thiopental and Brain-Injuries

Thiopental is a barbiturate used in traumatic brain injuries (TBIs) to reduce intracranial pressure (ICP) and to manage cerebral ischemia. As thiopental follows Michaelis-Menten kinetics, therapeutic drug monitoring (TDM) has been used in practice to improve efficacy and reduce adverse effects. However, its role is still debatable, and TDM is not widely practiced. Current evidence suggests that thiopental therapy may improve mortality and functional outcome in a subpopulation of patients with severe TBI with elevated ICP refractory to conventional medical therapy. Several analytical methods are available to quantify thiopental concentrations. This review uses a previously published 9-step decision-making algorithm to determine whether TDM of thiopental in TBI is warranted. There seems to be poor correlation between thiopental concentration and pharmacological response in terms of neurological response, ICP, electroencephalography, and drug toxicity. There is no established therapeutic range for thiopental continuous infusion due to a wide range of plasma concentrations corresponding to efficacy (25-50 mg/L) and toxicity (30-70 mg/L) and the resulting overlap between the 2. Thiopental exhibits intrapatient and interpatient variability due to age, obesity, renal and hepatic dysfunction, Michaelis-Menten kinetics, and hepatic enzyme autoinduction. Available evidence suggests that TDM of thiopental continuous infusion is not beneficial in improving efficacy or avoiding toxicity. There are however 2 possible scenarios in which TDM may provide additional information to sound clinical judgment. The first is providing patient-specific plasma target concentration to guide titration of therapy. The second scenario is differentiating between brain death and barbiturate-induced coma.

Topics: Age Factors; Brain Injuries; Clinical Trials as Topic; Coma; Critical Care; Decision Support Techniques; Drug Monitoring; Electroencephalography; GABA Modulators; Humans; Infusions, Intravenous; Intracranial Pressure; Thiopental

Transcranial Doppler and, if possible, measurement of intracranial pressure (ICP) allow preoperative diagnosis of acute intracranial hypertension (ICH) after brain trauma. The main goal of the anaesthesiologist is to prevent the occurrence of secondary brain injuries and to avoid cerebral ischaemia. Treatment of high ICP is mainly achieved with osmotherapy. High-dose mannitol administration (1.4 to 2 g/kg given in bolus doses) may be considered a better option than conventional doses, especially before emergency evacuation of a cerebral mass lesion. Hypertonic saline seems as effective as mannitol without rebound effect and without diuresis increase. Haemostasis should be normalized before neurosurgery and invasive blood pressure monitoring is mandatory. For anaesthesia induction, thiopental or etomidate may be used. In case of ICH, halogenated and nitrous oxide should be avoided. Until the dura is open, mean arterial pressure should be maintained around 90 mmHg (or cerebral perfusion pressure around 70 mmHg). If a long-lasting (several hours) extracranial surgery is necessary, ICP should be monitored and treatment of ICH should have been instituted before.

Topics: Acute Disease; Anesthesia, General; Blood Pressure; Brain Injuries; Brain Ischemia; Case Management; Combined Modality Therapy; Comorbidity; Contraindications; Diuretics, Osmotic; Etomidate; Humans; Hyperventilation; Intracranial Hypertension; Jugular Veins; Mannitol; Monitoring, Intraoperative; Monitoring, Physiologic; Nitrous Oxide; Oxygen; Preoperative Care; Saline Solution, Hypertonic; Thiopental; Tomography, X-Ray Computed; Ultrasonography, Doppler, Transcranial; Wounds and Injuries

A number of clinical studies have reported poor clinical outcomes for patients treated with barbiturate therapy in acute neurological and neurosurgical emergencies. Barbiturate therapy, as currently practised with thiopentone and pentobarbitone at least, is also associated with a prolonged post-infusion period of clinical unresponsiveness. Hence, the popularity of barbiturate therapy for sedation of critically ill neurological and neurosurgical patients has declined over the past decade. A retrospective study of traumatic brain injury patients treated at the Royal North Shore Hospital, Sydney, with high-dose thiopentone therapy between 1987 and 1997 has found disappointing results with a 1-month mortality outcome of 50% (14 of 28 patients). Nevertheless, barbiturate therapy remains a consideration for patients with severe cranial trauma in whom preferred treatments have failed to control intracranial or cerebral perfusion pressures. More favourable results ( approximately 10% 1-month mortality rate) were encountered for patients with refractory vasospasm complicating subarachnoid haemorrhage or intracerebral haemorrhage complicating supratentorial arteriovenous malformation resection. A well designed, prospective and randomised controlled trial may be of value in further determining the role of barbiturate therapy in acute neurovascular emergencies refractory to standard therapy.

Topics: Barbiturates; Brain Injuries; Craniocerebral Trauma; Emergencies; Humans; Hypnotics and Sedatives; Intracranial Pressure; Neurosurgery; Randomized Controlled Trials as Topic; Retrospective Studies; Status Epilepticus; Thiopental; Treatment Outcome; Vasospasm, Intracranial

The purpose of this research utilization article is to familiarize cardiovascular nurses with the Brain Resuscitation Clinical Trials (BRCTs) I and II and discuss the application of these trials to nursing practice. The BRCTs are a series of studies that examine the effects of selected interventions on neurologic outcome after cardiac arrest.

Topics: Brain Injuries; Calcium Channel Blockers; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Hypnotics and Sedatives; Lidoflazine; Thiopental; Trauma Severity Indices; Vasodilator Agents

Thiopental is a thiobarbiturate given in the case of brain injuries to reduce intracranial pressure and to manage cerebral ischemia. A pharmacokinetic model has been described previously in critically ill patients with a different therapeutic strategy. New treatment options prompted us to investigate if drug-drug interactions occur. A new model is proposed describing the influence of concomitant administration of esomeprazole on the distribution of thiopental.. The study population comprised 52 critically ill patients (body weight 47.1-114 kg) aged 18-78 years who had been admitted into the critical care unit for treatment of intracranial hypertension. A total mean dose of 282.8 ± 172.7 mg/kg was given in 96 ± 72 h. Pharmacokinetic analysis was performed by using a nonlinear mixed-effect population model.. A one-compartment open model with first-order elimination identified two covariates, namely, body weight on clearance and volume of distribution, and the administration of esomeprazole on volume of distribution. The mean values (% relative standard error) for total clearance (CL) and for central volume of distribution (Vd) in patients with and without concomitant esomeprazole were 5.3 L/h (9.2 %) and 256.1 (6.4 %) and 153.2 l (19.2 %), respectively.. Based on these results, we conclude that concomitant administration of esomeprazole increases the volume of distribution and the half-live of thiopental. This drug-drug interaction should be considered when a target concentration has to be reached.

Topics: Adolescent; Adult; Aged; Anti-Ulcer Agents; Brain Injuries; Critical Illness; Drug Interactions; Esomeprazole; Female; Humans; Hypnotics and Sedatives; Male; Middle Aged; Models, Biological; Proton Pump Inhibitors; Thiopental; Young Adult

Experimental research has demonstrated that the level of neuroprotection conferred by the various barbiturates is not equal. Until now no controlled studies have been conducted to compare their effectiveness, even though the Brain Trauma Foundation Guidelines recommend that such studies be undertaken. The objectives of the present study were to assess the effectiveness of pentobarbital and thiopental in terms of controlling refractory intracranial hypertension in patients with severe traumatic brain injury, and to evaluate the adverse effects of treatment.. This was a prospective, randomized, cohort study comparing two treatments: pentobarbital and thiopental. Patients who had suffered a severe traumatic brain injury (Glasgow Coma Scale score after resuscitation < or = 8 points or neurological deterioration during the first week after trauma) and with refractory intracranial hypertension (intracranial pressure > 20 mmHg) first-tier measures, in accordance with the Brain Trauma Foundation Guidelines.. A total of 44 patients (22 in each group) were included over a 5-year period. There were no statistically significant differences in ' baseline characteristics, except for admission computed cranial tomography characteristics, using the Traumatic Coma Data Bank classification. Uncontrollable intracranial pressure occurred in 11 patients (50%) in the thiopental treatment group and in 18 patients (82%) in the pentobarbital group (P = 0.03). Under logistic regression analysis--undertaken in an effort to adjust for the cranial tomography characteristics, which were unfavourable for pentobarbital--thiopental was more effective than pentobarbital in terms of controlling intracranial pressure (odds ratio = 5.1, 95% confidence interval 1.2 to 21.9; P = 0.027). There were no significant differences between the two groups with respect to the incidence of arterial hypotension or infection.. Thiopental appeared to be more effective than pentobarbital in controlling intracranial hypertension refractory to first-tier measures. These findings should be interpreted with caution because of the imbalance in cranial tomography characteristics and the different dosages employed in the two arms of the study. The incidence of adverse effects was similar in both groups.. (Trial registration: US Clinical Trials registry NCT00622570.).

Topics: Adolescent; Adult; Aged; Brain Injuries; Cohort Studies; Female; Humans; Intracranial Hypertension; Male; Middle Aged; Pentobarbital; Prospective Studies; Thiopental; Treatment Outcome; Young Adult

To study outcome from severe head injury (SHI: GCS < or = 8) and to investigate impact of prehospital factors and clinical intensive care parameters on outcome. To compare with former study results (1980-88) of our clinical setting.. Retrospectively, the history of 228 patients with SHI treated between 1988 and 1995 was looked into. The outcome was measured with the Glasgow Outcome Scale (GOS) post intensive care (median 9, min-max 2-77 days) and 6 months after trauma by a questionnaire. The GOS was related to age, Glasgow Coma Scale (GCS on the scene), prehospital hypotension and hypoxia (HH), intracranial pressure (ICP), cerebral perfusion pressure (CPP), intensive therapy including Tromethamine and/or Thiopentone. The rate of infections was determined.. Increasing age influences outcome negatively. Prehospital GCS and HH were significantly correlated with outcome. GOS of 30 patients with HH: GOS 1: 53%, GOS 2 + 3: 27%, GOS 4 + 5: 20%. GOS of 40 patients without HH: GOS 1: 25%, GOS 2 + 3: 10%, GOS 4 + 5: 65%. During intensive care the level of CPP (not ICP) as well as tromethamine and/or thiopentone treatment for control of elevated ICP were significantly correlated with outcome. Mortality rate in 32 patients with CPP < 50 mmHq was 69%, in 29 patients with CPP > 50 mmHg only 20%. Patients treated additionally with Tromethamine and Thiopentone because of uncontrollable intracranial hypertension showed a significantly worse outcome: GOS 1: 66%, GOS 2 + 3: 6%, GOS 4 + 5: 28%, compared to those who needed neither Tromethamine nor Thiopentone: GOS 1: 27%, GOS 2 + 3: 18%, GOS 4 + 5: 55%. Thiopentone treatment was not associated with an increased rate of pulmonary and other infections. In comparison to our former outcome study, covering the years 1980-88, we have not seen any improvements in outcome, despite modifications in intensive care protocols.. Prehospital hypotension and hypoxia have a significant negative impact on outcome by causing secondary brain damage. Despite various modifications in intensive care therapy an unchanged portion of secondary brain damage will not prove treatable. Therefore, prevention or early aggressive treatment of hypotension and hypoxia is the most promising way of improving outcome after severe head injury at the moment.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Brain Injuries; Child; Child, Preschool; Critical Care; Female; GABA Modulators; Glasgow Coma Scale; Humans; Infant; Intracranial Hypertension; Male; Middle Aged; Retrospective Studies; Risk Factors; Skull; Thiopental; Treatment Outcome; Tromethamine

Increased extracellular glutamate levels are related to glial and neuronal damage. Glutamate-mediated toxicity is limited by glial uptake and metabolic transformation of glutamate to glutamine and the energetic compounds alanine and lactate which are utilized by surrounding neurons. Under in vitro conditions, barbiturates have been shown to reduce glutamate uptake and its further metabolism, possibly impeding metabolic coupling between astrocytes and neurons. The aims were to investigate if under clinical conditions, the barbiturate thiopental reduces important detoxification of glutamate, resulting in lower CSF glutamine, alanine and lactate levels as opposed to patients receiving midazolam. During long-term administration of thiopental and midazolam, pathologically elevated ventricular CSF glutamate levels were associated with significantly increased glutamine and alanine levels up to 14 days after trauma. CSF lactate, however, remained normal. These data suggest that long-term administration of thiopental and midazolam under clinical conditions does not impede enzymatic activities responsible for detoxification and metabolism of glutamate.

Topics: Adolescent; Adult; Aged; Alanine; Brain Injuries; Cerebral Ventricles; Glutamic Acid; Glutamine; Humans; Hypnotics and Sedatives; Lactates; Midazolam; Middle Aged; Serine; Thiopental

Brain-injured patients are susceptible to secondary brain damage related to decreased cerebral perfusion pressure associated with edema formation and increased intracranial pressure (ICP). Whenever conventional therapy fails to reduce elevated ICP, barbiturate coma represents an additional intervention that may control ICP. In patients suffering from severe traumatic brain injury, cerebrospinal fluid levels of glutamate, hypoxanthine, and lactate were measured during barbiturate coma and correlated to electroencephalographic recordings and ICP.. Prospective, descriptive study.. Ten-bed surgical intensive care unit in a university hospital.. Twenty-one patients with severe traumatic brain injury (Glasgow Coma Scale score < or = 9); 11 required barbiturate coma because of refractory intracranial hypertension, and 10 were manageable with continuous administration of fentanyl and midazolam.. Thiopental was administered continuously for increased ICP within the first 24 hrs after trauma and adjusted to the burst-suppression pattern (four to six bursts per minute) on continuous electroencephalographic monitoring.. Glutamate and hypoxanthine were analyzed using high-performance liquid chromatography, whereas lactate was measured enzymatically. Patients requiring thiopental presented with significantly higher ICP, glutamate, and hypoxanthine levels than patients receiving fentanyl and midazolam (p < .05). Within the first 24 hrs, thiopental significantly reduced cerebrospinal fluid glutamate and hypoxanthine levels in all patients, i.e., the burst-suppression pattern was successfully induced (p < .001). Interestingly, in five patients cerebrospinal fluid glutamate increased to initial values again despite unchanged neuronal activity. In these patients, ICP, hypoxanthine, and lactate remained significantly elevated compared with the six patients with steadily decreasing cerebrospinal fluid glutamate, hypoxanthine, lactate, and ICP values (p < .02).. Barbiturate coma does not unequivocally preserve energetic stability despite successful suppression of neuronal activity. Despite the use of barbiturate coma in patients with refractory intracranial hypertension, persistent release or impaired uptake of glutamate may be associated with continuous anaerobic metabolism, as shown by increases in cerebrospinal fluid hypoxanthine and lactate levels.

Topics: Adolescent; Adult; Biomarkers; Brain Injuries; Electroencephalography; Female; Glutamic Acid; Humans; Hypnotics and Sedatives; Hypoxanthine; Intracranial Hypertension; Intracranial Pressure; Lactic Acid; Male; Middle Aged; Prospective Studies; Statistics, Nonparametric; Thiopental

Barbiturate coma is initiated in brain-injured patients whenever elevated intracranial pressure remains unresponsive to other therapeutical strategies. However, barbiturates alter cortical activity resulting in difficulties in clinical evaluation. Therefore, we investigated the impact of long-term thiopental administration on responsiveness to exteroceptive stimuli in relation to pharmacokinetics of thiopental in CSF and serum. Long-term infusion increases thiopental levels which remain elevated for 6 and 9 days in CSF and serum, respectively, after termination of its administration. Prolonged unresponsiveness to exteroceptive stimuli correlates with persisting thiopental in CSF and serum. Thus, quantitative analysis of thiopental in serum becomes indispensable in predicting the length of drug-induced neurological impairment and in avoiding misinterpretation of the neurological status.

Topics: Adolescent; Adult; Brain Injuries; Critical Care; Electroencephalography; Female; Humans; Hypnotics and Sedatives; Infusions, Intravenous; Intracranial Pressure; Male; Middle Aged; Thiopental; Time Factors

Barbiturate coma is employed in brain-injured patients whenever increases in intracranial pressure remain unresponsive to less aggressive therapeutic regimens. Barbiturate-mediated neuroprotection, however, is weakened by an increased infection rate related to barbiturate-induced immunosuppression. Co-administration of barbiturates with antibiotics known to induce bone marrow suppression could, in turn, potentiate barbiturate-mediated immunosuppression. Adverse drug reactions and interactions of thiopental with antibiotics in terms of leukopenia, infection rate, and bone marrow suppression were investigated.. White blood cells were measured daily, tracheobronchial secretion and urine were examined for bacterial growth twice a week or if an infection was suspected.. A total of 52 patients with severe isolated head injury were consecutively investigated. Due to increased intracranial pressure (ICP), which did not respond to analgosedation, barbiturate coma was performed in 23 cases. The other 29 patients remained analgosedated. Leukocytes and neutrophils were reversibly and significantly decreased in all patients, mostly sustained under thiopental. The pulmonary infection rate due to gram-negative organisms was nearly doubled during barbiturate coma. Reversible agranulocytosis and bone marrow suppression attributed to antibiotics developed in six patients after thiopental administration. Mortality rate, however, was not increased by these adverse effects.. Barbiturate coma may cause reversible leukopenia and an increased infection rate. Long-term administration of thiopental may also promote reversible antibiotic-induced bone marrow suppression. The mechanisms and site of interaction between thiopental and antibiotics cannot be assessed by the present study and remain to be clarified. However, during and after barbiturate coma, close monitoring of leukocytes and infections and careful selection of antibiotics is required.

Topics: Adult; Aged; Agranulocytosis; Alkyl and Aryl Transferases; Anti-Bacterial Agents; Bone Marrow; Brain Injuries; Coma; Critical Care; Female; Gram-Negative Bacterial Infections; Humans; Hypnotics and Sedatives; Immunosuppression Therapy; Leukopenia; Lung Diseases; Male; Middle Aged; Mitochondria, Liver; Neutrophils; Prospective Studies; Thiopental

This study was conducted on 10 pediatric patients in whom intracranial hypertension stemming from head injury was reduced by high-dose thiopental administered for a prolonged period. All children showed a favorable recovery of their neurological functions. The total dose normalized to body weight averaged 335 +/- 135 mg/kg, and the mean treatment duration was 93.0 +/- 37.1 h. Data analysis was modeled for each patient to cover all the doses on the whole plasma thiopental concentration-time curve, according to a one-compartment open model. A better fit was obtained using a linear model rather than a Michaelis-Menten elimination model. Model selection was guided by evaluation of the minimum objective function, the weighted residuals, and the Akaike criterion. Thiopental pharmacokinetic parameters in pediatric patients were compared with those determined in an adult control group with similar total doses and durations of treatment. No significant difference was found between the two groups in spite of a 33% decrease of the elimination half-life in children (11.7 +/- 5.7 h) compared with adults (17.5 +/- 9.03 h). The mean values obtained were 2.42 and 2.19 ml/min/kg for total clearance and 2.18 and 2.90 L/kg for Vd in pediatric and adult groups, respectively. The linear regression of pharmacokinetic parameters in terms of age was not significant. When high doses of thiopental were administered over a prolonged period, the pharmacokinetic parameters computed for pediatric patients did not differ from those obtained in adults.

Topics: Adolescent; Adult; Brain Injuries; Child; Child, Preschool; Female; Humans; Hypnotics and Sedatives; Intracranial Pressure; Male; Thiopental

Treatment resistant intracranial hypertension after severe head injury has a very high mortality with conventional therapy such as hyperventilation and mannitol infusions. In this report, we describe the use of large doses of thiopental as a means of treating such swelling. From a consecutive series of 107 severe head injuries with a Glasgow Coma Score (GCS) of 6 or below, we selected all patients below 40 years age with a progressive increase in intracranial pressure (ICP) to 40 mm Hg. The first 16 patients (mean age 20 years, mean GCS 4.3) were treated with deep barbiturate coma and hypothermia (32-35 degrees Celsius) until stable lowering of ICP was achieved. The next 15 patients received conventional intensive care and were in other respects very similar to the barbiturate group (mean age 26, mean GCS 5.2). After 9-12 months the outcome was classified according to the Glasgow Outcome Scale (GOS). Therapy with barbiturate coma resulted in 6 good/moderate outcomes, 3 severe and 7 dead/vegetative. Conventional treatment resulted in 2 good/moderate outcomes and 13 dead/vegetative. This is a highly significant difference and cannot easily be explained by more severe injuries or complications in the conventional group. Superior control of ICP was achieved by large doses of thiopental and the final outcome was better.

Topics: Adolescent; Adult; Brain Concussion; Brain Edema; Brain Injuries; Child; Child, Preschool; Clinical Trials as Topic; Dose-Response Relationship, Drug; Hematoma, Subdural; Humans; Intracranial Pressure; Prognosis; Pseudotumor Cerebri; Thiopental

Topics: Brain Injuries; Fentanyl; Humans; Intracranial Pressure; Intubation, Intratracheal; Lidocaine; Random Allocation; Succinylcholine; Suction; Thiopental

Intracranial pressure (ICP), arterial blood pressure (BP) and the calculated cerebral perfusion pressure (CPP) were investigated under standard conditions in 14 patients with severe brain injury. The influence of etomidate 0.3 mg/kg in comparison with thiopentone 6.0 mg/mg was evaluated both in patients with primarily elevated ICP (group I) and with an increase of ICP produced by nitrous oxide in oxygen (group II). In both groups of patients a marked ICP reduction (42%/26%) was produced by etomidate as well as by thiopentone. Whereas the reduction of CPP caused by thiopentone was enhanced by a moderate fall in BP, no influence on either BP or CPP was observed with etomidate. A regular fall in BP by about 10-15% was observed under nitrous oxide in oxygen alone, subsequently reducing the CPP by about 25%. These results emphasize the importance of the actions and interactions of different combinations of anesthetics in patients with acute brain injury in the prevention of further brain ischaemia. We believe that etomidate like thiopentone has brain protective properties in patients with cerebral hypoxia and must therefore be considered as an important therapeutic agent in such patients.

Topics: Blood Pressure; Brain Injuries; Brain Ischemia; Etomidate; Humans; Imidazoles; Intracranial Pressure; Nitrous Oxide; Thiopental

Ischemic and traumatic brain injury is associated with increased risk for death and disability. The inhibition of penumbral tissue damage has been recognized as a target for therapeutic intervention, because cellular injury evolves progressively upon ATP-depletion and loss of ion homeostasis. In patients, thiopental is used to treat refractory intracranial hypertension by reducing intracranial pressure and cerebral metabolic demands; however, therapeutic benefits of thiopental-treatment are controversially discussed. In the present study we identified fundamental neuroprotective molecular mechanisms mediated by thiopental. Here we show that thiopental inhibits global protein synthesis, which preserves the intracellular energy metabolite content in oxygen-deprived human neuronal SK-N-SH cells or primary mouse cortical neurons and thus ameliorates hypoxic cell damage. Sensitivity to hypoxic damage was restored by pharmacologic repression of eukaryotic elongation factor 2 kinase. Translational inhibition was mediated by calcium influx, activation of the AMP-activated protein kinase, and inhibitory phosphorylation of eukaryotic elongation factor 2. Our results explain the reduction of cerebral metabolic demands during thiopental treatment. Cycloheximide also protected neurons from hypoxic cell death, indicating that translational inhibitors may generally reduce secondary brain injury. In conclusion our study demonstrates that therapeutic inhibition of global protein synthesis protects neurons from hypoxic damage by preserving energy balance in oxygen-deprived cells. Molecular evidence for thiopental-mediated neuroprotection favours a positive clinical evaluation of barbiturate treatment. The chemical structure of thiopental could represent a pharmacologically relevant scaffold for the development of new organ-protective compounds to ameliorate tissue damage when oxygen availability is limited.

Topics: Animals; Brain Injuries; Brain Ischemia; Cell Death; Cell Hypoxia; Cell Line; Elongation Factor 2 Kinase; Humans; Hypnotics and Sedatives; Mice; Neurons; Oxygen; Peptide Elongation Factor 2; Protein Biosynthesis; Thiopental

To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality.. Retrospective chart and imaging review.. Children's Hospital, level 1 trauma center.. Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and <18 yr) with severe traumatic brain injury (presedation Glasgow Coma Scale ≤ 8 and head Maximum Abbreviated Injury Scale ≥ 4) that developed acute central diabetes insipidus between January 2000 and December 2011.. Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p < 0.001), as were a lower presedation Glasgow Coma Scale (p = 0.03), a lower motor Glasgow Coma Scale (p = 0.01), an occurrence of fixed pupils (p = 0.04), and a prolonged partial thromboplastin time (p = 0.04). Cerebral edema on the initial computed tomography, obtained in the first 24 hrs after injury, was the only imaging finding associated with death (p = 0.002). Survivors of central diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04).. The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.

Topics: Adolescent; Antidiuretic Agents; Brain Edema; Brain Injuries; Child; Child, Preschool; Coma; Deamino Arginine Vasopressin; Decompressive Craniectomy; Diabetes Insipidus, Neurogenic; Female; Glasgow Coma Scale; Humans; Hypnotics and Sedatives; Incidence; Intracranial Hypertension; Intracranial Pressure; Male; Monitoring, Physiologic; Partial Thromboplastin Time; Pupil Disorders; Radiography; Retrospective Studies; Thiopental; Time Factors

There have been case reports of hypokalaemia and hyperkalaemia on induction and cessation of thiopentone barbiturate coma for refractory intracranial hypertension, respectively. However, the incidence and characteristics are not well described.. We performed a retrospective review of all patients who received thiopentone barbiturate therapy for refractory intracranial hypertension during an 18-month period from January 2004 to June 2005 in our neurosurgical intensive care unit (ICU).. During this time period, 47 patients received thiopentone barbiturate therapy for refractory intracranial hypertension. Forty-two (89.4%) patients developed hypokalaemia after induction of barbiturate therapy. The median time to onset of hypokalaemia was 11 (6-23) h and time to nadir of serum potassium levels was 25 (15-41) h. Sixteen (34%) patients developed hyperkalaemia on weaning of barbiturate therapy. The peak serum potassium levels developed 31 (28-56) h after cessation. All patients who developed hyperkalaemia had been hypokalaemic previously. The mean potassium replaced during hypokalaemia was higher in patients who developed hyperkalaemia compared to those who did not (230 ± 135 vs. 66 ± 70, p < 0.001).. Hypokalaemia and hyperkalaemia are frequently associated with induction and cessation of thiopentone barbiturate coma. Serum potassium levels must be monitored vigilantly. Patients who develop hypokalaemia and receive large potassium replacement may be at greater risk of hyperkalaemia on cessation.

Topics: Anesthetics, Intravenous; Brain Injuries; Coma; Female; Humans; Hyperkalemia; Hypokalemia; Intensive Care Units; Intracranial Hypertension; Male; Middle Aged; Monitoring, Physiologic; Potassium; Retrospective Studies; Thiopental

Severe disturbance of potassium balance is a rare but life-threatening complication of therapeutic barbiturate coma. A 14-yr-old patient was treated with a thiopental infusion for management of increased intracranial pressure after severe head injury. The patient had persistent hypokalaemia during the thiopental infusion. On cessation of the infusion the patient rapidly developed a tachydysrhythmia associated with a serum K+ of 7.0. Possible mechanisms of this phenomenon are discussed. We conclude that aggressive treatment of hypokalaemia during barbiturate coma should be avoided, and advocate a tapering dose of thiopental and not abrupt cessation of an infusion. Severe disturbance of plasma potassium balance is a rare but life-threatening complication of therapeutic barbiturate coma. Awareness of this complication should be raised and management altered to less aggressive treatment of hypokalaemia occurring during thiopental infusion, with a tapering dose used on discontinuation to limit a rebound phenomenon.

Topics: Accidents, Traffic; Adolescent; Brain Death; Brain Injuries; Coma; Critical Care; Fatal Outcome; Female; Glasgow Coma Scale; Humans; Hyperkalemia; Hypnotics and Sedatives; Hypokalemia; Intracranial Pressure; Thiopental

To quantify the occurrence of high intracranial pressure (HICP) refractory to conventional medical therapy after traumatic brain injury (TBI) and to describe the use of more aggressive therapies (profound hyperventilation, barbiturates, decompressive craniectomy).. Prospective study of 407 consecutive TBI patients. Three neurosurgical intensive care units (ICU).. Intracranial pressure (ICP) was studied during the first week after TBI; 153 patients had at least 1 day of ICP>20 mmHg. Early surgery was necessary for 221 cases, and standard medical therapy [sedation, mannitol, cerebrospinal fluid (CSF) withdrawal, PaCO2 30-35 mmHg] was used in 135 patients. Reinforced treatment (PaCO2 25-29 mmHg, induced arterial hypertension, muscle relaxants) was used in 179 cases (44%), and second-tier therapies in 80 (20%). Surgical decompression and/or barbiturates were used in 28 of 407 cases (7%). Six-month outcome was recorded in 367 cases using the Glasgow outcome scale (GOS). The outcome was favorable (good recovery or moderate disability) in 195 cases (53%) and unfavorable (all the other categories) in 172 (47%). HICP was associated with worse outcome. Outcome for cases who had received second-tier therapies was significantly worse (43% favorable at 6 months, p=0.03).. HICP is frequent and is associated with worse outcome. ICP was controlled by early surgery and first-tier therapies in the majority of cases. Profound hyperventilation, surgical decompression and barbiturates were used in various combinations in a minority of cases. The indications for surgical decompression and/or barbiturates seem restricted to less than 10% of severe TBI.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Brain Injuries; Combined Modality Therapy; Craniotomy; Decompression, Surgical; Female; Glasgow Outcome Scale; Humans; Intensive Care Units; Intracranial Hypertension; Male; Middle Aged; Prospective Studies; Respiration, Artificial; Thiopental; Treatment Outcome

Controversy and speculation exist regarding intracranial pressure (ICP) changes produced by various combinations of rapid sequence intubation (RSI) agents. In this pilot study, we sought to develop a swine model to investigate these changes in classic RSI.. Eight adult swine were instrumented with arterial and intracranial pressure monitors. Four different versions of rapid sequence intubation were then performed sequentially in each animal in a crossover trial design: regimen 1, thiopental; regimen 2, thiopental and succinylcholine; regimen 3, lidocaine, thiopental, and succinylcholine; and regimen 4, pancuronium, lidocaine, thiopental, and succinylcholine. ICP and hemodynamic parameters were recorded and compared. Trials were excluded from analysis if baseline ICP measurements were unstable or if intubation was difficult.. Peak changes in ICP were noted at 2 to 3 minutes after administration of induction agents. Mean values for peak changes in ICP were as follows: regimen 1 (n = 5), 3.6 mm Hg (95% confidence interval [CI], 1.0-6.2 mm Hg); regimen 2 (n = 9), 13.6 mm Hg (95% CI, 9.6-17.6 mm Hg); regimen 3 (n = 2), 16.0 mm Hg (95% CI, -34.8-66.8 mm Hg); and regimen 4 (n = 3), 12.0 mm Hg (95% CI, -8.3-32.3 mm Hg).. The model is effective. It enables investigators to examine the aggregate ICP effects of combinations of RSI medications. RSI regimens with paralysis produced threefold increases in peak ICP change compared with the sedation-only regimen. Pretreatment agents did not affect ICP changes. Future investigations can examine other agents and add experimental manipulation of ICP to simulate head injury physiology. Additional parameters including cerebral metabolism and/or oxygenation may also be explored.

Topics: Animals; Brain Injuries; Cross-Over Studies; Disease Models, Animal; Emergency Treatment; Intracranial Pressure; Intubation, Intratracheal; Lidocaine; Pancuronium; Pilot Projects; Succinylcholine; Swine; Thiopental

Topics: Adult; Anesthesia, Intravenous; Brain Injuries; Electroencephalography; Evoked Potentials, Somatosensory; Female; Follow-Up Studies; Humans; Thiopental; Treatment Outcome

To report the occurrence of life-threatening hyperkalaemia following treatment with therapeutic thiopentone coma.. The neurosurgical intensive care units of Royal North Shore Hospital and Liverpool Hospital, Sydney, Australia.. Three patients treated with theraputic thiopentone coma. One patient with raised intracranial pressure secondary to a severe traumatic brain injury and two patients with refractory vasospasm secondary to subarachnoid haemorrhage. Two of the three patients developed hypokalaemia on starting thiopentone, which was resistant to potassium supplementation. All three patients developed severe hyperkalaemia during the recovery phase of coma. This was life-threatening in all three patients and fatal in one.. Severe hypokalaemia refractory to potassium therapy may occur during therapeutic thiopentone coma. Severe rebound hyperkalaemia may occur after cessation of thiopentone infusion. Protocols for the management of patients with therapeutic barbiturate coma should recognise this potentially serious complication.

Topics: Adult; Australia; Brain Injuries; Coma; Critical Illness; Female; Glasgow Coma Scale; Humans; Hyperkalemia; Hypnotics and Sedatives; Male; Middle Aged; Subarachnoid Hemorrhage; Thiopental; Treatment Outcome

Serial serum thiopentone concentrations were measured during and following completion of an intravenous infusion of thiopentone in 20 patients with neurosurgical emergencies. The concentration data from a further 55 patients who had had some such measurements were reviewed retrospectively. The patients received an infusion for longer than 24 hours at a rate adjusted to maintain EEG burst suppression. The data were interpreted in terms of thiopentone pharmacokinetics and used to produce statistical models relating to clinical outcomes. In these patients, the one-month mortality rate following commencement of thiopentone treatment was 20%; the mean durations of pupillary and motor unresponsiveness following cessation of an infusion were 22 and 91 hours, respectively. Predictors of a prolonged duration of motor unresponsiveness included a prolonged duration of pupillary unresponsiveness, a low thiopentone clearance and a high maximum serum concentration of thiopentone. From pooled logistic regression, median effective serum thiopentone concentrations (EC50) were found to be 50 mg x l(-1) for recovery of pupillary responsiveness and 12 mg x l(-1) for the recovery of motor responsiveness. Because prolonged high-dose thiopentone leads to prolonged residual serum concentrations, it is difficult to distinguish the residual pharmacological effects of thiopentone from the clinical condition. This study suggests that, based on EC50 values for responses, monitoring of post-infusion serum thiopentone concentrations may help determine whether a patient's clinical state is due to residual thiopentone pharmacological effects.

Topics: Adult; Brain Injuries; Cerebrovascular Disorders; Chromatography, High Pressure Liquid; Drug Monitoring; Electroencephalography; Emergencies; Female; Humans; Hypnotics and Sedatives; Infusions, Intravenous; Intracranial Hypertension; Intracranial Pressure; Logistic Models; Male; Middle Aged; Muscle Contraction; Neuroprotective Agents; Prospective Studies; Reflex, Pupillary; Retrospective Studies; Thiopental

Hypothermic circulatory arrest is a standard procedure for the treatment of aortic arch. However, there is a time limit for this procedure. There is now an urgent need to develop prophylactic measures to extend the time limit. We have used a pharmacological mixture of thiopental, nicardipine and mannitol for all patients undergoing circulatory arrest since 1991 to extend the safe limit. The purpose of this study was to analyze the neurological complications demonstrated by these patients and to evaluate the brain-protective effects of our measure.. The clinical records of 75 consecutive patients undergoing an aortic arch repair using a hypothermic circulatory arrest technique during the past 8 years were retrospectively reviewed. Systemic cooling was continued until a total disappearance of EEG activity. Prior to circulatory arrest, 15 or 30 mg/kg of thiopental, 20 mg of nicardipine and 300 ml of mannitol were infused into the venous reservoir of a cardiopulmonary bypass circuit. Graft replacement was performed in all patients and the extent of replacement was a total aortic arch in 43 patients, a distal aortic arch in 17, a hemiarch in 13 and a distal aortic arch and a total descending aorta in two.. The duration of circulatory arrest ranged from 16 to 80 min (mean 41.5 min), and it exceeded 45 min in 37 patients. Operative mortality was 10.7% and two patients died of stroke. Three patients had permanent and three other patients had transient neural deficits. The incidence of stroke was 8.0% as a whole, and no correlation between the incidence of neurological complications and the duration of circulatory arrest was found. A multivariate analysis showed that the duration of circulatory arrest was determined as a predictor of neither operative mortality nor postoperative stroke.. The findings of the present study suggest that our pharmacological brain protection appears to be effective for safely extending hypothermic circulatory arrest.

Topics: Adult; Aged; Aged, 80 and over; Aortic Aneurysm, Thoracic; Aortic Dissection; Aortic Rupture; Blood Vessel Prosthesis Implantation; Brain Injuries; Cardiopulmonary Bypass; Cause of Death; Diuretics, Osmotic; Drug Therapy, Combination; Electroencephalography; Humans; Hypnotics and Sedatives; Hypothermia, Induced; Mannitol; Middle Aged; Monitoring, Intraoperative; Nicardipine; Retrospective Studies; Thiopental; Time Factors; Treatment Outcome; Vasodilator Agents

Clinical strategy to maximize effectiveness and to minimize adverse influences remains to be determined for mild hypothermia therapy for traumatic brain injury. This study was conducted to evaluate the clinical feasibility of the titration method of mild hypothermia in severely head-injured patients in whom a reduction in intracranial pressure was regarded as the target effect.. Nine consecutive patients with severe head injury were studied. Patient age ranged between 18 and 66 years, Glasgow Coma Scale scores were equal to or less than 8, and intracranial pressures were equal to or greater than 20 mm Hg despite removal of intracranial hematoma and drugs, including glycerol and thiopental. During a maximum of 6 days of hypothermia therapy, jugular venous blood or cerebrospinal fluid temperature was titrated to reduce intracranial pressure to less than 20 mm Hg by means of repeated intragastric cooling with our nasoduodenal tube and surface cooling. The feasibility and the effects on systemic complications of this titration method of mild hypothermia were evaluated.. Intracranial pressure variably decreased from before to 3 hours after the beginning of all procedures of cooling. The mean intracranial pressure significantly decreased from 24 to 15 mm Hg with cooling, while temperature reduced an average of 2.0 degrees C. Four patients had systemic infection complications. Increased C-reactive protein and decreased platelet count were observed in all patients during hypothermia. The incidence of good recovery and moderate disability according to the Glasgow Outcome Scale was seven of nine patients.. The titration method of mild hypothermia to control intracranial hypertension in severely head-injured patients is clinically feasible. However, the method failed to reduce the incidence of infectious and hematological complications.

Topics: Adolescent; Adult; Aged; Brain Damage, Chronic; Brain Injuries; Combined Modality Therapy; Cross Infection; Cryotherapy; Dobutamine; Dopamine; Feasibility Studies; Female; Glasgow Coma Scale; Glycerol; Humans; Hypothermia, Induced; Intracranial Hypertension; Intubation, Gastrointestinal; Male; Middle Aged; Thiopental; Thrombocytopenia; Treatment Outcome

Thiopental monitoring was performed in 95 critically ill patients hospitalized for neurologic damage, High-dose thiopental was infused during long-term treatment. Total dose of 333 +/- 144 mg/kg (449 +/- 185 mg/kg for females and 302 +/- 113 mg/kg for men) were given in 125 +/- 43 hours. Plasma concentration-time data were analyzed according to a population pharmacokinetic approach with an initial group of 65 patients. Clearance (CL) and central volume of distribution (Vc) were modeled alone and under the influence of demographic covariates, assuming a two-compartment open model with first-order elimination. The final population models were as follows: CL (L/hr) = 11.7.weight (kg).age (yr)/(2136 + age2) and Vc = 1.52.weight (kg) + 44.8. Mean CL and Vc mean population estimates were 8.01 L/hr (133 ml/min or 2.02 ml/min/kg) and 145 L (2.19 L/kg). The predictive performance of the population modeling and parameters was evaluated with a bayesian fitting procedure in an independent validation set of 30 patients with similar physical and clinical characteristics. There was no statistically significant bias or imprecision between measured and predicted thiopental plasma concentrations in this validation group. Moreover, there was a good adequation (r = 0.939) between individual CL values predicted from the population formula and estimated with the bayesian approach.

Topics: Adolescent; Adult; Aged; Anticonvulsants; Brain Injuries; Female; Humans; Male; Middle Aged; Thiopental

1. Whole cell patch-clamp and extracellular field recordings were obtained from granule cells of the dentate gyrus in 400-microns-thick brain slices of the adult rat to determine the actions of the intravenous general anesthetic 2,6-diisopropylphenol (propofol) on acute neuronal survival and preservation of synaptic integrity after amputation of dendrites (dendrotomy), and to determine the role of gamma-aminobutyric acid-A (GABAA)-receptor-mediated inhibition in the neuroprotective effects of propofol. The actions of propofol were compared with those exerted by another widely used intravenous general anesthetic, 5-ethyl-5-[1-methylbutyl]-2-thiobarbituric acid (thiopental). 2. Propofol (10 microM) increased the frequency (control: 5.9 +/- 0.9 Hz, mean +/- SE; propofol: 10.5 +/- 1.3 Hz) and the single-exponential decay time constant (tau D) (control: 4.5 +/- 0.2 ms; propofol: 15.3 +/- 1.5 ms) of miniature inhibitory postsynaptic currents (mIPSCs) recorded in control neurons. Thiopental (25 microM) also increased the tau D (14.3 +/- 0.9 ms) of mISPCs, but had no effect on mIPSC frequency. Both anesthetics potentiated mIPSCs at low concentrations (propofol: 5 microM; thiopental: 1 microM). Propofol and thiopental did not change the peak amplitude and rise times of mIPSCs. 3. Propofol (10 microM) was able to depress the excitability of control granule cells, as determined by the reduction in the amplitude of the orthodromic population spikes. This depression could be prevented by the GABAA receptor antagonist bicuculline (50 microM), indicating that propofol reduces excitability via GABAA receptor functions. 4. Propofol and thiopental were neuroprotectant (assessed by antidromic population responses 2-5 h after injury) if present before and during the amputation of the granule cell dendrites. The protective actions were dose dependent, and at high doses (propofol: 200 microM; thiopental: 400 microM) the anesthetics were as neuroprotective against dendrotomy-induced cell death as 2-amino 5-phosphovaleric acid (APV) and 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX). The protective effects of the anesthetics were completely blocked with the GABAA receptor antagonists picrotoxin or bicuculline, and were mimicked by the GABAA receptor agonist muscimol (100 microM). 5. Propofol, in contrast to APV and CNQX, could not prevent the dendrotomy-induced Ca(2+)-dependent and long-lasting changes in mIPSC decay kinetics (appearance of a double-exponential, prolonged decay). 6

Topics: Acute Disease; Anesthetics, Intravenous; Animals; Brain Injuries; Dendrites; gamma-Aminobutyric Acid; In Vitro Techniques; Kinetics; Male; Neural Inhibition; Neurons; Neuroprotective Agents; Patch-Clamp Techniques; Propofol; Rats; Rats, Wistar; Synaptic Transmission; Thiopental

The effect of indomethacin, a cyclooxygenase inhibitor, was studied in the treatment of 10 patients with head injury and one patient with spontaneous subarachnoid hemorrhage, each of whom presented with high intracranial pressure (ICP) (34.4 +/- 13.1 mm Hg) and cerebral perfusion pressure (CPP) impairment (67.0 +/- 15.4 mm Hg), which did not improve with standard therapy using mannitol, hyperventilation, and barbiturates. The patient had Glasgow Coma Scale scores of 8 or less. Recordings were made of the patients' ICP and mean arterial blood pressure from the nurse's end-hour recording at the bedside, as well as of their CPP, rectal temperature, and standard therapy regimens. The authors assessed the effects of an indomethacin bolus (50 mg in 20 minutes) on ICP and CPP; an indomethacin infusion (21.5 +/- 11 mg/hour over 30 +/- 9 hours) on ICP, CPP, rectal temperature, and standard therapy regimens (matching the values before and during infusion in a similar time interval); and discontinuation of indomethacin treatment on ICP, CPP, and rectal temperature. The indomethacin bolus was very effective in lowering ICP (p < 0.0005) and improving CPP (p < 0.006). The indomethacin infusion decreased ICP (p < 0.02), but did not improve CPP and rectal temperature. The effects of standard therapy regimens before and during indomethacin infusion showed no significant changes, except in three patients in whom mannitol reestablished its action on ICP and CPP. Sudden discontinuation of indomethacin treatment was followed by significant ICP rebound. The authors suggest that indomethacin may be considered one of the frontline agents for raised ICP and CPP impairment.

Topics: Adolescent; Adult; Blood Pressure; Body Temperature; Brain Injuries; Carbon Dioxide; Cerebrovascular Circulation; Child; Cyclooxygenase Inhibitors; Female; Glasgow Coma Scale; Humans; Hyperventilation; Indomethacin; Infusions, Intravenous; Injections, Intravenous; Intracranial Pressure; Male; Mannitol; Pseudotumor Cerebri; Rectum; Subarachnoid Hemorrhage; Thiopental

The objective of this study was to analyze the effects of various anesthetics on the formation of brain edema resulting from a focal cryogenic lesion. Thirty rabbits (six per group) were anesthetized with isoflurane (1 minimum alveolar anesthetic concentration [MAC] 2.1 vol%), fentanyl (bolus 5 micrograms/kg; infusion rate 1.0-0.5 micrograms.kg-1.min-1), thiopental (32.5 mg.kg-1.h-1), or alpha-chloralose (50 mg/kg). Control animals (sham operation, no lesion) received alpha-chloralose (50 mg/kg). Regional cerebral blood flow (rCBF) in perifocal brain tissue was measured by H2-clearance. Animals anesthetized with isoflurane required support of arterial pressure by angiotensin II (0.15 micrograms.kg-1.min-1). Six hours after trauma the animals were killed. Formation of brain edema was studied by specific gravity of cortical gray matter, white matter, hippocampus, caudate nucleus, putamen, and thalamus. Brain tissue samples were collected at multiple sites close to and distant from the lesion. Mean arterial pressure, arterial PCO2 and PO2, hematocrit, body temperature, and blood glucose were not different between groups during the posttraumatic course (except for an increased arterial pressure with alpha-chloralose compared to thiopental 4-6 h after trauma). The specific gravity of cortical gray matter was significantly reduced up to a distance of 6 mm from the center of the lesion in animals anesthetized with isoflurane, thiopental, or alpha-chloralose and up to 9 mm in animals given fentanyl.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Anesthetics; Animals; Brain; Brain Edema; Brain Injuries; Cerebrovascular Circulation; Chloralose; Fentanyl; Intracranial Pressure; Isoflurane; Rabbits; Specific Gravity; Thiopental

Transcranial Doppler sonography (TCD) is a simple, noninvasive bedside procedure that can be repeated any time for the measurement of cerebral blood flow velocity in the great basal cerebral arteries. It is practicable in most severely head-injured patients in critical care. Flow patterns and pulsatility index (PI) resulting from maximal systolic and diastolic flow velocities and representing cerebrovascular resistance give quite an accurate impression of potential intracranial hypertension and the dependent cerebral perfusion pressure (CPP). With increasing intracranial pressure (ICP) and decreasing CCP, diastolic flow is progressively reduced. If ICP reaches the systemic diastolic blood pressure level, diastolic flow disappears. Oscillating (reverberating) flow patterns are seen when ICP increases further up to the arterial mean pressure level. The authors' own studies on 20 comatose patients with raised ICP showed typical changes in TCD parameters following different therapies for intracranial hypertension. Under continuous TCD monitoring of the middle cerebral artery, increases in maximal flow velocity (from 4% up to 102%, on average 27%) and mean flow velocity (from 18% up to 153%, on averaged 73%) were always observed after osmotherapy. In addition, a variable increase in negative frequencies was noted, probably due to increased turbulences. After barbiturate administration (thiopentone bolus of 0.3 g) a flow reduction was always seen [from -2% up to -25% (on average -13%) for maximal flow velocity and from -9% up to -30% (on average -19%) for mean flow velocity].(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Blood Flow Velocity; Brain; Brain Death; Brain Injuries; Carbon Dioxide; Critical Care; Humans; Intracranial Pressure; Pulsatile Flow; Thiopental; Ultrasonography, Doppler, Transcranial

These studies were conducted to determine the effect of anesthetic drugs on tissue perfusion and O2 supply in the brain with focal cerebral edema. Using an open cranium preparation, we studied the effects of isoflurane (I; 1 minimum alveolar anesthetic concentration), of fentanyl (F; 0.5-1 microgram.kg-1 x min-1), or of thiopental (T; 32.5 mg.kg-1 x h-1) on regional cerebral blood flow (rCBF) and regional brain tissue PO2 in albino rabbits (n = 6 per group) with a focal brain lesion (cold injury). The doses of anesthetics were sufficient to suppress nociception. rCBF (H2 clearance) and tissue PO2 (multiwire surface electrode) were studied adjacent to and distant from the lesion. Cerebral hyperemia developed immediately after trauma in all groups, although the flow increase did not attain statistical significance. rCBF was subsequently reduced by about 25% in the vicinity of the lesion. Distant from the trauma, a continuing hyperemia (+30%) was later observed in animals with isoflurane, whereas rCBF was decreased then by 10%-20% in animals with fentanyl, or was unchanged with thiopental. Brain tissue PO2 was increased with isoflurane in areas distant from the lesion, but decreased with fentanyl. However, with thiopental, the PO2 level had already been lowered before trauma with a subsequent tendency toward normalization. The heterogeneity of the tissue PO2 in fentanyl anesthesia, as well as the increased frequency of hypoxic PO2 values with thiopental, might have resulted from microcirculatory disturbances. Thus, although isoflurane seemed to facilitate hyperemia with an increased O2 supply to the brain, fentanyl tended to induce the opposite response. Although these properties suggest the potential to manipulate perfusion and O2 supply in cerebral ischemia or hyperemia after head injury, the effects of such measures on intracranial pressure, neurologic status, and outcome have yet to be proven.

Topics: Anesthetics; Animals; Brain Injuries; Cerebrovascular Circulation; Fentanyl; Isoflurane; Oxygen; Partial Pressure; Rabbits; Thiopental

Topics: Anesthesia, General; Animals; Brain; Brain Injuries; Cerebral Cortex; Fentanyl; Hypoxia; Isoflurane; Lung Diseases; Oxygen; Partial Pressure; Rabbits; Regional Blood Flow; Thiopental

This study reports on clinical outcome in 38 patients with severe head injuries (posttraumatic coma for 6 hours or more) treated with barbiturate coma because of intracranial hypertension. Eighteen patients died, 4 patients remained in a severely disabled or a chronic vegetative state, and 16 patients reached the levels good recovery/moderate disability. Six of these patients returned to work or school full time, 4 for half time and 3 were in a rehabilitation program. Fourteen patients were subjected to a comprehensive neuropsychological assessment. All patients except one exhibited varying degrees of cognitive dysfunction and 6 patients had signs of personality change. The quality of life for the majority of surviving patients was relatively good but the positive effects of barbiturate coma therapy in the age groups over 40 years appeared to be limited.

Topics: Adult; Brain Damage, Chronic; Brain Injuries; Child; Cognition Disorders; Critical Care; Disability Evaluation; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Glasgow Coma Scale; Humans; Male; Neurologic Examination; Neuropsychological Tests; Quality of Life; Survival Rate; Thiopental

This study reports all complications and side effects occurring in 38 patients with severe traumatic brain lesions treated with barbiturate coma because of a dangerous increase in intracranial pressure. The treatment was induced by intravenous infusion of thiopentone (5-11 mg.kg-1) followed by a continuous infusion of 4-8 mg.kg-1.h-1. The subsequent rate of thiopentone infusion was governed by the level of the intracranial pressure with the intention of keeping ICP below 20 mmHg (2.7 kPa). The duration of treatment was 1-15 days. Arterial hypotension occurred in 58%, hypokalemia in 82%, respiratory complications in 76%, infections in 55%, hepatic dysfunction in 87% and renal dysfunction in 47% of the patients. Twenty patients survived. Mortality in 17 patients was caused by an untreatable increase in intracranial pressure. In one patient complications due to barbiturate treatment may have contributed to the fatal outcome. In none of the other cases were the noted complications and side effects associated with any permanent symptoms or dysfunctions.

Topics: Adolescent; Adult; Bacterial Infections; Brain Injuries; Child; Female; Humans; Hypotension; Infusions, Intravenous; Intracranial Pressure; Kidney; Liver; Male; Middle Aged; Retrospective Studies; Sweden; Thiopental; Water-Electrolyte Imbalance

The effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and EEG monitored by Cerebral Function Monitor (CFM) were compared after bolus administration of mannitol (n = 55) and thiopentone (n = 67) to control intracranial hypertension in 18 severely head injured patients. Mannitol increased CPP in 89% of occasions and thiopentone in only 54% (p < 0.001). Thiopentone caused a mean increase in CPP +0.6 kPa (+5.0 +/- 1.6 mmHg) when the minimum pre-bolus voltage of CFM was above 4 microV and a fall in CPP -0.5 kPa (-4.1 +/- 1.6 mmHg) when cortical electrical activity was already severely depressed (p < 0.0002). When pre-bolus CFM was below 4 microV mannitol was superior to thiopentone. This different effect on CPP was due to a significantly greater fall in mean arterial pressure in the thiopentone sub-group -1.6 versus -0.3 kPa (-12.4 +/- 1.5 mmHg, -2.8 +/- 1.2 mmHg; p < 0.001). Severe and unpredictable hypotension occurred, particularly in the thiopentone low CFM sub-group. This symptomatic therapy seems inadequate but a targeted treatment of intracranial hypertension could be possible only with a more sophisticated monitoring, including continuous data on cerebral blood flow and adequacy to metabolic demand.

Topics: Adolescent; Adult; Brain Injuries; Child; Electroencephalography; Female; Humans; Intracranial Pressure; Male; Mannitol; Middle Aged; Monitoring, Physiologic; Pseudotumor Cerebri; Thiopental

The effect of pentobarbital was evaluated in 12 comatose brain injured patients (Glasgow coma scale < 7 at admission). Mean hemispheric cerebral blood flow (CBF) was studied following intravenous administration of 133Xenon. The results indicated a decrease in CBF, mean arterial pressure (MAP), intracranial pressure (ICP) and cerebral metabolic rate of oxygen (CMRO2). The increase in cerebral perfusion pressure (PP) was found only in patients with diffuse brain injury. The results supports the hypothesis that barbiturate therapy is more effective at reducing ICP while preserving CPP when the cause is a diffuse lesion.

Topics: Brain Injuries; Cerebrovascular Circulation; Female; Hemodynamics; Humans; Intracranial Pressure; Male; Oxygen Consumption; Thiopental

Blood flow velocity (BFV) of the MCA has been studied by TCD of 15 patients with non operated serious cranial trauma, treated with continuous barbiturate therapy. Without hemodynamic and ventilatory modifications (PaCO2), average BFV were lowered during the course of treatment and were raised significantly when it was stopped. This study poses the question of the indication and the methods of barbiturate treatment during serious cranial trauma.

Topics: Adult; Blood Flow Velocity; Brain Injuries; Cerebrovascular Circulation; Echoencephalography; Female; Humans; Male; Thiopental

Topics: Adult; Aged; Brain Injuries; Calorimetry, Indirect; Circadian Rhythm; Critical Care; Energy Intake; Energy Metabolism; Glasgow Coma Scale; Humans; Middle Aged; Oxygen; Parenteral Nutrition, Total; Respiration, Artificial; Retrospective Studies; Thiopental

Mean hemispheric cerebral blood flow (CBF) and intracranial pressure (ICP) were measured in 19 severely head-injured patients treated with barbiturate coma. The CBF was calculated from the clearance of tracer substance monitored by extracranial scintillation detectors after intravenous administration of xenon-133. In 11 of the patients cerebral arteriovenous oxygen differences were measured simultaneously. In all patients the effects of pronounced hyperventilation were recorded prior to initiation of barbiturate treatment. A normal CBF response to hyperventilation (delta CBF/delta PaCO2 greater than or equal to 1) was obtained in eight patients. In these patients induction of barbiturate coma was accompanied by physiological decreases in CBF and in the calculated cerebral metabolic rate of oxygen (CMRO2); they also exhibited a rapid and lasting decrease in ICP. A decreased or an abolished CO2 reactivity was recorded (delta CBF/delta PaCO2 less than 1) in 11 patients. In 10 of these 11 patients the physiological decreases in CBF and CMRO2 were not obtained during barbiturate treatment and the decrease in ICP was transitory. This study demonstrates a correlation between cerebral vasoreactivity, physiological effects of barbiturate therapy, and clinical outcome.

Topics: Adolescent; Adult; Brain; Brain Injuries; Carbon Dioxide; Cerebrovascular Circulation; Child; Coma; Female; Humans; Hyperventilation; Male; Middle Aged; Oxygen; Oxygen Consumption; Thiopental; Vascular Resistance

The value of EEG data and evoked potentials (EP), combined with the patient's clinical status, are important parameters used to document decerebration, but their reliability is at its best when the decerebration is nearly complete. Based on spectral analysis of the EEG we compiled criteria for the cerebral function with application of agents known to alter the normal EEG. We found very distinct and different pattern responses in spectral analysis of the EEG after the bolus injection of 100-500 mg Thiopental, correlating well with the patient's prognosis. In a study with 40 patients, those who showed a significant increase of power in all frequencies, especially a short lasting increase in beta (3-7 min) survived in 84%. On the other hand, all the patients who had a decrease of absolute power in all frequency band died, even when brainstem reflexes and various pain reactions were still present. Spectral analysis after Thiopental bolus injection also permits a very immediate assessment of slight improvements or deteriorations in the clinical course.

Topics: Adolescent; Adult; Aged; Brain Injuries; Child; Child, Preschool; Coma; Electroencephalography; Female; Humans; Male; Middle Aged; Prognosis; Thiopental

The clinical course and the intracranial pressure (ICP) changes in 66 severe head injury patients presenting bulk enlargement of one cerebral hemisphere within a few hours of trauma have been analyzed. These patients represent 11% of a series of 589 severe head injury cases studied with computerized tomography (CT). Cerebral hemisphere swelling, which was associated with an ipsilateral subdural haematoma of variable extent in 58 patients (88%), or a large epidural haematoma in 5 patients (7%), and occurred as an isolated lesion in 3 patients (4%), carried the highest incidence of uncontrollable intracranial hypertension, the highest mortality rate and the shortest survival period after trauma in the authors' severe head injury series. The high incidence of arterial hypotension and/or hypoxaemia at admission (48% of cases), and the severity of clinical presentation (82%) of patients scored 5 patients or less in the Glasgow Coma Scale, 77% had uni- or bilateral mydriasis and 82% initial ICP above normal limits) correlated with the very poor final outcome (85% mortality). Only one of the 12 patients with normal initial ICP continued to have low pressure throughout the course. High dose thiopental failed to control severe intracranial hypertension in 29 patients (44%) who had a fulminant, malignant course. A transient decrease in ICP elevation was achieved in 17 patients (26%) and a definitive control in 12 patients (18%), among them the 10 survivors in this series. In the authors experience once ICP is controlled, and unless haemodynamic instability compells action to the contrary, barbiturate should not be discontinued until a control CT scan shows complete disappearance of the mass effect.

Topics: Adolescent; Adult; Aged; Brain Edema; Brain Injuries; Child; Child, Preschool; Humans; Hypertension; Hypoxia; Infant; Intracranial Pressure; Male; Middle Aged; Thiopental; Tomography, X-Ray Computed

Combined infusion of high doses of lidocaine and thiopental in a comatose patient induced major latency and amplitude BAEP changes, which progressed to complete BAEP abolition. Responses returned to normal after drugs were discontinued. EEGs during the episodes showed long-lasting periods of activity suppression, but were never isoelectric. BAEPs are resistant to hypothermia and barbiturates, but must be interpreted cautiously in patients treated with a combination of anesthetic drugs that includes lidocaine.

Topics: Adult; Brain Injuries; Brain Stem; Coma; Drug Combinations; Evoked Potentials, Auditory; Female; Humans; Lidocaine; Thiopental

Propofol (Disoprivan) is a rapid and effective hypnotic comparable with etomidate. Up to now, the effects on intracranial pressure (ICP) have only rarely been investigated, especially in cases with pre-existing increased ICP [4, 18]. The aim of this study was the evaluation of ICP after i.v. propofol administration in comparison with thiopental. Method. Five patients were studied, all of whom had had isolated head trauma. All were on controlled ventilation and were unconscious. Depending on the result of computer tomography, an epidural pressure transducer was implanted. ICP, blood pressure (BP), and heart rate (HR) were measured before and 1, 3, 5, 10, and 15 min after 1 mg/kg propofol; subsequently 2 mg/kg thiopental were administered and the same parameters documented. Cerebral perfusion pressure (CPP) and mean arterial pressure (MAP) were calculated. Results. ICP decreased in all five cases 5 min after the initial values were measured. Two patients showed an ICP decrease after thiopental. BP was reduced markedly by propofol and very slightly by thiopental. The CPP showed a small decrease in four patients after propofol and in two after thiopental. Conclusions. The data now available permit the conclusion that both propofol and thiopental can be used in patients with possibly elevated ICP. The marked cardiovascular side effects of propofol must be taken into consideration.

Topics: Adolescent; Adult; Aged; Anesthesia; Blood Gas Analysis; Blood Pressure; Brain Injuries; Cerebrovascular Circulation; Humans; Intracranial Pressure; Middle Aged; Phenols; Propofol; Thiopental; Time Factors

Topics: Adolescent; Brain Injuries; Child; Child, Preschool; Coma; Female; Humans; Male; Pseudotumor Cerebri; Thiopental

The effects and indications of barbiturate therapy for brain protection, and prevention and reduction of the intracranial hypertension were investigated using an ultrashort acting barbiturate, thiamylal, in sixteen cases with intracranial lesions. Final outcome of the treatment revealed 8 good recoveries which were actively administered thiamylal during operation or immediately after. On the other hand, four cases, whose intracranial pressures (ICPS) of over 40 mmHg could not be controlled suffered brain death. Barbiturate therapy was not effective for brain protection of primary damaged lesions. It is concluded that barbiturate therapy may provide a satisfactory reduction of the intracranial hypertension in cases during the early postoperative stage or of under 40 mmHg initial ICP.

Topics: Adolescent; Adult; Aged; Brain Edema; Brain Injuries; Brain Neoplasms; Cerebral Hemorrhage; Child, Preschool; Female; Humans; Intracranial Aneurysm; Intracranial Arteriovenous Malformations; Male; Middle Aged; Postoperative Complications; Pseudotumor Cerebri; Thiamylal; Thiopental

Mean hemispheric cerebral blood flow (CBF) was studied in 11 comatose brain-injured patients following intravenous administration of xenon-133. Repeated measurements were performed in order to evaluate cerebral vasoreactivity following a decrease in PaCO2. In addition, the effect of induced barbiturate coma was evaluated in patients with intracranial hypertension. The cerebral vasoreactivity and the CBF response following induction of barbiturate coma varied. In patients with normal CO2 reactivity, barbiturate treatment was accompanied by a considerable decrease in CBF as compared to patients with decreased or abolished CO2 response. During barbiturate treatment the intracranial pressure (ICP) became normal in three of four patients with preserved CO2 response, but reached normal levels in only one of five patients with impaired CO2 reactivity. Patients whose ICP became normal recovered. The data suggest a positive correlation between CO2 reactivity and the effect of barbiturate treatment. Furthermore, preserved cerebral vasoreactivity after severe head injury may be of prognostic value.

Topics: Adolescent; Adult; Aged; Blood Pressure; Brain Injuries; Carbon Dioxide; Cerebrovascular Circulation; Female; Humans; Hypercapnia; Intracranial Pressure; Male; Middle Aged; Thiopental

Topics: Acute Disease; Adolescent; Adult; Aged; Brain Injuries; Female; Hemodynamics; Humans; Intracranial Pressure; Male; Middle Aged; Thiopental; Wounds and Injuries

Topics: Accidents; Adolescent; Adrenal Cortex Hormones; Adult; Aged; Brain Injuries; Child; Critical Care; Female; Humans; Male; Middle Aged; Suicide, Attempted; Thiopental; Time Factors

Topics: Animals; Brain Damage, Chronic; Brain Injuries; Cerebrovascular Disorders; Coma; Heart Arrest; Humans; Resuscitation; Thiopental

Thirty-eight patients with brain injury and mesencephalic coma, or a Glasgow score of less than 5, were treated routinely with Thiopental administered by electric syringe for a mean duration of 4 days. Follow up review criteria were based on clinical computed tomography and electroencephalographic data, as well as results of monitoring of intracranial pressure and assay of blood barbiturate levels. Global results indicated a mortality of 55.3% and reintegration of 34.2% of the patients. Results as a function of the different parameters of surveillance are discussed.

Topics: Adult; Brain Injuries; Coma; Decerebrate State; Female; Follow-Up Studies; Humans; Male; Mesencephalon; Thiopental

Topics: Adolescent; Anesthetics; Brain; Brain Injuries; Coma; Drug Therapy, Combination; Electroencephalography; Humans; Intracranial Pressure; Male; Monitoring, Physiologic; Pregnanediones; Thiopental

Topics: Adult; Bacterial Infections; Barbiturates; Brain; Brain Injuries; Candidiasis; Humans; Hypothermia, Induced; Intracranial Pressure; Lung Diseases; Monitoring, Physiologic; Respiratory Tract Infections; Thiopental

Topics: Adolescent; Adult; Alfaxalone Alfadolone Mixture; Brain Injuries; Child; Coma; Female; Humans; Intracranial Pressure; Male; Monitoring, Physiologic; Thiopental

Thiopental was used in long-term infusion (3-4.5 mg . kg-1 . h-1 during 4-8 days) to protect the brain from injury following trauma. Thiopental plasma concentrations were measured during infusion (48 patients) and after infusion (14 patients) to determine the kinetics of the drug in continuous infusion. All mean values were mean +/- SD. Steady state concentrations (Css) were 31.8 +/- 10.7 mg/l for an infusion rate of 3.05 +/- 0.37 mg . kg-1 . h-1 and 48.9 +/- 14.6 mg/l for a rate of 4.2 +/- 0.3 mg . kg-1 . h-1. Corresponding steady state clearance decreased when Css increased, indicating possible saturation of the metabolic enzymatic system. Michaelis-Menten kinetics were confirmed by postinfusion data that give, for higher Css, a nonlinear decay of log C versus time. First-order kinetics were only obtained with Css below 30 mg/l. The maximum rate of elimination (Vm) was 1.76 +/- 1.15 mg . l-1 . h-1 (n = 11), and the Michaelis constant (Km) was 26.7 +/- 22.9 mg/l (n = 11). Hepatic enzyme saturation was between 35 and 85%. The volume of distribution at steady state was 4.35 +/- 1.83 l/kg (n = 11). Apparent half-lives of elimination were between 18 and 36 h at the end of infusion, and predicted terminal half-lives were 10.15 +/- 5.43 h (n = 11). Phases of burst-suppression were observed on electroencephalographic traces for concentrations greater than 40 mg/l. The authors' results suggest that a continuous infusion at a dose of 4 mg . kg-1 . h-1 induces EEG changes consistent with a near-maximum reduction in cerebral metabolism. Because of the thiopental Michaelis-Menten kinetics at doses above 4 mg . kg-1 . h-1, the authors suggest that thiopental plasma concentrations be measured and/or the drug effect be measured with the EEG to prevent excessive thiopental overdosage, causing a prolonged recovery time.

Topics: Adolescent; Adult; Brain Injuries; Child; Electroencephalography; Female; Humans; Infusions, Parenteral; Kinetics; Male; Middle Aged; Muscle Contraction; Thiopental

Topics: Adolescent; Adult; Aged; Brain Injuries; Coma; Epilepsy, Tonic-Clonic; Humans; Hypoxia, Brain; Middle Aged; Neurosurgery; Postoperative Complications; Thiopental

Forty children with severe head injury were studies retrospectively. All were admitted to the medical center within 6 hours after injury. Seventeen had Glasgow Coma Scales of 3 to 4 and 23 scales of 5 to 7. Computerised tomography (CT) findings and coagulation abnormalities in the first 12 and intracranial pressure (ICP) in the first 24 hours after injury were examined in relation to the final result. Compressed basal cisterns in CT, presence of moderate to severe consumption coagulopathy (CC) and moderate to severe intracranial hypertension (ICP greater than 20 mmHg) all correlated significantly with fatal outcome. In contrast, survivors usually had patent basal cisterns on CT, normal coagulation data or only moderate CC and slight to rarely moderate intracranial hypertension. It is concluded that by using the proposed criteria, early assessment of severity and prediction of outcome after severe paediatric head injury is possible. In contrast to the Glasgow Coma Scale these criteria are applicable and retain predictive power also in children who receive early and intensive ICP-lowering therapy.

Topics: Adolescent; Blood Coagulation Tests; Brain Death; Brain Injuries; Child; Child, Preschool; Coma; Dexamethasone; Disseminated Intravascular Coagulation; Drug Therapy, Combination; Female; Furosemide; Humans; Infant; Infant, Newborn; Intracranial Pressure; Male; Mannitol; Phenobarbital; Prognosis; Thiopental; Tomography, X-Ray Computed

Topics: Brain Injuries; Critical Care; Fentanyl; Humans; Pupil; Thiopental

Thirty patients with an acute midbrain syndrome were treated by high dose barbiturate therapy. Of these patients 19 had a severe head injury. In 8 patients the symptoms of acute midbrain syndrome developed after subarachnoid haemorrhage. In three patients these symptoms were caused by postoperative swelling or ischaemia. The results of those patients, who were treated with barbiturates after head injury were much better than in 16 other patients, who had no barbiturates. The indications for high dose barbiturate therapy in neurosurgery are discussed with reference to other publications and to the pathophysiological effects of barbiturates.

Topics: Adolescent; Adult; Brain Diseases; Brain Injuries; Humans; Mesencephalon; Middle Aged; Neurosurgery; Postoperative Complications; Subarachnoid Hemorrhage; Syndrome; Thiopental

Massive intraoperative brain swelling is an infrequent but catastrophic occurrence. In this report, we describe the use of very large doses of thiopental as a means of treating such swelling. In our initial 11 cases (5 arteriovenous malformations, 4 hematomas, and 2 penetrating injuries), this approach produced the following outcomes: 6 patients made a good recovery, 2 are moderately disabled, 1 is severely disabled, and 2 are dead. These results indicate that this condition, which once was considered unmanageable, can indeed be managed and that treatment often results in an acceptable outcome. More recent experience in an additional 6 patients suggests that the use of planned deep thiopental anesthesia, with induced cerebral silence, during intracranial surgery may even prevent the occurrence of this phenomenon.

Topics: Brain Diseases; Brain Edema; Brain Injuries; Dose-Response Relationship, Drug; Hematoma, Epidural, Cranial; Hematoma, Subdural; Humans; Intracranial Arteriovenous Malformations; Intraoperative Complications; Prognosis; Thiopental

Pharmacologic protection should be used cautiously. The author reviews its rationale, use, and recommendations in three clinical conditions associated with ischemic brain damage: stroke, cardiac arrest, and head trauma.

Topics: Adult; Animals; Arterial Occlusive Diseases; Barbiturates; Brain Injuries; Brain Ischemia; Cats; Cerebral Arteries; Cerebrovascular Disorders; Dogs; Female; Heart Arrest; Humans; Intracranial Pressure; Male; Middle Aged; Models, Biological; Papio; Phenobarbital; Saimiri; Thiopental

Topics: Adolescent; Adult; Anesthesia, General; Brain Injuries; Child; Child, Preschool; Drug Therapy, Combination; Female; Humans; Hydroxybutyrates; Intracranial Pressure; Male; Sodium Oxybate; Thiopental

Topics: Adolescent; Brain Injuries; Child; Child, Preschool; Coma; Female; Humans; Infant; Intracranial Pressure; Male; Thiopental

The pathophysiology of brain trauma regarding disturbances of energy and transmitter metabolism, development of intra- and extracellular cerebral oedema are briefly outlined. Possible mechanisms of action of barbiturates in amelioration of cerebral ischaemia, decrease of cerebral metabolism, preservation of membrane stability, reduction of cerebral oedema and intracranial pressure are reviewed. We report on 6 patients with severe brain trauma due to head injury whose intracranial pressure despite conventional treatment with hyperventilation, steroids and osmotic diuresis remained above 25 mm Hg. They were infused with thiopentone 6--12 mg/kg x h for 6 to 15 days, to reduce cerebral electrical activity to the point of "burst suppression" in the electroencephalogram. Three patients survived, two of them regaining their previous good health. The results in these patients are discussed as regards thiopentone dosage and severity of trauma. Marked cardiovascular instability in one case and cholostatic jaundice due to barbiturate administration in two cases were the most important side effects. Barbiturate infusion seems to be indicated in brain trauma with sustained elevation of intracranial pressure above 25 mm Hg despite vigorous conventional therapy. Monitoring most essential to this aggressive treatment scheme comprises measurement of intracranial pressure and continuous observation of the EEG.

Topics: Adult; Barbiturates; Blood Pressure; Brain Edema; Brain Injuries; Electroencephalography; Energy Metabolism; Humans; Infusions, Parenteral; Intracranial Pressure; Male; Thiopental

A barbiturate protocol for control of raised intracranial pressure is presented in detail. Since the nursing staff may be responsible for maintaining cerebral perfusion and normal ICP with barbiturates, mannitol, fluids, and pressor agents, it was thought that a detailed description such as presented might be useful. We have shown that complex management protocols can easily be managed, even in smaller, non-university community hospitals. The present state of brain injury management by barbiturates, guided by ICP monitoring, even at this early stage of development, seems to show promise as the latest adjunct in the care of this difficult problem.

Topics: Brain Injuries; Humans; Infusions, Parenteral; Intracranial Pressure; Thiopental

Topics: Anesthesia, Intravenous; Angiotensin II; Animals; Blood; Blood Pressure; Brain; Brain Injuries; Carbon Dioxide; Cardiac Output; Cerebrospinal Fluid; Cerebrovascular Circulation; Dogs; Hemoglobinometry; Hydrogen-Ion Concentration; Hypoxia; Ketamine; Oxygen; Oxygen Consumption; Partial Pressure; Pressure; Regional Blood Flow; Respiration, Artificial; Respiratory Dead Space; Spirometry; Thiopental

Topics: Antidepressive Agents; Brain Injuries; Electroencephalography; Humans; Psychotic Disorders; Schizophrenia; Thiopental

Topics: Analgesia; Anesthesia; Anesthesia and Analgesia; Brain; Brain Injuries; Consciousness; Decerebrate State; Pain Management; Thiopental; Unconsciousness