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PubMedDate not supplied

Tolerance and efficacy of enteral nutrition in traumatic brain-injured patients induced into barbiturate coma.

BACKGROUND: There is a paucity of data evaluating the efficacy of nutrition support in traumatic brain-injured patients induced into barbiturate coma for refractory intracranial hypertension. Our objective was to evaluate the efficacy of enteral nutrition in a select group of trauma patients. METHODS: Prospective data were collected on severe traumatic brain-injured patients over a 4-year period. Patients were stratified by whether or not they were induced into a barbiturate coma. Barbiturate coma was defined as per American Association of Neurological Surgeons (AANS) guidelines. All patients were initially fed via the enteral route via a nasogastric feeding tube. Patients who did not tolerate feedings within 48 hours started receiving prokinetic agents. Feeding tolerance was defined as ability to tolerate enteral feedings with <150 mL of gastric residuals every 6 hours for >72 hours. RESULTS: Fifty-seven patients were induced into a barbiturate coma. All were victims of blunt-force trauma. Forty-two of 57 (74%) patients were men, with a mean age of 37+/-12 years and a mean injury severity score of 24+/-10. Thirty-eight of the 57 (67%) patients had an isolated traumatic brain injury. All 57 patients failed enteral nutrition via the nasogastric route after the first 48 hours of nutrition initiation after barbiturate coma was fully achieved by protocol criteria. Prokinetic agents demonstrated no improvement in feeding tolerance after the subsequent 48-72 hours. Of the 12 patients who had a postpyloric feeding tube placed, only 25% tolerated enteral nutrition for >48 hours. CONCLUSIONS: Patients with traumatic brain injury induced into barbiturate coma develop a significant ileus that is refractory to prokinetic agents. Only a marginal improvement is seen when the postpyloric route is obtained. Early parenteral nutrition should be considered in this patient population.

Adult↗
PubMed1990

Rhythmic coma in children.

We describe a syndrome of rhythmic coma in children that consists of an invariant, nonreactive, diffuse cortical activity of a specific frequency, such as alpha, beta, spindle, or theta, recorded from a comatose child. We report 11 cases of children who were found to be in rhythmic coma during their acute illnesses. Their ages ranged from 2 to 15 years, and their diagnoses included encephalitis, head trauma, seizures, near drowning, brain tumors, stroke, and metabolic derangements. The specific frequency of the electroencephalographic pattern, ie, alpha, beta, spindle, or theta, did not influence the outcome. The clinical outcome appeared to depend on the primary disease process rather than the electroencephalographic finding. The prognosis of alpha-frequency rhythmic coma as well as of rhythmic coma in general was better in children than in adults. The pathophysiology in children may be similar, ie, the interruption of reticulothalamocortical pathways by metabolic or structural abnormalities, but the expression of this deafferentation may be more varied in the developing brain. Thus, we propose the term rhythmic coma as a unified concept for alpha, beta, spindle, and theta coma in children.

Adolescent↗
PubMed1993

Valproate-induced coma: case report and literature review.

OBJECTIVE: To report a case of hyperammonemia without hepatic dysfunction as a possible cause of lethargy, stupor, and coma in a woman after valproic acid (VPA) administration, and discuss the possible different mechanisms of ammonia elevation and coma. CASE SUMMARY: A woman diagnosed with complex partial seizures that secondarily generalize was treated with phenytoin (PHT) 250 mg/d for 18 years. Three months before admission, this dosage was increased to 300 mg/d and phenobarbital (PB) 100 mg/d was added because the seizures were incompletely controlled. The patient developed a progressive inability to walk. She was diagnosed as having PHT intoxication. VPA therapy was begun while PHT was being tapered and progressive impairment of consciousness occurred. This evolved into a coma without focal neurologic signs, and was accompanied by isolated hyperammonemia without hepatic failure. DISCUSSION: Adverse effects attributable to VPA were reviewed in the literature. Occasionally, VPA may lead to severe secondary effects such as hepatic failure and coma. In these cases increased blood concentrations of transaminases, bilirubin, and ammonia have been found. Several reports have stressed the existence of hyperammonemic coma without biochemical evidence of hepatic failure, which is what occurred in our patient. This suggests that isolated hyperammonemia and hepatic failure after VPA treatment may have a different biochemical basis. CONCLUSIONS: VPA-induced coma with hyperammonemia and without evidence of hepatic failure should be considered in patients being treated with PHT or PB when VPA is administered concomitantly. This case report shows the importance of clinical monitoring and immediate drug discontinuation when drowsiness, gastrointestinal symptoms, or lethargy occur.

Ammonia↗
PubMed1988

EEG abnormality grades and subdivisions of prognostic importance in traumatic and anoxic coma in adults.

The EEG has long been established as an important laboratory test when assessing cerebral function in comatose states. During the last three decades, several grading scales regarding severity of the EEG abnormality in coma have been suggested to increase the prognostic power of the EEG for survival. Their main limitation was, that the majority of EEG abnormalities in coma fell in the middle of the five point scaling systems, i.e. Grade 3 abnormality on the five grade abnormality scales. In addition, it was considered that non-reactivity of EEG pattern in coma is confined only to the most advanced grades. The purpose of the present article is to define precisely the main five abnormality grades and their subdivisions, and to allocate them in five principal categories regarding their significance for survival. The five categories are: 1 = optimal, 2 = benign if persistent, 3 = uncertain, 4 = malignant if persistent, and 5 = fatal unless caused by drug effect or hypothermia. After the inclusion of more recently described coma patterns, it was possible to outline prognostic significance for survival in eleven types of abnormalities with assurance. Only four remain of uncertain prognostic significance. The EEG abnormalities as discussed in this article are generally applicable only to coma after diffuse brain trauma and cerebral hypoxia. However, they may also be found in some other diffuse encephalopathies associated with coma.

Alpha Rhythm↗
PubMed2005

Persistent but reversible coma in encephalitis.

INTRODUCTION: Nontraumatic coma in adults has a poor prognosis, and late recovery of consciousness is unlikely. Functional recovery is usually extremely poor. However, a few nontraumatic comatose patients have shown late recovery of both awareness and function. METHODS: A retrospective survey was conducted by reviewing the medical records of all inpatients to our department during the 1990s. Patients with persistent but reversible nontraumatic coma were identified according to the following criteria: (a) deep coma with a Glasgow Coma Scale (GCS) score of 7 or less on admission; (b) nontraumatic cause; (c) persistence of unconsciousness for longer than 1 month; and (d) subsequent recovery of GCS (total) to normal. The clinical spectrum of patients meeting these criteria was evaluated. RESULTS: Six patients (ages 16-75 years) met the criteria. Viral encephalitis was diagnosed in five (two with herpes simplex virus, two with cytomegalovirus, and one with Epstein-Barr virus or cytomegalovirus). Two young female patients with encephalitis manifested extremely protracted coma persisting for 3 and 18 months, respectively. Complications included nonconvulsive status epilepticus in two patients and relative overdose of clonazepam in one patient. CONCLUSION: Recognition of the clinical spectrum of persistent but reversible nontraumatic coma is important.

Adolescent↗
PubMed1976

Head injury in children and teenagers; functional recovery correlated with the duration of coma.

Residual impairments and mortality were assessed in 48 patients under 20 years of age at least two years after a traumatic head injury had caused coma lasting more than seven days. In this study the duration of coma was defined as the period of time when it is impossible to establish intellectual contact with the patient. A classification of functional levels 1 to 8 was used to identify the residual impairment and relate this impairment to the duration of coma for each patient. Of 30 patients who remained in coma less than three month, only one did not have independent ambulation with or without equipment at the time of his last follow-up evaluation. This was one parameter among others to show that the prognosis for recovery in this age group is much better than expected following severe head injury. These follow-up data, correlated with the duration of coma, can assist rehabilitation personnel in the prognostic planning for younger people with severe head injuries. Rehabilitation medicine needs to be involved in patient care during the period of coma to prevent contractures and other complications which often interfere with and delay later rehabilitation programs, making them more costly and less successful.

Adolescent↗
PubMed1992

[Comas in the emergency room of a central hospital].

The aim of the present prospective work was to study the etiologic diagnosis and prognosis of the comatose patients for whom a neurologic examination is requested. It included 148 consecutive cases admitted to the emergency room of a general hospital. Coma was caused by supratentorial lesions in 38%, subtentorial lesions in 10%, diffuse or metabolic brain dysfunction in 49%, and psychiatric disorder in 1% of the patients. CT scan was the most valuable ancillary exam, modifying the initial etiologic diagnosis in 42% of the cases on whom it was performed. Seventy percent of the patients died. Coma caused by structural lesions had a worse outcome than coma caused by diffuse or metabolic brain dysfunction (intoxications excluded), and this type of coma had a worse outcome than drug-induced coma. The presence of anisocoria, the number of brainstem reflexes present and the pattern of motor response, as well as the Glasgow Coma Scale score, predicted the outcome.

Adult↗
PubMed2005

Perioperative stroke and coma in Thai Anesthesia Incidents Study (THAI Study).

OBJECTIVES: To analyze perioperative stroke and coma using database of Thai Anesthesia Incidents Study (THAI Study) with regard to frequency, contributing factors, preventive and corrective strategies. MATERIAL AND METHOD: Details of perioperative neurological complications comprising stroke and coma in one year were recorded prospectively by attending anesthesiologists or nurse anesthetists in standardized record forms. All data were analyzed to identify contributing factors and preventive strategies. RESULTS: Among 172,592 anesthetics, there were 24 cases of coma, and 28 cases of stroke. Most cases of coma that eventually died (12/16 cases, 75%) had ASA physical status (ASA PS) ranging from 2E to 5E. Perioperative stroke was found mainly in patients with ASA PS 3 and most of the incidence (74%) occurred in patients who had no previous history of stroke. These patients already had pre-existing cardiovascular diseases and underwent high risk procedures. There were 54% of perioperative stroke cases that could be due to improper cardiovascular management and 42% due to improper emergency neurological management. CONCLUSION: The incidence of perioperative stroke and coma in this study was approximately 0.03%. The majority of cases had no prior stroke or coma, which suggested that a problem during perioperative period itself might predispose patients to these complications. Preventive strategies included quality assurance activity, improved communication, and practice guideline.

Adolescent↗
PubMed1990

[Prognostic value of electroencephalography in non-traumatic comas].

We recorded an EEG within the first few days of coma in 100 patients without history of trauma or drug intoxication, in 50 after cardiac arrest, and in 50 in coma of other, chiefly metabolic etiologies. The EEG findings were classified in 5 categories (I-V) in terms of increasing severity. We were especially interested in the question whether the degree of early EEG disturbances allows prognostic conclusions regarding the clinical fate of patients one month after the beginning of coma. It was found that very severe EEG changes (Grad IV-V) indicate a poor prognosis (death, persistent vegetative state or profound neurological deficits) in over 90% of coma both after cardiac arrest and of other etiologies. An EEG without very severe changes (grade I-III) does not allow definite prognostic conclusions. Depending on the etiology, recovery occurs in 10-33% of cases. The prognostic significance of certain EEG parameters can be summarized as follows: areactivity to external stimuli and the presence of an "alpha-coma" pattern are usually (but not necessarily) associated with a poor outcome. The same applies to coma patients with epileptiform patterns in the EEG and/or suffering from epileptic or myoclonic seizures. One-fourth of patients with triphasic EEG complexes recover completely.

Adolescent↗
PubMed1987

[Recurrent coma, papular mucinosis and benign dysglobulinemia].

A woman presented with a history of three regressive comas of undetectable etiology between the age of 52 and 57 years. An IgG lambda benign monoclonal dysglobulinemia was combined with a papular mucinosis (myxedematous lichen or the generalized form of Arndt-Gotton's scleromyxedema). In the 6 analogous cases documented in the literature the onset of coma occurred generally several weeks after an aggravation of the cutaneous lesions. The coma was preceded by an influenza-like syndrome followed by asthenia, malaise with vertigo and frequently epileptic seizures. During recovery, hallucinations and transient hepatic disorders were noted. Pruritus with pronounced hypereosinophilia preceded desquamation and regression of dermatologic lesions. These comas can lead to a fatal outcome (2 of 7 cases) or regress in 2 to 20 days usually without sequelae. The disease is probably of immunologic origin. The paraprotein or a serum factor could exert a direct toxic effect on brain. As in neurologic manifestations of malignant dysglobulinemia, explained initially by a "toxic encephalosis, clinical, angiography, biologic and immunologic data exist in favor of blood hyperviscosity. This hyperviscosity could result from polymer formation through intermediates immunoglobulins and other protein chains, or again from alteration of deformability of red cells by binding of paraprotein. Hyperviscosity syndromes are frequent in system diseases that are often associated with papular mucinosis. Whatever the exact mechanism of these "comas due to papular mucinosis", a logical choice is their treatment by immunosuppressants and plasmapheresis: in the case reported, the use of plasmapheresis as soon as premonitory signs had appeared probably prevented a fourth coma.

Alopecia↗
PubMedDate not supplied

Brainstem auditory evoked potentials in toxic, metabolic and anoxic coma.

The aim of this study was to evaluate the efficacy of brainstem auditory evoked responses as a prognostic tool in conditions of coma which interfere with cerebral metabolism. Thirteen patients in coma resulting from different systemic disorders (barbiturate intoxication, cardiac arrest, chronic hepatic insufficiency) were included in the study. Brainstem auditory evoked potentials were recorded and patients were graded according to the results. When used in conjunction with other clinical parameters (Glasgow Coma Scale), brainstem auditory evoked potentials provided a more reliable prognostic tool than the traditional EEG exam alone. A good correlation was found between electrophysiological data and clinical outcome not only in barbiturate (toxic) coma, but also in hepatic (metabolic) coma. Of particular significance was the disappearance of the components which follow wave III (grade 2), leading to a fatal outcome in all three patients in hepatic coma.

Adult↗
PubMedDate not supplied

[Alpha coma--a prognostic sign?].

We present a patient who has developed cardiac arrest after penetrating cardiac wound and consequent coma, with EEG characteristics of alpha coma. At the same time, auditory evoked potentials-brainstem (AEPB), subcortical and cortical were not within physiological range. During the sixth day of coma, alfa rhythm was substituted with theta and delta frequency, followed by the decreased amplitude and prolonged latency of AEPB and complete absence of cortical and subcortical responses. Lethal outcome occurred in the fifth week of coma with neurophysiological characteristics of complete brain dysfunction. Alpha coma, with EEG presentation that only resemble the normal neurophysiological cortical activity, is rather rare neurophysiological finding present mostly in cardiac arrest, metabolic disturbances and intoxication. It is probably caused by pathological pacers of alfa rhythm, so clinical presentation of alfa coma, specially in a case of cardiac arrest, does not predict a favourable outcome.

Alpha Rhythm↗
PubMed1980

[Electroencephalography in hepatic coma: therapy with hemoperfusion (author's transl)].

Six patients (two men and four women) aged between 15 and 60 years in hepatic coma stage IV and with very severe EEG changes were treated with hemoperfusion. The causes leading to coma were acute virus hepatitis A in two cases, hepatitis B in three cases, and Amanita intoxication in one case. Only the patient with Amanita intoxication survived. On admission to the hospital, there were very severe EEG changes of stage IV in all patients. They preceded the clinical manifestation of coma stage IV up to one day in half of the patients who were at most in coma stage II at this time. At the beginning of therapy better survival chances are reported in the lower coma stages. On the basis of the severely pathological EEG findings preceding the clinical coma in a proportion of the patients, an earlier start of therapy should thus be demanded.

Adolescent↗
PubMed2003

TPR-mediated interaction of RapC with ComA inhibits response regulator-DNA binding for competence development in Bacillus subtilis.

The Bacillus subtilis Rap family of proteins are characterized by protein-protein interaction modules containing the so-called tetratricopeptide repeats (TPRs). The six TPR motifs of RapC mediate its interaction with the pentapeptide inhibitor PhrC (ERGMT) or with its target protein ComA, a phosphorylation-dependent response regulator transcription factor for genetic competence. Our results show that RapC interaction with ComA inhibits the response regulator's ability to bind its target DNA promoter but does not affect its phosphorylation state. RapC binds equally well to ComA or to ComA approximately P. The PhrC pentapeptide binds to RapC and inhibits its interaction with ComA. The D195 residue in TPR3 and the P263 residue in TPR5 of RapC are critical for the interaction with PhrC as their mutation to asparagine or leucine, respectively, prevents peptide inhibitory activity. The RapC mechanism of regulating ComA activity is a new example of how TPR motifs and their structural organization have been adapted for different specific functions within the B. subtilis Rap family.

Amino Acid Motifs↗
PubMed2006

Modulation of the ComA-dependent quorum response in Bacillus subtilis by multiple Rap proteins and Phr peptides.

In Bacillus subtilis, extracellular peptide signaling regulates several biological processes. Secreted Phr signaling peptides are imported into the cell and act intracellularly to antagonize the activity of regulators known as Rap proteins. B. subtilis encodes several Rap proteins and Phr peptides, and the processes regulated by many of these Rap proteins and Phr peptides are unknown. We used DNA microarrays to characterize the roles that several rap-phr signaling modules play in regulating gene expression. We found that rapK-phrK regulates the expression of a number of genes activated by the response regulator ComA. ComA activates expression of genes involved in competence development and the production of several secreted products. Two Phr peptides, PhrC and PhrF, were previously known to stimulate the activity of ComA. We assayed the roles that PhrC, PhrF, and PhrK play in regulating gene expression and found that these three peptides stimulate ComA-dependent gene expression to different levels and are all required for full expression of genes activated by ComA. The involvement of multiple Rap proteins and Phr peptides allows multiple physiological cues to be integrated into a regulatory network that modulates the timing and magnitude of the ComA response.

Bacillus subtilis↗
PubMed1991

The primary role of comA in establishment of the competent state in Bacillus subtilis is to activate expression of srfA.

The establishment of genetic competence in Bacillus subtilis requires the genes of the competence regulon which function in the binding, processing, and transport of DNA. Their expression is governed by multiple regulatory pathways that are composed of the comA, comP, sin, abrB, spo0H, spo0K, spo0A, degU, and srfA gene products. Among these, srfA is thought to occupy an intermediate position in one of the pathways that controls late competence gene expression. The full expression of srfA requires the gene products of comP, comA, and spo0K. To determine the role of these genes in the regulation of competence development, the expression of the srfA operon was placed under control of the isopropyl-beta-D-thiogalactopyranoside (IPTG)-inducible promoter Pspac and the expression of the Pspac-srfA construct was examined in mutants blocked in early competence. By monitoring the IPTG-induced expression of Pspac-srfA with a srfA-lacZ operon fusion, it was observed that srfA expression was no longer dependent on the products of comP, comA, and spo0K. Production of the lipopeptide antibiotic surfactin in Pspac-srfA-bearing cells was induced in the presence of IPTG and was independent of ComP and ComA. Competence development was induced by IPTG and was independent of comP, comA, and spo0K in cells carrying Pspac-srfA. These results suggest that the ComP-ComA signal transduction pathway as well as Spo0K is required for the expression of srfA in the regulatory cascade of competence development. Studies of Pspac-srfA also examined the involvement of srfA in the growth stage-specific and nutritional regulation of a late competence gene.

Bacillus subtilis↗
PubMed1993

ComA, a phosphorylated response regulator protein of Bacillus subtilis, binds to the promoter region of srfA.

ComA is a response regulator protein of Bacillus subtilis which is required for the transcription of several genes which are involved in late-growth expression and in responses to environmental stress. Among these genes are degQ, gsiA, and srfA. The last is an operon needed for the development of genetic competence, surfactin production, and normal sporulation. We show here that partially purified ComA protein, isolated from an overproducing Escherichia coli strain, is phosphorylated in vitro by incubation with acetyl phosphate and that ComA could bind specifically to a DNA fragment containing the promoter of srfA and associated sequences. The binding affinity is enhanced when ComA is phosphorylated. DNase I protection analysis identified two protected sites located upstream from the srfA promoter. The presence of DNase I-hypersensitive bonds induced by ComA binding which are located between the protected sequences is consistent with a model for ComA action involving the bending of DNA.

Bacillus subtilis↗
PubMed1991

[Potentiation insulin coma therapy by regional and lateral electric stimulation].

Clinicopsychopathological and clinicostatistical methods were employed to explore reverse dynamics of psychopathological symptomatology in the course of insulin coma therapy of 200 schizophrenic patients. 90 patients received insulin coma therapy in combination with zonal and lateral stimulations by means of subsensory pulse current at a frequency of 1 to 30 Hz. Right hemispheral exposure potentiated antipsychotic action of insulin comas. After left hemispheral exposure insulin comas provoked temporary exacerbation of symptomatology. The new modification was called lateral potentiated insulin coma therapy. The use of the therapy made it possible to attain a more rapid reverse development of psychotic symptomatology, to reduce the number of comas required per treatment course, to raise the quality and duration of the remissions attained.

Combined Modality Therapy↗