Intracerebral microdialysis and bedside biochemical analysis in patients with fatal traumatic brain lesions
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 incre...
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Published in: | Acta anaesthesiologica Scandinavica Vol. 45; no. 8; pp. 977 - 985 |
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Munksgaard International Publishers
01-09-2001
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Abstract | 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 μl/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. |
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AbstractList | 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 μl/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. BACKGROUNDMicrodialysis 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. METHODSSeven 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. RESULTSDecreases 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. CONCLUSIONChanges 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 μl/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. 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. 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. 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. 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. |
Author | Hallström, A. Ståhl, N. Nordström, C. H. Mellergård, P. Ungerstedt, U. |
Author_xml | – sequence: 1 givenname: N. surname: Ståhl fullname: Ståhl, N. organization: Department of Clinical Neuroscience, Lund University Hospital and – sequence: 2 givenname: P. surname: Mellergård fullname: Mellergård, P. organization: Department of Clinical Neuroscience, Lund University Hospital and – sequence: 3 givenname: A. surname: Hallström fullname: Hallström, A. organization: Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden – sequence: 4 givenname: U. surname: Ungerstedt fullname: Ungerstedt, U. organization: Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden – sequence: 5 givenname: C. H. surname: Nordström fullname: Nordström, C. H. email: carl-henrik.nordstrom@swipnet.se organization: Department of Clinical Neuroscience, Lund University Hospital and |
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Keywords | Human Nervous system diseases Energy metabolism Craniocerebral Intracranial hypertension Diseases of the osteoarticular system Central nervous system Pyruvate Cardiovascular disease Exploration Glucose Glutamate Trauma Cerebral disorder Vascular disease Lactates Microdialysis Ischemia Central nervous system disease Skull disease Cerebrovascular disease Brain (vertebrata) |
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SubjectTerms | Adult Aged Biological and medical sciences Brain - metabolism Brain Injuries - metabolism Brain Ischemia - metabolism cerebral ischemia Energy Metabolism Female glucose Glucose - metabolism glutamate glycerol Glycerol - metabolism Head injury Humans Injuries of the nervous system and the skull. Diseases due to physical agents Intracranial Pressure Investigative techniques, diagnostic techniques (general aspects) lactate Lactic Acid - metabolism Male Medical sciences Medicin och hälsovetenskap Microdialysis Middle Aged Nervous system Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques pyruvate Pyruvic Acid - metabolism Traumas. Diseases due to physical agents |
Title | Intracerebral microdialysis and bedside biochemical analysis in patients with fatal traumatic brain lesions |
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