***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: INTRODUCTION Traumatic brain injury ( TBI ) is a leading cause of death and disability worldwide . Prophylactic hypothermia is effective in laboratory models , but clinical studies to date have been inconclusive , partly because of method ological limitations . Our Prophylactic Hypothermia Trial to Lessen Traumatic Brain Injury ( POLAR ) r and omised controlled trial is currently underway comparing early , sustained hypothermia versus st and ard care in patients with severe TBI . We describe our study protocol and the challenges in conducting prophylactic hypothermia research in TBI . DESIGN We aim to r and omise 500 patients to either prophylactic 33 ° C hypothermia initiated within 3 hours of injury and continued for at least 72 hours , or st and ard normothermic management .  Patients will be enrolled by paramedic services in the prehospital setting , or by emergency department staff at participating sites in Australia , New Zeal and and Europe . The primary outcome will be the eight-level extended Glasgow outcome scale ( GOSE ) , dichotomised to favourable and unfavourable outcomes at 6 months after injury . Secondary outcomes will include mortality at hospital discharge and at 6 months , ordinal analyses of 6-month GOSE outcomes , quality of life with health economic evaluations and the differential proportion of adverse events . We will predefine subgroup and interaction analyses . DISCUSSION After a run-in phase , recruitment for our main study began in December 2010 . When the study is completed , we aim to provide evidence on the efficacy of prophylactic hypothermia in TBI to guide clinicians in their management of this devastating condition BACKGROUND The inconsistent effect of hypothermia treatment on severe brain injury in previous trials might be because hypothermia was induced too late after injury . We aim ed to assess whether very early induction of hypothermia improves outcome in patients with severe brain injury . METHODS The National Acute Brain Injury Study : Hypothermia II ( NABIS : H II ) was a r and omised , multicentre clinical trial of patients with severe brain injury who were enrolled within 2·5 h of injury at six sites in the USA and Canada . Patients with non-penetrating brain injury who were 16 - 45 years old and were not responsive to instructions were r and omly assigned ( 1:1 ) by a r and om number generator to hypothermia or normothermia . Patients r and omly assigned to hypothermia were cooled to 35 ° C until their trauma assessment was completed . Patients who had none of a second set of exclusion criteria were either cooled to 33 ° C for 48 h and then gradually rewarmed or treated at normothermia , depending upon their initial treatment assignment . Investigators who assessed the outcome measures were masked to treatment allocation . The primary outcome was the Glasgow outcome scale score at 6 months . Analysis was by modified intention to treat . This trial is registered with Clinical Trials.gov , NCT00178711 . FINDINGS Enrolment occurred from December , 2005 , to June , 2009 , when the trial was terminated for futility . Follow-up was from June , 2006 , to December , 2009 . 232 patients were initially r and omised a mean of 1·6 h ( SD 0·5 ) after injury : 119 to hypothermia and 113 to normothermia . 97 patients ( 52 in the hypothermia group and 45 in the normothermia group ) did not meet any of the second set of exclusion criteria . The mean time to 35 ° C for the 52 patients in the hypothermia group was 2·6 h ( SD 1·2 ) and to 33 ° C was 4·4 h ( 1·5 ) . Outcome was poor ( severe disability , vegetative state , or death ) in 31 of 52 patients in the hypothermia group and 25 of 56 in the normothermia group ( relative risk [ RR ] 1·08 , 95 % CI 0·76 - 1·53 ; p=0·67 ) . 12 patients in the hypothermia group died compared with eight in the normothermia group ( RR 1·30 , 95 % CI 0·58 - 2·52 ; p=0·52 ) . INTERPRETATION This trial did not confirm the utility of hypothermia as a primary neuroprotective strategy in patients with severe traumatic brain injury Purpose : To evaluate the efficacy and safety of mild induced hypothermia for intracranial hypertension in patients with traumatic brain injury after decompressive craniectomy . Methods : A total of 60 adults with intracranial pressure ( ICP ) of more than 20 mm Hg after decompressive craniectomy were r and omly assigned to st and ard care ( control group ) or hypothermia ( 32 ° C‐35 ° C ) plus st and ard care . Then , ICP , cerebral perfusion pressure , Glasgow Outcome Scale score , and complications were assessed . Results : There was a significant difference in ICP and cerebral perfusion pressure between the 2 groups . Favorable outcomes occurred in 12 ( 40.0 % ) and 7 ( 36.5 % ) patients in the hypothermia and control groups , respectively ( P = .267 ) . Kaplan‐Meier curves revealed a marked difference in survival between the hypothermia and control groups ( P = .032 ) . There were significant differences in pulmonary infection and electrolyte disorders between the hypothermia and control groups ( P = .038 and .033 , respectively ) . Conclusion : Mild induced hypothermia can reduce intracranial hypertension after decompressive craniectomy , decreasing patient mortality . Hypothermia should be considered one of the main treatments for intracranial hypertension after decompressive craniectomy in patients with traumatic brain injury . HighlightsThis is a r and omized controlled trial research .Mild induced hypothermia therapeutics can reduce the intracranial hypertension after the decompressive craniectomy and can reduce the mortality of the patients BACKGROUND Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies , but the results were not definitive . To study this issue , we conducted a multicenter trial comparing the effects of hypothermia with those of normothermia in patients with acute brain injury . METHODS The study subjects were 392 patients 16 to 65 years of age with coma after sustaining closed head injuries who were r and omly assigned to be treated with hypothermia ( body temperature , 33 degrees C ) , which was initiated within 6 hours after injury and maintained for 48 hours by means of surface cooling , or normothermia . All patients otherwise received st and ard treatment . The primary outcome measure was functional status six months after the injury . RESULTS The mean age of the patients and the type and severity of injury in the two treatment groups were similar . The mean ( + /-SD ) time from injury to r and omization was 4.3+/-1.1 hours in the hypothermia group and 4.1+/-1.2 hours in the normothermia group , and the mean time from injury to the achievement of the target temperature of 33 degrees C in the hypothermia group was 8.4+/-3.0 hours . The outcome was poor ( defined as severe disability , a vegetative state , or death ) in 57 percent of the patients in both groups . Mortality was 28 percent in the hypothermia group and 27 percent in the normothermia group ( P=0.79 ) . The patients in the hypothermia group had more hospital days with complications than the patients in the normothermia group . Fewer patients in the hypothermia group had high intracranial pressure than in the normothermia group . CONCLUSIONS Treatment with hypothermia , with the body temperature reaching 33 degrees C within eight hours after injury , is not effective in improving outcomes in patients with severe brain injury Animal research suggests that moderate therapeutic hypothermia may improve outcome after a severe head injury , but its efficacy has not been established in humans . The authors r and omly assigned 40 consecutively treated patients with a severe closed head injury ( Glasgow Coma Scale score 3 to 7 ) to either a  hypothermia or a normothermia group .  Using cooling blankets and cold saline gastric lavage , patients in the hypothermia group were cooled to 32 degrees to 33 degrees C ( brain temperature ) within a mean of 10 hours after injury , maintained at that temperature for 24 hours , and rewarmed to 37 degrees to 38 degrees C over 12 hours . Patients in the normothermia group were maintained at 37 degrees to 38 degrees C during this time . Deep-brain temperatures were monitored directly and used for all temperature determinations . Intracranial pressure ( ICP ) , cerebral blood flow ( CBF ) , and cerebral metabolic rate for oxygen ( CMRO2 ) were measured serially for all patients . Hypothermia significantly reduced ICP ( 40 % ) and CBF ( 26 % ) during the cooling period , and neither parameter showed a significant rebound increase after patients were rewarmed . Compared to the normothermia group , the mean CMRO2 in the hypothermia group was lower during cooling and higher 5 days after injury . Three months after injury , 12 of the 20 patients in the hypothermia group had moderate , mild , or no disabilities ; eight of the 20 patients in the normothermia group had improved to the same degree . Both groups had a similar incidence of systemic complications , including cardiac arrhythmias , coagulopathies , and pulmonary complications . It is concluded that therapeutic moderate hypothermia is safe and has sustained favorable effects on acute derangements of cerebral physiology and metabolism caused by severe closed head injury . The trend toward better outcome with hypothermia may indicate that its beneficial physiological and metabolic effects limit secondary brain injury Recent experimental studies have demonstrated that mild hypothermia at about 34 degrees C can be effective in the control of intracranial hypertension . A r and omized controlled study of mild hypothermia was carried out in 33 severely head-injured patients . All patients fulfilled the following criteria : 1 ) persistent intracranial pressure ( ICP ) greater than 20 mm Hg despite fluid restriction , hyperventilation , and high-dose barbiturate therapy ; 2 ) an ICP lower than the mean arterial blood pressure ; and 3 ) a Glasgow Coma Scale score of 8 or less . The patients were divided into two groups : one received  mild hypothermia  ( 16 patients ) and one served as a control group ( 17 patients ) . Mild hypothermia significantly reduced the ICP and increased the cerebral perfusion pressure . Eight patients ( 50 % ) in the hypothermia group and three ( 18 % ) in the control group survived ( p < 0.05 ) , while five ( 31 % ) in the hypothermia group and 12 ( 71 % ) in the control group died of uncontrollable intracranial hypertension ( p < 0.05 ) . In five patients in the hypothermia group , cerebral blood flow was measured by the hydrogen clearance method and arteriojugular venous oxygen difference was evaluated before and during mild hypothermia . Mild hypothermia significantly decreased the cerebral blood flow , arteriojugular venous oxygen difference , and cerebral metabolic rate of oxygen ( p < 0.01 ) . The results of this preliminary investigation suggest that mild hypothermia is a safe and effective method to control traumatic intracranial hypertension and to improve mortality and morbidity rates PURPOSE We investigated the effects of therapeutic mild hypothermia on patients with severe traumatic brain injury after craniotomy ( TBI ) . METHODS Eighty patients with severe TBI after unilateral craniotomy were r and omized into a therapeutic hypothermia group with the brain temperature maintained at 33 degrees C to 35 degrees C for 4 days , and a normothermia control group in the intensive care unit . Vital signs , intracranial pressure , serum superoxide dismutase level , Glasgow Outcome Scale scores , and complications were prospect ively analyzed . RESULTS The mean intracranial pressure values of the therapeutic hypothermia group at 24 , 48 , and 72 hours after injury were much lower than those of the control group ( 23.49 + /- 2.38 , 24.68 + /- 1.71 , and 22.51 + /- 2.44 vs 25.87 + /- 2.18 , 25.90 + /- 1.86 , and 24.57 + /- 3.95 mm Hg ; P = .000 , .000 , and .003 , respectively ) . The mean serum superoxide dismutase levels of the therapeutic hypothermia group at days 3 and 7 were much higher than those of the control group at the same time point ( 533.0 + /- 103.4 and 600.5 + /- 82.9 vs 458.7 + /- 68.1 and 497.0 + /- 57.3 mug/L , respectively ; P = .000 ) . The percentage of favorable neurologic outcome 1 year after injury was 70.0 % and 47.5 % , respectively ( P = .041 ) . Complications , including pulmonary infections ( 57.5 % in the therapeutic hypothermia group vs 32.5 % in the control group ; P = .025 ) were managed without severe sequelae . CONCLUSIONS Therapeutic mild hypothermia provides a promising way in the intensive care unit for patients with severe TBI after craniotomy Aim of this study was to examine the hypothesis that only a subgroup of patients with lesser primary brain damage after severe head 
    Output:
    
High- quality studies show no significant difference in mortality , poor outcomes , or new pneumonia .
In addition , this review shows a place for fever control in the management of traumatic brain injury