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Armanni-Ebstein lesions of the kidney: diagnostic of death in diabetic coma?

In the period from January 1986 through April 1993, 47 cases with diabetes mellitus were autopsied at the Institute of Forensic Medicine, Odense University. In 26 cases, the diabetes had been treated with insulin, in 21 cases with oral medication or diet only. In eight insulin-dependent cases, tubular vacuolation was found in the kidneys, the so-called Armanni-Ebstein lesions. The circumstances of death and postmortem analyses of blood, urine and/or vitreous humor supported a presumed diabetic coma as the cause of death in these eight cases. Of the remaining 39 cases, six were too putrefied for histologic examination. In the remaining 33 cases and in a series of 20 non-diabetics, the cause of death was ascertained as illness (other than diabetes), traffic accidents, drowning or intoxication. In none of these cases was a diabetic coma suspected, and none of these cases showed tubular vacuolation in the kidneys. The authors conclude that tubular vacuolation of the kidneys strongly indicates death in diabetic coma.

Adult↗

Coma as presenting manifestation of Wernicke's encephalopathy.

A patient in whom coma was the presenting manifestation of Wernicke's encephalopathy is reported. Clinical reports on coma in Wernicke's encephalopathy are scarce, but postmortem studies have demonstrated that this form of presentation is often not recognized. The diagnosis of Wernicke's encephalopathy should be suspected in any patient presenting with coma of unclear etiology.

Coma↗

Recurrent coma and Lesch-Nyhan syndrome.

A patient with Lesch-Nyhan syndrome has had 3 recurrent episodes of coma, each associated with an acute illness. Extensive investigation for known causes of coma has failed to yield a diagnosis. Although coma is not generally recognized as a feature of Lesch-Nyhan syndrome, similar patients have been reported previously. This and other episodic phenomena observed in Lesch-Nyhan syndrome may be explained by the disruption of cellular energy metabolism due to purine depletion, consequent to lack of the purine salvage pathway normally provided by the hypoxanthine-guanine-phosphoribosyl-transferase enzyme.

Coma↗

Interobserver variation in the interpretation of SSEPs in anoxic-ischaemic coma.

OBJECTIVE: To study interobserver variation in the interpretation of median nerve SSEPs in patients with anoxic-ischaemic coma. METHODS: SSEPs of 56 consecutive patients with anoxic-ischaemic coma were interpreted independently by 5 experienced clinical neurophysiologists using guidelines derived from a pilot study. Interobserver agreement was expressed as kappa coefficients. RESULTS: Kappa ranged from 0.20 to 0.65 (mean 0.52, SD 0.14). Disagreement was related with noise level and failure to adhere strictly to the guidelines in 15 cases. The presence or absence of N13 and cortical peaks caused disagreement in 5 cases each. For recordings with a noise level of 0.25 microV or more, mean kappa was 0.34; for recordings with a noise level below 0.25 microV mean kappa was 0.74. CONCLUSIONS: Interobserver agreement for SSEPs in anoxic-ischaemic coma was only moderate. Since the noise level strongly influenced interobserver variation, utmost attention should be given to its reduction. If an artefact level over 0.25 microV remains, absence of N20 cannot be judged with sufficient certainty and the SSEP should be repeated at a later stage. SIGNIFICANCE: Because of its moderate interobserver agreement, great care has to be given to accurate recording and interpretation of SSEPs before using the recordings for non-treatment decisions.

Adult↗

Glasgow coma scale 7 or less surveillance program for brain death identification in Argentina: Epidemiology and outcome.

BACKGROUND: In Argentina, the rate of cadaveric organ donation per million inhabitants has recently increased to 10.5 (it was previously <7). PURPOSE: To overcome this challenge, the National Institute for Organ Donation and Transplantation (INCUCAI) created a proactive donor detection plan performed by intensive care unit (ICU) physicians (hospital transplantation coordinators) from 90 selected hospitals across the country. METHODS: A prospective, observational study of patients in severe coma status was conducted from September 2003 to December 2005. We enrolled hospitalized patients who displayed a Glasgow Coma Scale (GCS) of 7 or less and who were admitted to ICUs. Data included demographics, etiology of coma, cardiac arrest, brain death, discharge or derivation, and positive/negative donation. RESULTS: Among 9841 enrolled patients, we excluded 498 who were discharged to another hospital or had unknown outcomes, leaving 9343 for analysis including 64% males and 36% females of overall mean age 50 +/- 19 years (adults) and 5 +/- 4 years (children). Herein, we have highlighted the high risk of death during the first 2 days in the ICU of patients with GCS 7 or less. Gunshot to the head-injured patients and those with hemorrhagic strokes were less likely to survive. In this study, cardiac arrest events and organ donors (OD) GCS 7 or less ratios emerged as quality control markers of ICU care, unraveling problems of potential donor maintenance or inadequate policies. CONCLUSIONS: The GCS 7 or less surveillance program seemed to be a valuable tool for identifying organ donors and potentially treatable events, such as the high rate of cardiac arrest observed in this study.

Accidents, Traffic↗

Coma scales for children with severe falciparum malaria.

The Blantyre coma scale (BCS) is used to assess children with severe falciparum malaria, particularly as a criterion for cerebral malaria, but it has not been formally validated. We compared the BCS to the Adelaide coma scale (ACS), for Kenyan children with severe malaria. We examined the inter-observer agreement between 3 observers in the assessment of coma scales on 17 children by measuring the proportion of agreement (PA), disagreement rate (DR) and fixed sample size kappa (kappa n). We assessed the sensitivity and specificity of the scales in detecting events (seizures and hypoglycaemia) in 240 children during admission and the usefulness of the scales in predicting outcome. There was considerable disagreement between observers in the assessment of both scales (BCS: PA = 0.55, DR = 0.09 and kappa n = 0.27; ACS: PA = 0.36, DR = 0.31, and kappa n = 0.31), particularly with the verbal component of the BCS (kappa n = 0.02). Compared to the ACS, the BCS was more specific (0.85 for BCS and 0.80 for ACS), but less sensitive (0.25-0.69 vs. 0.38-0.88 respectively) in detecting events and was a worse predictor of neurological sequelae. The BCS provided a better overall assessment of a child's incapacity from falciparum malaria, but the ACS was more useful in assessing neurological disturbances.

Age Factors↗

Emergency treatment of neonatal hyperammonaemic coma with mild systemic hypothermia.

An infant aged 3 days presented with hyperammonaemic coma and seizures, which were found to be a result of a urea-cycle defect. Haemofiltration, alternative pathway metabolites, and glucose and insulin failed to lower the plasma ammonia concentration below 2000 micromol/L. The infant was then cooled to a rectal temperature of 34 degrees C for 48 h and put on haemofiltration for 12 h. Plasma ammonia fell to around 100 micromol/L and remained at this concentration after haemofiltration. He roused from his coma, breathed spontaneously, and resumed bottle feeding. Hypothermia may be therapeutic in such instances of metabolic coma because it lowers the enzymatic rate of production of the toxin while non-enzymatic methods remove the toxin.

Ammonia↗

Coma in the Wernicke-Korsakoff syndrome.

Four comatose patients were found to have the Wernicke-Krosakoff syndrome. All had a history of alcoholism, previous alcoholic neurological disease, and poor nutrition. Intravenous or nasogastric tube feeding without vitamin supplements precipitated coma in three. Examination showed a diffuse encephalopathy with intact pupillary light reflexes, no focal neurological signs, and absent doll's eye and caloric responses. The tendon reflexes were uniformly absent. Two patients were hypothermic and one was hypotensive. Although the level of consciousness improved in all after parenteral thiamine, three died and one was left disabled. The Wernicke-Korsakoff syndrome merits wider recognition as a cause of coma and empirical treatment with thiamine in cases of coma of unknown cause is recommended.

Coma↗

[Bilateral corneal endothelial decompensation after postsepticemia coma].

We report a case of unexplained bilateral corneal endothelial decompensation after a coma. A 71-year-old man with no medical history presented with bilateral endothelial decompensation that required penetrating keratoplasty of the left eye combined with cataract surgery. This coma was caused by septicemia originally due to staphylococcus infection following catheter placement in preparation for a CT scan. Visual acuity of the left eye was 20/400 and 20/100 in the right eye when the patient awoke from the coma. After examination, we noted only stromal thickening and Descemet membrane folds causing corneal edema predominating OS. The rest of the exam was normal. Six months after surgery, visual acuity improved to 20/25. The most probable physiopathological mechanism of this decompensation is an iatrogenic complication from drugs administered during the patient's stay in intensive care (oxacillin), but we cannot rule out direct aggression of a bacterium or its toxin or the decompensation of a preexisting pathology.

Aged↗

Protein ubiquitination in rat brain following hypoglycemic coma.

Hypoglycemic coma of 30 min duration selectively damages CA1 pyramidal neurons and the crest of dentate gyrus (DG) granule cells in hippocampus. Here, we show by high-resolution confocal microscopy and biochemical analysis that 30 min of hypoglycemic coma induces the ubiquitination and aggregation of several proteins in rat brain tissues. Protein ubiquitination and aggregation occurred in the CA1 and DG regions as early as the end of 30 min of hypoglycemic coma and lasted until neuronal death in the late recovery period after hypoglycemia. In comparison, the neurons surviving hypoglycemia were less affected. On western blots, ubiquitinated proteins (ubi-proteins) were present mainly in Triton-insoluble pellets, indicating that they are irreversibly aggregated. We conclude that proteins are ubiquitinated and aggregated in neurons after hypoglycemia prior to their death. We hypothesize that protein ubiquitination and aggregation may contribute to neuronal damage after hypoglycemia.

Animals↗

Prognosis in anoxic and traumatic coma.

This article presents a systematic review of the prognostic factors in coma caused by hypoxia and anoxia, and traumatic head injury. In the case of anoxic coma, poor prognosis can be determined very accurately at the bedside by the lack of brainstem reflexes assessed at day three post-insult. Electroencephalogram (EEG) and evoked potentials (i.e., auditory and somatosensory) detect additional patients with poor prognosis. Clinical examination is not as helpful in the case of traumatic coma. Evoked potentials performed within the first week detect approximately half of patients with a poor prognosis. EEG adds only a small amount of prognostic information.

Adult↗

Neurologic outcomes of pediatric epileptic patients with pentobarbital coma.

Status epilepticus is a life-threatening condition requiring emergent medical attention. Although initial therapies with antiepileptic drugs generally terminate seizures within 30 to 60 minutes, patients with refractory status epilepticus require additional intervention. High-dose pentobarbital has been the most commonly prescribed agent for the management of refractory status epilepticus in children. The objective of this research was to evaluate the association between the response of pentobarbital coma and neurologic outcomes in refractory status epilepticus. Twenty-three subjects were treated with pentobarbital coma for at least 48 hours. Medical records were reviewed to collect patient demographic information, responses to treatment, and neurologic outcomes. Among the 23 patients reviewed, 12 patients were controlled with pentobarbital (responders), six were unresponsive to pentobarbital (nonresponders), and five patients relapsed after discontinuation or during tapering of pentobarbital (relapser). The mortality rate among the relapser and nonresponder groups combined was 90.9%, but no deaths occurred among the responder group (P < 0.001). The survival rate was greater among toddlers compared with neonates or older children. Failure of seizure control after pentobarbital coma was associated with a poor prognosis. The potential for serious complications of pentobarbital therapy among neonates highlights the need for careful dosing in this age group.

Adolescent↗

Mycoplasma pneumoniae: a cause of coma in the absence of meningoencephalitis.

Mycoplasma pneumoniae encephalitis is a recognized cause of reversible coma in children. As an etiology of infectious encephalitis, it yields a relatively poorer prognosis than most other causes of infectious encephalopathies. Encephalitis is generally diagnosed by a constellation of clinical symptoms and confirmed by a cerebrospinal fluid (CSF) examination revealing cell pleocytosis and elevated protein. That Mycoplasma pneumoniae encephalopathy can occur in the presence of a normal CSF examination is less well appreciated. The authors report two children who presented with coma and normal CSF findings in whom a diagnosis of acute Mycoplasma pneumoniae infection was made. The two children both had rapid and complete recovery over several days. These cases exemplify that coma can result from acute infection with Mycoplasma pneumoniae in the absence of an inflammatory CSF response and that a normal CSF may herald a more favorable prognosis.

Child↗

[Importance of evoked potentials in the evolutive prognosis of coma during cerebral anoxia in adults].

Ten cases of postanoxic coma have been studied. A clinical neurological examination with study of brainstem reflexes and the EEG recording were made on the first day (J1), the third day (J3) and the tenth day (J10) after the start of the coma. A recording of the visual evoked potentials, the brainstem evoked potentials and the somatosensory potentials combined was made at the same time. A clinical examination is carried out one month after the coma when the patient survives. According to the initial clinical examination, we distinguished 3 groups of subjects. The results show that in group III the visual evoked potentials such as EEG have a slightly significant prognostic value; frequently the near outcome lead to death whereas EEG activity persists and the visual evoked potentials disappear later. On the other hand, the association of brainstem evoked potentials and somatosensory potentials clearly has a higher prognostic value in this group. The disappearance of the shortest brainstem responses and the cortical somatosensory responses is clearly an unfavourable prognosis. This disappearance associated with the end EEG activity is the absolute proof of brain death. On the other hand, the persistence of these responses is of a better prognosis at least on the survival level, but their degradation during evolution is unfavourable.

Adolescent↗

Response to selection for rapid chill-coma recovery in Drosophila melanogaster: physiology and life-history traits.

Resistance to low temperatures can vary markedly among invertebrate species and is directly related to their distribution. Despite the ecological importance of cold resistance this trait has rarely been studied genetically, mainly because low and variable fitness of offspring from cold-stressed mothers makes it difficult to undertake selection experiments and compare cold resistance of parents and offspring. One measure of cold resistance that varies geographically in Drosophila melanogaster and that is amenable to genetic analysis is chill-coma recovery. Three replicate lines of D. melanogaster were selected every second generation, for over 30 generations, for decreased recovery time following exposure to 0 degrees C. Correlated responses were scored to characterize underlying physiological traits and to investigate interactions with other traits. Lines responded rapidly to the intermittent selection regime with realized heritabilities varying from 33% to 46%. Selected lines showed decreased recovery time after exposure to a broad range of low temperatures and also had a lower mortality following a more severe cold shock, indicating that a general mechanism underlying cold resistance had been selected. The selection response was independent of plastic changes in cold resistance because the selected lines maintained their ability to harden (i.e. a short-term exposure to cool temperature resulted in decreased recovery time in subsequent chill-coma assays). Changes in cold resistance were not associated with changes in resistance to high temperature exposure, and selected lines showed no changes in wing size, development time or viability. However, there was a decrease in longevity in the selected lines due to an earlier onset of ageing. These results indicate that chill-coma recovery can be rapidly altered by selection, as long as selection is undertaken every second generation to avoid carry-over effects, and suggest that lower thermal limits can be shifted towards increased cold resistance independently of upper thermal limits and without tradeoffs in many life-history traits.

Acclimatization↗

Electrolyte shifts between brain and plasma in hypoglycemic coma.

Hypoglycemia of sufficient severity to cause cessation of EEG activity (coma) is accompanied by energy failure and by loss of ion homeostasis, the latter encompassing a marked rise in extracellular fluid (ECF) K+ concentration and a fall in ECF Ca2+ concentration. Presumably, ECF Na+ concentration decreases as well. In the present study, the extent that the altered ECF-plasma gradients give rise to net ion fluxes between plasma and tissue is explored. Accordingly, whole tissue contents of Ca2+, Mg2+, K+, and Na+ were measured. The experiments were carried out in anaesthetized and artificially ventilated rats given insulin i.p.; cerebral cortical tissue was sampled at the stage of slow-wave EEG activity, after 10, 30, and 60 min of coma (defined as isoelectric EEG), as well as after 1.5, 6, and 24 h of recovery. In the precomatose animals (with a slow-wave EEG pattern), no changes in electrolyte contents were observed. During coma, tissue Na+ content increased progressively and the K+ content fell (each by 20 mumol g-1 during 60 min). During recovery, these alterations were reversed within the first 6 h. The Mg2+ content remained unchanged. In spite of the appreciable plasma to ECF Ca2+ gradient, no significant calcium accumulation was observed. It is concluded significant calcium accumulation was observed. It is concluded that hypoglycemia leads to irreversible neuronal necrosis in the absence of gross accumulation of calcium in the tissue.

Animals↗

[Diabetic coma and Wernicke-Korsakoff syndrome. On the clinical significance of acquired thiamine deficiency].

Following consideration of the nosological role of hyperglycemic states in psychiatry the case report of a fifty-five year-old patient is presented suffering from fatty cell degeneration of the liver and a relapsing pancreatitis due to chronic alcoholism. After a long period of abstinence without previously known diabetes mellitus a sudden ketoacidotic coma developed with maximum serum glucose level of 2020 mg%. Having emerged during coma treatment Wernicke's encephalopathy passed into Korsakoff's syndrome the main features of which remained unchanged for more than one year. In this case thiamine deficiency of different pathogenetical origin is discussed: defective exogeneous availability due to malabsorption; depletion of endogeneous thiamine stores due to enlarged requirements for glucose oxidation during coma therapy; antimetabolic effects to thiamine by nitroimidazole-derivatives administered parenterally.

Alcohol Amnestic Disorder↗

Cerebral intraparenchymal pressure monitoring in non-traumatic coma: clinical evaluation of a new fibreoptic device.

Initial reporting and validation of the Camino miniaturised fibreoptic cerebral intraparenchymal pressure monitoring device has indicated that this tip transducing system (a) allows direct measurement of brain tissue pressure, (b) has a rapid response rate to intracranial changes and (c) correlates well with intraventricular pressure. However, there are no specific reports of this form of monitoring during non-traumatic coma in children, or any evaluation of change in clinical practice when compared with experience of other forms of invasive intracranial pressure monitoring. Over a 5-year-period (1985-1989) on the General Paediatric Intensive Care Unit, 74 children with presumed raised intracranial pressure complicating non-traumatic coma have had invasive intracranial pressure monitoring with a variety of devices. An intraventricular catheter was used in 16 patients, a subdural catheter in 6 patients, a subarachnoid screw in 35 patients and a fibreoptic intraparenchymal catheter in 17 patients. In 1985 to 1986 our preferred technique was the subarachnoid screw (33/49 patients monitored). Between 1987 and 1989 we have mainly used the Camino fibreoptic intraparenchymal monitoring system (17/25 patients monitored). In the whole series there were no cases of acute haemorrhage related to monitoring and only one patient developed infection and in this child an intraventricular catheter was used. The experience with the fibreoptic system has been favourable and the technique for insertion does not require additional expertise in comparison with standard subarachnoid screw pressure monitoring. Therefore in young children with raised intracranial pressure complicating non-traumatic coma, cerebral fibreoptic intraparenchymal pressure monitoring should be used in preference to standard subarachnoid screw pressure monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗