Clinical Information

Lactate dehydrogenase (LDH) activity is present in all cells of the body with the highest concentrations in the heart, liver, muscle, kidney, lung, and erythrocytes.

Pleural fluid:

Pleural fluid is normally present within the pleural cavity surrounding the lungs, serving as a lubricant between the lungs and inner chest wall. Pleural effusion develops when the pleural cavity experiences an overproduction of fluid due to increased capillary hydrostatic and osmotic pressure that exceeds the ability of the lymphatic or venous system to return the fluid to circulation. Laboratory-based criteria are often used to classify pleural effusions as either exudative or transudative. Exudative effusions form due to infection or inflammation of the capillary membranes allowing excess fluid into the pleural cavity. Patients with these conditions benefit from further investigation and treatment of the local cause of inflammation. Transudative effusions form due to systemic conditions such as volume overload, end stage kidney disease, and heart failure that can lead to excess fluid accumulation in the pleural cavity. Patients with transudative effusions benefit from treatment of the underlying condition.(1) Measurement of LDH in body fluids is primarily indicated to aid in the differentiation of transudative and exudative effusions as LDH activity is considered an indicator of the extent of inflammation. Dr. Richard Light derived criteria in the 1970s for patients with pleural effusions that are still used today.(2)

The criteria include the measurement of total protein and LDH in pleural fluid and serum. Exudates are defined as meeting one of the following criteria:

1. Pleural fluid-to-serum protein ratio above 0.5

2. Pleural fluid LDH above two-thirds the upper limit of normal serum LDH

3. Pleural fluid-to-serum LDH ratio above 0.6

Pericardial fluid:

The routine analysis of LDH to differentiate exudative and transudative pericardial effusions is not considered helpful.(3)

Peritoneal fluid:

Spontaneous bacterial peritonitis or ascitic fluid infection is common (12%) at the time of admission of a patient with cirrhosis and ascites. The diagnosis is made in the presence of an elevated ascitic fluid absolute polymorphonuclear (PMN) leukocyte count (ie, >250 cells/mm(3) [0.25 x 10(9)/L]) without an evident intra-abdominal, surgically treatable source of infection.(4)

Secondary bacterial peritonitis (ie, ascitic fluid infection caused by a surgically treatable intra-abdominal source) can masquerade as spontaneous bacterial peritonitis. Signs and symptoms do not help separate patients who need surgical intervention from those who have spontaneous bacterial peritonitis and need only antibiotic treatment. In contrast, the initial ascitic fluid analysis and the response to treatment can assist with this important distinction. The characteristic analysis in the setting of free perforation is PMN count of 250 cells/mm(3) (usually many thousands) or higher, multiple organisms (frequently including fungi and enterococcus) on Gram stain and culture, and at least 2 of the following criteria: total protein above 1 g/dL, LDH above the upper limit of normal for serum, and glucose below 50 mg/dL. Studies have reported higher than 95% sensitivity but low specificity using these criteria; a computerized tomographic scan was diagnostic in 85% of patients with secondary peritonitis.(5)