Hyperglycemia, Cerebrospinal Fluid Lactic Acidosis, and Cerebral Blood Flow in Severely Head-injured Patients

Abstract

Cerebrospinal fluid (CSF) lactate concentration is known to increase during the acute phase after severe head injury. To determine the influence of glycemia or cerebral ischemia on this lactate increase, we studied 69 head-injured patients aged 28.7 +/- 15.4 (SD) years with a mean Glasgow coma score of 5.7 +/- 1.7 (SD). They were intubated, paralyzed, and artificially respired. We measured lactate and glucose concentrations in ventricular CSF (VCSF), arterial blood, and jugular bulb blood for 5 days. Samples were obtained within 12 hours after injury and at regular 12-hour intervals. These patients were not treated for hypo- or hyperglycemia. Cerebral blood flow (CBF) was also measured within 12 hours and at 12- to 48-hour intervals. Hyperglycemia was found consistently within 12 hours after injury (224 +/- 98 mg/dl, P less than 0.001), and mild hyperglycemia persisted during the entire period of study. The VCSF glucose course was parallel to that in blood (the initial VCSF glucose value was 128 +/- 37 mg/dl, P less than 0.001). The blood lactate value was also elevated during the first 12 hours (4.2 +/- 2.0 mmol/litre, P less than 0.001), normalizing within 24 to 36 hours. The VCSF lactate course was independent from that of the blood lactate value. It was significantly elevated within 12 hours after injury (5.3 +/- 2.6 mmol/litre, P less than 0.001) and remained so during the 5 days of study. A high initial VCSF glucose value was associated with a high initial VCSF lactate value. However, a high VCSF lactate concentration was present even when the glucose value was close to the normal level.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma glucose level in Nigerian Africans with head injury

“…Studies have shown that the glucose concentration, as well as the hormones thought to be responsible for the increase, may still be high within this period. 3,10,12,21 The present study will form a template for further studies to confirm our findings. There is a need to determine the glucose concentrations in other parts of sub-Saharan Africa to confirm if there is little or no rise in glucose concentrations in blacks with head injury.…”

Effects of glycaemic control on cerebral neurochemistry in primary intracerebral haemorrhage

“…19,20 During hypoxic and hyperglycaemic conditions, central nervous system (CNS) cells in perihaemorrhagic penumbra are unable to metabolise the excess glucose due to mitochondrial membrane dysfunction. 21 Anaerobic glycolysis takes place, leading to excessive accumulation of lactate and hydrogen ions, which results in tissue acidosis [22][23][24] and increased production of oxygen free radicals, respectively. 25,26 In addition, intracellular acidosis leads to neuronal cell destruction by triggering a cascade of events that may involve activation of calcium entry into cells, lipolytic release of cytotoxic free fatty acids and excitatory amino acids such as glutamates.…”

“…Improved oxygenation in neuronal cells drives the mitochondrial Kreb's cycle, in which excess glucose is metabolised. 21,32 The uptake of pyruvate into Kreb's cycle decreases the cytosolic redox state and oxygen free radical production, thus maintaining phosphorylation potential, and limits energy depletion during ischaemia. 28,29 This leads to a reduction in cerebral EC pyruvate level in the intensive group of patients.…”

Effects of magnesium sulfate on tissue lactate and malondialdehyde levels in experimental head trauma

“…In previous human and animal studies on brain ischemia and trauma, interest has been focused on two groups of energy-related metabolites; pyruvate and lactate, which is involved in glucose metabolism, and the purine metabolites hypoxanthine and xanthine [1,2,4,19].…”