Evolution of Idiopathic Pleural Effusion: A Prospective, Long-term Follow-up Study

doi:10.1378/chest.109.6.1508

Chest

Volume 109, Issue 6, June 1996, Pages 1508-1513

https://doi.org/10.1378/chest.109.6.1508 Get rights and content

The management of idiopathic pleural effusion remains controversial. Because the long-term evolution of this entity is not well known, two different approaches, aggressive and conservative, have been proposed. We conducted a 10-year study of the evolution of idiopathic pleural effusion.

Methods

Between 1984 and 1994, we prospectively studied 40 consecutive patients (30 men and 10 women; mean [±SD] age, 53.8±19.4 years) with exudative pleural effusion undiagnosed after exhaustive evaluation. The pleural fluid adenosine deaminase level was below 43 IU/L in all; periodic chest radiographs and clinical evaluation were carried out in all patients for a mean of 62 months (range, 36 to 108 months). Further diagnostic procedures were performed whenever the effusion recurred or when indicated by the clinical picture.

Results

Effusions resolved in a mean time of 5.6 months (range, 7 days to 48 months). Five patients (12.5%) had one or more relapses of their pleural effusion, and in a further 5 (12.5%), the effusion persisted unchanged for more than 1 month. In 32 cases (80%), no potential cause of the effusion was detected. The diagnoses in the remaining eight cases were asbestos pleural effusion in three, pulmonary adenocarcinoma in one, mesothelioma in one, congestive heart failure in one, liver cirrhosis in one, and rheumatoid arthritis in one. Tuberculosis was not detected in any of the cases, although 19 patients initially had positive tuberculin tests.

Conclusions

Most idiopathic pleural effusions follow a benign course. Our results support conservative treatment of patients with idiopathic pleural effusion. Antituberculous treatment does not appear to be warranted, regardless of tuberculin test results, if the pleural fluid adenosine deaminase level is not elevated.

Section snippets

Patients

Between January 1984 and March 1991, 394 patients with pleural effusion were admitted to our department. Initial studies included the following: medical history to rule out exposure to asbestos or previous drug ingestion; complete physical examination; blood analysis; chest radiograph; and tuberculin test. Studies on pleural fluid obtained by thoracentesis included the following: determination of the levels of glucose, protein, adenosine deaminase, and lactate dehydrogenase; bacteriologic study

RESULTS

Baseline clinical and radiologic data for the 40 patients (30 men and 10 women) at diagnosis are shown in Table 2. A summary of the pleural fluid findings and the procedures used in the diagnostic workup are shown in Table 3. In the 19 patients with positive tuberculin tests, the pleural fluid was lymphocytic in 16 and polymorphonuclear in 3. In the 21 patients with negative tuberculin tests, the pleural fluid was lymphocytic in 19 and polymorphonuclear in 2. All patients had adenosine

DISCUSSION

The results of this study show that an idiopathic pleural effusion with no clinical or radiologic evidence of malignancy resolves spontaneously, albeit on occasions (12%) after a prolonged period of time or several relapses. A major finding in this study was that none of the patients developed tuberculosis during the follow-up period, despite the fact that 19 patients had a positive tuberculin test. The current recommendation for antituberculous treatment for patients with idiopathic pleural

ACKNOWLEDGMENT

The writers thank Cristina O'Hara for help with translation.

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To appropriately manage the pleural effusion, it is important to first determine its cause [1]. The most common causes of exudative pleural effusion include malignancy, tuberculosis, and pneumonia [4]. Less frequently, contiguous spread from adjacent infection, such as a liver abscess or pancreatitis, can give rise to pleural effusions [1].
Pleural effusions are associated with a variety of disease states, rendering the differential diagnosis challenging. Spondylodiscitis is an uncommon disease, and its prompt diagnosis can reduce morbidity and mortality. However, an atypical manifestation of the disease, such as pleural effusion, can result in delayed diagnosis. A 76-year-old woman presented with back pain and right pleural effusion. Magnetic resonance imaging revealed paravertebral soft tissue infiltration, with enhancement of bone marrow and intervertebral disk at the T8 and T9 levels, suggesting spondylodiscitis. In patients with exudative pleural effusion, spondylodiscitis may be the cause, so careful analysis of imaging is necessary.
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The most common postbiopsy causes include the following: tuberculosis, malignant mesothelioma or metastatic carcinoma, asbestos pleural diseases, heart failure, liver cirrhosis, postradiation effusion, trauma, parapneumonic effusion, and autoimmune disease. Most important is malignancy which occurs in between 8 and 20% of the cases probably as a consequence of a failure to sample diagnostic tissue [1-3,6,7,10-12,20,21]. Persistence of the effusion, weight loss, fever, and large size of the effusion usually are harbingers of a subsequent malignant diagnosis [20].
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A pleural biopsy without granulomatous inflammation or tumour cells is interpreted as ‘non-specific pleuritis’ (NSP), a diagnosis without any specificity, often frustrating for physicians. However, varying histological features are found in NSPs with unknown significance. The aim of this study was to describe the detailed microscopic features of NSP and correlate them with the underlying aetiology. One hundred patients diagnosed with NSP after pleural biopsy were retrospectively evaluated. A benign cause of pleural effusion was attributed. Histological features evaluated were inflammation, fibrosis, vascular proliferation, haemorrhage, fibrin, oedema and mesothelial hyperplasia. A semi-quantitative scoring was applied. Bacterial-caused and autoimmune disease-associated NSPs showed a higher score followed by viral and drug-induced conditions, while pneumothorax and cardiac-induced NSPs showed a lower score (p<0.0001). The degree of fibrosis was higher in bacterial NSP, and the type of fibrosis was cellular in this group (p=0.006). Vascular proliferation differed between groups (p<0.0001), and was higher in bacterial NSP. Histological findings differ significantly between the varying aetiologies of NSP, and this may be used to suggest the cause of the effusion.

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: revision accepted December 20

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Chest

Clinical Investigations: The PleuraEvolution of Idiopathic Pleural Effusion: A Prospective, Long-term Follow-up Study

Methods

Results

Conclusions

Section snippets

Patients

RESULTS

DISCUSSION

ACKNOWLEDGMENT

Chest

Chest

Chest

Chest

Chest

Chest

Chest

Ann Thorac Surg

Am J Med

Clin Chest Med

Am Heart J

Pleural effusion: a diagnostic dilemma

JAMA

Pleural effusion: laboratory test in 300 cases

Thorax

Pleural effusions

Mayo Clin Proc

The pleura

Am Rev Respir Dis

Pleural diseases

Initial tuberculous pleuritis in the Finnish Armed Forces in 1939–1945 with special reference to eventual post pleuritic tuberculosis

Acta Tuberc Scand

Primary serofibrinous pleural effusion in military personnel

Am Rev Tuberc

Clinical Investigations: The Pleura
Evolution of Idiopathic Pleural Effusion: A Prospective, Long-term Follow-up Study