Ascites and pleural fluid

Published on 02/03/2015 by admin

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Last modified 22/04/2025

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64

Ascites and pleural fluid

Ascites

Serum-ascites albumin gradient

The serum-ascites albumin gradient (SAAG) is defined as the serum albumin concentration minus the ascitic fluid albumin concentration. The SAAG correlates directly with the portal pressure. Patients with a wide SAAG (defined as ≥11 g/L) have portal hypertension, whereas patients with a narrow SAAG (<11 g/L) do not (Table 64.1).

Table 64.1

Serum-ascites albumin gradient

Wide (>11 g/L) Narrow (<11 g/L)
Chronic liver disease (cirrhosis) Peritoneal carcinomatosis
Veno-occlusive disease Reduced plasma oncotic pressure (e.g. nephrotic syndrome)
Massive hepatic metastases Secondary peritonitis
Congestive cardiac failure Tuberculous peritonitis
Spontaneous bacterial peritonitis  

Sometimes causes of ascites that are normally associated with a narrow gradient will occur in patients with portal hypertension, in which case the gradient will be wide. In these situations additional analyses may assist with the differential diagnosis. For example, abnormalities of pH, lactate, glucose and/or lactate dehydrogenase (LDH) may point towards an inflammatory process; increased lymphocytes in the ascitic fluid may point towards tuberculosis, lymphomas or fungal infections of the peritoneum; and malignant cells are found in nearly all patients with peritoneal carcinomatosis (where the tumour directly involves the peritoneum).

Peritonitis

Cirrhotic patients with ascites are prone to develop peritonitis, usually without an obvious focus of infection (so-called spontaneous bacterial peritonitis or SBP). Less commonly, identifiable sources of infection, e.g. perforated viscus or intra-abdominal abscess, are responsible (secondary infection). Laboratory investigations can assist in three ways. First, they may be used to predict who is going to develop SBP. Second, they may permit rapid detection of infection. Third, they may help to differentiate SBP from secondary infection.

SBP or secondary infection?

Secondary peritonitis tends to be more severe than SBP, probably because of the heavier bacterial load. This severity is reflected in the ascitic fluid biochemistry (Table 64.2). Bacteria and neutrophils consume glucose, anaerobic metabolism of which results in the production of lactate, which correlates inversely with pH. Lysis of stimulated neutrophils results in the release of LDH and other cellular proteins, with a consequent rise in the ascitic fluid total protein concentration.

Table 64.2

Spontaneous bacterial peritonitis compared with secondary infection

Ascitic fluid parameter Spontaneous bacterial peritonitis Secondary
Glucose (mmol/L) >2.8 <2.8
Lactate dehydrogenase <upper limit of reference interval >upper limit of reference interval
Total protein (g/L) <10 >10

Pleural fluid

Transudate or exudate?

Clinicians usually request pleural fluid analysis because they want to know what is causing an effusion. In some cases, a specific cause is suspected, but much more frequently the question is posed in more general terms, by asking if the effusion is a transudate or an exudate. The underlying assumption is that fluid formed by ‘exudation’ from inflamed or tumour-infiltrated pleura is likely to be high in protein, whereas fluid formed by ‘transudation’ from normal pleura due to an imbalance in hydrostatic and oncotic forces is likely to be low in protein; in general terms, exudates are more likely to reflect local pathology, and to warrant further investigation. The criteria established by Light and colleagues in 1972, and subsequently modified, continue to be applied widely in classifying pleural fluids as exudates or transudates. They are summarized in Table 64.3.

Application of Light’s criteria in routine practice sometimes results in the misclassification of transudates as exudates. For this reason, alternative markers have been proposed e.g. pleural fluid cholesterol. However, there is no single test, or combination of tests, which is clearly better than modified Light’s criteria. In addition, analysis of pleural fluid protein and LDH alone usually produces the same categorization of pleural effusions as modified Light’s criteria; thus a blood sample may not always be necessary.

Is it empyema?

Infection of the pleural space usually occurs in association with bacterial pneumonia, and manifests initially as an exudative pleural effusion. If this does not resolve, it can become purulent (when it is referred to as empyema). Empyema is resistant to antibiotic therapy and often only amenable to surgical drainage. So when pleural fluid is frankly purulent or turbid on sampling, insertion of a chest tube is clearly indicated. If it is not clear that an empyema is developing, biochemical analysis may be helpful, in exactly the same way as it is in distinguishing between SBP and secondary infection – bacteria and neutrophils in the pleural fluid consume glucose, and anaerobic metabolism increases with heavier bacterial loads. This results in the production of lactate, which correlates inversely with pH. A pleural fluid pH of less than 7.2 is a very useful predictor of empyema.

Other questions

image Malignant pleural effusions. As with ascites, finding malignant cells in pleural fluid indicates the presence of malignancy, although only 70% of patients with malignant effusions will have positive cytology. Again, measurement of tumour markers in pleural fluid is rarely indicated. This in part reflects the utility of other modalities of investigation in the diagnosis of malignancy, e.g. imaging.

image Is it chyle? Chyle is the fluid found in intestinal lymphatics during absorption of food postprandially. Chylothorax is defined as lymphatic fluid (chyle or lymph) in the pleural space; it usually results from the leak or rupture of the thoracic duct or one of its major divisions. There is no unique marker for chyle, although chylomicrons are relatively specific, except postprandially. Triglycerides are more readily measured than chylomicrons and are widely used instead.

Pleural fluid glucose

For reasons that are not entirely clear, pleural effusions in patients with rheumatoid arthritis characteristically have very low concentrations of glucose; the explanations usually given – consumption of glucose by inflammatory and other cells, or altered pleural permeability to glucose – are not very convincing, since concentrations are relatively normal in other connective tissue disorders like systemic lupus erythematosus. Glucose concentrations are sometimes low in other conditions such as empyema, malignancy and tuberculosis, but are sufficiently variable that they are not diagnostically useful in these contexts.

Ascites and pleural fluid

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