Recently, two large studies have demonstrated that therapeutic hypothermia can improve outcome in patients with post-anoxic brain injury, following cardiac arrest.[11
] On the other hand, although some previous studies for TBI showed that mild hypothermia therapy was associated with a better clinical outcome, this treatment remains highly controversial, especially in patients with severe traumatic head injury. One well designed, multi-centered, randomized controlled trial (RCT), in 2001, did not show any effect on the outcome, in the overall patient group, although decreases in intracranial pressure were noted in the hypothermia group.[13
] This study has been criticized based on its methodology: Treatment was started late, and cooling was slow (average time to target temperature >8 h).[14
] Furthermore, there were problems with hypotension, hypovolemia, electrolyte imbalance, and hyperglycemia in the treatment group. Marshall[15
] criticized the study for inter-center inconsistencies in patient management and the lack of specialized neurointensive care at some of the study centers. Based on these problems, a new study has been initiated that includes hypothermic and normothermic groups of patients with severe TBI (GCS3-8), in whom, hypothermia of 33°C is being achieved within 4 h after injury, and maintained for 48 h, in patients who are 16-45 years old. Rewarming is being initiated in 48 h, after reaching the target temperature. Hypotension will be promptly treated with vasopressors.[16
It has been shown that even very brief episodes of mild hypotension and/or hypovolemia can adversely affect the outcome.[17
] Great care should be taken to avoid all the potentially harmful effects of hypothermia and to prevent even the briefest episodes of hypovolemia and hypotension. Indeed, in this study, CVP was kept relatively constant during initiation, but with decreasing temperature, urinary volume increased, and dehydration deteriorated. In addition, AP was kept relatively constant during initiation, but with decreasing temperature, SVRI increased, and cardiac output deteriorated. CPP is the difference between the MAP and ICP. Therefore, similarly, CPP was kept relatively constant during initiation, but with decreasing temperature, SVRI increased, and cardiac output deteriolated. During the initiation of hypothermia, systemic circulation disturbance might result in cerebral ischemia. It is thought that we have to monitor these parameters carefully. If we recognize abnormal value in these parameters, we are able to treat systemic circulation disturbance with volume displacement and vasopressors or vasodilators.
It has been well known that the cardiac output decreases linearly with hypothermia, to approximately 60% of control values at a body temperature of 32-33°C.[18
] The reduction in cardiac output was due mainly to the decrease in heart rate and the volume of circulating blood, since the stroke volume was decreased to a much lesser extent.[19
] The causes for bradycardia during hypothermia are thought to be the direct effects of cooling on sinus nodes or the atrium of the heart, metabolic reduction in accordance with body temperature drop, and a possible mediation of vagal nerves. It was found that a suppression of the baroreflex of HR, but not sympathetic nerve activity, during hypothermia, may indicate the direct effects of hypothermia on the heart.[20
] Therefore, there is less possibility that a decrease in HR, during hypothermia, results from metabolic reduction. These adverse events can occur as side effects of cooling, but are quite easily preventable, with proper intensive care, and thus, should not be regarded as inevitable consequences of hypothermic treatment. Actually, it was reported that moderate hypothermia improved neurological outcome of severe TBI patients so far, as their cardiac output was maintained in normal-hyperdynamic range.[21
Recently, from experimental and clinical research, we have learned that the neurological outcome is not an effect of the primary damage occurring at the moment of injury. The primary injury develops into secondary injuries triggered by various biochemical and hemodynamic processes influenced, for example, by episodes of intracranial hypertension, systemic hypotension, and hypoxia.[22
] And so, in addition to the intracranial environment monitoring, monitoring of systemic circulation are mandatory for adequate treatment of patients with severe brain damage. But each of these monitoring devices is separate and independent making simultaneous evaluation of blood flow and metabolic changes in both cerebral and systemic circulation not feasible. We have used the monitoring system using a personal computer system.[23
] With this system in real time, we can manage intaracranial and systemic changes instantaneously, by a way of combined monitoring of brain damage setting. There are many parameters provided by using these multimodality monitoring devices. It is important clinically to observe a trend change of parameters with time. Our monitoring system allows by way of a trend graph to display trend changes on the same screen at the same time. In particular, this becomes important during on-going hypothermia treatment. As a result, we are able to detect an abnormality while monitoring, and treat promptly.