Lower extremity weakness is associated with elevated blood and cerebrospinal fluid glucose levels following multibranched endovascular aortic aneurysm repair.

OBJECTIVE: Hyperglycemia is associated with worsened clinical outcomes after central nervous system injury. The purpose of this study was to examine the association between lower extremity weakness (LEW) and the glucose levels of blood and cerebrospinal fluid (CSF) in patients undergoing multibranched endovascular aneurysm repair (MBEVAR) of thoracoabdominal and pararenal aortic aneurysms. METHODS: Blood and CSF samples were collected preoperatively, immediately after aneurysm repair, and on postoperative day 1 in 21 patients undergoing MBEVAR. Data on demographics, operative repair, complications, and outcomes were collected prospectively. RESULTS: There were 21 patients who underwent successful MBEVAR. Two patients had pre-existing paraplegia from prior open aortic surgery and were excluded from the current analysis. The mean age was 73 ± 8 years, and 15 of 19 (79%) were men. In the postoperative period, 7 of 19 (37%) patients developed LEW. This was temporary in 5 of 19 (26%) patients and permanent in 2 of 19 (11%) patients. The LEW group was older than the non-LEW group (77 ± 6 vs 70 ± 9 years, respectively; P = .10), had a lower preoperative glomerular filtration rate (58.6 ± 18.5 vs 71.4 ± 23.5 mL/min per 1.73 m2; P = .24), and was more likely to be taking a statin (100% vs 67%, respectively; P = .13), but these did not reach statistical significance. There was no significant difference in the prevalence of diabetes mellitus, hypertension, coronary artery disease, lung disease, or peripheral artery disease between the LEW and non-LEW groups. There was also no difference in operative time, blood loss, contrast material volume, or fluoroscopy times between the two groups. Preoperative blood and CSF glucose levels were similar in those with and without LEW. During the postoperative period, glucose values in the blood and CSF were significantly higher in those patients who developed LEW compared with those who did not develop LEW. In all patients with LEW, the elevation in the blood or CSF glucose level preceded the development of LEW. In a multivariable logistic regression model, CSF glucose concentration on postoperative day 1 was significantly and independently associated with the development of LEW (odds ratio, 2.30 [1.03-5.14] per 10 mg/dL increase in CSF glucose; P = .04). CONCLUSIONS: Elevated blood glucose and CSF glucose levels are associated with postoperative LEW in patients undergoing MBEVAR. The protective effect of euglycemia deserves further study in patients at risk for spinal cord ischemia.

Serum glucose adjusted cut-off values for normal cerebrospinal fluid/serum glucose ratio: implications for clinical practice.

BACKGROUND: Calculation of the cerebrospinal fluid/serum glucose (CSF/SGlu) ratio is part of the routine CSF work-up, however, different cut-off values ranging from 0.3 to 0.5 have been suggested so far to distinguish physiological from pathological conditions. The objective of this study was to determine cut-off values for normal CSF/SGlu ratio dependent on serum glucose concentrations. METHODS: We screened our database for paired CSF and serum samples, which have been collected by lumbar puncture, were processed within 1 h after withdrawal, showed cell count <15/3, erythrocyte count <1500/3 and normal CSF total protein resulting in 1036 sample pairs. Glucose concentrations in CSF and serum were measured by enzymatic spectrophotometry. RESULTS: Median glucose concentration in CSF was approximately 60% of that in serum. CSF/SGlu ratios negatively correlated with serum glucose levels (R=-0.586, p<0.001) and cut-off values for normal CSF/SGlu ratio defined as the 5th percentile were 0.5 for patients with serum glucose concentrations <100 mg/dL, 0.4 for those with a glucose level of 100-149 mg/dL and 0.3 for serum glucose concentrations ≥150 mg/dL. CONCLUSIONS: CSF/SGlu ratio inversely correlates with serum glucose concentrations in a non-linear manner. These findings suggest that cut-off values for normal CSF/SGlu ratio must be adjusted to serum glucose levels, probably explaining the considerably varying cut-offs that have been reported so far.

Hyperglycemia, cerebrospinal fluid lactic acidosis, and cerebral blood flow in severely head-injured patients.

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)

Hemichorea-hemiballismus associated with nonketotic hyperglycemia: a possible role of inflammation.

Three cases of hemichorea-hemiballismus (HC-HB) associated with nonketotic hyperglycemia were reported. Of them two patients presented as HC-HB and the remaining one as generalized chorea-ballismus (CB). Brain MRI showed characteristic T1-weighted high-intensity lesions in the contralateral or bilateral striatum without edema or mass effect. They all had a prior history of respiratory or urinary infection. Cerebrospinal fluid test in two patients showed an elevation of protein concentration with normal cell and an increased IgG content and elevated IgG index or 24 h IgG intrathecal synthesis rate. These results suggested that inflammation within the central nervous system may participate in the pathogenesis of chorea and ballismus induced by NKH.

Ascertaining hypoglycorrhachia in an acute patient.

A study was undertaken in an urgent clinical setting to determine whether the use of a cerebrospinal fluid (CSF) to blood glucose ratio is appropriate for describing the relationships between CSF glucose and blood glucose in patients who had not fasted. Blood glucose levels were obtained before a lumbar puncture in 79 adults who had normal CSF findings. Regression analysis of CSF glucose and blood glucose levels of these patients who had not fasted, as well as data from four published studies of normal blood and CSF glucose levels, indicated that a ratio was not a valid measure of the normal relationship between CSF and blood. Only when the blood glucose level was between 89 and 115 mg/dL was the relationship within the expected "ratio" of 0.60 to 0.70. In hyperglycemic states, the normal relationship may be substantially lower than 0.50. a nomogram is presented which is useful in determining hypoglycorrhachia when the patient is hyperglycemic.

Pattern of CSF glucose concentration after induced hyperglycaemia in patients with acute meningitis and evidence of cerebrospinal canal obstruction.

The pattern of glucose CSF concentration after induced hyperglycaemia was studied in 14 patients suffering from acute meningitis and 10 having meningism, as judged by normal CSF. Four out of the first group of patients had symptoms and signs likely to be due to cerebrospinal canal obstruction after the acute phase of the disease was over. When the patterns of CSF glucose concentration of the two groups were compared it was noted that patients suffering from acute meningitis showed generally a quicker and more profound rise of glucose levels after induced hyperglycaemia than patients with meningism. In four cases CSF glucose levels showed a partial or complete failure to rise, despite adequate increase of blood glucose concentration. Subsequent investigation revealed permanent obstruction of the cerebrospinal canal in three of the cases. The usefulness of serial CSF glucose estimations after induced hyperglycaemia as an early screening test for cases with possible obstruction is discussed.

Influence of hyperglycemia on cerebral adenosine production during ischemia and reperfusion.

We hypothesized that systemic hyperglycemia would alter cerebral adenosine concentrations during ischemia and reperfusion. In the present study, we analyzed brain tissue and cerebrospinal fluid (CSF) from hyperglycemic and normoglycemic rats before ischemia, after 15 min of incomplete forebrain ischemia, and during 60 min of reperfusion. Hyperglycemic rats received 3 g/kg of 17% D-glucose intraperitoneally, which increased blood glucose to 357 +/- 23 mg/100 ml compared with 128 +/- 12 mg/100 ml in normoglycemic rats. Brain tissue was sampled by the freeze-blow technique, and CSF was obtained by collecting cortical perfusate from the closed cranial window. Tissue and CSF were analyzed for adenosine and its metabolites inosine and hypoxanthine, and tissue was also analyzed for adenine nucleotides. Hyperglycemia significantly attenuated the increase in brain tissue and CSF adenosine and its metabolites during ischemia while preserving adenine nucleotide concentrates. This attenuation of ischemic adenosine production persisted after 5 min of reperfusion in tissue and throughout 60 min of reperfusion in CSF. Because adenosine, a cerebral vasodilator, can inhibit the release of neuronal excitotoxins as well as affect neutrophil-endothelial interactions, adenosine has been proposed as an endogenous neuroprotector. Thus the attenuation of adenosine and its metabolites may be a factor in the pathogenesis of increased ischemic brain injury associated with systemic hyperglycemia.