to hypoxemia
(1) Anxiety, restlessness, emotional lability
(2) Headache, feeling of fullness in the head
3. Physical findings
a. Signs of alveoli collapse
(1) Diminished breath sounds in lower lung fields
(2) Unequal chest excursion or, if severe, total absence of chest wall movement on the affected side
b. Signs of resultant hypoxemia
(1) Cyanosis, cool extremities
(2) Oliguria
(3) Decreased bowel sounds, constipation
c. Signs of pleural space expansion within the chest
(1) Trachea deviated away from the side with the pleural effusion.
(2) Displaced point of maximal impulse (apical pulse) shifted, especially if pleural effusion is on the left.
B. Diagnostic Tests
1. Initial screening
a. Chest x-ray
(1) Anterior-posterior view usually adequate unless effusion is loculated in a single area, then lateral decubitus x-ray may be helpful (Antunes et al., 2003).
(2) Best results if taken with patient in the upright position; supine x-rays will cause the fluid to track the length of the lung field and appear as haziness rather than a fluid filling the base of the lung.
(3) Reveals blunted diaphragmatic dome, reduced opacity in the lung field due to alveolar collapse, fluid meniscus with possible tracking up the side of the pleural space.
b. Clinical examination
(1) Confirms severity as determined by chest excursion
(2) Assists the clinician to determine the work of breathing the patient is exerting to achieve compensation and a marginally normal oxygenation
(3) Assists in assigned severity of symptomatology to the diagnostic test finding
2. Definitive diagnosis
a. Chest tomography (CT) scan.
(1) Helpful to differentiate interstitial and pleuritic processes that may be occurring simultaneously
(2) Identifies loculated effusions; may allow external skin marking for needle thoracentesis localization
b. Ultrasound is especially helpful at localization of small effusions.
3. Histopathologic diagnosis
a. Thoracentesis fluid collection
(1) Transudative versus exudative—It is unclear whether existing criteria for defining effusions in these two categories can be used as a definitive diagnostic tool, or to even guide therapeutic decisions; however, it is considered standard management to send pleural fluid for chemistry to classify the effusion characteristics. An overview of the defining features of transudative and exudative effusions is included in Table 36-1.
TABLE 36-1 Transudative Versus Exudative Effusions | ||||||||||||||||||||||||||||||||||
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