Refractory intracranial hypertension and "second-tier" therapies in traumatic brain injury.

OBJECTIVE: To quantify the occurrence of high intracranial pressure (HICP) refractory to conventional medical therapy after traumatic brain injury (TBI) and to describe the use of more aggressive therapies (profound hyperventilation, barbiturates, decompressive craniectomy). DESIGN: Prospective study of 407 consecutive TBI patients SETTING: Three neurosurgical intensive care units (ICU). MEASUREMENTS AND RESULTS: Intracranial pressure (ICP) was studied during the first week after TBI; 153 patients had at least 1 day of ICP>20 mmHg. Early surgery was necessary for 221 cases, and standard medical therapy [sedation, mannitol, cerebrospinal fluid (CSF) withdrawal, PaCO2 30-35 mmHg] was used in 135 patients. Reinforced treatment (PaCO2 25-29 mmHg, induced arterial hypertension, muscle relaxants) was used in 179 cases (44%), and second-tier therapies in 80 (20%). Surgical decompression and/or barbiturates were used in 28 of 407 cases (7%). Six-month outcome was recorded in 367 cases using the Glasgow outcome scale (GOS). The outcome was favorable (good recovery or moderate disability) in 195 cases (53%) and unfavorable (all the other categories) in 172 (47%). HICP was associated with worse outcome. Outcome for cases who had received second-tier therapies was significantly worse (43% favorable at 6 months, p=0.03). CONCLUSIONS: HICP is frequent and is associated with worse outcome. ICP was controlled by early surgery and first-tier therapies in the majority of cases. Profound hyperventilation, surgical decompression and barbiturates were used in various combinations in a minority of cases. The indications for surgical decompression and/or barbiturates seem restricted to less than 10% of severe TBI.

Intracranial pressure monitoring in intensive care: clinical advantages of a computerized system over manual recording.

INTRODUCTION: The presence of intracranial hypertension (HICP) after traumatic brain injury (TBI) affects patient outcome. Intracranial pressure (ICP) data from electronic monitoring equipment are usually calculated and recorded hourly in the clinical chart by trained nurses. Little is known, however, about how precisely this method reflects the real patterns of ICP after severe TBI. In this study, we compared hourly manual recording with a validated and continuous computerized reference standard. METHODS: Thirty randomly selected patients with severe TBI and HICP admitted to the neuroscience intensive care unit (Policlinico University Hospital, Milan, Italy) were retrospectively studied. A 24-hour interval with ICP monitoring was randomly selected for each patient. The manually recorded data available for analysis covered 672 hours corresponding to 36,492 digital data points. The two methods were evaluated using the correlation coefficient and the Bland and Altman method. We used the proportion test to analyze differences in the number of episodes of HICP (ICP > 20 mm Hg) detected with the two methods and the paired t test to analyze differences in the percentage of time of HICP. RESULTS: There was good agreement between the digitally collected ICP and the manual recordings of the end-hour values. Bland and Altman analysis confirmed a mean difference between the two methods of 0.05 mm Hg (standard deviation 3.66); 96% of data were within the limits of agreement (+7.37 and -7.28). The average percentages of time of ICP greater than 20 mm Hg were 39% calculated from the digital measurements and 34% from the manual observations. From the continuous digital recording, we identified 351 episodes of ICP greater than 20 mm Hg lasting at least five minutes and 287 similar episodes lasting at least ten minutes. Conversely, end-hour ICP of greater than 20 mm Hg was observed in only 204 cases using manual recording methods. CONCLUSION: Although manually recorded end-hour ICP accurately reflected the computerized end-hour and mean hour values, the important omission of a number of episodes of high ICP, some of long duration, results in a clinical picture that is not accurate or informative of the true pattern of unstable ICP in patients with TBI.

Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: a microdialysis study.

OBJECT: The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). METHODS: After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue. After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 +/- 18 to 122.6 +/- 45.2 mm Hg (p < 0.0001), whereas brain lactate dropped from its baseline (3.21 +/- 2.77 mmol/L), reaching its lowest value (2.90 +/- 2.58 mmol/L) after 3 hours of hyperoxia (p < 0.01). Pyruvate dropped as well, from 153 +/- 56 to 141 +/- 56 micromol/L (p < 0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 +/- 1.22 to 4.15 +/- 0.76 m/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p < 0.01), but the lactate/pyruvate ratio did not change. CONCLUSIONS: Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.

Analysis of propofol/remifentanil infusion protocol for tumor surgery with intraoperative brain mapping.

BACKGROUND: There is no general consensus about the best anesthesiologic approach to use during craniotomies with intraoperative brain mapping, and large prospective studies evaluating the complications associated with different approaches are lacking. Objective of this study was to prospectively collect and evaluate data about a large series of consecutive asleep-awake and asleep-asleep craniotomies. METHODS: We analyzed 238 consecutive procedures from January 2005 to December 2008. During asleep-awake procedures, patients were initially ventilated through a laryngeal mask which was removed to allow language testing. During asleep-asleep procedures, patients remained sedated and intubated to permit motor testing. RESULTS: In asleep-awake craniotomies [n=135, age 42 y (range: 16 to 72 y), American Society of Anesthesiologists classification (ASA) 1 (1 to 3), and body mass index 24.2+/-3.7 kg/m], 43% of the procedures were free of complications. Most common complications were hypertension (27%) and brief clinical seizures (16%), but also hypotension (10%), vomiting (7%), brief periods of apnea (4%), and agitation (6%) were observed. In 7% of the procedures, seizures required pharmacologic treatment. Fifty-nine percent of the asleep-asleep procedures [n=103, age 51 y (range: 21 to 76 y), ASA 1 (1 to 3), body mass index 25.4+/-3.9 kg/m, P<0.05 vs. asleep-awake] were free of complications. Clinical seizures were observed in 31% of the cases. The administration of boluses of hypnotics was rarely necessary (6%) and safer because of secured airways. CONCLUSIONS: With this study, we demonstrated the feasibility and safety of our protocols on large prospective case series. Asleep-awake protocol can be safely used when intraoperative language mapping is planned, whereas an asleep-asleep protocol with secured airway might be preferred when motor testing only is required.