Pleural effusion J90

Between the two pleural leaves, in the pleural cavity (cavitas pleuralis), there is physiologically a serous fluid of approx. 5 - 10 ml. On the one hand, this fluid enables the pleural sheets to slide during inspiration and expiration, and at the same time connects the two pleural sheets to each other by capillary force.

The physiological fluid present in the pleural space flows into the space from several places: from the interstitium of the lung via the visceral pleura, from the pleural capillaries of the parietal pleura, from the lymphatics located in the thoracic wall and from the peritoneal cavity.

Resorption occurs via the lymphatic vessels of the parietal pleura. In this way, the complete fluid 1x/h is completely renewed.

Furthermore, in pleural effusion, a pathologic amount of fluid is found in the pleural cavity because either the resorption capacity of the pleura is decreased and/or pleural fluid production is increased.

Pleural effusion may also develop into empyema. In this case, an infection occurs in a pre-existing pleural effusion. As a result, the effusion fluid becomes macroscopically purulent. In the initial so-called exudative phase, there is an influx of neutrophil granulocytes. This is followed by the fibropulent phase with progressive fibrin formation. In the acidic, hypoxic environment of the pleural effusion, the granulocyte defense is severely limited, which allows the infection to progress.

see also pleural puncture

s.a. Pleura

There are 2 different forms of effusions: exudate and transudate, whose origin and composition differ. The differentiation between the two forms is decisive for the further diagnosis (see below).

1. transudate

During transudate, the pleura itself is not diseased; it is rather systemic factors that play a role here. An increase in capillary pressure in the great circulation leads to an increased secretion of the parietal pleura. In addition, there is also an increase in capillary pressure in the small circulation, which reduces reabsorption in the visceral pleura. The increase in pressure also has an influence on lymph drainage, which is also reduced.

2. exudate

With exudate, local factors influence the development of the effusion. Disease of the pleura leads to an increase in capillary permeability in the parietal pleura and thus to an increase in exudate.

The protein and cell content of the exudate is significantly increased compared to the physiologically occurring fluid in the pleural gap. As a result, the already increased exudate can be additionally absorbed even more poorly.

For the differentiation between transudate/exudate see below under Diagnosis

Empyema with parapneumonic effusion

The parapneumonic effusion in combination with bacterial pneumonia is probably the most common exudative effusion in our latitudes. It can develop into an empyema.

Empyema is also described in the context of pleuritis, lung abscesses, bronchiectasis, after trauma or thoracic surgery, etc.

Pleural effusion is one of the most common diseases in clinical medicine, the frequency of which increases significantly with age. Precise figures for Germany are not available. In the USA, the incidence is approximately 500,000 cases per year, figures that might also apply to Central European countries.

Empyema has a special position among the effusions. About 50 % of patients with bacterial pneumonia develop a parapneumonic effusion. In 5 % of these patients an empyema develops in the course of the disease. Empyema has a bad prognosis if it is detected too late or is not treated adequately. In young, previously healthy patients the mortality rate is 8 - 15 %. In older patients or in patients with severe pre-existing conditions the mortality rate rises to 40 - 70%.

The most frequent cause of pleural effusion < 40 years is tuberculosis.

The 3 most common diseases that lead to a transudate in western countries are:

• decompensated left heart failure
• Pulmonary embolism
• Cirrhosis of the liver

Possible other causes are:

• atelectasis
• nephrotic syndrome
• Sarcoidosis
• The three most common diseases that lead to exudate in western countries are:
• pneumonia
• Malignancies
• Pulmonary embolism (can lead to both exudate and transudate)

Possible other causes are:

• infectious diseases (especially tuberculosis)
• Collagenoses / Vasculitides
• lymphatic systemic diseases
• endocrinological diseases
• iatrogenic

Empyema

A large number of pathogens can be found in empyema. In formerly healthy individuals, the pathogens are usually S. pneumoniae, S. pyogenes or S. aureus. Anaerobic infections are mainly found after aspiration pneumonia, lung abscesses, oropharyngeal or gastrointestinal infections. S. aureus or Gram-negative pathogens are particularly common after thoracic surgery. Staphylococci predominate in the hematothorax.

However, tuberculosis and fungi have also been described as pathogens of empyema.

• Dyspnoea, especially under stress
• possibly pain in case of pleuritis (depending on breathing) or tumour
• sometimes also dry dry cough
• otherwise symptoms of the underlying disease

Sonography:

For the ultrasound examination the patient should be seated if possible. However, any fluid in the thoracic cavity can also be visualized while lying down. Even the smallest amounts of fluid in the thoracic cavity (from approx. 20 ml) can be detected by ultrasound, better than by X-ray. The extent of the effusion, the mobility when changing position and even the presence of fibrin septum can be assessed well. A possible puncture should ideally always be performed under sonographic control.

Thorax X-ray in 2 planes:

The X-ray image allows the localisation and extension of the effusion to be assessed. However, only effusions of approx. 100 ml or more can be displayed here (when the image is taken lying down and with the lateral beam). In the case of a p.a. image taken in a standing position, only effusions of approx. 200 ml or more can be displayed.

Blood gases:

The blood gases are generally not altered, since an effusion does not lead to ventilation/perfusion inhomogeneity. The situation is different, however, when re-expansion edema occurs (possible complication of a pleural drainage). In this case a distinct hypoxia develops. For this reason, re-expansion edema can always be ruled out in the case of sudden onset of hypoxaemia.

Lung function:

Usually we find a restrictive disorder due to the effusion. Here, the extent of the restriction, in particular the reduction of vital capacity, corresponds to about one third to one fifth of the amount of pleural effusion. Conversely, an effusion drainage of one litre leads to an improvement of the vital capacity of about 200 - 300 ml. The efficiency of the therapy can therefore be assessed well by the course of the vital capacity.

Thoracoscopy:

Should only be carried out in cases where the diagnosis is unclear. The effusion fluid can thus be aspirated immediately under visual control. Therapeutic interventions such as talcumpoid draping for malignant effusion are also possible.

Bloody effusions should be centrifuged immediately. If the hematocrit reaches more than half of the blood hematocrit, we speak of a hematothorax. A bloody effusion is always - until proven otherwise - suspected to be malignant.

Differentiation between exudate and transudate:

Exudate must meet at least 1 of the following criteria:

• pleural fluid/serum protein content > 0,5
• LDH in the pleural fluid/serum LDH > 0.6
• LDH in pleural fluid is more than two thirds of the upper standard limit of serum LDH.

However, up to 25 % of transudates are erroneously identified as exudates using these criteria. If the clinical situation is more in favour of exudate, it is recommended that the protein concentration in serum and in the pleural fluid be determined simultaneously. If the gradient is more than 31g/l (3.1g/dl), this is a clear indication that exudate is not possible. If it is indeed an exudate, the following additional diagnostic measures are indicated:

Macroscopic description of the puncture (turbidity, colour, possible blood admixture, etc.)

Glucose content:

• Glucose/serum < 0.5 indicates malignancy, rheumatoid arthritis, empyema, lupus erythematosus, tuberculosis, oesophageal rupture)
• very low or not measurable indicates parapneumonic effusion, empyema or rheumatoid arthritis

Amylase activity:

• Pleural Amylase > Serum Amylase is indicative of acute or chronic pancreatitis, esophageal rupture or malignancy

triglycerides:

• >100 mg/dl Chylothorax or Pseudochylothorax

tumor markers:

• can often be specific depending on the tumour, but are not very sensitive

LDH:

• > 1000IU/l Empyema, parasitoses, rheumatoid arthritis, occasionally malignancies

Adenosine deaminase or also ADA:

• Tuberculosis

protein:

• >4 g/dl tuberculous process
• > 7 g/dl Multiple myeloma

Determination of the pH value:

• pH between 7.0 and < 7.2 Malignancy, rheumatoid arthritis, pneumatic effusion
• pH <7.0 plus leucocytosis indicates a lactate cause and thus an empyema
• pH increase speaks for the degradation of glucose and thus probably for bacteria.

Microbiological examination:

• obligatory in cases of inflammatory effusion or empyema; Note: is often negative, although later on bacterial genesis is confirmed (the inhibitors in the effusion are so strong that they prevent the growth of bacteria in the laboratory)

Cytology:

• In case of unclear effusions it is recommended to take a smear (Gram staining) immediately, because this way information about the number of granulocytes and lymphocytes can be obtained relatively easily and also information about whether malignant cells are present.

Neutrophil granulocytes:

• < 5000/µl chronic exudates (malignancies, tuberculosis)
• 10.000 - 50.000 /µl (acute pancreatitis, lupus erythematosus, uncomplicated parapneumonic effusions)
• >50.000 /µl (complicated parapneumonic effusions

lymphocytes:

• 50 - 70 % (in about half of the cases malignancies)
• > 85 % (rheumatoid arthritis, tuberculosis, lymphoma, empyema, yellow nail syndrome)

Eosinophil granulocytes:

• > 10 % (relatively unspecific, speaks rather against tuberculosis)

Mesothelial cells:

• < 5 %: unspecific
• > 5 %: probably due to tuberculosis

Note:

By treatment with diuretics and thus by thickening the blood, a transudate can become a (sham) exudate. However, in this case we also find an increased serum protein. Conversely, in the case of inflammation or overhydration, an exudate can be mistaken for a transudate.

• Pleural empyema with:
• pleural rind or pleural calluses
• restrictive lung disease

The therapy depends on the underlying disease. Empyema usually also responds well to the therapy of pneumonia.

However, if the effusion does not recede quickly or has a layer thickness of more than 10 mm, therapeutic puncture of the empyema is recommended at an early stage.

Occasionally there are also recurrences after the puncture. In this case a drainage should be applied and possibly a pleural lavage with a fibrinolytic agent (e.g. 250,000 IU of streptokinase or 100,000 IU of urokinase) should be performed. Alternatively, a thoracoscopy with adhesiolysis would be possible.

If all these measures remain ineffective, a decortication should be considered as the last resort.

The prognosis depends on the causal disease.

Empyema has a poor prognosis if it is detected too late or is not treated adequately. In young, previously healthy patients, the mortality rate is 8 - 15 %. In older patients or in patients with severe pre-existing conditions the mortality rate rises to 40 - 70%.

1. Cafarotti S et al (2016) Physiology and Pathophysiology of the Pleura S 14-19
2. Gerok W et al.(2007) Die Innere Medizin - Reference work for the medical specialist S 473-475
3. Herold G et al (2017) Internal Medicine S 429-431
4. Kasper DL et al (2015) Harrison's Principles of Internal Medicine S 1716-1719
5. Kasper DL et al (2015) Harrison's Internal Medicine S 2101-2103
6. Köhler D et al (2010) Pneumology S 182-189
7. Loscalzo J et al (2011) Harrison's Lung Medicine and Intensive Care S 254-257
8. Piper W et al (2013) Internal Medicine S 251-252
9. Schmidt G et al.(2004) Course book Ultrasound S 281
10. Suttrop N et al (2004) Infectious diseases S 138-141