BACKGROUND: Microdialysis with bedside biochemical analysis was used to monitor cerebral biochemical alterations that precede and accompany increase in intracranial pressure (ICP), resulting in a complete cessation of cerebral blood flow. METHODS: Seven patients, who died due to an untreatable increase in ICP, were included. The patients originate from a large, consecutive series of severely head injured patients (n: 95) monitored with intracerebral microdialysis (perfusion rate 0.3 microl/min). One microdialysis catheter was inserted via a separate burr hole frontally to that used for the intraventricular catheter ("better" position) and one catheter was inserted into cerebral cortex surrounding an evacuated focal contusion or underlying an evacuated haematoma ("worse" position). Biochemical analyses of glucose, lactate, glycerol, urea, glutamate, and pyruvate were performed at the bedside. All samples were frozen for subsequent HPLC (high-performance liquid chromatography) analyses of amino acids and ions. RESULTS: Decreases in glucose and pyruvate and increases in lactate, glycerol, glutamate, and lactate/pyruvate (la/py) ratio characterized cerebral ischaemia. The measured markers give information regarding substrate availability (glucose), redox state of the tissue (la/py ratio), degradation of glycerophospholipids in cell membranes (glycerol), and extracellular concentration of excitatory amino acids (glutamate). In the "worse" position biochemical deterioration occurred before the increase in ICP. In the "better" position biochemical deterioration was usually observed after the increase in ICP. CONCLUSION: Changes of cerebral energy metabolism that accompany cerebral ischaemia follow a certain pattern and may be detected at the bedside by intracerebral microdialysis before the secondary damage causes an increase in ICP.
BACKGROUND: Microdialysis with bedside biochemical analysis was used to monitor cerebral biochemical alterations that precede and accompany increase in intracranial pressure (ICP), resulting in a complete cessation of cerebral blood flow. METHODS: Seven patients, who died due to an untreatable increase in ICP, were included. The patients originate from a large, consecutive series of severely head injured patients (n: 95) monitored with intracerebral microdialysis (perfusion rate 0.3 microl/min). One microdialysis catheter was inserted via a separate burr hole frontally to that used for the intraventricular catheter ("better" position) and one catheter was inserted into cerebral cortex surrounding an evacuated focal contusion or underlying an evacuated haematoma ("worse" position). Biochemical analyses of glucose, lactate, glycerol, urea, glutamate, and pyruvate were performed at the bedside. All samples were frozen for subsequent HPLC (high-performance liquid chromatography) analyses of amino acids and ions. RESULTS: Decreases in glucose and pyruvate and increases in lactate, glycerol, glutamate, and lactate/pyruvate (la/py) ratio characterized cerebral ischaemia. The measured markers give information regarding substrate availability (glucose), redox state of the tissue (la/py ratio), degradation of glycerophospholipids in cell membranes (glycerol), and extracellular concentration of excitatory amino acids (glutamate). In the "worse" position biochemical deterioration occurred before the increase in ICP. In the "better" position biochemical deterioration was usually observed after the increase in ICP. CONCLUSION: Changes of cerebral energy metabolism that accompany cerebral ischaemia follow a certain pattern and may be detected at the bedside by intracerebral microdialysis before the secondary damage causes an increase in ICP.
Authors: Frantz R Poulsen; Mette Schulz; Anne Jacobsen; Åse B Andersen; Lykke Larsen; Wilhelm Schalén; Troels H Nielsen; Carl-Henrik Nordström Journal: Neurocrit Care Date: 2015-04 Impact factor: 3.210
Authors: Michael Roslin; Roger Henriksson; Per Bergström; Urban Ungerstedt; A Tommy Bergenheim Journal: J Neurooncol Date: 2003-01 Impact factor: 4.130