Increase of
ketone body concentration in plasma is induced by various factors such as onset of diabetes. Secretion of excessive stress
hormone including
catecholamine is responsible for stimulation of lipolysis which increases plasma
ketone body concentration.
Catecholamine levels reflect the severity of the neurologic insult, so this is a basis for the use of
catecholamine measurements as a physiological marker of patient outcome. Twenty-seven patients with severe
head injury and twenty-five healthy volunteers were enrolled in this study, but patients with diabetes or
liver dysfunction were excluded. The patients with severe
head injury consisted of 19 with focal injury and 8 with diffuse injury. The outcome was as follows; 14 patients died and 13 patients survived. We collected arterial blood samples as promptly as possible after onset of severe
head injury and measured the following: 1, base excess; 2,
beta-hydroxybutyrate; 3,
acetoacetate; 4,
lactate; 5,
epinephrine; 6,
norepinephrine. The
ketone body (
beta-hydroxybutyrate +
acetoacetate) concentration in plasma was significantly elevated in patients with severe
head injury. The increment of
beta-hydroxybutyrate levels was greater than that of
acetoacetate levels, resulting decreased arterial
ketone body ratio (AKBR;
acetoacetate/
beta-hydroxybutyrate). We demonstrated that plasma
ketone body concentrations were elevated and the AKBR decreased in severe head-injured patients. Elevation of
catecholamine has been reported as a stress reaction in severe
head injury.
Catecholamine is most potent in stimulating lipolysis, and ketogenesis. Therefore, the
ketonemia observed in severe
head injury is most likely to be induced by elevation of
catecholamine levels. The degree of
ketonemia may be an index of the severity of severe
head injury.