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PubMedDate not supplied

Intensive therapy for hepatic coma.

Of 45 patients observed in the ICU with severe acute hepatic insufficiency, 15 patients were in hepatic coma. All patients received combined treatment consisting of standard conservative methods (drug therapy) and surgical methods for temporary support of liver function (hemodialysis, exchange blood transfusion, pig liver perfusion). Intensive therapy which began during the early phase of hepatic coma enabled us to bring six patients out of the coma, four of whom completely recovered. These studies showed that of the diseases causing hepatic coma, the worst results were obtained with viral hepatitis. This may be explained both by the extensive liver damage and marked metabolic disturbances, which led to failure of other vital organs and systems. At present, the combined therapy contributes to a greater percentage of recovery of patients with hepatic failure and coma.

Adrenal Cortex Hormones↗
PubMed2001

Involvement of acetyl phosphate in the in vivo activation of the response regulator ComA in Bacillus subtilis.

Development of genetic competence in Bacillus subtilis is regulated by ComP--ComA, a two-component signal transduction system. The response regulator ComA is primarily activated by ComP, a histidine kinase that mediates response to nutrient conditions and cell density, and the activated ComA is required for transcription of the srf operon, which is essential for the development of genetic competence and surfactin production. In this study we suggested that the ComA could also be activated by a small molecule phospho-donor, acetyl phosphate. Examination of srfA-lacZ expression indicated that a significant amount of srfA expression still occurs in the comP mutant during growth in a sporulation medium containing excess glucose. Analysis of a comP and pta mutant suggests that srfA activation seen in the comP mutant is dependent on the expression of pta, which encodes phosphotransacetylase (Pta). As Pta is responsible for the catalysis for conversion of acetyl coenzyme A to acetyl phosphate, we conclude that the expression of srfA seen in the comP mutant is mainly due to the activation of ComA by acetyl phosphate.

Bacillus subtilis↗
PubMed1979

[Eliciting factors and clinical picture of hepatic coma in 152 patients with cirrhosis of the liver (author's transl)].

Exogenous hepatic coma was found 102 times (group A) and a combination of exogenous and endogenous hepatic coma 50 times (group B) in 152 patients with hepatic coma. The most frequent eliciting factors in group A were too high a protein supply and gastrointestinal hemorrhage and diuretics, in group B necrotic exacerbations and infections, 2/3 of them having severe portal hypertension with ascites and esophageal varices at the same time. A typical fetor hepaticus was found in only 25% of group A and 50% in group B. 10% had a primary liver cell carcinoma. The prognosis depends largely on the stage of the coma and the treatment of the eliciting factors. Altogether 50 of the 152 hepatic coma patients died. The most frequent complication was a terminal renal failure which no longer responded to therapy.

Acute Kidney Injury↗
PubMed1991

Serum levels of short-chain fatty acids in cirrhosis and hepatic coma.

Short-chain fatty acids cause reversible coma in animals and may contribute to the pathogenesis of the hepatic coma in humans. The concentrations of short-chain fatty acids in peripheral venous blood were significantly elevated in 15 patients with hepatic encephalopathy caused by cirrhosis (362 +/- 83 mumol/L; mean +/- S.E.M.) compared with 17 cirrhotic patients without encephalopathy (178 +/- 57 mumol/L) and 11 normal individuals (60 +/- 8 mumol/L). However, no correlation between the depth of coma and the level of short-chain fatty acids was found after repetitive measurements in the coma group. Compared with normal individuals, all short-chain fatty acids, except valerate, were elevated in patients with hepatic encephalopathy, whereas only the concentrations of isobutyrate and isovalerate were significantly elevated in cirrhotic patients without encephalopathy. The concentrations of short-chain fatty acids in 21 nonencephalopathic cirrhotic patients who underwent catheterization were equally distributed in the aorta (187 +/- 56 mumol/L), the hepatic vein (212 +/- 75 mumol/L), the azygos vein (140 +/- 37 mumol/L) and the renal vein (135 +/- 43 mumol/L) compared with peripheral venous blood (178 +/- 57 mumol/L). This study does not support the idea that short-chain fatty acids are of major importance in the pathogenesis of hepatic coma in patients with cirrhosis.

Adult↗
PubMed1981

[Acute experimental (endogenous) hepatic coma and the clinical syndrome of acute hepatocellular injury].

In search of the adequate experimental model for creating endogenous coma, the characteristics of which would be identical to the clinical picture of acute hepatic coma in men, the ischaemic method of experimentally originated acute endogenous hepatic coma was applied. The experiment was carried out on 12 dogs in which the terminolateral portocaval shunt with ligation of all the collateral of the arterial irrigation leading to the liver was performed, while the double ligation was performed on the hepatic artery. After the animals had emerged from the postoperative state of shock, the hepatic artery was ligated in local anesthesia and the created state was controlled by clinical observations and laboratory tests. Experimentally created acute endogenous hepatic coma achieved by applying ischaemic method proved to be a good model. Its true value manifested itself in the clinical picture as well as in the laboratory findings which resembled considerably the state of acute hepatic coma in men.

Acute Disease↗
PubMed2004

[Diffusion-weighted magnetic resonance imaging in hypoglycemic coma].

Hypoglycemia is a classic cause of coma and can result in irreversible neuronal loss. Until now, the main prognostic factors were depth of hypoglycemia and duration of coma. We report the case of a 55-Year-old woman who suffered severe hypoglycemic coma with abnormal cortico- subcortical diffusion weighted MR images. These MRI abnormalities preceded severe atrophy of these cerebral areas. This findings suggests that diffusion abnormalities in hypoglycemic coma may be related to neuronal loss and may thus have prognostic value.

Alcoholism↗
PubMed2002

Barbiturate coma for intracranial hypertension: clinical observations.

PURPOSE: To determine the neurologic outcome of patients with intracranial hypertension treated with barbiturate-induced coma. MATERIALS AND METHODS: The records of 49 patients who were admitted to a 31-bed medicosurgical intensive care unit over a 5-year period in whom a barbiturate coma was induced to control intracranial hypertension were analyzed retrospectively. Analysis included assessment of the response to barbiturate coma and evaluation of the long-term neurologic outcome according to the Glasgow Outcome Scale (GOS). RESULTS: Intracranial hypertension was caused by head trauma in 28 patients and subarachnoid hemorrhage in 21 patients. Eight of the head trauma patients and 5 of the patients with subarachnoid hemorrhage survived their hospital stay. The survivors were younger than the nonsurvivors, and had a good neurologic status after 1 year (except for 2 patients who died 1 and 3 months after discharge, respectively). There was no significant difference in the Glasgow Coma Score (GCS) on admission between the survivors and the nonsurvivors. The long-term outcome at 1 year was markedly better in the patients who had experienced a subarachnoid hemorrhage than in the trauma patients.

Adolescent↗
PubMed2005

Should catatonia be part of the differential diagnosis of coma?

The descriptions of catatonia are complex and unclear. More than 40 different signs and symptoms have been included, but coma is not among them. Recently, a case report of coma in relation to catatonia was presented. We report two further cases where coma was a part of this syndrome of disturbed motility. They were successfully treated with ECT. Consequently, we suggest that catatonia may be a differential diagnosis of coma.

Adult↗
PubMed1997

Successful treatment by direct hemoperfusion of coma possibly resulting from mitochondrial dysfunction in acute valproate intoxication.

PURPOSE: We evaluated the efficacy of direct hemoperfusion (DHP) for treatment of acute valproate (VPA) intoxication and speculate on the biochemical perturbations that suggest a mechanism of coma induced by VPA overdose. PATIENT AND METHODS: The comatose patient was hospitalized approximately 6 h after ingesting 18 g VPA. DHP, with 200 g activated charcoal, was performed for 6 h. The plasma concentrations of VPA and Glasgow coma scale scores after admission were estimated. Before and after DHP, urine samples were tested in serial fashion for VPA metabolites, organic acids, and acyl carnitine esters of fatty acids. RESULTS: Plasma VPA was efficiently adsorbed on activated charcoal. The patient's plasma concentration of VPA decreased from 471 microg/ml (2,830 microM) to 45 microg/ml (270 microM), at which point the patient became alert. The half-life (t1/2) of VPA was calculated as 4.4 h before DHP and as 1.8 h during DHP. Before DHP, lactate and VPA-glucuronide markedly increased in urine samples, but beta-keto-VPA, a major mitochondrial metabolite, was not detected. Urinary excretion of carnitine esters of medium chain (C8-C10) dicarboxylic acids was increased. After DHP, lactate and VPA-glucuronide decreased, but a significant amount of beta-keto-VPA was demonstrated. Carnitine esters of medium chain dicarboxylic acids were decreased. CONCLUSIONS: DHP with activated charcoal was effective treatment for the patient with acute VPA intoxication and coma. The onset of coma may have been related to inhibition of beta-oxidation in the mitochondria, which was reversible by elimination of plasma VPA by DHP.

Acute Disease↗
PubMed1992

Motor and somatosensory evoked potentials in coma: analysis and relation to clinical status and outcome.

Central sensory and motor conduction were studied in 23 comatose and three brain-dead patients. Motor evoked potentials (MEPs) to transcranial magnetic (magMEP) and electrical (elMEP) stimulation were recorded from the hypothenar muscle, and somatosensory evoked potentials (SEPs) were recorded after median nerve stimulation. Comparison of clinical with evoked potential (EP) findings revealed: 1) a painful stimulus applied to the skin of the arm lowered excitation threshold to cortical stimulation and was a prerequisite to obtain MEPs in 14 instances; 2) only in braindead patients were all EPs abolished simultaneously and bilaterally; 3) MEPs (p less than or equal to 0.05, chi 2-Test), but not necessarily SEPs (p greater than 0.1) were preserved in the arms that showed normal motor reaction during clinical examination; 4) no correlation was found between EP findings and the Glasgow Coma Scale (GCS). The results of clinical and EP testing were examined in the light of the patient's outcome 10 months later: 1) fatal outcome was predicted by a GCS of three (38% of cases, p less than or equal to 0.05, Fisher's exact test), abolished brainstem- or papillary reflexes (38%, p less than or equal to 0.05), the combination of these clinical signs (54%, p less than or equal to 0.01), bilateral abolition of elMEPs (38%, p less than or equal to 0.05), magMEPs (38%, p less than or equal to 0.05), or SEPs (23%, p greater than 0.1), or a combination of clinical and EP data (85%, p less than or equal to 0.0005); 2) good outcome was predicted by a GCS of greater than or equal to 8 only in post-traumatic coma, and EPs did not help to predict fatal outcome of coma; 1) if this appears impossible on the basis of clinical data alone; 2) if a second indicator is needed to confirm a clinical impression; 3) SEPs may be first evaluated during the acute stage of coma treatment, because they can be recorded in the presence of anaesthetic or relaxant agents; 4) MEP may be studied if outcome prediction remains ambiguous, and if the clinical situation allows for discontinuation of these agents.

Adolescent↗
PubMed1992

The role of immediate operative intervention in severely head-injured children with a Glasgow Coma Scale score of 3.

In an attempt to improve and expedite the care of head-injured children, data have been published recommending burr hole exploration in lieu of computed tomography for children with signs of brain stem compression or with a Glasgow Coma Scale score of 3. Exploratory burr holes revealed a high incidence of subdural hematomas, and removal of the hematomas improved survival. We are reporting 19 consecutive children with Glasgow Coma Scale scores of 3. Coma score evaluation was confounded by intubation, sedation, pharmacological paralysis, and posttraumatic seizures. We found no radiographical or postmortem pathological evidence of intracranial hemorrhage, which would warrant operative intervention. A high incidence of multisystem injuries and high cervical spine injuries would have made early intervention both dangerous and inappropriate. Although there is a definite role for emergency trephination, routine exploratory burr holes for children with a Coma score of 3 is not justified.

Accidents, Traffic↗
PubMedDate not supplied

The effectiveness of coma arousal intervention.

Thirty-one patients who were in coma or persistent vegetative state two weeks after sustaining a severe head injury were entered into a coma arousal programme. The coma arousal protocol called for a sequence of vigorous multisensory stimulations to be applied to the patient by a relative for up to eight hours a day for seven days a week. An independent study team monitored two patient outcomes, the time taken to obey a simple command on two consecutive occasions 24 hours apart and patients' score on the Glasgow Outcome Scale 10-12 months post-injury. Outcomes were compared with an historical reference group chosen from the literature, consisting of 135 similarly classified patients. Differences between the pilot study and the reference group patients on initial characteristics suggested that the pilot study patients might have the more favourable outcomes, independent of treatment effect. The sample size was sufficient to detect a 40% improvement in recovery rate. No significant improvements were noted in either the time to obey a simple command (p greater than 0.2) or in the Glasgow Outcome Scale (p greater than 0.25), although the observed difference in the latter group was 11% in favour of the pilot study patients. This study was unable to find any evidence that coma arousal, for all its arduous patient contact, had a markedly better outcome compared with conventional treatment.

Adolescent↗
PubMed2001

[Point systems for evaluating coma in patients with injuries of the central nervous system (CNS)].

Paper reviews various coma scales which are used to monitor consciousness after sustaining severe injuries of CNS. Glasgow Coma Scale, at present the most frequently used, was compared to recently developed scales, which are more useful for monitoring persistent comas, allows to evaluate discrete changes in patient's state more precisely and to predict the outcome. The necessity of evoked potentials' measurements, such as Trigeminal-Auditory Glasgow (Coma Scale) has been stressed.

Brain Injuries↗
PubMed1991

Childhood coma in Ibadan. Relationship to socio-economic factors.

According to the literature, socio-economic factors may contribute more to geographic variations in the aetiology and prognosis of childhood coma than has previously been recognised. This prospective study involving 118 children with strictly defined coma demonstrated that the commonest causes of coma in Ibadan were cerebral malaria (55%), meningitis (13%) and encephalitis (10%). The prognosis was poor. Forty-three (36%) of 118 cases died and 75 (64%) survived, including 23 who showed neurologic deficits. Noteworthy prognostic indices of coma were the aetiology of the condition, the presence of severe anaemia, hypoglycaemia and pneumonia. The findings are discussed in the context of the socio-economic background of children in the tropics.

Child, Preschool↗
PubMed1981

Nonketotic hyperosmolar coma in two diabetic children.

Two diabetic children with nonketotic hyperosmolar coma were treated successfully. In one of the patients, plasma-free fatty acids, insulin, C-peptide and two lipolytic hormones (growth hormone and cortisol) were measured serially during the coma. Free fatty acids, insulin, C-peptide, growth hormone and cortisol levels were within normal ranges and subsequently these levels did not change significantly. The results suggest that the normal levels of lipolytic hormones may account for the normal plasma free fatty acids and the absence of ketosis found in children with nonketotic hyperosmolar coma, in contrast to the elevated levels of lipolytic hormones and ketone bodies in ketoacidotic diabetic coma.

C-Peptide↗
PubMed1977

[Two cases of nonketotic hyperosmolar coma in neurosurgery (author's transl)].

Hyperosmolar nonketotic coma is characterized by hyperglycemia, hyperosmolarity and dehydration in the absence of ketoacidosis. Two cases of hyperosmolar nonketotic coma, in which both the patients recovered, were presented. One of the cases was a 59-year-old female who had suffered from a metastatic brain tumor. After removal of the tumor, the patient's condition improved for a period. This was followed by a period of frequent vomiting, subsequently followed by coma. The laboratory data showed the absence of ketoacidosis in the blood sugar measured at 672 mg/dl and serum osmolarity at 343.1 mOsm./kg. The other case was a 74-year-old female who was admitted to the clinic because of cerebral thrombosis. Her caloric in-take was restricted and insulin was administered because of a mild diabetes mellitus which occured after admission. Then she entered a hyperosmolar non-ketotic coma. The laboratory data revealed blood sugar to be 1068 mg/dl and serum osmolarity to be 418 mOsm./kg. Immediately after large amounts of intravenous drip infusion and insulin were administerd, she recovered from the syndrome. The clinical observations and the pathogenesis of this syndrome were discussed.

Aged↗
PubMed1997

[Hypoxic-ischemic coma in children. Factors related to the prognosis].

OBJECTIVE: The purpose of this study was to analyze the etiology, evolution and predictive value of clinical variables and complementary explorations in children admitted to a PICU with hypoxic-ischemic coma. PATIENTS AND METHODS: A retrospective review (1991-1996) of 24 children with hypoxic-ischemic coma admitted to the pediatric ICU of a reference hospital was performed. Clinical data on admission and results of complementary explorations (EEG and neuroimaging techniques) were collected and the findings compared according to the evolution and underlying pathophysiological mechanism. RESULTS: Non-reactive and dilated pupils, existence of neurohypophyseal disorders and isoelectric EEGs were exclusively found in dead patients. A score of 3-4 on the Glasgow Coma Score was obtained more frequently in groups with the worse evolution (exitus and surviving with sequelae), as well as positive findings with neuroimaging techniques and the appearance of seizures, though without meaningful differences. More significant was the existence of associated problems, which was more frequent in groups with a negative evolution. The differences among the pathophysiological groups were not meaningful. Global mortality in the series studied was 41.6%, with 29.2% of the survivors having neurological sequelae and 29.2% being healthy. CONCLUSIONS: Hypoxic-ischemic coma in children has a high mortality and morbility. The prognosis for each patient is based on the clinical facts and complementary explorations. No isolated data allows the establishment of the final outcome with certainty.

Brain Ischemia↗
PubMed1993

End-stage Alzheimer's disease. Glasgow Coma Scale and the neurologic examination.

OBJECTIVE: To characterize the cognitive and neurologic features of patients with end-stage Alzheimer's disease using a standard neurologic examination and the Glasgow Coma Scale. DESIGN: Case series. SETTING: Local community nursing homes. PATIENTS: Forty patients with Alzheimer's disease were drawn from previously enrolled subjects in the Rochester Alzheimer's Disease Project with Clinical Dementia Rating scores of 3, 4, or 5. MAIN OUTCOME MEASURES: Scores on the Glasgow Coma Scale and cognitive screening examinations and the prevalence of neurologic manifestations such as primitive reflexes and extrapyramidal signs were compared across the Clinical Dementia Rating groups. RESULTS: When compared with patients in the Clinical Dementia Rating stages 3 and 4, patients with a stage 5 scored significantly lower on the Glasgow Coma Scale, with the discriminating subscales being verbal and motor responses. Primitive reflexes, myoclonus, and dyskinesia were increasingly prevalent in the more terminal stages. Cognitive screening assessments did not discriminate between groups. CONCLUSIONS: Rudimentary neurologic functions can be readily assessed and, when viewed together with the Glasgow Coma Scale, may circumvent the "floor effect" frequently encountered when using the currently available cognitive and functional scales and, thereby, better define patients with end-stage Alzheimer's disease.

Aged↗