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==Classification==
==Classification==
Pleural effusion may be classified according to composition of pleural fluid by Light's criteria into two subtypes: Exudate and transudate. An increase in plasma osmotic pressure or elevated systemic or pulmonary hydrostatic pressure are alterations that lead to the formation of transudate. In contrast, an exudate results from inflammation and infectious disease of the pleural surface, as seen in tuberculosis and pneumonia with effusion, or other disease of the pleural surface as seen in malignancy, pancreatitis, pulmonary infarction, or systemic lupus erythematosus.
Light's criteria classifies pleural fluid as an exudate if at least one of the following three criteria is fulfilled:<ref name="pmid4642731">{{cite journal| author=Light RW, Macgregor MI, Luchsinger PC, Ball WC| title=Pleural effusions: the diagnostic separation of transudates and exudates. | journal=Ann Intern Med | year= 1972 | volume= 77 | issue= 4 | pages= 507-13 | pmid=4642731 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4642731  }} </ref>
*Pleural fluid protein/serum protein ratio greater than 0.5, or
*Pleural fluid LDH/serum LDH ratio greater than 0.6, or
*Pleural fluid LDH greater than two-thirds the upper limits of the laboratory's normal serum LDH
Pleural effusion may also be classified according to the appearance of pleural fluid, and etiology of the pleural fluid.
Example; [[Serous fluid]], ([[hydrothorax]]) [[Blood]], ([[hemothorax]]) [[Chyle]], ([[chylothorax]]) [[Pus]], ([[pyothorax]] or [[empyema]])


==Pathophysiology==
==Pathophysiology==

Revision as of 21:00, 5 October 2016

Pleural effusion Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Overview

Pleural effusion is defined as the presence of excessive fluid in the pleural cavity resulting from transudation or exudation from the pleural surfaces. In normal conditions, the pleural space contains a small amount of fluid (≈0.3 mL·kg-1)[1][2][3] maintained by a complex interplay of hydrostatic pressures and lymphatic drainage, which allows for steady liquid and protein turnover.[4] Pathological processes may lead to the development of pleural effusions by causing disequilibrium between the rates of pleural fluid formation, pleural permeability and pleural fluid absorption. Pleural effusion may be secondary to pleural processes, pulmonary disorders, systemic conditions, and medications. A systematic approach with a comprehensive clinical history and physical examination is required for establishing the etiology.

Historical Perspective

Pleural infection was first described by Hippocrates as far back as 460-370 B.C.[5] During this time open chest drainage was the sole treatment modality and was associated with high mortality.

In 1300s, Guy de Chauliac also called Guido or Guigo de Cauliaco, a surgeon of medieval France, commented with surprise on the lack of ancient writings concerning thoracic wounds and the disagreements on the treatment of these wounds. Lanfranc of Paris, William of Bologna, and Roland of Parma advocated that open treatment of penetrating thoracic wounds using tents and drains allow blood and decaying organic materials to escape however, Henri de Mondeville was of different opinion that immediate closure of wounds helps to prevent heat loss and air entry.[6]

During the early 1500s, Giovanni da Vigo, an Italian surgeon and physician of Pope Julius II, was one of the first surgeons to discuss firearm wounds to the chest.[6]

IN 1873, Playfair gave the first description of a water-seal chest drainage system in the treatment of a child with thoracic empyema.[7]

In 1875, Gotthard Bülau a German Internist described the use of closed water-seal chest drainage to treat an empyema, as an alternative to the standard rib resection and open tube drainage. He punctured the pleura membrane with trocar and introduced a rubber catheter into the pleural cavity. The free end of the catheter inserted in a bottle one-third full of solution allowing pus to flow freely from the chest into the bottle.[8][9]

Closed chest tube drainage was experimentally practised during the influenza epidemic in 1917–19 when open surgical drainage was associated with a high mortality rate. This coincided with world war I and the resultant crisis of streptococcal pneumonia and empyema.[10]

In 1950, Vincenzo Monaldi an Italian Pulmonologist suggested draining the thoracic cavity with a more superior approach at the second or third intercostal space.[11]

The modern three chamber thoracic drainage system was first described by Howe in 1952 but not widely employed at the time.[12]

Closed chest tube drainage became the standard of treatment from late 1950.[13]

Classification

Pleural effusion may be classified according to composition of pleural fluid by Light's criteria into two subtypes: Exudate and transudate. An increase in plasma osmotic pressure or elevated systemic or pulmonary hydrostatic pressure are alterations that lead to the formation of transudate. In contrast, an exudate results from inflammation and infectious disease of the pleural surface, as seen in tuberculosis and pneumonia with effusion, or other disease of the pleural surface as seen in malignancy, pancreatitis, pulmonary infarction, or systemic lupus erythematosus.

Light's criteria classifies pleural fluid as an exudate if at least one of the following three criteria is fulfilled:[14]

  • Pleural fluid protein/serum protein ratio greater than 0.5, or
  • Pleural fluid LDH/serum LDH ratio greater than 0.6, or
  • Pleural fluid LDH greater than two-thirds the upper limits of the laboratory's normal serum LDH

Pleural effusion may also be classified according to the appearance of pleural fluid, and etiology of the pleural fluid. Example; Serous fluid, (hydrothorax) Blood, (hemothorax) Chyle, (chylothorax) Pus, (pyothorax or empyema)

Pathophysiology

Healthy individuals have less than 15 ml of fluid in each pleural space. Normally, fluid enters the pleural space from the capillaries in theparietal pleura, from interstitial spaces of the lung via the visceral pleura, or from the peritoneal cavitythrough small holes in the diaphragm. This fluid is normally removed by lymphatics in the visceral pleura, which have the capacity to absorb 20 times more fluid than is normally formed. When this capacity is overwhelmed, either through excess formation or decreased lymphatic absorption, a pleural effusion develops.

Causes

Differentiating Pleural Effusion from other Diseases

Evaluation of a patient with a pleural effusion requires a thorough clinical history and physical examination in conjunction with pertinent laboratory tests and imaging studies. Thoracentesis should not be performed for bilateral effusions in a clinical setting strongly suggestive of a transudate unless there are atypical features or they fail to respond to therapy. Pleural fluid should always be sent for protein, lactate dehydrogenase, Gram stain, cytology and microbiological culture.[15] Additional studies which may be indicated in selected cases include pH, glucose, acid-fast bacilli and tuberculosis culture, triglycerides, cholesterol, amylase, and hematocrit. Light's criteria is applied to distinguish the fluid between transudative or exudative.[14] A broad array of underlying conditions result in exudative effusions, while a limited number of disorders are assoicated with transudative effusions, which include congestive heart failure, cirrhosis, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, urinothorax, atelectasis, constrictive pericarditis, trapped lung, superior vena caval obstruction, and duropleural fistula.

Epidemiology and Demographics

In the United States, up to one million patients develop parapneumonic effusions annually, and approximately 100,000 patients undergo pleurodesis for recurrent pleural effusions per year.[16] Pleural effusion is reported to have an incidence of 0.32% in a study among the general population in central Bohemia. Congestive heart failure accounts for nearly 50% of cases, with malignancy, pneumonia and pulmonary emboli as the next three leading causes.[17] However, the distribution of causes is largely dependent on the population studied.

Risk Factors

Natural History, Complications, and Prognosis

Diagnosis

Symptoms

  • [Disease name] is usually asymptomatic.
  • Symptoms of [disease name] may include the following:
  • [symptom 1]
  • [symptom 2]
  • [symptom 3]
  • [symptom 4]
  • [symptom 5]
  • [symptom 6]

Physical Examination

  • Patients with [disease name] usually appear [general appearance].
  • Physical examination may be remarkable for:
  • [finding 1]
  • [finding 2]
  • [finding 3]
  • [finding 4]
  • [finding 5]
  • [finding 6]

Laboratory Findings

  • There are no specific laboratory findings associated with [disease name].
  • A [positive/negative] [test name] is diagnostic of [disease name].
  • An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
  • Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

Chest X Ray

Chest films acquired in the lateral decubitus position (with the patient lying on their side) are more sensitive, and can pick up as little as 50 ml of fluid. At least 300 ml of fluid must be present before upright chest films can pick up signs of pleural effusion (e.g., blunted costophrenic angles).

CT

MRI

Other imaging findings

Other diagnostic studies

Treatment

Medical Therapy

  • There is no treatment for [disease name]; the mainstay of therapy is supportive care.
  • The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
  • [Medical therapy 1] acts by [mechanism of action 1].
  • Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

  • Surgery is the mainstay of therapy for [disease name].
  • [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
  • [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
  • Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].


References

  1. Noppen M (2004). "Normal volume and cellular contents of pleural fluid". Paediatr Respir Rev. 5 Suppl A: S201–3. PMID 14980271.
  2. Noppen M, De Waele M, Li R, Gucht KV, D'Haese J, Gerlo E; et al. (2000). "Volume and cellular content of normal pleural fluid in humans examined by pleural lavage". Am J Respir Crit Care Med. 162 (3 Pt 1): 1023–6. doi:10.1164/ajrccm.162.3.9910050. PMID 10988124.
  3. Noppen M (2001). "Normal volume and cellular contents of pleural fluid". Curr Opin Pulm Med. 7 (4): 180–2. PMID 11470970.
  4. Miserocchi G (1997). "Physiology and pathophysiology of pleural fluid turnover". Eur. Respir. J. 10 (1): 219–25. PMID 9032518. Unknown parameter |month= ignored (help)
  5. FRANCE, JOHN (2010). [URL: http://www.jstor.org/stable/10.7722/j.ctt7zstnd Journal of Medieval Military History: Volume VIII] Check |url= value (help). Boydell Press, Boydell & Brewer. p. 206. ISBN 9781843835967.
  6. 6.0 6.1 LINDSKOG GE (1961). "Some historical aspects of thoracic trauma". J Thorac Cardiovasc Surg. 42: 1–11. PMID 13762404.
  7. Munnell ER (1997). "Thoracic drainage". Ann Thorac Surg. 63 (5): 1497–502. PMID 9146363.
  8. Meyer JA (1989). "Gotthard Bülau and closed water-seal drainage for empyema, 1875-1891". Ann Thorac Surg. 48 (4): 597–9. PMID 2679468.
  9. Van Schil PE (1997). "Thoracic drainage and the contribution of Gotthard Bülau". Ann Thorac Surg. 64 (6): 1876. PMID 9436605.
  10. Peters RM (1989). "Empyema thoracis: historical perspective". Ann Thorac Surg. 48 (2): 306–8. PMID 2669652.
  11. Knobloch K (2008). "eComment: A tribute to Gotthard Bulau and Vincenzo Monaldi". Interact Cardiovasc Thorac Surg. 7 (6): 1159. doi:10.1510/icvts.2008.181750A. PMID 19029391.
  12. HOWE BE (1951). "Evaluation of chest suction with an artificial thorax". Surg Forum: 1–7. PMID 14931188.
  13. Monaghan SF, Swan KG (2008). "Tube thoracostomy: the struggle to the "standard of care"". Ann Thorac Surg. 86 (6): 2019–22. doi:10.1016/j.athoracsur.2008.08.006. PMID 19022041.
  14. 14.0 14.1 Light RW, Macgregor MI, Luchsinger PC, Ball WC (1972). "Pleural effusions: the diagnostic separation of transudates and exudates". Ann Intern Med. 77 (4): 507–13. PMID 4642731.
  15. Hooper C, Lee YC, Maskell N (2010). "Investigation of a unilateral pleural effusion in adults: British Thoracic Society Pleural Disease Guideline 2010". Thorax. 65 Suppl 2: ii4–17. doi:10.1136/thx.2010.136978. PMID 20696692. Unknown parameter |month= ignored (help)
  16. Light, Richard J. (2007). Pleural diseases. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-6957-4.
  17. Marel M, Zrůstová M, Stasný B, Light RW (1993). "The incidence of pleural effusion in a well-defined region. Epidemiologic study in central Bohemia". Chest. 104 (5): 1486–9. PMID 8222812. Unknown parameter |month= ignored (help)

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