Abstract
IntroductionMaintaining arterial blood glucose within tight limits is beneficial in critically ill patients. Upper and lower limits of detrimental blood glucose levels must be determined.MethodsIn 69 patients with severe traumatic brain injury (TBI), cerebral metabolism was monitored by assessing changes in arterial and jugular venous blood at normocarbia (partial arterial pressure of carbon dioxide (paCO2) 4.4 to 5.6 kPa), normoxia (partial arterial pressure of oxygen (paO2) 9 to 20 kPa), stable haematocrit (27 to 36%), brain temperature 35 to 38°C, and cerebral perfusion pressure (CPP) 70 to 90 mmHg. This resulted in a total of 43,896 values for glucose uptake, lactate release, oxygen extraction ratio (OER), carbon dioxide (CO2) and bicarbonate (HCO3) production, jugular venous oxygen saturation (SjvO2), oxygen-glucose index (OGI), lactate-glucose index (LGI) and lactate-oxygen index (LOI). Arterial blood glucose concentration-dependent influence was determined retrospectively by assessing changes in these parameters within pre-defined blood glucose clusters, ranging from less than 4 to more than 9 mmol/l.ResultsArterial blood glucose significantly influenced signs of cerebral metabolism reflected by increased cerebral glucose uptake, decreased cerebral lactate production, reduced oxygen consumption, negative LGI and decreased cerebral CO2/HCO3 production at arterial blood glucose levels above 6 to 7 mmol/l compared with lower arterial blood glucose concentrations. At blood glucose levels more than 8 mmol/l signs of increased anaerobic glycolysis (OGI less than 6) supervened.ConclusionsMaintaining arterial blood glucose levels between 6 and 8 mmol/l appears superior compared with lower and higher blood glucose concentrations in terms of stabilised cerebral metabolism. It appears that arterial blood glucose values below 6 and above 8 mmol/l should be avoided. Prospective analysis is required to determine the optimal arterial blood glucose target in patients suffering from severe TBI.
Highlights
Maintaining arterial blood glucose within tight limits is beneficial in critically ill patients
Arterial blood glucose significantly influenced signs of cerebral metabolism reflected by increased cerebral glucose uptake, decreased cerebral lactate production, reduced oxygen consumption, negative lactate-glucose index (LGI) and decreased cerebral CO2/HCO3 production at arterial blood glucose levels above 6 to 7 mmol/l compared with lower arterial blood glucose concentrations
Prospective analysis is required to determine the optimal arterial blood glucose target in patients suffering from severe Traumatic brain injury (TBI)
Summary
Maintaining arterial blood glucose within tight limits is beneficial in critically ill patients. These changes occur in parallel and sequentially They are associated with metabolic and energetic disturbances [1,2], due to impaired perfusion [3]; increased glycolysis [4] with increased lactate production [5]; regionally altered glucose uptake [6] and impaired glucose metabolism due to changes in enzymatic and mitochondrial activity [6,7,8,9,10]; functional derangements as observed in cortical spreading depolarisations (CSD) [11]; excitotoxicity with disturbed ionic homeostasis and activated intracellular destructive secondary cascades [12]; and increased activity of neurons and astrocytes [13]. Hypoxia and anaemia, changes in blood glucose levels induce additional damage In this context, hyperglycaemia induces local acidosis [15,16] and oxidative stress, promotes oedema formation, impairs nitric oxide-mediated vasodilatation [17] and activates inflammation as reflected by increased leucocyte infiltration [18]. Hypoglycaemia increases glutamate release [19], induces metabolic impairment [19], and promotes generation of CSD which, in turn, generates and aggravates exisiting oedema [20]
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