thiopental and Coma

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

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

To assess survival after cardiac arrest and to determine whether age is an independent determinant of late mortality or poor neurologic outcome.. Analyses using results of Brain Resuscitation Clinical Trial I (1979 to 1984) and Brain Resuscitation Clinical Trial II (1984 to 1989), two randomized, double-blind studies of outcome following cardiac arrest.. A multicenter study in 12 acute care hospitals in nine countries (Brain Resuscitation Clinical Trial I), and 24 hospitals in eight countries (Brain Resuscitation Clinical Trial II).. A total of 774 patients who were initially comatose after successful resuscitation from cardiac arrest. The analyses include both in- and out-of-hospital cardiac arrests.. The 6-month mortality rate for the entire group was 81%. Mortality rate was 94% for the oldest group (> 80 yrs) compared with 68% for the youngest group (< or = 45 yrs) (p < .01). Other independent predictors of mortality were history of diabetes mellitus, inhospital arrests, arrest time of > 5 mins, history of congestive heart failure, a noncardiac cause of arrest, and cardiopulmonary resuscitation time of > 20 mins. Of the 774 patients, 27% recovered good neurologic function. There was no statistically significant difference in neurologic recovery rates by age. Multivariate analysis showed that independent predictors of good neurologic recovery were: no history of diabetes mellitus, a cardiac cause of arrest, short arrest time, and short cardiopulmonary resuscitation time.. Increasing age was a factor in postresuscitation mortality, but was not an independent predictor of poor neurologic outcome.

Topics: Age Factors; Aged; Aged, 80 and over; Cardiopulmonary Resuscitation; Coma; Double-Blind Method; Female; Glasgow Coma Scale; Heart Arrest; Humans; Lidoflazine; Male; Middle Aged; Neurologic Examination; Prognosis; Risk Factors; Thiopental

When a patient resuscitated from cardiac arrest remains unconscious the clinician would like to have a reliable early method for predicting the outcome. The objective of our study was to predict cerebral outcome after cardiac arrest by clinical neurological examination. The data were drawn from an international multicentre controlled clinical trial of thiopentone. Twelve hospitals in nine countries took part. 262 comatose cardiac arrest survivors were followed up for one year. These patients were given advanced life support (American Heart Association guidelines) followed by intensive care to a standardised protocol. Glasgow and Glasgow-Pittsburgh coma scores and their constituent signs were recorded at fixed times. Outcome was taken to be the best cerebral performance at any time during follow-up, and for that purpose we used cerebral performance categories (CPC 1-5) of the Glasgow outcome categories. A poor outcome (CPC 3-5) could be predicted immediately after reperfusion (at entry into the study) with an accuracy ranging from 52% to 84% for various signs and scores. On the third day it was possible to identify severely disabled or permanently comatose survivors without false predictions using both coma scores and several of their constituent variables. The best predictor was absence of motor response to pain. This modelling exercise now needs to be repeated on a new series of patients but the results do suggest that, after 3 days, stringent ethical criteria can be met and used in decision-making about termination of care in comatose cardiac arrest survivors.

Topics: Brain; Cardiopulmonary Resuscitation; Coma; False Positive Reactions; Female; Follow-Up Studies; Glasgow Coma Scale; Heart Arrest; Humans; International Cooperation; Male; Middle Aged; Neurologic Examination; Predictive Value of Tests; Prognosis; Prospective Studies; Survivors; Thiopental; Treatment Outcome; Withholding Treatment

Levels of brain creatine phosphokinase (CPK), glutamic oxalic transaminase, lactate dehydrogenase, and lactate in lumbar cerebrospinal fluid (CSF) were analyzed as an adjunctive study in a randomized clinical trial evaluating the effects of thiopental loading intravenously in comatose survivors of cardiac arrest. Three hospitals participated and a total of 62 cases of enzyme changes were studied. Enzyme levels but not lactate were higher at 48 hours than at 24 hours after restoration of spontaneous circulation. All enzymes were highly correlated with one another at 24 and 48 hours (P < .001). There was a significant negative correlation between cerebral recovery and increased CPK levels at 24 hours (P < .05), and a highly significant correlation with all three enzyme levels at 48 hours (P < .0001). The increase of cytosolic enzyme activity in lumbar CSF reflects permanent brain damage, and there is a relationship between activity levels and cerebral outcome.

Topics: Aspartate Aminotransferases; Brain Chemistry; Coma; Creatine Kinase; Heart Arrest; Humans; Injections, Intravenous; L-Lactate Dehydrogenase; Lactates; Lactic Acid; Prognosis; Survivors; Thiopental; Time Factors

After restoration of spontaneous circulation and adequate oxygenation, 262 comatose survivors of cardiac arrest were randomly assigned to receive standard brain-oriented intensive care or the same standard therapy plus a single intravenous loading dose of thiopental (30 mg per kilogram of body weight). The study was designed to have an 80 percent probability of detecting a 20 percent reduction in the incidence of permanent postischemic cerebral dysfunction. Base-line characteristics were similar in the two treatment groups. At the end of one year of follow-up, there was no statistically significant difference between treatment groups in the proportion of patients who died (77 percent of the thiopental vs. 80 percent of the standard-therapy group), survived with "good" cerebral recovery (20 percent of the thiopental vs. 15 percent of the standard-therapy group), or survived with permanent severe neurologic damage (2 percent of the thiopental vs. 5 percent of the standard-therapy group). The results of this study do not support the use of thiopental for brain resuscitation after cardiac arrest.

Topics: Adolescent; Adult; Aged; Brain Damage, Chronic; Brain Ischemia; Child; Child, Preschool; Clinical Trials as Topic; Coma; Female; Follow-Up Studies; Heart Arrest; Humans; Infant; Male; Middle Aged; Random Allocation; Resuscitation; Thiopental

The Brain Resuscitation Clinical Trial (BRCT) was established as a multi-institutional, clinical study of brain resuscitation. The BRCT was designed to test the hypothesis that the addition of thiopental loading to the protocol of standard therapy for cardiac arrest survivors, comatose at 10-50 minutes after restoration of spontaneous circulation, would significantly increase the number of patients recovering good cerebral function. Twelve hospitals in nine countries collaborated in this randomized, controlled clinical trial. The study was designed to take into account numerous problems including the reliability of information on complex events surrounding cardiac arrest, the difficulty of maintaining uniform treatment protocols, and the difficulty of obtaining informed consent within the constraints of the time the therapy was hypothesized to be effective. The major outcome measurements of the study were neurological status at the end of various time intervals following resuscitation and the best neurological performance ever attained during follow-up. Mortality and other untoward events were closely monitored to establish treatment safety. Of the 262 patients entered into the study between 1979 and 1982, 45% were over 65 years of age, and 75% were men. The majority of the arrests (74%) occurred out of hospital, and major pathology underlying arrest was cardiac. Arrest time was greater than 5 minutes in 36% of the patients. As a result of randomization, patient characteristics at entry as well as the characteristics associated with the brain insult in the standard group were similar to those in the thiopental group.

Topics: Aged; Clinical Trials as Topic; Coma; Critical Care; Data Collection; Follow-Up Studies; Heart Arrest; Humans; Hypoxia, Brain; Infusions, Parenteral; Injections, Intravenous; Male; Methods; Neurologic Examination; Random Allocation; Recurrence; Research Design; Resuscitation; Thiopental; Time Factors

In patients with gamma-hydroxybutyrate (GHB) use disorder (GUD), withdrawal can have a fulminant course with rapid progression of severe, potentially life-threatening complications.

Topics: Benzodiazepines; Coma; Humans; Male; Middle Aged; Sodium Oxybate; Substance Withdrawal Syndrome; Thiopental

The aim was to study the effects of barbiturate coma treatment (BCT) on intracranial pressure (ICP) and intracranial compensatory reserve (RAP index) in children (< 17 years of age) with traumatic brain injury (TBI) and refractory intracranial hypertension (RICH).. High-resolution monitoring data were used to study the effects of BCT on ICP, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and RAP index. Four half hour long periods were studied: before bolus injection and at 5, 10, and 24 hours thereafter, respectively, and a fifth tapering period with S-thiopental between < 100 and < 30 μmol/L. S-thiopental concentrations and administered doses were registered.. Seventeen children treated with BCT 2007-2017 with high-resolution data were included; median age 15 (range 6-17) and median Glasgow coma score 7 (range 3-8). Median time from trauma to start of BCT was 44.5 h (range 2.5-197.5) and from start to stop 99.0 h (range 21.0-329.0). Median ICP was 22 (IQR 20-25) in the half hour period before onset of BCT and 16 (IQR 11-20) in the half hour period 5 h later (p = 0.011). The corresponding figures for CPP were 65 (IQR 62-71) and 63 (57-71) (p > 0.05). The RAP index was in the half hour period before onset of BCT 0.6 (IQR 0.1-0.7), in the half hour period 5 h later 0.3 (IQR 0.1-0.7) (p = 0.331), and in the whole BCT period 0.3 (IQR 0.2-0.4) (p = 0.004). Eighty-two percent (14/17) had favorable outcome (good recovery = 8 patients and moderate disability = 6 patients).. BCT significantly reduced ICP and RAP index with preserved CPP. BCT should be considered in case of RICH.

Topics: Adolescent; Anticonvulsants; Arterial Pressure; Barbiturates; Brain Injuries, Traumatic; Cerebrovascular Circulation; Child; Coma; Convulsive Therapy; Female; Humans; Intracranial Hypertension; Intracranial Pressure; Male; Retrospective Studies; 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

We report on the long-term follow-up of a patient with refractory non-convulsive SE who was successfully treated with VNS. A 7-year old girl with a medical history of thrombosis in the right internal cerebral vein and right thalamic bleeding 8 days after birth, developed epilepsy at the age of 13 months. At the age of 6 she presented with a refractory non-convulsive SE. A vagus nerve stimulator was placed after 11 days of thiopental-induced coma. Three days after VNS implantation, the thiopental-induced coma was successfully withdrawn and electroencephalography showed normalization one week after start of VNS. After a follow-up of 13 months she remains seizure-free and AEDs have been partially tapered. This case illustrates a potential acute abortive effect with sustained long-term seizure reduction of VNS in a 7-year old girl who presented with refractory non-convulsive SE.

Topics: Child; Coma; Electric Stimulation Therapy; Electroencephalography; Female; Humans; Status Epilepticus; Thiopental; Treatment Outcome; Vagus Nerve Stimulation

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

Sodium thiopental in the comatogenic (but not soporogenic) dose caused hyperammoniemia in rats. Blood ammonium level increased 3-fold within 3 h and 5-fold within 18 h. Blood urea level increased by one-third within 18 h against the background of unchanged creatinine level and hematocrit. Urinary excretion of ammonium did not decrease, while its release with exhaled air increased, indicating intensification of ammonium formation in the body. Barbiturate coma did not change the slope of curves of dose-dependent increase of ammonium or urea levels in the blood of rats injected with ammonium acetate, which attested to the absence of appreciable disorders in the ammonium detoxifying function of the liver. Ammonium hyperproduction could be caused by gastrointestinal stasis verified by X-ray examination and confirmed by correlation between blood urea level and stool retention in narcotized rats.

Topics: Ammonia; Animals; Coma; Female; Gastrointestinal Motility; Hyperammonemia; Rats; Thiopental

Under modeling of thiopental coma influence of sodium succinate and (or) external warming for the support of normal body temperature (isothermal regimen) on the gas exchange, blood gas content, acid-base status and survival rate was studied in rats. In the absence of therapy hypothermia was developed (-9.4 degrees C), O(2) consumption decreased by a factor 5, oxygenation of arterial blood (pO(2)) did not change while that of venous blood increased, where with arteriovenous oxygen tension gradient decreased by half. Blood tension of carbon dioxide (pCO(2)) increased twice, respiratory and metabolic acidosis was developed. Survival rate under absence of a therapy was 42%, with isolated use of isothermal regimen or succinate therapy alike-50%; with their use in combination drastically increased up to 92%. Succinate increased arteriovenous gradient of pO(2), decreased deficit of buffer bases, increased bicarbonate concentration. At isothermal regimen accumulation of CO(2) in the blood was diminished, its excretion was increased, pH of blood approached normal values. Combined use of both therapy agents increased O(2) consumption and potentiated their positive influence on acid-base status. The implication is that hypothermia restrains effect of succinate in barbiturate coma; prevention of hypothermia in combination with succinate administration is highly effective method of experimental therapy of barbiturate intoxication.

Topics: Anesthetics, Intravenous; Animals; Blood Gas Analysis; Body Temperature; Carbon Dioxide; Coma; Female; Hypothermia; Lethal Dose 50; Oxygen; Oxygen Consumption; Rats; Succinic Acid; Thiopental; Time Factors

Fulminant hyperammonaemia as a threshold effect of coma-inducing dose of sodium thiopental has been revealed in rats. Blood ammonia content increased progressively after the introduction of 1.0 LD(50) (but not 0.8 LD(50)) of sodium thiopental three times in 3h and five times in 18h. The urinary ammonia excretion was not impaired while the volatilization of ammoniac from the body of ST-treated rats was higher, giving evidence of the augmentation of ammonia production. Blood urea increased by one third despite of insignificant alterations of haematocrit and blood creatinine. Ammonia hyperproduction in the digestive tract could result from gastrointestinal stasis, which has been verified by roentgenography and confirmed by correlation of hyperammonaemia with the stool retardation. In thiopental coma rats the slope of a dose-dependent increase of the blood ammonia and the blood urea after the intraperitoneal injection of ammonium acetate did not exceed that in intact animals. So the ammonia hyperproduction in the digestive tract could be the main contributing cause of fulminant hyperammonaemia in rats with thiopental coma and thus be involved into pathogenesis of the coma.

Topics: Acetates; Ammonia; Animals; Blood Urea Nitrogen; Coma; Defecation; Dose-Response Relationship, Drug; Gastrointestinal Contents; Gastrointestinal Tract; Hyperammonemia; Hypnotics and Sedatives; Injections, Intraperitoneal; Intestinal Obstruction; Rats; Thiopental; Time Factors

In rats with experimental thiopental coma rectal temperature decreased by 9.4 degrees C, oxygen consumption 5-fold, and arteriovenous Po(2)gradient decreased 2-fold within 3 h; CO(2)accumulated in the blood and mixed type acidosis developed. Administration of sodium succinate under these conditions increased arteriovenous Po(2)gradient and reduced manifestations of metabolic acidosis. Maintenance of normal body temperature (warming) corrected primarily manifestations of respiratory acidosis. Each therapeutic agent reduced inhibition of O(2)consumption by 1/4; animal survival tended to increase from 42 to 50%. Combined use of these treatments potentiated the antiacidotic effect and increased survival to 92%. The authors conclude that hypothermia inhibits the therapeutic effect of succinate in barbiturate coma.

Topics: Acidosis, Respiratory; Animals; Body Temperature; Carbon Dioxide; Coma; Female; Oxygen; Oxygen Consumption; Rats; Succinates; Thiopental; Time Factors

Topics: Acidosis; Adult; Anesthetics, Intravenous; Coma; Conscious Sedation; Critical Care; Fatal Outcome; Female; Fever; Humans; Hyperkalemia; Infusions, Intravenous; Male; Propofol; Rare Diseases; Syndrome; Thiopental; Time Factors

Isoniazid is an anti-tuberculosis drug, used commonly for treatment and prophylaxis of tuberculosis. Acute isoniazid intoxication is characterized by a clinical triad consisting of metabolic acidosis resistant to treatment with sodium bicarbonate, seizures which may be fatal and refractory to standard anticonvulsant therapy, and coma. Treatment requires admission to the intensive care unit for ventilatory support, management of seizures and metabolic acidosis. Pyridoxine, in a dose equivalent to the amount of isoniazid ingested, is the only effective antidote. We report the successful treatment of two isoniazid intoxication cases: the case of a child developing an accidental acute isoniazid intoxication and an adult case of isoniazid intoxication with the intent of suicide.

Topics: Acidosis; Acute Disease; Adolescent; Anticonvulsants; Antitubercular Agents; Charcoal; Child; Coma; Diazepam; Female; Gastric Lavage; Humans; Intubation, Intratracheal; Isoniazid; Pyridoxine; Seizures; Sodium Bicarbonate; Suicide, Attempted; Thiopental; Vitamin B Complex

We describe a patient who entered a stuporous state after receiving benzodiazepine treatment for generalized tonic-clonic status epilepticus. A diagnosis of generalized NCSE with tonic seizures was made on the basis of the clinical picture and response to barbiturate anaesthetic, although the EEG pattern was not typical of the changes previously described in tonic seizures-tonic status epilepticus. This report discusses the differential diagnosis of postictal stupor, nonconvulsive status epilepticus with tonic seizures and sedation caused by the emergency treatment of status epilepticus, and summarizes the literature on tonic seizures and tonic status epilepticus.

Topics: Adult; Anticonvulsants; Benzodiazepines; Coma; Diagnosis, Differential; Electroencephalography; Epilepsy, Complex Partial; Epilepsy, Generalized; Epilepsy, Tonic-Clonic; Female; Humans; Learning Disabilities; Phenobarbital; Seizures; Status Epilepticus; Thiopental; Valproic Acid

Refractory status epilepticus (RSE) is a critical medical condition with high mortality. Although propofol (PRO) is considered an alternative treatment to barbiturates for the management of RSE, only limited data are available. The aim of this study was to assess PRO effectiveness in patients with RSE.. We retrospectively considered all consecutive patients with RSE admitted to the medical intensive care unit (ICU) between 1997 and 2002 treated with PRO for induction of EEG-monitored burst suppression. Subjects with anoxic encephalopathy showing pathological N20 on somatosensory evoked potentials were excluded.. We studied 31 RSE episodes in 27 adults (16 men, 11 women; median age, 41.5 years). All patients received PRO, and six also subsequently thiopental (THP). Clonazepam (CZP) was administered with PRO, and other antiepileptic drugs (AEDs) concomitant with PRO and THP. RSE was successfully treated with PRO in 21 (67%) episodes and with THP after PRO in three (10%). Median PRO injection rate was 4.8 mg/kg/h (range, 2.1-13), median duration of PRO treatment was 3 days (range, 1-9), and median duration of ICU stay was 7 days (range, 2-42). In 24 episodes in which the patient survived, shivering after general anesthesia was seen in 10 episodes, transient dystonia and hyperlipemia in one each, and mild neuropsychological impairment in five. The seven deaths were not directly related to PRO use.. PRO administered with CZP was effective in controlling most of RSE episodes, without major adverse effects. In this setting, PRO may therefore represent a valuable alternative to barbiturates. A randomized trial with these drug classes could definitively assess their respective role in RSE treatment.

Topics: Adult; Anesthetics, Intravenous; Anticonvulsants; Clonazepam; Coma; Dose-Response Relationship, Drug; Drug Therapy, Combination; Electroencephalography; Female; Humans; Infusions, Intravenous; Male; Monitoring, Physiologic; Propofol; Retrospective Studies; Status Epilepticus; Thiopental; Treatment Outcome

Rats poisoned with one LD50 of thiopental or amytal are shown to increase oxygen consumption when intraperitoneally given sucinate, malate, citrate, alpha-ketoglutarate, dimethylsuccinate or glutamate (the Krebs cycle intermediates or their precursors) but not when given glucose, pyruvate, acetate, benzoate or nicotinate (energy substrates of other metabolic stages etc). Survival was increased with succinate or malate from control groups, which ranged from 30-83% to 87-100%. These effects were unrelated to respiratory depression or hypoxia as judged by little or no effect of succinate on ventilation indices and by the lack of effect of oxygen administration. Body cooling of comatose rats at ambient temperature approximately 19 degrees C became slower with succinate, the rate of cooling correlated well with oxygen consumption decrease. Succinate had no potency to modify oxygen consumption and body temperature in intact rats. A condition for antidote effect of the Krebs intermediate was sufficiently high dosage (5 mmol/kg), further dose increase made no odds. Repeated dosing of succinate had more marked protective effect, than a single one, to oxygen consumption and tended to promote the attenuation of lethal effect of barbiturates. These data suggest that suppression of whole body oxygen consumption with barbiturate overdose could be an important contributor to both body cooling and mortality. Intermediates of Krebs cycle, not only succinate, may have a pronounced therapeutic effect under the proper treatment regimen. Availability of Krebs cycle intermediates may be a limiting factor for the whole body oxygen consumption in barbiturate coma, its role in brain needs further elucidation.

Topics: Amobarbital; Animals; Antidotes; Body Temperature; Citric Acid Cycle; Coma; Female; Hypnotics and Sedatives; Hypothermia; Injections, Intraperitoneal; Oxygen Consumption; Poisoning; Rats; Succinic Acid; Thiobarbiturates; Thiopental

Krebs cycle intermediates normalized gas exchange and decreased the mortality rate in rats with barbiturate coma. Treatment with other substrates including glucose and products of glycolysis was ineffective. Oxygen inhalation had no effect on oxygen consumption and indexes of external respiration. Our results suggest that deficiency of endogenous intermediates of the Krebs cycle, but not disturbances in oxygen mass transfer, serves as a limiting factor for oxygen consumption in rats with barbiturate coma.

Topics: Animals; Citric Acid Cycle; Coma; Female; Oxygen; Oxygen Consumption; Oxygen Inhalation Therapy; Rats; Succinates; Thiopental

Injection of sodium succinate in doses of 5 or 10 mmol/kg (but not 1 mmol/kg) intensified oxygen consumption in rats with sodium thiopental-induced coma. Injection of SDH inhibitor (sodium malonate) inhibited gas exchange and abolished the effect of sodium succinate. The effect of succinate on rat survival was positive, while that of malonate was negative, but manifested only as a trend. The critical role of succinate oxidation in preventing lethal complications of barbiturate-induced coma is proved.

Topics: Animals; Coma; Female; Hypnotics and Sedatives; Malonates; Oxygen Consumption; Rats; Respiration; Succinic Acid; Survival Rate; Thiopental

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

In an earlier study on the effect of mild hypothermia (34 degrees C) on the cerebral metabolic rate for oxygen (CMRO2) in rats, we used norepinephrine (NE) to support arterial blood pressure while inducing isoelectricity on the electroencephalogram (EEG) with thiopental (TP). Even with administration of sufficient TP to reduce a fully active EEG to an isoelectric EEG, CMRO2 was often unchanged. Based on this observation, we hypothesized that NE had activated CMRO2 despite thiopental coma. Therefore, we studied the effect of NE compared with donor blood (DB) infusion to maintain arterial blood pressure during TP-induced isoelectric EEG on whole-brain CBF (H2 clearance) and CMRO2 during normothermia (38 degrees C) and mild hypothermia (34 degrees C) in rats during 70% N2O/30% O2 analgesia. Cerebral blood flow (CBF) and CMRO2 were measured in four groups of rats at 38 degrees C followed by measurements at either 38 degrees C (two groups) or 34 degrees C (two groups) and during TP-induced EEG isoelectricity. Within each of the two groups at 38 degrees C and 34 degrees C, arterial pressure was sustained by either DB (n = 10) or NE (n = 9) infusion. At 38 degrees C, CMRO2 in the DB and NE groups was 7.92 +/- 1.05 and 6.4 +/- 0.80 mL x 100 g-1.min-1 and decreased to 50% of normal (3.95 +/- 0.70 and 3.32 +/- 0.40 mL x 100 g-1.min-1, respectively) during TP isoelectricity for a functional:basal CMRO2 distribution of 50% +/- 4% and 50% +/- 4%. At 34 degrees C, CMRO2 values in the DB and NE groups were 6.31 +/- 1.41 and 5.41 +/- 2.02 mL x 100 g-1.min-1, respectively. During TP-induced isoelectricity, CMRO2 values in both groups were reduced to 2.37 +/- 0.43 and 3.55 +/- 1.27 mL x 100g-1.min-1, respectively, resulting in a functional:basal CMRO2 distribution of 61%:38% in the DB group and the reverse, or 27%:73%, in the Ne group. Basal CMRO2 was significantly (P < 0.05) larger in the NE-infused rats. These results suggest that NE infusion, by increasing CMRO2 during mild hypothermia, could nullify its protective effects in the ischemic brain.

Topics: Adrenergic alpha-Agonists; Analgesics; Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Blood Pressure; Blood Transfusion; Body Temperature; Brain; Brain Ischemia; Cerebrovascular Circulation; Coma; Electroencephalography; Hypothermia; Hypothermia, Induced; Male; Neuroprotective Agents; Nitrous Oxide; Norepinephrine; Oxygen Consumption; Rats; Rats, Wistar; Thiopental

Brainstem reflexes were examined in 23 children treated with thiopentone infusion and correlated with serum thiopentone concentrations. The results suggest that if all brainstem reflexes are lost with a serum thiopentone concentration less than 40 mg/l, it is unlikely to be due to the thiopentone alone. Other causes including brain death need to be considered.

Topics: Adolescent; Brain Death; Brain Stem; Child; Child, Preschool; Coma; Humans; Infant; Infant, Newborn; Reflex; 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

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

Preterminal BAEP changes were studied until brain death in 8 head-injured patients out of a series of 38 comas monitored by means of a system allowing high-rate sequential recording. Two different modalities of BAEP degradation were disclosed: (1) simultaneous latency increase of all components associated with a decrease of cerebral perfusion pressure (CPP), consistent with ongoing ischaemia of the posterior fossa; (2) deterioration of brain-stem components (waves III-V) with preserved or even enhanced wave I. The latter pattern was not consistently associated with any haemodynamic change and might be related to mechanical factors causing rostro-caudal deterioration of brain-stem function. The time course of BAEP degradation ranged from a few minutes to more than 10 h. In the case of slow preterminal evolution definitely pathological trends were identified even when individual BAEPs were still within normal limits. Such trends would have remained unnoticed in single BAEP records. Hypothermia and anaesthetic drugs were found to induce falsely alarming BAEP changes very similar to those seen during preterminal evolution. Our results suggest that continuous brain-stem monitoring could be helpful for management of comatose head-injured patients.

Topics: Blood Pressure; Body Temperature; Brain Death; Brain Stem; Cerebrovascular Circulation; Coma; Data Display; Evoked Potentials, Auditory; Humans; Image Processing, Computer-Assisted; Intensive Care Units; Intracranial Pressure; Lidocaine; Methods; Monitoring, Physiologic; Thiopental

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

Topics: Anesthesia; Barbiturates; Brain; Cardiopulmonary Bypass; Coma; Heart Arrest; Humans; Statistics as Topic; Thiopental

Topics: Barbiturates; Coma; Craniocerebral Trauma; Humans; Thiopental

The aim of this study was to determine the feasibility of inducing a prolonged coma in severely asphyxiated newborn babies by the infusion of high dose thiopentone. In six severely asphyxiated babies the electroencephalograph (EEG) and blood pressure were monitored continuously. Thiopentone was infused at a rate sufficient to suppress completely the EEG providing the mean blood pressure remained above 35 mm Hg; it was continued until there was no evidence of cerebral oedema for 24 hours. In two the infusion was stopped prematurely because of hypotension that was unresponsive to treatment. In the other four a deep coma was maintained for a median duration of 127 hours. All developed pharmacodynamic tolerance to the thiopentone and showed non-linear elimination kinetics. Three babies died; the three survivors have moderate to severe handicap. It was concluded that with full intensive care it is possible to induce a deep coma; the outcome does not seem to be improved, however, and the incidence of complications was high.

Topics: Asphyxia Neonatorum; Coma; Feasibility Studies; Female; Humans; Infant, Newborn; Kinetics; Male; Thiopental

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

Topics: Aged; Ambulatory Care; Coma; Emergency Medical Technicians; Follow-Up Studies; Heart Arrest; Humans; Middle Aged; Prognosis; 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: Adolescent; Adult; Alfaxalone Alfadolone Mixture; Brain Injuries; Child; Coma; Female; Humans; Intracranial Pressure; Male; Monitoring, Physiologic; Thiopental

Three anoxic comatose children had EEG alpha-like activity and in two of them mu rhythm was recorded. The paradoxical appearance of these electrical activities in comatose children seems to indicate a grave prognosis. A possible role for barbiturate treatment in this phenomenon is not excluded.

Topics: Alpha Rhythm; Child; Child, Preschool; Coma; Electroencephalography; Female; Humans; Male; Prognosis; 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

The effect of barbiturate coma upon regional cerebral blood flow (RCBF) and ultimate neurologic outcome was examined after total cerebral ischemia (TCI). TCI was induced in dogs using a relatively noninvasive double-occlusion balloon technique; cardiopulmonary protection was provided during the period of ischemia. RCBF was measured using 15-mu radioactively labeled microspheres. A reproducible pattern of impaired reperfusion of the central nervous system (CNS) was observed in control animals after the restoration of cerebral perfusion pressure after TCI. This pattern was accentuated by the administration of pentothal to induce barbiturate coma. The additional depression in RCBF in those animals receiving pentothal was most prominent in cortical gray matter and brainstem structures at 3 and 6 h after TCI. It was also observed in cortical white matter. No untreated animal surviving TCI achieved a neurologic functional level better than persistent vegetative (decerebrate) survival over 1 wk of observation. Animals receiving 90 mg/kg body weight of pentothal post-TCI demonstrated irreversible cardiogenic shock related to the myocardial depressant effect of the drug. Animals receiving 40 to 60 mg/kg of pentothal post-TCI demonstrated a survival rate similar to that of untreated animals. Although this study did not establish the possible effectiveness of barbiturate coma in improving residual neurologic damage after TCI, the data do demonstrate that any possible effectiveness in this model is not associated with any improvement in the markedly decreased cerebral perfusion after TCI.

Topics: Animals; Brain Ischemia; Cerebrovascular Circulation; Coma; Dogs; Hemodynamics; Regional Blood Flow; Thiopental

A gaschromatographic method is presented for the determination of thiopental (and of its metabolite pentobarbital) in cases of severe head injuries treated by induction of therapeutic barbiturate coma. To 1 ml serum the internal standard and saturated ammonium sulphate solution are added. The mixture is extracted by chloroform and the concentrated organic phase is injected into the gaschromatograph (stationary phase: SP 2510 DA). Imprecision from day to day: Coefficient of variation 7.7%; recovery 97%. The specificity was checked by comparison with the retention time of more than 80 drugs. One determination is accomplished within 1 hour.

Topics: Barbiturates; Chromatography, Gas; Coma; Humans; Thiopental

Seven patients treated with deep sustained barbiturate narcosis to protect the brain and control intracranial hypertension underwent extensive monitoring. The epidural intracranial pressure (EDP) and arterial blood pressure (BP) were recorded continuously; serial records of the EEG, somatosensory evoked potential (SEP) and internal carotid artery (ICA) flow velocities by pulsed Doppler technique were obtained. Serum barbiturate levels leading to full suppression of the EEG did not change the central conduction time nor the configuration of the evoked responses. Monitoring the intracranial pressure (ICP), BP, and thereby, the cerebral perfusion pressure (CPP) gave valuable information on the patients' state and served as a guide for dosage and timing of barbiturate therapy, and facilitated supervision of adequate ventilation. Recording of EEG and SEP, monitoring of the CPP and ICA Doppler investigation offer prognostic information in these cases. When clinical deterioration occurs, these methods can predict and, in combination, give ample evidence for development of brain tamponade. Premature as well as unnecessarily deferred 4-vessel angiography, therefore, can be avoided.

Topics: Barbiturates; Blood Pressure; Brain; Cerebrovascular Circulation; Coma; Electroencephalography; Evaluation Studies as Topic; Evoked Potentials, Somatosensory; Humans; Intracranial Pressure; Monitoring, Physiologic; Prognosis; Thiopental

EEGs and somatosensory evoked responses from the brachial plexus, neck and scalp were recorded in seven comatose patients on continuous thiopentone infusion. Although pathological in five of the patients, the evoked responses were present in all. Additional amounts of thiopentone producing a full suppression of all spontaneous EEG activity had no effects either on the configuration of the evoked responses or on the central conduction times. This resistance of the somatosensory evoked responses to a deep and sustained thiopentone narcosis makes it a useful test in comatose patients receiving this treatment.

Topics: Adolescent; Adult; Child; Coma; Delta Rhythm; Electroencephalography; Evoked Potentials, Somatosensory; Humans; Prognosis; Pseudotumor Cerebri; Reaction Time; Theta Rhythm; Thiopental

The present studies evaluated the effect of phenobarbital, pentobarbital, and thiopental at concentrations comparable to those attained during therapeutic barbiturate-induced coma, on in vitro mitogen-induced lymphocyte activation. Lymphocytes from normal volunteers were incubated for 72 hours in culture medium containing mitogen (phytohemagglutinin) and a range of concentrations of the barbiturates (5 to 833 microgram/ml). Three parameters of lymphocyte activation (mitogen-induced blast transformation, 3H-thymidine incorporation, and cell proliferation) were all suppressed by the barbiturates. The suppression was dose-dependent. The greatest suppression was caused by the short-acting barbiturate, thiopental. Lymphocyte responses were much less affected by the long-acting barbiturate, phenobarbital. The intermediate-acting barbiturate, pentobarbital, was also intermediate in its ability to inhibit lymphocyte activation. The two-to threefold difference between the effects of thiopental and pentobarbital on lymphocyte function may have direct clinical relevance, since it is primarily these two agents that are employed to induce therapeutic "barbiturate coma." Since lymphocyte suppression appears to be much more marked in the presence of thiopental, these observations support a role for the other barbiturates in programs of induced coma.

Topics: Barbiturates; Blood Proteins; Cell Division; Coma; Humans; Lymphocyte Activation; Lymphocytes; Mitogens; Pentobarbital; Phenobarbital; Thiopental

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

Six children who remained in deep coma after immersion accidents in fresh water received therapy to maintain normal intracranial pressure (ICP). This involved controlled ventilation to ensure hypocapnia and hyperoxaemia, maintenance of low normothermia, fluid restriction, dexamethasone (1-1.5 mg/kg initially, 1-1.5 mg/kg/day as maintenance) and barbiturates (phenobarbitone and thiopentone). The latter were given in a wide range of dosage. Increased ICP was common to all patients, but could always be kept at acceptable levels. All patients suffered from pulmonary oedema; three developed broncho-pneumonia and two developed adult respiratory distress syndrome. All children survived with good recovery, two needed active rehabilitation for several months.

Topics: Accidents; Child; Child, Preschool; Coma; Critical Care; Female; Fresh Water; Humans; Hypothermia, Induced; Immersion; Infant; Intracranial Pressure; Male; Monitoring, Physiologic; Near Drowning; Phenobarbital; Pulmonary Edema; Resuscitation; Thiopental

Topics: Anti-Inflammatory Agents, Non-Steroidal; Child; Child, Preschool; Coma; Dexamethasone; Encephalitis; Female; Humans; Infant; Male; Phenobarbital; Positive-Pressure Respiration; Seizures; Thiopental

Topics: Adult; Coma; Female; Humans; Infusions, Parenteral; Seizures; Thiopental

Topics: Adult; Anesthesia, Intravenous; Cerebrospinal Fluid Shunts; Coma; Diazepam; Humans; Male; Nitrous Oxide; Pseudotumor Cerebri; Thiopental

Topics: Adolescent; Blood Pressure; Brain Diseases; Brain Neoplasms; Child; Child, Preschool; Coma; Craniocerebral Trauma; Female; Humans; Hypothermia, Induced; Intracranial Pressure; Male; Middle Aged; Pentobarbital; Perfusion; Respiration, Artificial; Skull Fractures; Thiopental

Topics: Acidosis; Aged; Anesthesia, General; Cholangitis; Cholecystectomy; Cholecystitis; Coma; Emergencies; Female; Humans; Hyperglycemia; Infusions, Parenteral; Insulin; Nitrous Oxide; Osmolar Concentration; Thiopental

Topics: Acidosis; Aged; Anesthesia, General; Blood Glucose; Cerebrovascular Disorders; Coma; Female; Humans; Hyperglycemia; Nitrous Oxide; Osmolar Concentration; Thiopental; Time Factors

Topics: Adult; Anesthesia, Endotracheal; Atropine; Coma; Female; Halothane; Humans; Kidney Transplantation; Male; Nephrectomy; Nitrous Oxide; Postoperative Complications; Respiration, Artificial; Seizures; Succinylcholine; Thiopental; Toxiferine; Transplantation, Homologous

Topics: Adult; Amobarbital; Barbiturates; Coma; Female; Humans; Pentobarbital; Phenobarbital; Thiopental

Topics: Anesthesia; Barbital; Barbiturates; Coma; Insulin; Psychotherapy; Shock; Sodium; Thiopental