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Pleural effusion

Aug 22, 2013

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. Definition:A pleural effusion is an excessive accumulation of fluid in the pleural space. It can be detected on X-ray when 300 mL or more of fluid is present and clinically when 500 mL or more is present. The chest X-ray appearances range from the obliteration of the costophrenic angle to dense

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Pleural Effusion

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Definition:. A pleural effusion is an excessive accumulation of fluid in the pleural space. It can be detected on X-ray when 300 ml or more of fluid is present and clinically when 500 ml or more is present. The chest X-ray appearances range from the obliteration of the costo-phrenic angle to dense

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Approach to Pleural Effusion

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An interesting case of undiagnosed pleural effusion

Pleural effusions are commonly encountered in the clinical practise of both respiratory and nonrespiratory specialists. An estimated 1–1.5 million new cases in the USA and 200 000–250 000 new cases of pleural effusions are reported from the UK each year [1]. Analysis of the relevant clinical history, physical examination, chest radiography and diagnostic thoracentesis is useful in identifying the cause of pleural effusion in majority of the cases [2]. In a few cases, the aetiology may be unclear after the initial assessment. The list of diseases that may account for a persistent undiagnosed pleural effusion is long [3]. We present an interesting case of undiagnosed pleural effusion that was encountered in our hospital.

Short abstract

Pulmonary embolism is an important cause of undiagnosed pleural effusion http://ow.ly/HDLx30bVVa7

Pleural effusions are commonly encountered in the clinical practise of both respiratory and nonrespiratory specialists. An estimated 1–1.5 million new cases in the USA and 200 000–250 000 new cases of pleural effusions are reported from the UK each year [ 1 ]. Analysis of the relevant clinical history, physical examination, chest radiography and diagnostic thoracentesis is useful in identifying the cause of pleural effusion in majority of the cases [ 2 ]. In a few cases, the aetiology may be unclear after the initial assessment. The list of diseases that may account for a persistent undiagnosed pleural effusion is long [ 3 ]. We present an interesting case of undiagnosed pleural effusion that was encountered in our hospital.

Case presentation

A 33-year-old male presented to our hospital with a history of sudden-onset, pleuritic, right-sided chest pain of 2 days’ duration. It was not associated with fever, cough, dyspnoea, wheeze or haemoptysis. There was no history of swelling in the lower extremities, weight loss or anorexia. There was no history of any significant comorbidities. He was a smoker (8 pack-years). He had no history of drug abuse.

On examination, his temperature was 37.2°C, pulse was 77 beats⋅min −1 , respiratory rate was 22 breaths⋅min −1 , blood pressure was 112/66 mmHg and oxygen saturation measured by pulse oximetry was 98% on room air. There was no pallor, clubbing, pedal oedema, icterus or lymphadenopathy. The breath sounds were absent in the infrascapular and infra-axillary areas on the right side. No adventitious sounds were heard on either side of the chest. The remaining systemic examination was unremarkable.

Investigations revealed a haemoglobin level of 16.4 g⋅dL −1 , and total leukocyte count of 8870 cells⋅mm −3 with a differential count of 62% neutrophils, 28% lymphocytes, 7% monocytes, 2% eosinophils and 1% basophils. The platelet count was 160 000 cells⋅mm −3 . Creatinine, electrolytes and liver function tests were normal. The ECG was unremarkable and cardiac enzymes were within normal limits. Chest radiograph ( figure 1 ) showed a mild, right-sided pleural effusion, blunting of the left costophrenic angle, no shift of mediastinal position and no lung parenchymal opacities.

Frontal chest radiograph.

What is the next step in management?

Bilateral effusions that are of unequal size, unresponsive to therapy and associated with pleuritic chest pain or fever should be subjected to diagnostic thoracentesis [ 4 ].

He was subjected to a diagnostic thoracentesis, which showed 6.5 g·L −1 protein (corresponding serum proteins were 7.3 g·L −1 ), and lactate dehydrogenase (LDH) concentration was 820 U⋅L −1 (corresponding serum LDH was 563 U⋅L −1 ) and that of glucose was 7 mmol⋅L −1 . The erythrocyte count was 2 700 000 cells⋅µL −1 , and leukocytes count was 3400 cells⋅µL −1 with 53% neutrophils, 42% lymphocytes and 5% monocytes. The Gram stain and cultures were sterile. There were no acid-fast bacilli seen in smears and real-time PCR for Mycobacterium tuberculosis was negative. The cytological examination showed no malignant cells.

He was treated with antibiotics and analgesics. 48 h after admission, the patient complained of severe, left-sided chest pain in the night. It was nonradiating and not associated with sweating, nausea or vomiting. There was no haemodynamic compromise and the patient was normoxaemic. There were reduced breath sounds in both infrascapular and infra-axillary areas. An ECG was performed ( figure 2 ).

1) Describe the ECG findings.

2) What is the differential diagnosis for these findings?

1) The ECG showed a normal sinus rhythm with an S-wave in lead I, and a Q-wave and an inverted T-wave in lead III. This pattern is the S1Q3T3 pattern. There was an inverted T-wave in V1.

2) The S1Q3T3 pattern is a sign of acute cor pulmonale. The differential diagnosis for this condition includes acute pulmonary embolism (PE), pneumothorax, acute bronchospasm and left posterior fascicular block. Severe pneumonia may also show this pattern in almost 10% of cases [ 5 ]. It is seen in 12–50% of cases of acute PE [ 6 ]. This pattern has 54% sensitivity, 62% specificity, 80% positive predictive value and 33% negative predictive value for the diagnosis of acute PE.

Serial cardiac enzymes were normal. Chest radiography was also repeated ( figure 3 ).

Describe the chest radiograph.

The second chest radiograph showed an increase in the pleural effusion on the left side, while the right-sided effusion was the same. There were no fresh lung parenchymal opacities.

The patient had a bout of cough associated with mild haemoptysis and fever of up to 38°C. The possibility of PE was entertained. The revised Geneva score for the assessment of the clinical probability of PE was 5, suggesting that there was an intermediate probability of an embolism. Therefore, a D-dimer test was ordered and the level was found to be 3.6 mg⋅L −1 (normal range 0.09–0.33 mg⋅L −1 ). In line with the diagnostic algorithm for patients with suspected, not high-risk PE proposed by the European Society of Cardiology [ 7 ], the patient was subjected to computed tomographic pulmonary angiography (CTPA), which showed filling defects in the both lower and upper lobar arteries, right middle lobe, and lingular arterial branches consistent with an acute PE. There was no right ventricle enlargement seen in the four-chamber view of the heart by CTPA, which was suggestive that there was no right ventricular dysfunction ( figure 4 ).

a) CTPA showing filling defects in both the upper and left lower lobar pulmonary arteries suggestive of bilateral pulmonary embolism. Bilateral, mild pleural effusion is also seen. b) CTPA showing no enlargement of the right ventricle with a normal position of the interventricular septum suggesting no evidence of right ventricle dysfunction.

How would you manage this patient?

Once a diagnosis of acute PE is confirmed, further optimal management depends on stratifying the patient into classes of disease severity in such a way that the initial treatment is planned according to the individual’s early death risk. The clinical tools used to stratify patients into high, intermediate and low risk of early mortality are the presence of shock or hypotension, Pulmonary Embolism Severity Index (PESI) and imaging, as well as laboratory markers of right ventricular dysfunction. PESI classes I–II represent low-risk patients who may be managed with anticoagulants and considered for early discharge from the hospital. If there is any doubt about the presence of right ventricular dysfunction even in patients belonging to PESI class I–II, further imaging and laboratory testing of right ventricular function should be done [ 8 ]. PESI class III–IV patients with normal blood pressure, and imaging and/or laboratory evidence of right ventricular dysfunction need to be put on anticoagulation and monitored for haemodynamic parameters. Primary reperfusion therapy should be considered in these patients when clinical signs of a haemodynamic compromise appear.

The patient was found to be in PESI class I. This, combined with there being no signs of right ventricular dysfunction on CTPA and normal troponin levels, was suggestive of a low risk of adverse early outcome. He was given enoxaparin 7 days, followed by dabigatran. Blood and sputum cultures were eventually found to be sterile. The autoimmune/vasculitis screen was negative. Gradually, over the next few days, the patient’s fever subsided and his chest pain resolved completely. He was continued on dabigatran and a repeat chest radiograph at the last follow-up showed a complete resolution of the pleural effusion on left side with a residual blunting of right costophrenic angle ( figure 5 ). A pleural fluid acid-fast bacillus culture showed no growth of any organism after 6 weeks of incubation.

The evaluation of a persistent, undiagnosed pleural effusion begins with the classification of the pleural fluid as a transudative or exudative effusion. Light’s criteria are the best way to differentiate transudates from exudates. In approximately 15–30% cases, transudates are misclassified as exudates. These false-positive exudates are usually seen in patients receiving diuretics. Analysis of protein and albumin gradients in these patients can accurately detect transudative nature of the pleural effusion [ 9 ]. Malignancy, pneumonia, tuberculosis, PE, fungal infections, pancreatic pseudocysts and intra-abdominal abscess are some of the diseases likely to produce exudative pleural effusions [ 3 ]. Special tests on the pleural fluid help in identifying the cause of the pleural effusion in many cases. Measurement of adenosine deaminase or γ-interferon helps in the diagnosis of pleural tuberculosis. If a lymphoma is suspected, flow cytometry helps in establishing the diagnosis [ 10 ]. In cases of suspected chylothorax, pleural fluid cholesterol and triglycerides help in confirming the diagnosis [ 4 ]. Spiral computed tomography of the chest is recommended in the evaluation of undiagnosed pleural effusions. Parenchymal infiltrates and masses, pleural thickening and masses, mediastinal lymphadenopathy, and PE can be diagnosed with these scans. If the diagnosis is still elusive, thoracoscopy and pleural biopsy are recommended [ 11 ].

Acute PE is the third most frequent cardiovascular syndrome after myocardial infarction and stroke [ 8 ]. It is a cause of significant acute and long-term morbidity and mortality worldwide. Approximately one-third of the cases of PE die in the first 30 days. Early diagnosis and appropriate treatment can reduce the mortality to <10%. Pleural effusions occur in 19–61% of cases of PE [ 12 ]. Most of the series of pleural effusions that have been investigated with thoracentesis have <5% of cases attributable to PE. In a recent publication, 1.8% of the cases of pleural effusion were caused by PE [ 13 ]. The possible reasons for this discrepancy are [ 14 ]:

• Most of the effusions related to PE are too small to warrant a thoracentesis
• It is not considered as a possibility while investigating cases of undiagnosed pleural effusion
• Most of the patients with moderate to high suspicion of PE are immediately anticoagulated by the time the diagnosis is established and thoracentesis is not indicated in such a situation

PE is the most overlooked entity in patients with pleural effusion. A substantial number of cases of undiagnosed pleural effusions may be caused by acute PE.

The release of vascular endothelial growth factor and other inflammatory mediators causes an increase in the pulmonary capillary permeability. The resultant fluid in the interstitial space traverses the visceral pleura and accumulates in the pleural cavity, causing an exudative pleural effusion. This is the most plausible explanation for the presence of pleural effusion in patients with acute PE. There is long list of risk factors for a patient developing acute PE. These include a recent history of surgery, previous venous thromboembolism, immobilisation due to any cause, trauma, malignancy, and hereditary and acquired thrombophilia, such as prothrombin G20210A mutation or activated protein C resistance. Advanced age, obesity, pregnancy, the post partum period, central venous catheters and acute infections are some of the other factors implicated in the causation of acute PE. One-fifth of the cases of acute PE have no identifiable risk for its occurrence.

PE may present as pulmonary infarction with pleuritic chest pain and/or haemoptysis, isolated dyspnoea or circulatory collapse. In a large study of 4145 patients with PE, pleural effusion was found in 27% of cases with pulmonary infarction, 16% cases with circulatory collapse and 12% cases with isolated dyspnoea [ 15 ]. Pleuritic chest pain is the most important symptom in patients presenting with PE and pleural effusion, occurring in more than three-quarters of the cases. Thus, the presence of pleuritic chest pain in a patient with pleural effusion should raise a strong suspicion of acute PE. Dyspnoea is the other common symptom, seen in almost 70% of cases of pleural effusion secondary to acute PE. It is usually out of proportion to the size of the pleural effusion. Cough and fever may be seen in half the cases of pleural effusion with PE. ∼15% of the cases may have haemoptysis [ 14 ]. Our patient had pleuritic chest pain, haemoptysis (suggesting pulmonary infarction), fever and cough.

Pleural effusion associated with PE are usually maximal by the third day and any enlargement of effusion after this period or contralateral occurrence of effusion is suggestive of recurrent embolism [ 12 ], as was seen in our case. The pleural effusion is small and unilateral in majority of the patients, but it maybe bilateral in one-third of patients [ 16 ]. In a study of 141 patients with unilateral pleural effusion subjected to CTPA after a comprehensive clinical assessment including a diagnostic thoracentesis, 6.4% of cases were found to have PE. Almost all these cases were found to have cytologically proven malignant pleural effusion. PE was not found to be a primary cause of effusion in these cases. The authors concluded that pulmonary emboli are not a common cause of unilateral pleural effusion but may be frequently seen in patients having a concomitant pleural malignancy. They advocated the use of CTPA and pleural-phase imaging for patients presenting with a pleural effusion and suspected pleural malignancy [ 17 ]. Up to one-third of the cases may have loculated effusions. This is usually a result of a delay in the diagnosis of the PE. Systemic anticoagulants may be helpful in the resolution of these loculated collections [ 18 ].

Pleural fluid analysis reveals exudative fluid, which shows an increase in the erythrocyte count >10 000 cells⋅µL −1 in most of the cases [ 19 ]. There may be an increase in the leukocyte count and neutrophilic preponderance. A few patients may also have pleural fluid eosinophilia. Our patient had an exudative effusion with increased erythrocyte and leukocyte counts, and predominant neutrophils in the pleural fluid.

The treatment of pleural effusion associated with PE is similar to that of any other patient of PE, and depends on risk stratification and consequent further management. Anticoagulation is the mainstay of therapy in all cases. The presence of haemorrhagic effusion is not a contraindication for anticoagulation or thrombolysis [ 12 ]. The pleural effusion gradually resolves with anticoagulant therapy, as was seen in our case. If the pleural effusion increases in size or appears on the contralateral side, it is suggestive of a recurrent thromboembolism, infection in the pleural cavity or haemothorax [ 14 ].

Pleural effusions are commonly seen in association with acute PE. It should be entertained as an important possibility while investigating a case of undiagnosed exudative pleural effusion presenting with a pleuritic chest pain. These effusions are generally unilateral but may also be bilateral especially if there is a recurrent thromboembolism. The pleural effusion associated with acute PE show a good response to systemic anticoagulant therapy.

Conflict of interest None declared

JOY SHEN-WAGNER, MD, CHRISTINE GAMBLE, MD, AND PHYLLIS MACGILVRAY, MD

Am Fam Physician. 2023;108(5):464-475

Author disclosure: No relevant financial relationships.

Pleural effusion affects 1.5 million patients in the United States each year. New effusions require expedited investigation because treatments range from common medical therapies to invasive surgical procedures. The leading causes of pleural effusion in adults are heart failure, infection, malignancy, and pulmonary embolism. The patient's history and physical examination should guide evaluation. Small bilateral effusions in patients with decompensated heart failure, cirrhosis, or kidney failure are likely transudative and do not require diagnostic thoracentesis. In contrast, pleural effusion in the setting of pneumonia (parapneumonic effusion) may require additional testing. Multiple guidelines recommend early use of point-of-care ultrasound in addition to chest radiography to evaluate the pleural space. Chest radiography is helpful in determining laterality and detecting moderate to large pleural effusions, whereas ultrasonography can detect small effusions and features that could indicate complicated effusion (i.e., infection of the pleural space) and malignancy. Point-of-care ultrasound should also guide thoracentesis because it reduces complications. Computed tomography of the chest can exclude other causes of dyspnea and suggest complicated parapneumonic or malignant effusion. When diagnostic thoracentesis is indicated, Light's criteria can help differentiate exudates from transudates. Pleural aspirate should routinely be evaluated using Gram stain, cell count with differential, culture, cytology, protein, l-lactate dehydrogenase, and pH levels. Additional assessments should be individualized, such as tuberculosis testing in high-prevalence regions. Parapneumonic effusions are the most common cause of exudates. A pH level less than 7.2 is indicative of complicated parapneumonic effusion and warrants prompt consultation for catheter or chest tube drainage, possible tissue plasminogen activator/deoxyribonuclease therapy, or thoracoscopy. Malignant effusions are another common cause of exudative effusions, with recurrent effusions having a poor prognosis.

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Pleural Effusions

Table of contents.

Updated April 2022

Authors: Neha Deshpande, MD 1 ,  Ryan Murphy, MD 2 Executive Editor: Yilin Zhang, MD 1

1 Assistant Professor, Department of Medicine, University of Washington 2 Clinical Instructor, Department of Medicine, Division of Pulmonary and Critical Care Medicine

• Describe criteria differentiating pleural effusions into transudative and exudative effusions.  
• Generate a differential diagnosis for each transudative and exudative effusions and associate diagnoses with characteristic pleural fluid studi es.  
• Create a framework for the management of parapneumonic effusions.  

Teaching Instructions

Plan to spend at least 30-60 minutes preparing for this talk by using the Interactive Board and the Teaching Instructions. Click through the graphics animations to become familiar with the flow and content of the talk. All clickable elements will be denoted by a shaded rounded rectangle and a mouse cursor. 

Begin with reviewing the objectives for the session. We recommend progressing in order, though this gives you the flexibility  to deliver  more focused teaching. The talk can be presented in one of two ways:

• Project the “Interactive Board” OR
• Reproduce your own drawing of the presentation on a whiteboard/ Chalkboard

The anticipated time for the content of this talk is about 15 min. With cases, 25-30 min. 

Title Page :  Introduce the ways to identify a pleural effusion on imaging (blunted costophrenic angle, meniscus on CXR). Ask your learners which pleural effusions warrant further evaluation.  Click on the button to reveal the answer . 

Objective 1 – Describe criteria differentiating pleural effusions into transudative and exudative effusions. ( Light's Criteria)

The first step in the evaluation of a pleural effusion is to perform  a n   ultrasound-guided  diagnostic thoracentesis and obtain pleural fluid . Light’s criteria compare the pleural fluid LDH and protein to serum LDH and protein and  differentiate transudative (non-inflammatory) from exudative ( inflammatory) effusions.  Light's criteria has a sensitivity of 98% and specificity of 83%. However, it is not accurate in the setting of diuretic use or in with high pleural RBC counts (> 10k) which can falsely elevate LDH. 

Bonus learning:  The serum albumin – pleural albumin gradient can also be used to identify a transudative process (gradient > 1.2). 

Additional  standard  and specialized pleural fluid studies can further characterize the  effusion  and  help diagnose the underlying etiology.  Ask your learners to review Light’s criteria ( click “Light's criteria” to reveal ).  Ask them how many of  Light’s criteria need to be met in order to define an exudative process.  Then, ask your learners which additional pleural fluid studies they would send.  Click on “pleural studies” and “specialized tests” to reveal additional information.   

Bonus learning:  To learn more about any of these studies, you may click on the “bonus information” button to navigate to a page with detailed information on each test.

Objective 2  – Challenge your learners to list off some causes of transudative and exudative effusions before moving onto the differential slide. ( Differential)

Navigate to the Differential slide by either clicking on the “Differential” page in the left hand table of contents or on the “transudate” or “exudate” buttons. Challenge your learners to list off some causes of transudative and exudative effusions before moving onto the differential slide . 

• Transudative effusions – Click on “transudate” to reveal a differential. Typically caused by volume overload (heart failure, renal failure) or cirrhosis. Hypoalbuminemia can also result in third spacing to the pleural space.  
• M ycobacterial tuberculosis pleural effusions, AFB stain and  culture from pleural fluid are not  sensitive, and pleural biopsy for tissue stain and culture is diagnostic.  An adenosine deaminase study can also be suggestive of a tuberculous infection. 
• For malignant effusions, higher volume therapeutic thoracenteses increase the diagnostic yield. The sensitivity of an initial thoracentesis for malignant effusion is ~ 60%. The sensitivity increases to ~ 75% with a second large volume thoracentesis.

Objective 3 – Create a framework for the management of parapneumonic effusions. ( Management )

Further characterization of parapneumonic effusions into uncomplicated and complicated effusions is critical because this  distinction determines management.  Ask your learners how  to classify parapneumonic effusions based on the  pr esence of  septations  and/or loculations on imaging, low  pleural fluid  pH and glucose, and  frank  pus and/or bacteria  on gram stain ( click on each of these pleural findings to reveal classification of parapneumonic effusions ) . 

• Uncomplicated parapneumonic effusions – these are effusions without loculations, septations and do not meet other criteria for complicated parapneumonic effusion or empyema. Click on “uncomplicated parapneumonic effusion to reveal treatment. Emphasize that uncomplicated effusions are treated with antibiotics alone.
• Complicated parapneumonic effusions – Complicated effusions have loculations, septations, low pH < 7.2 or low glucose.  Click on complicated effusion to reveal management.
• Empyema – Empyema is diagnosed based on presence of frank pus or positive pleural culture. Contrast the management of complicated effusions and empyema from uncomplicated effusions. Complicated effusions and empyemas require drainage of the pleural space for effective treatment. The  treatment  of a complicated pleural effusion  is multi-disciplinary , and often  needs  interventional  radiology, pulmonology, and thoracic surgery consultation .

Ask learners to list mechanisms of complex pleural fluid drainage. Click on “antibiotics and drainage” to reveal additional information. Depending on the complexity of the effusion, less-invasive  pigtail placement  may be sufficient. For heavily loculated effusions, a larger-bore chest tube may  be more appropriate.  For empyema, more-invasive  surgical  procedures such as video-associated thoracic surgery  (VATS)  or  open  decortication  are likely to be needed. 

Instillations of  tPA  and  dornase  through the pleural catheter  can augment drainage, however, this has not been shown to decrease mortality ,  and  more data about the optimal timing of surgery is needed.  A randomized controlled trial comparing outcomes of fibrinolytic therapy to early VATS decortication is planned.  

Cases  – There are a total of 3 cases. After reading through the stem, have your learners request work-up and click on the corresponding section. Not all tests are needed in every case.

Interactive Board

Take home points.

• Light’s criteria are used to distinguish transudative and exudative pleural effusion s.  
• Transudat ive effusions  develop  from non-inflammatory  conditions (such as heart, renal, and liver failure)  and  e xudative effusions   typically  result  from inflammatory diseases (such as infections, malignancy, autoimmune diseases).
• Parapneumonic effusions are further differentiated into complicated and uncomplicated effusions by the presence of loculations, low pH, and low glucose. Complicated parapneumonic effusions  and empyema  require drainage for effective   treatment   and  consultation with  multiple subspecialties.  
• Light RW. Clinical practice. Pleural effusion. NEJM. 2002; 346(25):1971-1977. 
• Feller-Kopman D and Light R. Pleural  d isease. NEJM. 2018 ;378(8):740-51. DOI: 10.1056/NEJMra1403503.  
• Porcel JM and Light RW. Pleural  effusions . Disease-a-Month.  2013;59:29 -57 . DOI: 10.1016/j.disamonth.2012.11.002.  
• ClinicalTrials.gov [Internet]. Bethesda (MD): National Library  of Medicine (US). 2018 Jul 26  – .  Identifier  NCT03583931, Early Intervention for  c omplicated  p arapneumonic  e ffusion : randomized controlled trial for fibrinolytic therapy versus VATs decortication; [cited 2020 Dec 16]; [about  8 pages]. Available from: https://clinicaltrials.gov/ct2/show/NCT03583931.  
• Heffner JE. Diagnostic evaluation of a pleural effusion in adults: Initial testing. In Uptodate, Finaly G (Ed), UpToDate, Waltham, MA. (Accessed on Dec 17, 2020).
• [email protected]

Patient confidentiality is a priority.  No case presented here contains uniquely identifying characteristics, nor do the cases reflect the presentation or care of any one individual.  Rather, they represent a compilation of similar cases adapted to achieve the greatest educational value and generalizability.

The authors pro­vide this content for educational pur­poses only. This content is not intended, nor should it be used as medical advice.

The content on this site does not necessarily represent the opinions of the principal author, team or their employer.

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Getting to the heart of pleural effusions: a case study

Affiliation.

• 1 St. Boniface General Hospital, Winnipeg, Manitoba, Canada. [email protected]
• PMID: 19845808
• DOI: 10.1111/j.1745-7599.2009.00431.x

Purpose: To provide nurse practitioners (NPs) with an overview of the physiology, pathophysiology, clinical presentation, and comprehensive assessment, as well as the differential diagnosis process and initial management of patients with unilateral pleural effusions.

Data sources: A review of the scientific literature was performed on pleural effusions, using Pub Med, Medline, and CINAHL. The case study of a patient with a pleural effusion related to heart failure is used to integrate this knowledge into clinical practice.

Conclusions: Pleural effusions are common sequelae of numerous pathophysiological processes.

Implications for practice: Knowledge of the underlying physiological and pathophysiological mechanisms enables the NP to obtain an accurate and comprehensive assessment, establishes a differential diagnosis, and provides the timely initial management necessary to optimize patient care outcomes.

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