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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.

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Aditya Vedantam, Claudia S. Robertson and Shankar P. Gopinath

OBJECTIVE

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.

METHODS

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.

RESULTS

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).

CONCLUSIONS

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.

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Aditya Vedantam, Claudia S. Robertson and Shankar P. Gopinath

OBJECTIVE

Early withdrawal of life-sustaining treatment due to expected poor prognosis is responsible for the majority of in-house deaths in severe traumatic brain injury (TBI). With increased focus on the decision and timing of withdrawal of care in patients with severe TBI, data on early neurological recovery in patients with a favorable outcome is needed to guide physicians and families.

METHODS

The authors reviewed prospectively collected data obtained in 1241 patients with head injury who were treated between 1986 and 2012. Patients with severe TBI, motor Glasgow Coma Scale (mGCS) score < 6 on admission, and those who had favorable outcomes (Glasgow Outcome Scale [GOS] score of 4 or 5, indicating moderate disability or good recovery) at 6 months were selected. Baseline demographic, clinical, and imaging data were analyzed. The time from injury to the first record of following commands (mGCS score of 6) after injury was recorded. The temporal profile of GOS scores from discharge to 6 months after the injury was also assessed.

RESULTS

The authors studied 218 patients (183 male and 35 female) with a mean age of 28.9 ± 11.2 years. The majority of patients were able to follow commands (mGCS score of 6) within the 1st week after injury (71.4%), with the highest percentage of patients in this group recovering on Day 1 (28.6%). Recovery to the point of following commands beyond 2 weeks after the injury was seen in 14.8% of patients, who experienced significantly longer durations of intracranial pressure monitoring (p = 0.001) and neuromuscular blockade (p < 0.001). In comparison with patients with moderate disability, patients with good recovery had a higher initial GCS score (p = 0.01), lower incidence of anisocoria at admission (p = 0.048), and a shorter ICU stay (p < 0.001) and total hospital stay (p < 0.001). There was considerable improvement in GOS scores from discharge to follow-up at 6 months.

CONCLUSIONS

Up to 15% of patients with a favorable outcome after severe TBI may begin to follow commands beyond 2 weeks after the injury. These data caution against early withdrawal of life-sustaining treatment in patients with severe TBI.

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Aditya Vedantam, Claudia S. Robertson and Shankar P. Gopinath

OBJECTIVE

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).

METHODS

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.

RESULTS

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).

CONCLUSIONS

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.

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Manuela Cormio, Alex B. Valadka and Claudia S. Robertson

Object. The aim of this study was to investigate the incidence of elevated (≥ 75%) jugular venous oxygen saturation (SjvO2) and its relationship to cerebral hemodynamic and metabolic parameters and to outcome after severe head injury.

Methods. Data from 450 severely head injured patients admitted to the Neurosurgical Intensive Care Unit of Ben Taub General Hospital were analyzed retrospectively. The SjvO2 was measured in blood obtained from indwelling jugular bulb catheters. Patients were classified into the following categories: high (Group I), normal (Group II), or low SjvO2 (Group III) if their mean SjvO2 over the duration of monitoring was 75% or higher, 74 to 56%, or 55% or lower, respectively.

A high SjvO2 occurred in 19.1% of patients. There was no consistent relationship between SjvO2 and simultaneous cerebral blood flow (CBF) or cerebral perfusion pressure measurements. Compared with Groups II and III, the patients in Group I had a significantly higher CBF and lower cerebral metabolic rate of oxygen (CMRO2). In Group I, the outcomes were death or persistent vegetative state in 48.8% of patients and severe disability in 25.6%. These outcomes were significantly worse than for patients in Group II. Within Group I, the patients with a poor neurological outcome were older and more likely to have suffered a focal head injury; they demonstrated a lower CMRO2 and a greater rate of cerebral lactate production than the patients who attained a favorable outcome.

Conclusions. Posttraumatic elevation of SjvO2 is common but cannot be automatically equated with hyperemia. Instead, elevated SjvO2 is a heterogeneous condition that is associated with poor outcome after head injury and may carry important implications for the management of comatose patients.