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 artifically 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 < 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/ml, P < 0.001). The blood lactate value was also elevated during the first 12 hours (4.2 ± 2.0 mmol/litre, P < 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 < 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. Arterial-venous differences (AVDs) of glucose and lactate indicated an uptake of glucose by the brain and a washout of lactate from the brain during the 5 days of study. Cerebral ischemia, as evidenced by low CBF or high arterial-venous difference of oxygen or both, was uncommon in this study. When it occurred, it was not related to a high VCSF lactate concentration. Short term hyperglycemia after severe head injury may be related to a 'stress' response to injury. Hyperglycemia coupled with impaired oxidative metabolism may be the cause of the initial high blood lactate value. The VCSF lactate increase outlasts the acute responses to injury. Increased VCSF lactate concentrations may reflect a dysfunctional cellular metabolism caused by the injury itself, aggravated by secondary insults. Although it is possible that hyperglycemia potentiates brain lactic acidosis after head injury, the high VCSF lactate value seems to be unrelated to global ischemia. VCSF lactic acidosis seems to be due to an inability of the central nervous system cells to metabolize the excess or even normal levels of substrate.
|Original language||English (US)|
|Number of pages||6|
|State||Published - 1987|
ASJC Scopus subject areas
- Clinical Neurology