Claudia S. Robertson and Robert G. Grossman
✓ The effect of insulin-induced reduction in blood glucose to 65 ± 20 mg/dl (mean ± standard deviation) on recovery of electrophysiological function and extracellular lactate concentration was studied in a rabbit model of spinal cord ischemia. These results were compared to findings in animals with spinal cord ischemia that either were fasted overnight (fasted group: blood glucose 97 ± 26 mg/dl) or had no pretreatment (control group: blood glucose 172 ± 65 mg/dl). The aorta was occluded until the postsynaptic waves of the spinal somatosensory evoked potentials (SSEP's) had been absent for 20 minutes, a period of ischemia that produces paraplegia in 100% of untreated rabbits. The total aortic occlusion time was not significantly different in the three groups. Recovery of the SSEP's was significantly better in the insulin-treated animals than in the fasted or control animals. The N3 wave of the SSEP's, which has been found to correlate best with neurological recovery, returned to 65% ± 48% of the preischemia amplitude in the insulin-treated animals, compared to 40% ± 34% in the fasted group and 26% ± 24% in the control animals. Extracellular lactate concentration in the spinal cord increased immediately after occlusion of the aorta, reached a plateau as the postsynaptic waves disappeared from the SSEP's, and then increased a second time during the first 15 minutes of reperfusion. The peak lactate concentration during ischemia and during reperfusion correlated with the preischemia glucose concentration (r = 0.60336 and r = 0.76930, respectively). Lactate concentration in the spinal cord was higher during ischemia and throughout the first 2 hours of reperfusion in the control and fasted animals than in the insulin-treated animals. During the 2nd hour of reperfusion, lactate concentration was significantly higher in the control animals than in the fasted animals. Reduction in blood glucose with insulin improves recovery of electrophysiological function after spinal cord ischemia, probably because of reduced lactic acid production, especially during the early reperfusion period.
Aditya Vedantam, Claudia S. Robertson, and Shankar P. Gopinath
Hypernatremia is independently associated with increased mortality in critically ill patients. Few studies have evaluated the impact of hypernatremia on early mortality in patients with severe traumatic brain injury (TBI) treated in a neurocritical care unit.
A retrospective review of patients with severe TBI (admission Glasgow Coma Scale score ≤ 8) treated in a single neurocritical care unit between 1986 and 2012 was performed. Patients with at least 3 serum sodium values were selected for the study. Patients with diabetes insipidus and those with hypernatremia on admission were excluded. The highest serum sodium level during the hospital stay was recorded, and hypernatremia was classified as none (≤ 150 mEq/L), mild (151–155 mEq/L), moderate (156–160 mEq/L), and severe (> 160 mEq/L). Multivariate Cox regression analysis was performed to determine independent predictors of early mortality.
A total of 588 patients with severe TBI were studied. The median number of serum sodium measurements for patients in this study was 17 (range 3–190). No hypernatremia was seen in 371 patients (63.1%), mild hypernatremia in 77 patients (13.1%), moderate hypernatremia in 50 patients (8.5%), and severe hypernatremia in 90 patients (15.3%). Hypernatremia was detected within the 1st week of admission in 79.3% of patients (n = 172), with the majority of patients (46%) being diagnosed within 72 hours after admission. Acute kidney injury, defined as a rise in creatinine of ≥ 0.3 mg/dl, was observed in 162 patients (27.6%) and was significantly associated with the degree of hypernatremia (p < 0.001). At discharge, 148 patients (25.2%) had died. Hypernatremia was a significant independent predictor of mortality (hazard ratios for mild: 3.4, moderate: 4.4, and severe: 8.4; p < 0.001). Survival analysis showed significantly lower survival rates for patients with greater degrees of hypernatremia (log-rank test, p < 0.001).
Hypernatremia after admission in patients with severe TBI was independently associated with greater risk of early mortality. In addition to severe hypernatremia, mild and moderate hypernatremia were significantly associated with increased early mortality in patients with severe TBI.
Roukoz B. Chamoun, Claudia S. Robertson, and Shankar P. Gopinath
A Glasgow Coma Scale (GCS) score of 3 on presentation in patients with severe traumatic brain injury due to blunt trauma has been recognized as a bad prognostic factor. The reported mortality rate in these patients is very high, even approaching 100% in the presence of fixed and dilated pupils in some series. Consequently, there is often a tendency to treat these patients less aggressively because of the low expectations for a good recovery. In this paper, the authors' purpose is to report their experience in the management of this patient population, analyzing the mortality rate, prognostic factors, and functional outcome of survivors.
The authors performed a retrospective review of patients who presented between 1997 and 2007 with blunt head trauma and a GCS score of 3. Demographics, mechanism of injury, examination, blood alcohol level, associated injury, intracranial pressure (ICP), surgical procedures, and outcome were all recorded.
A total of 189 patients met the inclusion criteria and were included in this study. The overall mortality rate was 49.2%. At the 6-month follow-up, 13.2% of the entire series achieved a good functional outcome (Glasgow Outcome Scale [GOS] score of 1 or 2).
The patient population was then divided into 2 groups: Group 1 (patients who survived ) and Group 2 (patients who died ). Patients in Group 1 were younger (mean 33.3 ± 12.8 vs 40.3 ± 16.97 years; p = 0.002) and had lower ICP on admission (mean 16.3 ± 11.1 vs 25.7 ± 12.7 mm Hg; p < 0.001) than those in Group 2. The difference between the 2 groups regarding sex, mechanism of injury, hypotension on admission, alcohol, surgery, and associated injuries was not statistically significant.
The presence of bilateral fixed, dilated pupils was found to be associated with the highest mortality rate (79.7%). Although not statistically significant because of the sample size, pupil status was also a good predictor of the functional outcome at the 6-month follow-up; a good functional outcome (GOS Score 1 or 2) was achieved in 25.5% of patients presenting with bilateral reactive pupils, and 27.6% of patients presenting with a unilateral fixed, dilated pupil, compared with 7.5% for those presenting with bilateral fixed, nondilated pupils, and 1.4% for patients with bilateral fixed, dilated pupils.
Overall, 50.8% of patients survived their injury and 13.2% achieved a good functional outcome after at 6 months of follow-up (GOS Score 1 or 2). Age, ICP on admission, and pupil status were found to be significant predictive factors of outcome. In particular, pupil size and reactivity appeared to be the most important prognostic factor since the mortality rate was 23.5% in the presence of bilateral reactive pupils and 79.7% in the case of bilateral fixed, dilated pupils. The authors believe that patients having suffered traumatic brain injury and present with a GCS score of 3 should still be treated aggressively initially since a good functional outcome can be obtained in some cases.
Guy L. Clifton, Claudia S. Robertson, and Sung C. Choi
✓ A nomogram is presented for estimation of energy expenditure at the bedside in comatose patients during the first 2 weeks after brain injury. In analysis of 312 days of energy expenditure in 57 patients, a combination of Glasgow Coma Scale (GCS) score, heart rate (HR), and days since injury (DSI) was found with multiple regression analysis to provide good prediction of resting metabolic expenditure (RME) according to the following relationship: %RME = 152 − 14(GCS score) + 0.4(HR) + 7(DSI) (n = 111, r = 0.7, p < 0.001). In non-comatose patients, predictive ability was less strong due to inability to measure truly rested values, but HR and GCS score could be used to predict energy expenditure by this relationship: %RME = 90 − 3 (GCS score) + 0.9 (HR) (n = 135, r = 0.47, p < 0.001). In six patients, paralysis was found to decrease energy expenditure to between 100% and 125% of expected. Movement or stimulation had little effect on energy expenditure in patients who could localize stimuli but increased rested values by 20% in posturing patients.
Analysis of fasted balance periods of nitrogen excretion in 22 patients based on 273 days of measurement showed a significant relationship between creatinine-height index (an index of muscle mass) and nitrogen excretion, but no relationship between nitrogen excretion and weight, temperature, and RME. Levels of retention of nitrogen with feeding could not be predicted by any of these variables. Feeding of the individual comatose patient is best guided at present by estimation of energy expenditure using a nomogram and periodic measurement of urinary nitrogen excretion.
Aditya Vedantam, Claudia S. Robertson, and Shankar P. Gopinath
Few studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).
The authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.
Twenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).
In the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.