Cerebrospinal Fluid Glucose and Lactate Levels After Subarachnoid Hemorrhage: A Multicenter Retrospective Study

Abstract

Background: In patients with subarachnoid hemorrhage (SAH), abnormalities in glucose and lactate metabolism have been described using cerebral microdialysis. Glucose and lactate concentrations in cerebrospinal fluid (CSF) are more easily accessible, but scarce data are available in this setting. The aim of this study is to assess the relationship of CSF glucose and lactate with blood concentrations and with unfavorable neurological outcome after SAH. Methods: A retrospective cohort study was conducted in 5 European University intensive care units. Patients aged 18 years and above who were admitted after a nontraumatic SAH over a 4-year period (2011 to 2014) were included if they had an external ventricular drain placed, daily analysis of CSF including glucose (±lactate) concentrations for 1 to 4 consecutive days, and concomitant analysis of glucose and lactate concentrations in the arterial blood. Results: A total of 144 patients were included in the final analysis (median age: 58 [49 to 66] y; male sex: 77/144). Median time from admission to external ventricular drain placement was 1 (0 to 3) day; median Glasgow Coma Scale on admission was 10 (7 to 13), and CT-scan Fisher scale was 4. A total of 81 (56%) patients had unfavorable neurological outcome at 3 months (Glasgow Outcome Scale ≤3). There was a weak correlation between blood and CSF glucose (r 2=0.07, P=0.007), and between blood and CSF lactate levels (r 2=0.58, P<0.001) on day 1, which were not influenced by insulin therapy. The presence of shock and low CSF glucose/lactate ratio were the only independent predictors of unfavorable outcome. Conclusions: CSF glucose and lactate levels poorly correlated with blood concentrations. Low CSF glucose/lactate ratio was associated with poor neurological outcome.

Osteopontin in post-subarachnoid hemorrhage pathologies

“…This leads to mitochondrial impairment, inflammatory or oxidative reactions, ionic gradient breakdown, glutamate-mediated excitotoxicity, stress signaling and finally to cell deaths [50]. After SAH, decreasing CSF glucose-to-lactate ratios were reported to be accompanied by unfavorable outcomes [51], but the role of extracellular lactate is still controversial if the lactate supports basal metabolism in neurons or contributes to neurotransmission activity per se [52,53]. Recently, it has been revealed that neurons and glia orchestrate a metabolic reaction to sustain energy demands and the redox balance of neuronal activities or cause post-stroke brain injuries such as aquaporin 4-medated brain edema and neuronal apoptosis, which may be reduced by hypothermia-induced suppression of metabolic activity [50,[53][54][55][56].…”

Alpha-Ketoglutarate Alleviates Neuronal Apoptosis Induced by Central Insulin Resistance through Inhibiting S6K1 Phosphorylation after Subarachnoid Hemorrhage

“…For hyperglycemia after SAH, the effects of insulin treatment are not satisfied even with a high risk of hypoglycemia [ 8 ]. Targeted treatment of central IR seems to be a better way to improve energy metabolism disorders with a lower risk of hypoglycemia [ 36 ].…”

“…Glucose transport and metabolism can serve as important regulatory points in the early apoptotic cascade [6]. A number of studies have shown that SAH patients with or without a history of diabetes will have transient hyperglycemia after bleeding, which seriously affects the prognosis [7][8][9]. Researchers proposed that insulin resistance (IR) after SAH was the direct cause of this phenomenon [9,10], but the mechanisms remain unclear.…”

Fluid metabolic pathways after subarachnoid hemorrhage

“…In patients with poor prognosis, the types and concentrations of amino acids in the CSF were increased, and phospholipid biosynthesis, steroid biosynthesis and fatty acid metabolism were up‐regulated (Li et al., 2019). Taccone et al performed metabolomic analysis of CSF from SAH patients and found that a low glucose/lactate ratio was associated with poor prognosis (Taccone et al., 2020). There are two major sources of glutamate in CSF after SAH.…”