The KEB represents an equation for calculating the fictitious average number of ATP molecules produced in the CSF compartment from one molecule of glucose, and we used it successfully as a new parameter for evaluating energy metabolism status in the CSF.

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The simultaneous cytological and metabolic investigation of various extravascular body fluids (EBFs) provides clinically relevant information about the type and intensity of the immune response in particular organ systems. The oxidative burst of professional phagocytes with the concomitant production of reactive oxygen species consumes a large amount of oxygen and is the cause of switch to the development of anaerobic metabolism. We assessed the relationships between percentages of neutrophils, aerobic and anaerobic metabolism, and tissue damage via the determination of aspartate aminotransferase catalytic activities (AST) in cerebrospinal fluid (CSF), pleural effusions (PE), abdominal effusions (AE), and synovial fluids (SF). EBFs with 0.0–20.0% neutrophils: 83.0% aerobic and 1.3% strongly anaerobic cases with median of AST = 13.8 IU/L in CSF; 68.0% aerobic and 9.0% strongly anaerobic cases with median of AST = 20.4 IU/L in PE; 77.5% aerobic and 10.5% strongly anaerobic cases with median of AST = 18.0 IU/L in AE; 64.1% aerobic and 7.7% strongly anaerobic cases with median of AST = 13.8 IU/L in SF. EBFs with 80.0–100.0% neutrophils: 4.2% aerobic and 73.7% strongly anaerobic cases with median of AST = 19.2 IU/L in CSF; 7.4% aerobic and 77.3% strongly anaerobic cases with median of AST = 145.2 IU/L in PE; 11.8% aerobic and 73.7% strongly anaerobic cases with median of AST = 61.8 IU/L in AE; 25.5% aerobic and 38.2% strongly anaerobic cases with median of AST = 37.2 IU/L in SF. The significant presence of neutrophils, concomitant strong anaerobic metabolism, and elevated AST in various EBFs are reliable signs of damaging purulent inflammation.

Background Simultaneous cytological and metabolic investigation of the pleural effusion provides clinically relevant information about the type and intensity of immune response in the pleural cavity. Methods We investigated 1329 pleural effusions from patients with different pathological changes in the pleural cavity. Evaluated parameters were differential cell count of neutrophils, eosinophils, lymphocytes and monocytes, and values of the coefficient of energy balance. Results We found the lowest numbers of cells and the highest coefficient of energy balance values in patients with heart failure and sepsis; relatively high frequency of eosinophils and slightly decreased coefficient of energy balance values in patients with pneumothorax and haemothorax; the predominance of lymphocytes and low coefficient of energy balance values in patients with tuberculous pleuritis; the predominance of neutrophils and variable coefficient of energy balance values in patients after chest surgery; the highest presence of neutrophils and very low coefficient of energy balance values in patients with chest empyema and the predominance of lymphocytes and normal to low coefficient of energy balance values in patients with pleural malignancy. Conclusions Our findings in patients with heart failure and sepsis suggest the absence of inflammation in the pleural cavity. We observed the manifestation of tissue repair in patients with pneumothorax and haemothorax. Patients with tuberculous pleuritis were predominantly characterized by T cell-driven immune response and oxidative burst of macrophages. We found different intensities of immune responses to the chest surgery. The typical finding in patients with empyema was oxidative burst of neutrophils. In patients with pleural malignancy, weak cytotoxic inflammation predominates together with the intensive inflammation characterized by oxidative burst of macrophages.

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.