Simulation of propofol anaesthesia for intracranial decompression using brain hypothermia treatment

<p>Abstract</p> <p>Background</p> <p>Although propofol is commonly used for general anaesthesia of normothermic patients in clinical practice, little information is available in the literature regarding the use of propofol anaesthesia for intracranial decompression using brain hypothermia treatment. A novel propofol anaesthesia scheme is proposed that should promote such clinical application and improve understanding of the principles of using propofol anaesthesia for hypothermic intracranial decompression.</p> <p>Methods</p> <p>Theoretical analysis was carried out using a previously-developed integrative model of the thermoregulatory, hemodynamic and pharmacokinetic subsystems. Propofol kinetics is described using a framework similar to that of this model and combined with the thermoregulation subsystem through the pharmacodynamic relationship between the blood propofol concentration and the thermoregulatory threshold. A propofol anaesthesia scheme for hypothermic intracranial decompression was simulated using the integrative model.</p> <p>Results</p> <p>Compared to the empirical anaesthesia scheme, the proposed anaesthesia scheme can reduce the required propofol dosage by more than 18%.</p> <p>Conclusion</p> <p>The integrative model of the thermoregulatory, hemodynamic and pharmacokinetic subsystems is effective in analyzing the use of propofol anaesthesia for hypothermic intracranial decompression. This propofol infusion scheme appears to be more appropriate for clinical application than the empirical one.</p

Revising a dogma: ketamine for patients with neurological injury?

We evaluated reports of randomized clinical trials in the perioperative and intensive care setting concerning ketamine's effects on the brain in patients with, or at risk for, neurological injury. We also reviewed other studies in humans on the drug's effects on the brain, and reports that examined ketamine in experimental brain injury. In the clinical setting, level II evidence indicates that ketamine does not increase intracranial pressure when used under conditions of controlled ventilation, coadministration of a gamma-aminobutyric acid (GABA) receptor agonist, and without nitrous oxide. Ketamine may thus safely be used in neurologically impaired patients. Compared with other anesthetics or sedatives, level II and III evidence indicates that hemodynamic stimulation induced by ketamine may improve cerebral perfusion; this could make the drug a preferred choice in sedative regimes after brain injury. In the laboratory, ketamine has neuroprotective, and S(+)-ketamine additional neuroregenerative effects, even when administered after onset of a cerebral insult. However, improved outcomes were only reported in studies with brief recovery observation intervals. In developing animals, and in certain brain areas of adult rats without cerebral injury, neurotoxic effects were noted after large-dose ketamine. These were prevented by coadministration of GABA receptor agonists. IMPLICATIONS: Ketamine can be used safely in neurologically impaired patients under conditions of controlled ventilation, coadministration of a {gamma}-aminobutyric acid receptor agonist, and avoidance of nitrous oxide. Its beneficial circulatory effects and preclinical data demonstrating neuroprotection merit further animal and patient investigation

[Therapeutic hypothermia after traumatic brain injury or subarachnoid hemorrhage. Current practices of German anaesthesia departments in intensive care]

BACKGROUND: We aimed to explore current practices in use of therapeutic hypothermia after traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH) in intensive care of adults. METHODS: Questionnaires were sent to anaesthesia department chairs in German hospitals with neurosurgical care in January 2004 with a survey focussing on cooling procedures, temperature measurement, depth and duration of hypothermia, and rewarming after therapy. RESULTS: 99 (67%) questionnaires on TBI and 95 (64%) on SAH could be analysed. Hypothermia was used in 39% after TBI and 18% after SAH. Its aims were neuroprotection in approximately 45% and control of refractory intracranial hypertension in approximately 50%. However, in most cases (69% TBI, 59% SAH) hypothermia was used in less than a quarter of patients treated. A criterion for hypothermia was severe disease in approximately 40% and refractory intracranial hypertension in approximately 50%. Temperatures were targeted to 36-34 degrees C in 77% after TBI and 88% after SAH. In more than 80%, bladder temperatures were measured. For induction of hypothermia, surface cooling was applied in approximately 90%. The duration of hypothermia was 24-48 h in 62% after TBI and 29% after SAH. Cooling was orientated at the intracranial pressure (ICP) in 31% after TBI and 47% after SAH, and was used for more than 48 h in approximately 25%. After hypothermia was stopped, a rewarming rate of 0.5 degrees C/h was applied in 38% after TBI and 53% after SAH. In approximately 35%, rewarming was orientated at the ICP, and in 33% after TBI and 24% after SAH, it was performed over 24 h. After SAH, spontaneous rewarming was used in 24%. CONCLUSION: Therapeutic hypothermia is used in 39% after TBI and 18% after SAH in the intensive care of German anaesthesia departments. There is no standard in management, and there is wide variation in practices of duration of cooling and rewarming. For patients' benefit, evidence-based recommendations on therapeutic hypothermia should be published by the appropriate medical societies in the German language

Hypertonic saline solutions for treatment of intracranial hypertension.

PURPOSE OF REVIEW: This review aims to provide an update on recent knowledge gained on hypertonic saline solutions for the treatment of intracranial hypertension. Explanatory approaches to the mechanisms underlying the edema-reducing effects of the solutions are outlined, practical aspects of use are presented, and trials that assessed their clinical utility are highlighted. RECENT FINDINGS: With an established trauma system, hypertonic saline added to conventional fluid resuscitation did not improve long-term outcome in multiple injury with hypotension and brain trauma. In intensive care, hypertonic saline reduced intracranial hypertension after subarachnoid haemorrhage, brain trauma, and a variety of other brain diseases, including cerebral edema in acute liver failure. SUMMARY: Hypertonic saline solutions have evolved as an alternative to mannitol or may be used in otherwise refractory intracranial hypertension to treat raised intracranial pressure. With high osmolar loads, the efficacy of the solution is enhanced, but no simple relationship between the saline concentration and the clinical effects of a solution is established. Caution is advised with high osmolar loads because they carry increased risks for potentially deleterious consequences of hypernatremia or may induce osmotic blood-brain barrier opening with possibly harmful extravasation of the hypertonic solution into the brain tissue

Hypothermia after traumatic brain injury. Report of the Neuroonaesthesia Working Group of the German Society of Anaesthesiology and Intensive Care Medicine

The benefit of therapeutic hypothermia after traumatic brain injury in adult patients remains a controversial issue in the literature. Nevertheless, there is widespread use of cooling after head trauma. In published clinical trials, hypothermia is used for the prevention of secondary brain injury or the reduction of intracranial hypertension which cannot be controlled otherwise. In approximately half of these studies, hypothermia resulted in a better outcome. The US multicenter trial published in 2001 did not show any improvement in the outcome for patients with severe head injury after hypothermic treatment with a core temperature of 33 degreesC for 48 hours in comparison to normothermic patients. However, due to certain features in this study, the information it provides is limited. Several meta-analyses from the years 2001, 2002 and 2003 did not show any effect of mild to moderate short-term hypothermia. Two meta-analyses published in 2003 explored the effects of depth and duration of hypothermia as well as the effect of rewarming. In the case of hypothermia lasting at least 24 hours, the risk of death was reduced by 19% and with a duration of at least 48 hours there was a 30% reduction in the risk of death. Additionally, hypothermia lasting at least 48 hours decreased the risk of a poor neurologic outcome by 35%. The combination of a target temperature range of 32-33 degreesC, hypothermia lasting at least 24 hours, and rewarming within 24 hours also reduced the risk of a poor neurologic outcome. An overview of the studies currently available does not permit the definition either of standards or of therapeutic guidelines for the routine use of hypothermia after traumatic brain injury. If hypothermia is applied as a preventive measure, treatment should be based on the criteria associated with therapeutic benefit in the meta-analyses