Abstract
Hyperglycolysis is a known phenomenon after severe subarachnoid hemorrhage (SAH) and after brain injury. It is characterized by decreased oxidative metabolism and relatively increased anaerobic glycolysis. Metabolic suppressive therapy reduces the cerebral metabolic rate of oxygen (CMRO2) and the cerebral metabolic rate of glucose (CMRGluc). If CMRO2 is suppressed after SAH, withdrawal of metabolic suppressive therapy could lead to the accumulation of lactate. In this project, we assessed the relationship between the withdrawal of metabolic suppressive therapy and cerebrospinal fluid (CSF) lactate concentration. A prospective observational database containing 262 patients with SAH was retrospectively analyzed. CSF lactate levels were compared with the daily dose of metabolic suppressive therapy. Outcome was assessed with the Glasgow Outcome Scale (GOS). In 56% of patients an increase in CSF lactate (mean: 3.2 ± 0.9 mmol/L) after withdrawal of metabolic suppressive therapy was observed. Mean Glasgow Outcome Score (GOS) was lower in patients with an increase in CSF lactate concentration (>0.5 mmol/L) after withdrawal of metabolic suppressive therapy (p = 0.095). In 88% of patients who died during the first 30 days after SAH, a CSF lactate elevation of more than 0.5 mmol/L after withdrawal of metabolic suppressive therapy was found (p = 0.071).
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References
Baughman VL, Hoffman WE, Albrecht RF, Miletich DJ (1987) Cerebral vascular and metabolic effects of fentanyl and midazolam in young and aged rats. Anesthesiology 67:314–319
Bederson JB, Connolly ES Jr, Batjer HH, Dacey RG, Dion JE, Diringer MN, Duldner JE Jr, Harbaugh RE, Patel AB, Rosenwasser RH (2009) Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 40:994–1025
DeSalles AA, Kontos HA, Becker DP, Yang MS, Ward JD, Moulton R, Gruemer HD, Lutz H, Maset AL, Jenkins L et al (1986) Prognostic significance of ventricular CSF lactic acidosis in severe head injury. J Neurosurg 65:615–624
Glenn TC, Kelly DF, Boscardin WJ, McArthur DL, Vespa P, Oertel M, Hovda DA, Bergsneider M, Hillered L, Martin NA (2003) Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism. J Cereb Blood Flow Metab 23:1239–1250
Hoekema D, Schmidt RH, Ross I (2007) Lumbar drainage for subarachnoid hemorrhage: technical considerations and safety analysis. Neurocrit Care 7:3–9
Mori K, Nakajima K, Maeda M (1993) Long-term monitoring of CSF lactate levels and lactate/pyruvate ratios following subarachnoid haemorrhage. Acta Neurochir (Wien) 125:20–26
Oertel M, Kelly DF, Lee JH, Glenn TC, Vespa PM, Martin NA (2002) Metabolic suppressive therapy as a treatment for intracranial hypertension – why it works and when it fails. Acta Neurochir Suppl 81:69–70
Oertel M, Kelly DF, Lee JH, McArthur DL, Glenn TC, Vespa P, Boscardin WJ, Hovda DA, Martin NA (2002) Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury. J Neurosurg 97:1045–1053
Oertel MF, Schwedler M, Stein M, Wachter D, Scharbrodt W, Schmidinger A, Boker DK (2007) Cerebral energy failure after subarachnoid hemorrhage: the role of relative hyperglycolysis. J Clin Neurosci 14:948–954
Seitz HD (1976) Gas levels and biochemical changes in cerebrospinal fluid after experimental brain injury: its effect on cerebral circulation and cerebral metabolism as well as its management. Z Exp Chir 9:341–354
Seitz HD, Ocker K (1977) The prognostic and therapeutic importance of changes in the CSF during the acute stage of brain injury. Acta Neurochir (Wien) 38:211–231
Shimoda M, Yamada S, Yamamoto I, Tsugane R, Sato O (1989) Time course of CSF lactate level in subarachnoid haemorrhage. Correlation with clinical grading and prognosis. Acta Neurochir (Wien) 99:127–134
Shiogai T, Nara I, Saruta K, Hara M, Saito I (1999) Continuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia. Acta Neurochir Suppl 75:49–55
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Stein, M., Schomacher, J., Scharbrodt, W., Preuss, M., Oertel, M.F. (2012). Cerebrospinal Fluid Lactate Concentration After Withdrawal of Metabolic Suppressive Therapy in Subarachnoid Hemorrhage. In: Schuhmann, M., Czosnyka, M. (eds) Intracranial Pressure and Brain Monitoring XIV. Acta Neurochirurgica Supplementum, vol 114. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0956-4_64
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DOI: https://doi.org/10.1007/978-3-7091-0956-4_64
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