Energy Dysfunction as a Predictor of Outcome after Moderate or Severe Head Injury: Indices of Oxygen, Glucose, and Lactate Metabolism

The purpose of this study was to determine if the relationship between abnormalities in glucose, lactate, and oxygen metabolism were predictive of neurologic outcome after moderate or severe head injury, relative to other known prognostic factors. Serial assessments of the cerebral metabolic rates for glucose, lactate, and oxygen were performed using a modified Kety-Schmidt method. In total, 31 normal control subjects were studied once, and 49 TBI patients (mean age 36±16 years, median GCS 7) were studied five times median per patient from postinjury days 0 to 9. Univariate and multivariate analyses were performed. Univariate analysis showed that the 6-month postinjury Glasgow Outcome Scale (GOS) was most strongly associated with the mean cerebral metabolic rate of oxygen (CMRO2) ( P = 0.0001), mean arterial lactate level ( P = 0.0001), mean arterial glucose ( P = 0.0008), mean cerebral blood flow (CBF), ( P = 0.002), postresuscitation GCS ( P = 0.003), and pupillary status ( P = 0.004). Brain lactate uptake was observed in 44% of all metabolic studies, and 76% of patients had at least one episode of brain lactate uptake. By dichotomized GOS, patients achieving a favorable outcome (GOS 4-5) were distinguished from those with an unfavorable outcome (GOS1-3) by having a higher CMRO2 ( P = 0.003), a higher rate of abnormal brain lactate uptake relative to arterial lactate levels ( P = 0.04), and lesser degrees of blood-brain barrier damage based on CT findings ( P = 0.03). Conclusions: During the first 6 days after moderate or severe TBI, CMRO2 and arterial lactate levels are the strongest predictors of neurologic outcome. However, the frequent occurrence of abnormal brain lactate uptake despite only moderate elevations in arterial lactate levels in the favorable outcome patients suggests the brain's ability to use lactate as a fuel may be another key outcome predictor. Future studies are needed to determine to what degree nonglycolytic energy production from alternative fuels such as lactate occurs after TBI and whether alternative fuel administration is a viable therapy for TBI patients.

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Prognostic significance of ventricular CSF lactic acidosis in severe head injury

Journal of Neurosurgery ◽

10.3171/jns.1986.65.5.0615 ◽

1986 ◽

Vol 65 (5) ◽

pp. 615-624 ◽

Cited By ~ 118

Author(s):

Antonio A. F. DeSalles ◽

Hermes A. Kontos ◽

Donald P. Becker ◽

Mildred S. Yang ◽

John D. Ward ◽

...

Keyword(s):

Head Injury ◽

Lactic Acidosis ◽

Severe Head Injury ◽

Clinical Course ◽

Lactate Concentration ◽

Ventricular Catheter ◽

Good Outcome ◽

Poor Outcome ◽

Csf Lactate ◽

Lactate Levels

✓ Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an important role in the clinical course of severe head injury. Ventricular CSF lactate concentration was studied in 19 patients during the first 5 days after severe head injury. All patients were intubated, paralyzed, and artificially ventilated so that PaCO2 was kept at 33.2 ± 5.0 mm Hg and PaO2 at 122 ± 18 mm Hg (mean ± standard deviation). The mean Glasgow Coma Scale score on admission was 5.73 ± 2.42. The first CSF sample was drawn within 18 hours after head injury. Over the first 4 days postinjury, patients with a poor outcome had significantly higher ventricular CSF lactate levels than did those with moderate disabilities or a good outcome. Patients showing favorable outcome had a significant decrease in ventricular CSF lactate levels 48 hours after injury. This decrease was not observed in patients with a poor outcome. Increased ventricular CSF lactate concentration was also reliably associated with increased intracranial pressure (ICP). Ventricular CSF lactate levels did not correlate with the magnitude of intraventricular bleeding. Arterial and jugular venous blood lactate levels, although high after head injury, were usually lower than the levels in the ventricular CSF and reached a normal range by the 3rd day following head trauma. At that time, the ventricular CSF lactate concentration was still above normal in patients with a poor outcome but had decreased to normal in patients with moderate disabilities or a good outcome. Ventricular CSF pH did not generally correlate with the ventricular CSF lactate concentration in patients under controlled ventilation; however, in a few patients close to death or with ventricular infection, a correlation was noted. Ventricular CSF lactate levels were not related to cerebral blood flow. In this study, profiles of ventricular CSF lactate concentration are defined in relation to the patients' clinical course and outcome. High ventricular CSF lactate concentration is present within 18 hours after severe head injury. Its decrease to normal in the following 48 hours is a reliable sign of clinical improvement; however, ventricular CSF lactate levels that are persistently high or that increase over time indicate the patient's deterioration. Serial assessment of ventricular CSF for acid-base status and metabolites in head-injured patients with a ventricular catheter already placed for ICP monitoring is useful in the evaluation of prognosis and clinical course.

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Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury

Neurosurgical FOCUS ◽

10.3171/foc.1999.6.5.1 ◽

1999 ◽

Vol 6 (5) ◽

pp. E1

Author(s):

Matthias Menzel ◽

Egon M. R. Doppenberg ◽

Alois Zauner ◽

Jens Soukup ◽

Michael M. Reinert ◽

...

Keyword(s):

Head Injury ◽

Brain Tissue ◽

Severe Head Injury ◽

Early Period ◽

Control Cohort ◽

Brain Tissue Oxygenation ◽

Glucose Levels ◽

The Mean ◽

Lactate Levels ◽

Inspired Oxygen

Object Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2). Methods In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2) was increased to 441 ± 88 mm Hg over a period of 6 hours by raising the FiO2 from 35 ± 5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mm Hg). The mean brain PO2 levels increased in the O2-treated patients up to 359 ± 39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period. Conclusions Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.

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Effects of Pegorgotein on Neurologic Outcome of Patients With Severe Head Injury

JAMA ◽

10.1001/jama.1996.03540070034027 ◽

1996 ◽

Vol 276 (7) ◽

pp. 538 ◽

Cited By ~ 117

Author(s):

Byron Young

Keyword(s):

Head Injury ◽

Severe Head Injury ◽

Neurologic Outcome

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Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury

Journal of Neurosurgery ◽

10.3171/jns.1999.91.1.0001 ◽

1999 ◽

Vol 91 (1) ◽

pp. 1-10 ◽

Cited By ~ 233

Author(s):

Matthias Menzel ◽

Egon M. R. Doppenberg ◽

Alois Zauner ◽

Jens Soukup ◽

Michael M. Reinert ◽

...

Keyword(s):

Head Injury ◽

Brain Tissue ◽

Severe Head Injury ◽

Control Cohort ◽

Content Type ◽

Glucose Levels ◽

The Mean ◽

Lactate Levels ◽

Inspired Oxygen ◽

Fine Print

Object. Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2).Methods. In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2 was increased to 441 ± 88 mm Hg over a period of 6 hours by raising the FiO2 from 35 ± 5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mm Hg).The mean brain PO2 levels increased in the O2-treated patients up to 359 ± 39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period.Conclusions. Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.

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