Acute Severe Head Injury Research Articles

Factors influencing outcome in head injury patients with glasgow coma scale

Background: Over the years in the emergency department, it has been generally observed that the overall outcome in severe head injury patients is very poor. Hence, a study was conducted in traumatic brain injury patients with a Glasgow Coma Scale (GCS) <8, in which various factors that affect outcome in severe head injury patients were analyzed. Objective: The objective of the study was to understand the various factors influencing outcome in patients with severe head injury (GCS ≤8). Subjects and Methods: This was a prospective study, conducted on 350 consecutive acute severe head injury patients with a GCS ≤8. Thirteen independent factors expected to affect prognosis of severe head injury patients were analyzed and studied. Multivariate analysis was used to include adjustment for prognostic variables. Positive predictive value and strong association of the data were analyzed using cumulative percentage, Chi-square test, and cross-tabulation. Results: From the study, it was observed that male population, older age group patients, low GCS on arrival, train accidents, increased time interval, poor motor response, sluggish or absent pupillary reaction to light, absence of dolls eye movement, presence of comorbidities and other severe traumatic injury of major organs, poor glycemic status, and altered coagulation profile were associated with poor outcome in patients. Conclusions: A keen evaluation of patient profile before taking definitive management decisions is recommended, so as to improve the outcome in severe head injury patients. This is because, there are certain factors such as glycemic statuses of the patient, hemoglobin level, and coagulation profile that are modifiable, and if identified and corrected early, could improve the prognosis of the patients to a large extent.

Investigation on the cause and treatmene strategies for patients with severe acute head injury causes encephalocele

Objective To investigate the causes and treatment strategies of intraoperative encephalocele brain injury.Meethods 55 traumatic brain injury patients with intraoperative encephalocele were selected,the clinical data were retrospectively analyzed.Results 55 patients undergoing acute encephalocele reasons including widespread severity of brain contusion,acute brain swelling(19cases),delayed intracranial hematoma(28 cases),the late herniation,hematoma too long(4 cases),traumatic shock and hypotension leading to cerebral ischemia,hypoxia (4 cases).Assessed by GOS outcome at discharge:Good 3 cases,moderate disability in 5 cases,8 cases of severe disability,vegetative five cases,of whom 34 died.Conclusion Delayed intracranial hematoma,acutebrain swelling is an acute intraoperative encephalocele main reason.Clear intraoperative brain injury causes acute encephalocele,take appropriate measures as soon as possible,in order to achieve better results and reduce mortality. Key words: Meningocele ; Craniocrebral trauma; Intraoperative complications

Barbiturates for acute traumatic brain injury.

Raised intracranial pressure (ICP) is an important complication of severe brain injury, and is associated with high mortality. Barbiturates are believed to reduce ICP by suppressing cerebral metabolism, thus reducing cerebral metabolic demands and cerebral blood volume. However, barbiturates also reduce blood pressure and may, therefore, adversely effect cerebral perfusion pressure. To assess the effects of barbiturates in reducing mortality, disability and raised ICP in people with acute traumatic brain injury. To quantify any side effects resulting from the use of barbiturates. The following electronic databases were searched on 26 September 2012: CENTRAL (The Cochrane Library), MEDLINE (Ovid SP), PubMed, EMBASE (Ovid SP), PsycINFO (Ovid SP), PsycEXTRA (Ovid SP), ISI Web of Science: Science Citation Index and Conference Proceedings Citation Index-Science. Searching was not restricted by date, language or publication status. We also searched the reference lists of the included trials and review articles. We contacted researchers for information on ongoing studies. Randomised controlled trials of one or more of the barbiturate class of drugs, where study participants had clinically diagnosed acute traumatic brain injury of any severity. Two review authors screened the search results, extracted data and assessed the risk of bias in the trials. Data from seven trials involving 341 people are included in this review.For barbiturates versus no barbiturate, the pooled risk ratio (RR) of death from three trials was 1.09 (95% confidence interval (CI) 0.81 to 1.47). Death or disability, measured using the Glasgow Outcome Scale was assessed in two trials, the RR with barbiturates was 1.15 (95% CI 0.81 to 1.64). Two trials examined the effect of barbiturate therapy on ICP. In one, a smaller proportion of patients in the barbiturate group had uncontrolled ICP (68% versus 83%); the RR for uncontrolled ICP was 0.81 (95% CI 0.62 to 1.06). In the other, mean ICP was also lower in the barbiturate group. Barbiturate therapy results in an increased occurrence of hypotension (RR 1.80; 95% CI 1.19 to 2.70). For every four patients treated, one developed clinically significant hypotension. Mean body temperature was significantly lower in the barbiturate group.In one study of pentobarbital versus mannitol there was no difference in death between the two study groups (RR 1.21; 95% CI 0.75 to 1.94). Pentobarbital was less effective than mannitol for control of raised ICP (RR 1.75; 95% CI 1.05 to 2.92).In one study the RR of death with pentobarbital versus thiopental was 1.78 (95% CI 1.03 to 3.08) in favour of thiopental. Fewer people had uncontrollable ICP with thiopental (RR 1.64; 95% CI 1.03 to 2.60). There was no significant difference in the effects of pentobarbital versus thiopental for death or disability, measured using the Glasgow Outcome Scale (RR 1.31; 95% CI 0.88 to 1.94), or hypotension (RR 0.95; 95% CI 0.81 to 1.12). There is no evidence that barbiturate therapy in patients with acute severe head injury improves outcome. Barbiturate therapy results in a fall in blood pressure in one in four patients. This hypotensive effect will offset any ICP lowering effect on cerebral perfusion pressure.

Chapter 11. Barbiturates

Chapter 11. Barbiturates

Relationship between oxyhemoglobin saturation in internal jugular vein (cerebral extraction of oxygen) and prognosis of head injury

Objective To observe blood gas analysis of internal carotid artery and internal jugular vein to calculate the cerebral extraction of oxygen, and to investigate the relationship between oxyhemoglobin in internal jugular vein, cerebral extraction of oxygen, and the prognosis of patients with head injury. Method Seventy patients with acute severe head injury in ICU of Taizhou People Hospital were studied, and another 80 patients with mild head injury were enrolled as controls. Twenty-four hours after first aid such as keeping airway open and circulatory and ventilation support, and emergency craniotomy, the blood samples from internal carotid artery and internal jugular vein were collected for blood gas analysis including SaO2, PaO2, SjvO2, PJVO2 > PaCO2, PJVCO2, SaO2-SjvO2, Pa-jvCCO2, CaO2-CjvO2 and Ca-jvO2/CaCO2 (CEO2, cerebral oxygen extraction). Results There were significant differences in SjvO2, PjvO2, Sa-jvO2, Pa-jvO2 Ca-jvO2 and CEO2 between two groups. Conclusions The SjvO2 and CEO2 represent the cerebral oxygen uptake and oxygen consumption precisely, and they can be used to predict the outcome of patients with severe craniocerebral trauma commendabiy. Key words: Severe head injury; Cerebral oxygen metabolism; Blood gas analysis; Relation analysis

Relationship between Plasma Cortisol Levels and Stress Ulcer following Acute and Severe Head Injury

Objective: This study was designed to investigate the relationship between plasma cortisol levels and stress ulcer following acute severe head injury. Patients and Methods: The plasma cortisol levels were prospectively measured by radioimmunoassay in 68 patients following acute head injury. The diagnosis of stress ulcer was based on clinical evidence and was confirmed by endoscopic examination. Results: Patients with stress ulcer and gastrointestinal bleeding (n = 30, 44.1%) were older than those without stress ulcer(38.2 ± 7.9 vs. 28.3 ± 9.7 years, p < 0.01). The combined rate of poor recovery and death in the stress ulcer patients (70.0%) was significantly higher than in the nonulcer patients (42.1%, p = 0.02). On each of the first 3 days following the head injury, the average plasma cortisol levels in the stress ulcer patients were higher than in the nonulcer patients (p < 0.01). Univariate analysis showed a positive relationship between plasma cortisol on admission and stress ulcer (r = 0.329, p = 0.01). Logistic regression analysis revealed that plasma cortisol levels on admission (OR = 2.326, 95% CI = 1.982–2.466) and age (OR = 1.064, 95% CI = 0.861–1.219) were independent predictors of stress ulcer. Conclusions: The data showed that acute severe head injury was associated with a significant increase in plasma cortisol. Plasma levels of cortisol and age were independent predictors of stress ulcer following acute head injury.

Balance of cytokines in patients with severe head injury

Dynamic study of the blood levels of cytokines (interleukins IL-1β, IL-6, IL-1O and TNFalfa) was carried out in 40 patients with different outcomes of acute severe head injury. It was shown that severe head trauma resulted in the disbalance of pro- and antiinflammatory cytokines. During the first 24 hours, the direction of pathologic shifts did not differ between different patient groups and was characterized by the increase in IL-1β, IL-6 and IL-10 concentrations. By week 3, the decrease in concentrations of both pro- and anti-inflammatory cytokines was found in patients who had been discharged from the hospital for ambulant therapy. In cases of fatal outcome, deterioration of general condition of patients was combined with the decrease in IL-1β concentration and the considerable increase in IL-6 and IL-10 concentrations, which may be regarded as one of unfavorable prognostic signs of head injury.

Commentary: Brunker C. (2006). Assessment of sedated head‐injured patients using the Glasgow Coma Scale: an audit

AbstractThe Glasgow Coma Scale (GCS) is widely used to assess head‐injured patients. However, patients with acute severe head injury are typically managed with varying doses of sedative drugs that may interfere with GCS assessments. There is a question as to whether GCS assessments are useful and justified when the patient is sedated. The limited literature available is briefly reviewed. The aim of the audit described in this paper was to gain an overview of current practice among the neuroscience intensive care units in the UK, in search of any consensus. Thirty questionnaires were distributed and 23 returned (a 77% response). The results show considerable variations in practice and, in particular, differences between those units that treat only neuroscience patients and those that manage general intensive care patients as well. This audit demonstrates a lack of clear consensus and highlights the need for more research. Abstract reprinted from the British Journal of Neuroscience Nursing, volume 2, Brunker C, ‘Assessment of sedated head‐injured patients using the Glasgow Coma Scale: an Audit.’, pages 276–280. © 2006, reproduced with permission from MA Healthcare Limited.

Effect of hyperoxia on cerebral metabolic rate for oxygen measured using positron emission tomography in patients with acute severe head injury

Effect of hyperoxia on cerebral metabolic rate for oxygen measured using positron emission tomography in patients with acute severe head injury

Effect of hyperoxia on cerebral metabolic rate for oxygen measured using positron emission tomography in patients with acute severe head injury

Recent observations indicate that traumatic brain injury (TBI) may be associated with mitochondrial dysfunction. This, along with growing use of brain tissue PO2 monitors, has led to considerable interest in the potential use of ventilation with 100% oxygen to treat patients who have suffered a TBI. To date, the impact of normobaric hyperoxia has only been evaluated using indirect measures of its impact on brain metabolism. To determine if normobaric hyperoxia improves brain oxygen metabolism following acute TBI, the authors directly measured the cerebral metabolic rate for oxygen (CMRO2) with positron emission tomography before and after ventilation with 100% oxygen. Baseline measurements of arterial and jugular venous blood gases, mean arterial blood pressure, intracranial pressure, cerebral blood flow (CBF), cerebral blood volume, oxygen extraction fraction, and CMRO2 were made at baseline while the patients underwent ventilation with a fraction of inspired oxygen (FiO2) of 0.3 to 0.5. The FiO2 was then increased to 1.0, and 1 hour later all measurements were repeated. Five patients were studied a mean of 17.9 +/- 5.8 hours (range 12-23 hours) after trauma. The median admission Glasgow Coma Scale score was 7 (range 3-9). During ventilation with 100% oxygen, there was a marked rise in PaO2 (from 117 +/- 31 to 371 +/- 99 mm Hg, p < 0.0001) and a small rise in arterial oxygen content (12.7 +/- 4.0 to 13.3 +/- 4.6 vol %, p = 0.03). There were no significant changes in systemic hemodynamic or other blood gas measurements. At the baseline evaluation, bihemispheric CBF was 39 +/- 12 ml/100 g/min and bihemispheric CMRO2 was 1.9 +/- 0.6 ml/ 100 g/min. During hyperoxia there was no significant change in either of these measurements. (Values are given as the mean +/- standard deviation throughout.) Normobaric hyperoxia did not improve brain oxygen metabolism. In the absence of outcome data from clinical trials, these preliminary data do not support the use of 100% oxygen in patients with acute TBI, although larger confirmatory studies are needed.

Assessment of sedated head-injured patients using the Glasgow Coma Scale: An audit

The Glasgow Coma Scale (GCS) is widely used to assess head-injured patients. However, patients with acute severe head injury are typically managed with varying doses of sedative drugs which may interfere with GCS assessments. There is a question as to whether GCS assessments are useful and justified when the patient is sedated. The limited literature available is briefly reviewed. The aim of the audit described in this paper was to gain an overview of current practice among the neuroscience intensive care units in the UK, in search of any consensus. Thirty questionnaires were distributed and 23 returned (a 77% response). The results show considerable variations in practice and, in particular, differences between those units that treat only neuroscience patients and those that manage general intensive care patients as well. This audit demonstrates a lack of clear consensus and highlights the need for more research.

Cardiac Arrest due to Severe Hypokalemia during Barbiturate Coma Therapy in a Patient with Severe Acute Head Injury: A case report

An emergency left frontotemporal craniectomy with direct neck clipping and hematoma removal was performed in a 36-year-old man with a ruptured left middle cerebral artery aneurysm and sylvian hematoma. Because of severe brain swelling postoperatively, we induced barbiturate coma therapy to treat his intractable brain swelling. He had an initial loading dose of sodium thiopental (5 mg/kg) followed by continuous infusion of sodium thiopental (5 mg/kg/hour). The lowest potassium concentration recorded during the barbiturate coma therapy was 1.1 mmol/L; necessitating treatment with cardiac massage, epinephrine, and atropine because of asystole and severe bradycardia. However, he did not recover from cardiac arrest. We present here a case of cardiac arrest due to severe life threatening hypokalemia that occurred during barbiturate coma therapy. (Korean J Anesthesiol 2006; 50: S 71~3)

Severe hypokalemia occurring during barbiturate coma therapy in a patient with severe acute head injury

Acta Anaesthesiologica ScandinavicaVolume 49, Issue 6 p. 883-884 Severe hypokalemia occurring during barbiturate coma therapy in a patient with severe acute head injury S-H. Ok, S-H. OkSearch for more papers by this authorY-W. Chung, Y-W. ChungSearch for more papers by this authorJ-T. Sohn, Corresponding Author J-T. Sohn * Ju-Tae Sohn, MD Department of Anesthesia, Institute of Health Sciences Gyeongsang National University College of Medicine 90 Chilam-dong Jinju, 660–702 Korea e-mail: jtsohn@nongae.gsnu.ac.krSearch for more papers by this authorJ-M. Jung, J-M. JungSearch for more papers by this authorY-K. Chung, Y-K. ChungSearch for more papers by this author S-H. Ok, S-H. OkSearch for more papers by this authorY-W. Chung, Y-W. ChungSearch for more papers by this authorJ-T. Sohn, Corresponding Author J-T. Sohn * Ju-Tae Sohn, MD Department of Anesthesia, Institute of Health Sciences Gyeongsang National University College of Medicine 90 Chilam-dong Jinju, 660–702 Korea e-mail: jtsohn@nongae.gsnu.ac.krSearch for more papers by this authorJ-M. Jung, J-M. JungSearch for more papers by this authorY-K. Chung, Y-K. ChungSearch for more papers by this author First published: 06 May 2005 https://doi.org/10.1111/j.1399-6576.2005.00728.xCitations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume49, Issue6July 2005Pages 883-884 RelatedInformation

Postmortem endoscopy of the ocular fundus: A valuable tool in forensic postmortem practice

Pathological changes of the ocular fundus in acute severe head or extracranial injury are difficult to document. In vivo examination usually has to be carried out under intensive care conditions. Postmortem ophthalmoscopy is usually impeded by rapid blurring of the cornea. Therefore, endoscopic fundal photography has been applied by using a pars plana approach during forensic postmortem procedures. This technique provides fundoscopic pictures of high quality as a valuable supplement for subsequent macro- and histopathological preparations and sections. Different patterns of fundoscopic findings seem to correspond to different types of injuries such as craniocerebral trauma, traumatic asphyxia and decompression sickness, and may allow some insight into the respective pathogenetic mechanism.

Intravenous lignocaine as pretreatment for intubation of patients with acute severe head injury

Intravenous lignocaine at a dose of 1.5–2.0 mg/kg is frequently included in intubation protocols for patients with acute severe head injury. This literature review attempts to provide an evidence base for this. A Medline search and review of all relevant articles post-1966 was undertaken. There is evidence that lignocaine has a beneficial effect on intracranial and intraocular pressures. Neuroprotection is demonstrated in some animal models. There is, however, no evidence that lignocaine improves outcome. This article recommends using lignocaine in pre-intubation for patients where a rise in intraocular pressure is a concern (e.g. penetrating eye injury), but cannot, on evidence alone, justify its inclusion in head injury protocols.

Measurements of cortical cellular pH by intracranial tonometer in severe head injury.

To evaluate the cortical cellular damage in acute severe head injury, we measured the cortical cellular pH by using an intracranial tonometer made in our institution. Prospective, 3.5-yr data collection. University hospital trauma intensive care unit. Severely head-injured patients (n = 29) with Glasgow Coma Scale score <8. Routine emergency neurologic procedure. We made 98 measurements of cortical cellular pH by intracranial tonometer in 29 severely head-injured patients in the acute phase. Each patient's intracranial pressure was recorded, and in 16 patients, the saturation of jugular venous oxygen was monitored. The outcome at 6 months after injury was significantly better in patients having a cortical cellular pH of >7.2 than those with <7.2. The cerebral perfusion pressure and cortical cellular pH correlated significantly (p < .0001). Our study suggests the usefulness of measurement of cortical cellular pH by intracranial tonometer for evaluating the severity of focal anaerobic cerebral metabolism and predicting patient prognosis.

Barbiturates for acute traumatic brain injury.

Raised intracranial pressure (ICP) is an important complication of severe brain injury, and is associated with a high mortality rate. Barbiturates are believed to reduce intracranial pressure by suppressing cerebral metabolism, thus reducing cerebral metabolic demands and cerebral blood volume. However, barbiturates also reduce blood pressure and therefore may adversely effect cerebral perfusion pressure. To assess the effects of barbiturates in reducing raised intracranial pressure, mortality and morbidity in people with acute traumatic brain injury. To quantify any side effects resulting from the use of barbiturates. The review draws largely on the search strategy developed for the Cochrane Injuries Group as a whole. However, in addition the Cochrane Library was searched in December 1996 using the text terms "barbiturate*," "pentobarb*," "phenobarb*," "head," and "brain." An updated search was done in April 1999. Randomised or quasi randomised trials of any one or more of the barbiturate class of drugs (amobarbital, barbital, hexobarbital, mephobarbital, methohexital, murexide, pentobarbital, phenobarbital, secobarbital, thiobarbiturate) where study participants had a clinically diagnosed acute traumatic brain injury of any severity. The reviewer extracted the data and assessed the quality of allocation concealment in the trials. The pooled relative risk for death (barbiturate vs no barbiturate) was 1.09 (95%CI 0.81 to 1.47). The pooled effect of barbiturates on adverse neurological outcome, measured using the Glasgow Outcome Scale (death, persistent vegetative state or severe disability) was 1.15 (95% 0.81 to 1.64). Two studies examined the effect of barbiturate therapy on intracranial pressure. In the study by Eisenberger et al, a smaller proportion of patients in the barbiturate group had uncontrolled ICP (68% vs 83%). The relative risk for uncontrolled ICP was 0.81 (95%CI 0.62 to 1.06). Similarly, in the study by Ward et al, mean ICP was lower in the barbiturate treated group. Barbiturate therapy results in an increase in the occurrence of hypotension (RR=1.80 95%CI 1.19 to 2.70). For every four patients treated one will develop clinically significant hypotension. Mean body temperature was significantly lower in the barbiturate treated group. Schwartz et al compared pentobarbital with mannitol in the control of intracranial pressure. Pentobarbital was less effective than mannitol for control of raised ICP. 68% of patients in the pentobarbital treated group required a second drug for the treatment of raised intracranial pressure compared to 39% in the mannitol treated group (RR=1.75 95%CI 1.05 to 2.92). There was no substantial difference in mortality between the two study groups (RR=1.18 95%CI 0.73 to 1.92). There is no evidence that barbiturate therapy in patients with acute severe head injury improves outcome. Barbiturate therapy results in a fall in blood pressure in 1 in 4 treated patients. The hypotensive effect of barbiturate therapy will offset any ICP lowering effect on cerebral perfusion pressure.

Decompressive surgery in acute head injuries: where should it be performed?

In Norway, most patients with severe head injuries are transported to, and operated in, the neurosurgical unit of the regional university hospital. However, some patients are still occasionally operated on in county central hospitals by orthopedic or general surgeons who do not have neurosurgical expertise. The aim was to analyze this surgical activity outside the neurosurgical units. Data were collected from two sources: a nation-wide survey and the records of all patients with a severe head injury occurring within Vestfold county (1987-1996). The Norwegian county central hospitals perform each only 2.5 to 3 surgical evacuations of intracranial hematomas per year. In Vestfold county, a total of 161 patients were hospitalized alive with an acute severe head injury. One third of the patients (54 patients) underwent decompressive surgery, mostly evacuations of intracranial hematomas. The patients operated on in the central hospital had a significantly worse outcome than the patients who were transferred to and operated on in the neurosurgical unit of the regional hospital. Only patients with extracerebral hematomas were operated on in the central hospital. Patients with an extradural (epidural) hematoma had a better outcome than patients with an acute subdural hematoma. Based on the surgery records and preoperative and postoperative computed tomographic scans, one third of the operations (10 operations) in the central hospital were classified retrospectively as inadequate, because the hematoma was not evacuated or found or because the surgeons did not achieve control of the perioperative bleeding. The overall mortality rate was 29.8%. The present study indicates that, in Norway and countries with a similar hospital system, it must be difficult for general and orthopedic surgeons to achieve and maintain the skills required for emergency operations in patients with acute severe head injuries. Thus, it is probably to the patients' benefit to improve the general hospitals' competency and speed in the detection of candidates for surgical decompression, and stress the importance of these patients being transferred without unnecessary delay to a neurosurgical unit.

Cerebral ischemia in acute severe head injury studied by XE-CT-CBF

Cerebral ischemia in acute severe head injury studied by XE-CT-CBF

CO(2) and indomethacin vasoreactivity in patients with head injury.

The purpose of this study was to compare the effect of hyperventilation and indomethacin on cerebral circulation, metabolism and pressures in patients with acute severe head injury in order to see if indomethacin may act supplementary to hyperventilation. Fourteen severely head injured patients entered the study. Intracranial pressure (ICP), mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored continuously. Within the first four days after the trauma the CO(2) and indomethacin vasoreactivities were studied by measurements of cerebral blood flow (CBF) (Cerebrograph 10a, intravenous (133)Xe technique) and arterio-venous difference of oxygen (AVdO(2)). Ischaemia was evaluated from changes in CBF, saturation of oxygen in the jugular bulb (SvjO(2)), lactate and lactate/oxygen index (LOI). Data are presented as medians and ranges, results are significant unless otherwise indicated. Before intervention ICP was well controlled ,(14.8 (9-24) mmHg) and basic CBF level was 39.1 (21.6-75.0) ml/100 g/min). The arterio-venous oxygen differences were generally decreased (AVdO(2) = 4.3 (1.8-8.1) ml/100 ml) indicating moderate luxury perfusion. Levels of CMRO(2) were decreased (1.54 (0.7-3.2) ml/100 g/min) as well. During hyperventilation (delta PaCO(2)=0.88 (0.62-1.55) kPa) CBF decreased with 11.8 (-33.4-29.7) %/kPa and ICP decreased with 3.8 (0-10) mmHg. AVdO(2) increased 34.0 (4.0-139.2) %/kPa, MABP was unchanged, CMRO(2) and CPP increased (delta CPP = 3.9 (-10-20) mmHg). AVD (lactate) and LOI were unchanged. No correlations between CBF responses to hypocapnia and outcomes were observed. An i.v. bolus dose of indomethacin (30 mg) decreased CBF 14.7 (-16.7-57.4)% and ICP decreased 4.3 (-1-17) mmHg. AVdO(2) increased 27.8 (-40.0-66.7)%, MABP (delta MABP = 4.9 (-2-21) mmHg) and CPP (delta CPP = 8.7 (3-29) mmHg) increased while CMRO2 was unchanged. No changes in AVd (lactate) and LOI indicating cerebral ischaemia were found. Compared to hyperventilation (changes per 1 kPa, at PaCO(2) level = 4.05 kPa) the changes in MABP, CPP and CBF were significantly greater after indomethacin, while the changes in AVdO(2), ICP, SvjO(2) and LOI were of the same order of magnitude. No correlation between relative reactivities to indomethacin and CO(2), evaluated from changes in CBF and AVdO(2), or between the decrease in ICP after the two procedures were found. Thus, some patients reacted to indomethacin but not to hyperventilation, and vice versa. These results suggest that indomethacin and hyperventilation might act independently, or in a complementary fashion in the treatment of patients with severe head injury.