Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Coma”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

Severe traumatic coma in infancy and childhood: results after surgery and resuscitation.

This study deals with 390 cases of severe traumatic coma in infancy, childhood and youth, aged between 4 months and 19 years. Cases in which unconsciousness lasted less than 24-48 hours have not been considered here. 161 patients were operated upon for intracranial space-occupying lesions or for open head injury: extradural haematomas 60; extradural haematomas + brain lacerations and/or subdural haematomas 16; acute subdural haematomas 18; brain laceration 36; open head injuries 17; decompressive operations, hydromas and contusions 14. 102 patients recovered and 59 died. 229 subjects were given only to resuscitation treatment. 164 recovered and 65 died. Recovery and mortality rate are discussed in relation to the pathologicial lesions and to the clinical picture (severity, evolution and duration of coma). Overall mortality rate was 31%. Mortality was higher in operated patients (36.6%) and lower in patients in whom space-occupying lesions were not demonstrated by angiography and who underwent only resuscitation treatment (28%). The lowest rate was observed in cases of extradural haematoma (25.4%) and open head injury (23%). Highest mortality rate have been observed in cases of decerebrated coma (with or without signs of low brain stem impairment). Complete recovery can be achieved even after prolonged decerebration. 31 patients showed the typical picture of the "apallic syndrome": in 28 cases after prolonged decerebrated coma, in 3 cases after coma without decerebration. Of our 31 cases, 4 died, 4 are still in a chronic apallic state and 23 recovered. Of these, 10 patients had a remarkable recovery and 13 remained severely disabled.

Adolescent↗
PubMed2002

No more coma cocktails. Using science to dispel myths & improve patient care.

It should be clear from this discussion that coma cocktails are a bad idea and should be immediately abandoned. In fact, the indiscriminate use of the coma cocktail may indeed harm patients, EMS has evolved to a point where any EMS provider should be able to reasonably determine the most likely cause of coma, or, in a worst-case scenario, narrow the cause to but a few possibilities. Certainly, patients with bona fide hypoglycemia should receive IV glucose. Because the consequences of prolonged hypoglycemia are severe, if there's a doubt about whether hypoglycemia is present, then glucose should be empirically administered. Naloxone should be used only for those cases in which a narcotic overdose appears likely. Similarly thiamine administration should be limited to patients suspected of chronic alcohol abuse and who exhibit at least one of the three symptoms of WE described above. Flumazenil has no role in the routine treatment of coma unless the patient is known to not be benzodiazepine dependent and the overdose is known to result only from benzos--two very difficult requirements to verify in the back of an ambulance at 2 a.m. Coma cocktails are bad medicine. Let's banish them from our EMS armamentarium.

Coma↗
PubMed1992

[Decrease in the incidence of epidural hematomas surgically treated during coma after a lucid interval. Is this an index of quality of care?].

The level of consciousness prior to surgery has been analyzed in a series of 64 patients suffering epidural hematoma (EDH) who underwent surgery during the period from July 1987 to June 1989. The percentage of cases which underwent surgery in coma after a lucid interval have been compared in different periods of time (1978-80, 1981-82, 1983-84 and July 1987 to June 1989). During the period from July 1987 to June 1989 surgery was performed on: 15 patients (23.5%) in coma from the moment of accident, 8 patients (12.5%) underwent surgery in coma but after a lucid interval and 41 patients (64.1%) were conscious. During the different periods of time the number of patients undergoing surgery in coma after a lucid interval were the following: 1979-80, 9 cases (26.5%); 1981-82, 17 cases (43.6%); 1983-84, 8 cases (20%) and during the last period, 1987-89, 7 cases (15.2%). The difference between the percentage of patients intervened in coma after a lucid interval in the previously referred periods of time was statistically significant (p 0.05).

Coma↗
PubMedDate not supplied

[Biochemical analysis of the vitreous body of the eye in post-mortem diagnosis of diabetic coma].

The biochemical test of the vitreous body (VB) may be used in post-mortem diagnosis of diabetes mellitus and diabetic coma. Concentrations of glucose, lactate, keton bodies in the VB of the eye do not depend on duration of post-mortem period. Methods of diagnosis of hyperglycemic, hypoglycemic and ketoacidotic comas in the postmortem period are proposed. VB glucose over 17 mmol/l is a specific marker indicating death due to diabetic coma with hyperglycemia. Blood lactate under 16 mmol/l and glucose absence in the VB specifically mark death of hypoglycemic coma. In death of diabetic coma with ketoacidosis, a sharp rise in the level of VB ketonic bodies was observed.

Biochemistry↗
PubMed1978

[Alcoholic coma by accidental poisoning in children].

Among comas of toxic origin, in children, alcoholic coma due to accidental poisoning is uncommon compared with comas due to drugs or household products. It is however important to make an early diagnosis, for this is a severe from of poisoning, liable to cause irreversible cerebral lesions if not treated very quickly. It almost always causes a flask coma, without localising signs, hypothermia and hypoglycemia, but hypoglycemic comas are not always of alcoholic origin, and only measurement of blood alcohol gives a definite diagnosis.

Accidents, Home↗
PubMedDate not supplied

Catecholamines in the rat brain during hypoglycemic convulsions and coma.

The purpose of the study was to investigate the relation between the catecholamines: noradrenaline and dopamine in the rat brain on one hand and hypoglycemic convulsions and coma on the other. Concentrations of noradrenaline in the hypothalamus, brain stem and cerebral cortex were decreased during hypoglycemic convulsions and were lower during coma than those during convulsions. Dopamine concentration in the striatum was decreased during convulsions and coma. It was shown that the decrease in concentration of catecholamines was a result of hypoglycemia but not of insulin action itself. Clonidine- alpha 2 agonist accelerated occurrence and prolonged duration of hypoglycemic convulsions. Haloperidol-dopamine receptor blocker had no effect on the time of occurrence or duration of convulsions and coma. The results indicate that noradrenaline may exert an inhibitory influence on hypoglycemic convulsions. No evidence has been provided to support involvement of dopamine in the control of hypoglycemic convulsions and coma.

Animals↗
PubMed1989

[Early prognosis in severe cranio-cerebral trauma using the Glasgow Coma Score and evoked potentials].

During 72 h following severe head injury, 103 patients in acute posttraumatic coma were assessed by clinical examinations (documented by Glasgow Coma Score) and brain stem auditory evoked potentials (BAEP) as well as short-latency somatosensory evoked potentials (SEP) following median-nerve stimulation. Patient outcomes were classified at 6 months or more according to the following categories: good recovery, severely disabled or vegetative, and brain dead. Patients who had died of systemic complications (pneumonia, septicemia, renal failure, etc.) were excluded from the study. The Glasgow Coma Score was reliable in forecasting a favorable outcome; all patients with a Score over 9 points had a good recovery. The Glasgow Coma Score was not reliable in predicting an unfavorable outcome, however; some patients with the lowest possible Glasgow Coma Score (3 points) at the early clinical examination survived with good recovery. The BAEPs were reliable predictors of an unfavorable outcome; the outcome was unfavorable when a missing wave V or more missing waves pointed toward a secondary brainstem lesion. Normal BAEPs were not reliable, however, in predicting a favorable outcome. SEP data served as a prognostic indicator of unfavorable as well as favorable outcomes. In summary, evoked potentials add valuable information to the clinical examination in assessing a patient's outcome after severe head injury.

Acute Disease↗
PubMed1981

[Coma states induced by craniocerebral injuries in children. Review of 20 cases].

From a total of three-hundred and fifty-six children admitted into the Department of Pediatrics at the Hospital Clínico of the University of Granada during of period of two years, twenty cases that needed admittance in critical pediatrics care unit are revised. Organic etiology that provoked coma, time of appearance, intensity, evolution, complications and short term outcome are analysed. A comparison is made of the incidences and prognosis of this type of coma with that of other authors presenting therapeutic outline carried. Two large evolutive groups; one which consisted of nine patients which entered into coma immediately after injury. The second group includes those patients which had lucid period before entering into coma. Following conclusions have been withdrawn: Severity and duration of coma does not have a definite relationship with the existence of a mass-lesion. Presence of an associated--mass-lesion is a sign of grave prognosis. For a good therapeutic response the following approaches are necessary: Immediate assistance monitoring and periodic or systematic maintenance of extracranial variants diagnostic, and treatment of the primary causing factor.

Brain Injuries↗
PubMed1980

The outcome of prolonged coma in childhood.

The outcome of prolonged, nontraumatic coma (greater than five days) in 16 children is reviewed to determine operational clinical parameters which may assist in both clinical decision making and counseling of parents. The children were evaluated by physical and neurologic examinations and school reports one to five years after coma. Six children are normal, six have minor handicaps (attention deficit disorder, minor motor disorders, mild retardation, personality disorders), and four have sustained major sequelae (severe retardation, uncontrolled seizures, blindness). Anoxia, as an etiology of coma and the need for assisted ventilation, were significant indicators of a less than normal outcome. Our results suggest that elevated intracranial pressure of greater than two days duration and deep coma of greater than two weeks were indicators of an abnormal outcome. In view of the improving technical capability to care for these children, but limited past experience, clearly defined and uniform criteria are needed both to assess children during coma and to evaluate them upon recovery.

Adolescent↗
PubMed1997

[A protocol for the assessment of patients with coma of unknown origin].

OBJECTIVE: Evaluation of the applicability of a protocol designed for the quick and efficient management of patients with coma of unknown origin (CUO). METHODS: Every patient admitted to our Emergency Department with the diagnosis of CUO was evaluated with our diagnostic protocol. The first diagnostic steps included evaluation of the hemodynamic and respiratory situation, Glasgow Coma Scale, basic neurologic and clinical examination, as well as blood withdrawal, for analysis of metabolic and toxicologic parameters. If indicated, cranial computer tomography (CCT) and/or lumbar puncture were performed. RESULTS: Within the study period from 1. 1. 1995 until 30. 9. 1996, 122 patients (65 males, median age 50 years, 25 and 75 percentile: 33; 69) were included. Blood analysis and the toxicological screening were diagnostic effective in 66 patients, clinical examination and body temperature in one case each, CCT in 50 patients and lumbar puncture in 2 patients. By the use of this diagnostic protocol 51 neurologic, 38 toxicologic, 28 metabolic and 2 infectious causes of coma were diagnosed (98%). Etiology of 2 of the comas remained unclear. CONCLUSION: By using our protocol, 98% of the causes of CUO were clarified. The main causes of coma were of neurological, toxicological and metabolic origin. CCT and the blood analysis were the most important procedures leading to a final diagnosis.

Adult↗
PubMed1987

The dust distribution within the inner coma of comet P/Halley 1982i: encounter by Giotto's impact detectors.

Analysis of the data from Giotto's Dust Impact Detection System experiment (DIDSY) is presented. These data represent measurement of the size of dust grains incident on the Giotto dust shield along its trajectory through the coma of comet P/Halley on 1986 March 13/14. First detection occurred at some 287000 km distance from the nucleus on the inbound leg; the majority of the DIDSY subsystems remained operational after closest approach (604 km) yielding the last detection at about 202000 km from the nucleus. In order to improve the data coverage (and especially for the smallest grains, to approximately 10(-19) kg particle mass), data from the PIA instrument has been combined with DIDSY data. Flux profiles are presented for the various mass channels showing, to a first approximation, a 1/R2 flux dependence, where R is the distance of the detection point from the cometary nucleus, although significant differences are noted. Deviations from this dependence are observed, particularly close to the nucleus. From the flux profiles, mass and geometrical area distributions for the dust grains are derived for the trajectory through the coma. Groundbased CCD imaging of the dust continuum in the inner coma at the time of encounter is also used to derive the area of grains intercepted by Giotto. The results are consistent with the area functions derived by Giotto data and the low albedo of the grains deduced from infrared emission. For the close encounter period (-5 min to +5 min), the cumulative mass distribution function has been investigated, initially in 20 second periods; there is strong evidence from the data for a steepening of the index of the mass distribution for masses greater than 10(-13) kg during passage through dust jets which is not within the error limits of statistical uncertainty. The fluences for dust grains along the entire trajectory is calculated; it is found that extrapolation of the spectrum determined at intermediate masses (cumulative mass index alpha = 0.85) is not able to account for the spacecraft deceleration as observed by the Giotto Radio Science Experiment and by ESOC tracking operations. Data at large masses (>10(-8) kg) recently analysed from the DIDSY data set show clear evidence of a decrease in the mass distribution index at these masses within the coma, and it is shown that such a value of the mass index can provide sufficient mass for consistency with the observed deceleration. The total particulate mass output from the nucleus of comet P/Halley at the time of encounter would be dependent on the maximum mass emitted if this change in slope observed in the coma were also applicable to the emission from the nucleus; this matter is discussed in the text. The flux time profiles have been converted through a simple approach to modeling of the particle trajectories to yield an indication of nucleus surface activity. There is indication of an enhancement in flux at t approximately -29 s corresponding to crossing of the dawn terminator, but the flux detected prior to crossing of the dawn terminator is shown to be higher than predicted by simple modelling. Further enhancements corresponding to jet activity are detected around +190 s and +270 s.

Astronomical Phenomena↗
PubMed1988

Regional brain GABA metabolism and release during hepatic coma produced in rats chronically treated with carbon tetrachloride.

Hepatic coma was induced in rats chronically treated with CCl4, by means of a single injection of ammonium acetate. The activities of glutamate decarboxylase (GAD) and GABA transaminase (GABA-T), as well as the synaptosomal uptake and release of [3H]GABA, were measured in the following brain areas of the comatose rats: cortex, striatum, hypothalamus, hippocampus, midbrain and cerebellum. Hepatic coma was associated with a general decrease of GAD activity, whereas GABA-T activity was diminished only in the hypothalamus, striatum and midbrain. During hepatic coma, the K+-stimulated [3H]GABA release was notably diminished in the striatum and cerebellum, whereas a significant increase was observed in the hippocampus. [3H]GABA uptake increased in most regions after CCl4 treatment, independently of the presence of coma. The results indicate that GABAergic transmission seems to be decreased in most cerebral regions during hepatic coma.

4-Aminobutyrate Transaminase↗
PubMed1980

CNS tryptamine metabolism in hepatic coma.

Lumbar CSF indoleacetic acid (IAA) was higher in patients with cirrhosis of the liver than in controls. It was also higher in CSF of patients in coma than in those with hepatic cirrhosis but not in coma. There was a strong correlation (r = 0.89, p less than 0.01) between the grade of hepatic coma and CSF IAA. These data indicate that there is an association between elevated CNS tryptamine metabolism and hepatic coma. How far changes in the metabolism of tryptamine and other trace amines are relevant to the induction of hepatic coma or are simply a reflection of advanced liver dysfunction is unclear.

Adult↗
PubMed1979

A longitudinal study of tryptophan involvement in hepatic coma.

Previous cross-sectional studies have demonstrated that hepatic coma is associated with abnormally high levels of plasma free tryptophan. Establishment of a more definitive relationship between this biochemical abnormality and hepatic coma requires an evaluation of biochemical changes in individual patients as they undergo alterations in the function of their central nervous systems. The present report is an evaluation of tryptophan and substances believed to influence its entry into the brain in six patients whose clinical status progressed from hepatic coma to complete recovery. Consistent significant decreases in plasma free tryptophan and free fatty acids were demonsrated to occur as the patients recovered. No consistent changes, however, were found in the plasma levels of the amino acids which have been reported to compete with tryptophan for transport across the blood-brain barrier, except for leucine which was significantly decreased in all six patients upon recovery from coma. Assay of lumbar cerebrospinal fluid for both tryptophan and the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), showed no consistent changes as the patients recovered from hepatic coma.

Adult↗
PubMed2001

Identification and characterization of novel competence genes comA and exbB involved in natural genetic transformation of Pseudomonas stutzeri.

After transposon mutagenesis we identified a novel gene (comA) of Pseudomonas stutzeri which is essential for natural genetic transformation. The putative amino acid sequence is similar to ComA orthologs of other transformable bacteria including Neisseria gonorrhoeae (ComA), Haemophilus influenzae (Rec-2), Bacillus subtilis (ComEC) and Streptococcus pneumoniae (CelB). Downstream of comA two partially overlapping open reading frames termed exbB and exbD were found coding for putative proteins similar to proteins required for macromolecule uptake in Escherichia coli and present in other Gram-negative bacteria. Insertional inactivation of exbB decreased the transformability to 20% of that of the wild type. The binding of 3H-labeled DNA and its uptake into a DNase-resistant state in the comA and exbB strains were similar to the wild type, suggesting that these proteins are involved in a late step of transformation, presumably in the translocation of DNA from the periplasm into the cytosol. The question of whether the translocation process occurs separately from the step of single-strand formation is discussed.

Amino Acid Sequence↗
PubMed1977

[Extracorporeal perfusion with baboon liver in the treatment of hepatic coma (author's transl)].

In 11 patients with hepatic coma (stage IV and V according to Abouna) extracorporeal haemoperfusion using the Scribner shunt (radial or profunda femoris artery) was performed over 12 to 27 hours with 22 baboon and one human livers. Eight patients emerged from coma, six of them showed sufficient regeneration of the diseased liver. Four patients were discharged as cured, one patient died of acute pancreatic necrosis, a further one due to bleeding from an old gastric ulcer. In the 2 remaining patients the coma recurred within 48 hours. Tree patients never came round from coma. After perfusion no antibodies against baboon proteins were demonstrable in the patients. Thus there is very little danger of an anaphylactic reaction when perfusion is repeated. The titre of preformed cytotoxic antibodies against baboon cells in patients' serum rises only after 1-2 weeks and decreases again after 4 weeks. In our experience extracorporeal liver perfusion with baboon or human livers is the most promising method for treatment of hepatic coma.

Adult↗
PubMed1984

Grade I Reye's syndrome--outcome and predictors of progression to deeper coma grades.

We studied 83 biopsy-proved cases of Grade I Reye's syndrome to determine the outcome, possible clinical or laboratory predictors of progression to deeper coma grades, and hepatic ultrastructural findings. Seventy-eight patients had no change in coma grade during hospitalization, whereas five (6 per cent) had progression to deeper coma grades. All the patients survived without sequelae except one who sustained severe brain damage. The mean (+/- S.E.) level of serum ammonia on admission was significantly higher (P = 0.005) in patients whose disease progressed to deeper neurologic grades (291 +/- 42 micrograms per deciliter) than in those whose disease did not so progress (53 +/- 5 micrograms per deciliter), and the corrected prothrombin time was significantly more prolonged (P = 0.005) in patients with progressing coma (3.9 +/- 0.5 seconds) than in those whose coma grade did not change (1.6 +/- 0.2 seconds). The combination of a prothrombin time 3 seconds or longer than that of the control and a serum level of ammonia on admission of 100 micrograms per deciliter or more correctly predicted progression in 71.5 per cent of the cases (sensitivity, 100 per cent; specificity, 97.6 per cent). Our findings suggest that the prognosis is excellent for survival without sequelae in Grade I Reye's syndrome (98.8 per cent) when management includes hospital surveillance and intravenous glucose and electrolyte infusion.

Ammonia↗
PubMed1976

L-dopa in hepatic coma.

The use of L-Dopa in hepatic coma has been the subject of numerous reports since 1970. The following represents our experience with a rather heterogenous group of patients treated at the Massachusetts General Hospital over the past 4 years. Thirty-five patients with severe liver disease, a mean age of 53 +/- 3.5 years, including nutritional cirrhosis with acute coma and acute hepatitis were treated. Four patients were judged grade III, 31 patients grade IV. All patients had previously been treated with protein restriction, orally administered non-absorbable antibiotics, fluid and electrolytes, and in some cases, steroids. L-Dopa was given orally in 21 patients, and as a retention enema in 14. Thirteen of the 35 patients did not respond to therapy. Seventeen responded, but did not survive, and 5 patients responded and survived. There was no difference between any of the groups as far as dosage of L-Dopa and clinical features. The one striking finding as the differences between groups was the time of initiation of L-Dopa therapy. In Group I, the survivors, therapy was started within 1.4 +/- 0.8 days after the onset of coma. In Group II, there was an initiation of therapy at 6.7 +/- 1.6 days, and in the non-responders 9.5 +/- 1.6 days. These differences are highly significant. The results suggest that coma may pass from a reversible to an irreversible stage, and that L-Dopa therapy initiated early in the course of hepatic coma, may be of some benefit.

Alcoholism↗