***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: OBJECT Deepening sedation is often needed in patients with intracranial hypertension . All widely used sedative and anesthetic agents ( opioids , benzodiazepines , propofol , and barbiturates ) decrease blood pressure and may therefore decrease cerebral perfusion pressure ( CPP ) .  Ketamine is a potent , safe , rapid-onset anesthetic agent that does not decrease blood pressure . However , ketamine 's use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure ( ICP ) . Based on anecdotal clinical experience , the authors hypothesized that ketamine does not increase-but may rather decrease-ICP . METHODS The authors conducted a prospect i ve , controlled , clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center . All patients were se date d and mechanically ventilated prior to inclusion in the study . Children with sustained , elevated ICP ( > 18 mm Hg ) resistant to first-tier therapies received a single ketamine dose ( 1 - 1.5 mg/kg ) either to prevent further ICP increase during a potentially distressing intervention ( Group 1 ) or as an additional measure to lower ICP ( Group 2 ) . Hemodynamic , ICP , and CPP values were recorded before ketamine administration , and repeated- measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration . RESULTS The results of 82 ketamine administrations in 30 patients were analyzed . Overall , following ketamine administration , ICP decreased by 30 % ( from 25.8 + /- 8.4 to 18.0 + /- 8.5 mm Hg ) ( p < 0.001 ) and CPP increased from 54.4 + /- 11.7 to 58.3 + /- 13.4 mm Hg ( p < 0.005 ) . In Group 1 , ICP decreased significantly following ketamine administration and increased by > 2 mm Hg during the distressing intervention in only 1 of 17 events . In Group 2 , when ketamine was administered to lower persistent intracranial hypertension , ICP decreased by 33 % ( from 26.0 + /- 9.1 to 17.5 + /- 9.1 mm Hg ) ( p < 0.0001 ) following ketamine administration . CONCLUSIONS In ventilation-treated patients with intracranial hypertension , ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions , without lowering blood pressure and CPP . These results refute the notion that ketamine increases ICP .  Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension , and it can possibly be used safely in trauma emergency situations Introduction Endotracheal suctioning ( ETS ) is essential for patient care in an ICU but may represent a cause of cerebral secondary injury . Ketamine has been historically contraindicated for its use in head injury patients , since an increase of intracranial pressure ( ICP ) was reported ; nevertheless , its use was recently suggested in neurosurgical patients . In this prospect i ve observational study we investigated the effect of ETS on ICP , cerebral perfusion pressure ( CPP ) , jugular oxygen saturation ( SjO2 ) and cerebral blood flow velocity ( mVMCA ) before and after the administration of ketamine . Methods In the control phase , ETS was performed on patients se date d with propofol and remifentanil in continuous infusion . If a cough was present , patients were assigned to the intervention phase , and 100 γ/kg/min of racemic ketamine for 10 minutes was added before ETS . Results In the control group ETS stimulated the cough reflex , with a median cough score of 2 ( interquartile range ( IQR ) 1 to 2 ) . Furthermore , it caused an increase in mean arterial pressure ( MAP ) ( from 89.0 ± 11.6 to 96.4 ± 13.1 mmHg ; P < 0.001 ) , ICP ( from 11.0 ± 6.7 to 18.5 ± 8.9 mmHg ; P < 0.001 ) , SjO2 ( from 82.3 ± 7.5 to 89.1 ± 5.4 ; P = 0.01 ) and mVMCA ( from 76.8 ± 20.4 to 90.2 ± 30.2 cm/sec ; P = 0.04 ) . CPP did not vary with ETS . In the intervention group , no significant variation of MAP , CPP , mVMCA , and SjO2 were observed in any step ; after ETS , ICP increased if compared with baseline ( 15.1 ± 9.4 vs. 11.0 ± 6.4 mmHg ; P < 0.05 ) . Cough score was significantly reduced in comparison with controls ( P < 0.0001 ) . Conclusions Ketamine did not induce any significant variation in cerebral and systemic parameters . After ETS , it maintained cerebral hemodynamics without changes in CPP , mVMCA and SjO2 , and prevented cough reflex . Nevertheless , ketamine was not completely effective when used to control ICP increase after administration of 100 γ/kg/min for 10 minutes Spreading depolarizations are waves of mass neuronal and glial depolarization that propagate across the injured human cortex . They can occur with depression of neuronal activity as spreading depressions or isoelectric spreading depolarizations on a background of absent or minimal electroencephalogram activity . Spreading depolarizations are characterized by the loss of neuronal ion homeostasis and are believed to damage functional neurons , leading to neuronal necrosis or neurological degeneration and poor outcome . Analgesics and sedatives influence activity-dependent neuronal ion homeostasis and therefore represent potential modulators of spreading depolarizations . In this exploratory retrospective international multicentre analysis , we investigated the influence of midazolam , propofol , fentanyl , sufentanil , ketamine and morphine on the occurrence of spreading depolarizations in 115 brain-injured patients . A surface electrode strip was placed on the cortex , and continuous electrocorticographical recordings were obtained . We used multivariable binary logistic regression to quantify associations between the investigated drugs and the hours of electrocorticographical recordings with and without spreading depolarizations or clusters of spreading depolarizations . We found that administration of ketamine was associated with a reduction of spreading depolarizations and spreading depolarization clusters ( P < 0.05 ) . Midazolam anaesthesia , in contrast , was associated with an increased number of spreading depolarization clusters ( P < 0.05 ) . By using a univariate odds ratio analysis , we also found a significant association between ketamine administration and reduced occurrence of isoelectric spreading depolarizations in patients suffering from traumatic brain injury , subarachnoid haemorrhage and malignant hemispheric stroke ( P < 0.05 ) . Our findings suggest that ketamine-or another N-methyl-d-aspartate receptor antagonist-may represent a viable treatment for patients at risk for spreading depolarizations . This hypothesis will be tested in a prospect i ve study Objective : The manual injection of a bolus of opioid in patients with brain injury induces an increase in intracranial pressure related to a decrease in mean arterial pressure . Such an effect has not been observed with the use of ketamine . The use of target-controlled infusion would minimize or suppress this adverse effect of opioid . This study evaluated the effects of an increase in plasma concentrations of sufentanil or ketamine administered by target-controlled infusion on cerebral hemodynamics . Design : Prospect i ve , r and omized study . Setting : Intensive care unit in a trauma center . Patients : Thirty patients with severe traumatic brain injury . Interventions : Patients were assigned to receive sedation consisting of sufentanil-midazolam or ketamine-midazolam using target-controlled infusion . Twenty-four hours after the onset of sedation , the target concentrations of sufentanil or ketamine were doubled for 15 mins . Blood sample s were collected to determine the actual plasma concentration of sufentanil and ketamine , before and 15 mins after concentration change . Measurements and Main Results : The baseline values of intracranial pressure and cerebral perfusion pressure were similar in both groups . The two-fold increase in drug concentrations did not involve a significant change for intracranial pressure , cerebral perfusion pressure , and mean velocity of middle cerebral artery in both the ketamine and the sufentanil groups . The measured plasma concentrations of sufentanil and ketamine  were 0.4 ± 0.2 ng/mL and 2.6 ± 2.2 & mgr;g/mL , respectively , before the increase in concentrations and 0.7 ± 0.4 ng/mL and 5.5 ± 3.8 & mgr;g/mL after . Conclusions : The present study shows that the increase in sufentanil or ketamine plasma concentrations using a target-controlled infusion is not associated with adverse effects on cerebral hemodynamics in patients with severe brain injury . The use of target-controlled infusion could be of interest in the management of severely brain-injured patients . However , there is a need for specific pharmacokinetic models design ed for intensive care unit patients Summary Ketamine was supposed to be contra-indicated in head injured patients although it possesses numerous advantages over other commonly used analgosedative drugs . Referring to these potential advantages and the lack of definitive data about its effect upon ICP , CPP or neurological development , we conducted a prospect i ve study in which moderate or severely head injured patients ( n=35 ) were prospect ively allocated to receive treatment either with a combination of ketamine and midazolam or fentanyl and midazolam . The initial dose was 6.5 mg/kg/day midazolam , 65 mg/kg/day ketamine or 65 μg/kg/day fentanyl and was later adjusted due to clinical requirements for a period of 3 to 14 days . Comparably high dosages of detamine have been found necessary ( 104 mg/kg/day).Four patients from the ketamine group ( n=17 ) and 5 from the control group ( n=18 ) were withdrawn during treatment due to persistent ICP above 25 mm Hg , countermeasured by barbiturate coma . Two more patients were withdrawn due to development of cardiovascular arrest ( ketamine group ) and multi organ failure . A comparison of the remaining patients revealed a lower requirement of catecholamines ( significant on first day , p<0.05 ) , an on average 8 mm Hg higher cerebral perfusion pressure and a 2 mm Hg higher intracranial pressure in the fentanyl group . Enterai food intake was better in the study group . The outcome was comparable in both groups with or without inclusion of withdrawn patients Background : The potential adverse effects of ketamine in neurosurgical anesthesia have been well established and involve increased intracranial pressure ( ICP ) and cerebral blood flow . However , reexamination of ketamine is warranted because data regarding the effects of ketamine on cerebral hemodynamics are conflicting . Methods : Eight patients with traumatic brain injury were studied . In all patients , ICP monitoring was instituted before the study . Control of ICP ( less than 25 mmHg ) , hemodynamic values , and blood gas tension ( partial pressure of carbon dioxide in arterial blood between 35–38 mmHg ) was obtained with propofol infusion ( 3 mg [ center dot ] kg sup ‐1 [ center dot ] h sup ‐1 ) and mechanical ventilation . The effects of three doses of ketamine , 1.5 , 3 , and 5 mg/ kg , respectively , on ICP , cerebral perfusion pressure , jugular vein bulb oxygen saturation , middle cerebral artery blood flow velocity , and electric activity of the brain ( EEG ) were measured . The three doses were administered intravenously at 6‐h intervals over 30 s through a central venous line . Systemic and cerebral hemodynamics and end‐tidal carbon dioxide were continuously monitored and recorded at 1‐min intervals throughout the 30‐min study periods . Results : Ketamine , in all three doses studied ( 1.5 , 3 , and 5 mg/kg ) was associated with a significant decrease in ICP ( mean + /‐ SD : 2 + /‐ 0.5 mmHg [ P < 0.05 ] , 4 + /‐ 1 mmHg [ P < 0.05 ] , and 5 + /‐ 2 mmHg [ P < 0.05 ] ) among the study patients regardless of the ketamine dose used . There were no significant differences in cerebral perfusion pressure , jugular vein bulb oxygen saturation , and middle cerebral artery blood flow velocity . Ketamine induced a low‐amplitude fast‐activity electroencephalogram , with marked depression , such as burst suppression . Conclusions : These results suggest that ketamine may not adversely alter cerebral hemodynamics of mechanically ventilated head‐trauma patients se date d with propofol . These encouraging results should be confirmed in larger groups of similar patients Objective The aim of the study was to compare the safety concerning cerebral hemodynamics of ketamine and sufentanil used for sedation of severe head injury patients , both drugs being used in combination with midazolam 
    Output:
    
We found no evidence of harm during ketamine use in patients suffering from acute brain injury