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At least 847 records · Page 47Linked to original sources
PubMed1981

Prognostic indicators in pediatric near-drowning: the Glasgow coma scale.

The records of 101 drowning or near-drowning victims admitted to Children's Hospital of Los Angeles (CHLA) between January 1975 and June 1978 were reviewed. The admission Glasgow coma score could be assigned retrospectively to 94 patients. A low score (less than 5) predicted a high risk group of patients with 80% mortality or permanent neurological sequelae. A high score (greater than or equal to 6) defined a low risk group of patients with no deaths or severe neurological sequelae. The Glasgow coma scale may be a useful tool for predicting the outcome of near-drowning victims in the pediatric age group.

Child↗
PubMed1981

Metabolic turnover in the reticular activating system in ammonia induced coma.

Previous studies have implicated the ascending reticular activating system (RAS) as playing a vital role in ammonia induced coma. It has been shown, for example, that cells of the RAS have selective decreases in the level of energy metabolites such as ATP and phosphocreatine as compared to adjacent tissue during ammonia induced encephalopathy. To determine the utilization rate of metabolites during ammonia induced coma, we have examined the turnover rate of four key energy metabolites in 20-22 gram mice. Results from this study show decreases in the turnover of glucose, glycogen, and phosphocreatine. The derived value for the turnover of energy metabolites was decreased by 49% as compared to that of control mice. These data suggest that energy utilization is decreased at a time when the physiological output of the RAS is also diminished and the animal is comatose.

Adenosine Triphosphate↗
PubMed1981

Silent duodenal perforation. A difficult diagnosis in iatrogenic barbiturate coma.

Iatrogenic barbiturate coma for the control of intracranial hypertension is a relatively new addition to the neurosurgeon's therapeutic armamentarium. Although initial studies are quite promising, the induction of coma, especially for prolonged periods (ranging from days to weeks), is a major therapeutic endeavor which requires sophisticated monitoring of both neurological and physiological function. A multidisciplinary approach prevents many possible complications of this form of therapy and facilitates treatment when untoward physiological complications do occur. The following case report illustrates one such complication.

Accidents, Traffic↗
PubMedDate not supplied

Myxedema coma in the elderly.

BACKGROUND: Myxedema coma in the elderly, although uncommon, is frequently overlooked and has a high mortality rate. Signs and symptoms are many and are often insidious. Nearly every organ system is involved. Prompt recognition and treatment are mandatory for a successful outcome. METHODS: A case study is presented. Using the key words "myxedema" with the word "aged," MEDLINE files were searched from 1989 to present. Articles dating before 1989 were accessed from the reference lists of the more recent articles. RESULTS AND CONCLUSIONS: This review describes the signs and symptoms of myxedema coma in the elderly. Epidemiology and histopathology of the disorder are discussed. Prompt recognition and emergency medical treatment are essential for a successful outcome. Prevention requires screening of elderly patients at risk for hypothyroidism and assuring thyroid hormone replacement therapy.

Aged↗
PubMed1995

[Japan coma scale in the prediction of outcome after early surgery for aneurysmal subarachnoid hemorrhage].

The value of the 10-grade Japan Coma Scale (JCS) as a means of evaluating patients undergoing early aneurysm surgery was assessed in terms of its relationship to surgical outcome. The 13-grade Glasgow Coma Scale (GCS) was also assessed, and comparisons were made between the two. A series of 765 patients who underwent aneurysm surgery within 7 days after hemorrhage were evaluated both by JCS and GCS immediately prior to surgery, and outcome was assessed by the Glasgow Outcome Scale (GOS) 6 months postoperatively. Both the JCS and GCS scores were significantly correlated with surgical outcome (JCS vs GOS: rs = 0.586, GCS vs GOS: rs = 0.615, p < 0.001). There was no significant difference between the correlation coefficients for outcome of the JCS and GCS. In general, the better the JCS or GCS score was, the better the surgical outcome was, however, outcome among those with a JCS score of 3 was poorer than among those with a score of 10, 20, or 30. The results of this study indicate that both JCS and GCS are useful in predicting surgical outcome, but the GCS may be better than the JCS because of the problem with the score of 3 in the latter.

Acute Disease↗
PubMed1994

[Diagnosis of metabolic coma in children].

This article describes the metabolic investigations to be applied in any clinical situation consistent with a late acute form of inborn error of metabolism: unexplained coma with or without focal neurological manifestations, recurrent vomiting with lethargy, episodes of ataxia with or without behaviour disorder, fits of psychiatric troubles. In each of these situations, careful medical history is of major importance searching for previous clinical manifestations such as episodes of coma, ataxia or vomiting, anorexia, failure to thrive, developmental delay, all very suggestive of metabolic disorder. The association of neurological symptoms and abnormal hepatic tests is also of great value and must not lead to the diagnosis of Reye's syndrome without considering a metabolic defect of fatty acid oxidation, urea cycle, respiratory chain, or Wilson's disease. When looking for an etiological origin, it is mandatory to collect all the biological information at the same time, also knowing that metabolic abnormalities may be mild and transitory, and that many of them are non specific (metabolic acidosis, hyperlactacidemia, hyperammonemia, hepatic tests disturbances) being encountered in collapsus, shock and multiple organ failure syndrome.

Acute Disease↗
PubMed1993

[Awakening from traumatic coma and its future. 3 phases of dynamic reconstruction].

After the question of TC patient's survival in Intensive Care Units, many other questions, during-coma awakening phase, appear to family, care team, and the patient himself i.e. will the patient be handicapped or will he be as before? which after-effects of this passage? The vital functions and autonomy conquest goes with a permanent adjustment of psychical functions for keeping together an "exploded" subject. Each patient's singular history, its expression and meanings, are catched into initial trauma, coma, intensive care and awakening phase framework. Clinical observations leads to describe three evolutive periods, specific of awakening but also bound up with each other.

Brain Injuries↗
PubMed1993

[Plea for interactive rehabilitation during coma].

The question of head trauma reasons, and the shock of traditional family and therapeutic references, make the authors examine clinic coma evolution till awakening. From signs of libidinal values collected by care-team, another way during coma and till life recovery, is rebuilt.

Brain Injuries↗
PubMed1993

[Coma--resuscitation--unconsciousness. Approach to a difficult triple connection].

Clinical observations as well as words pronounced by brain injured patients in coma awaking phases attest the emergence of an unconscious psychic register, which arises at the time of coma and resuscitation, and takes an active part in their perspective background during the subsequent phases. Reported clinical fragments illustrate the interconnections between this unconscious register and the various physiological breakdowns suffered by patients as well as their attempts to recover this background.

Adult↗
PubMed1994

Nonketotic hyperosmolar coma in children.

Nonketotic hyperosmolar diabetic coma is well known in adults, but infrequently reported in children. This syndrome is associated with a 20-70% mortality rate. We report the successful treatment of a 12.5 year old girl with a hyperglycemic (1,800 mg/dl glucose) nonketotic hyperosmolar diabetic coma and summarize the reported cases in the literature.

Child↗
PubMedDate not supplied

[Embolism in an elderly diabetic patient following hyperosmolar coma].

The authors report a case of hemiballismus in an old patient with diabetes and hypertension, developed after a non ketotic hyperosmolar coma episode. In agreement with the recent literature, the syndrome is not always caused by a single Luys body lesion, but also by complex scattered lesions demonstrable only by RMN. A possible pathogenetic role of the recent non ketotic hyperosmolar diabetic coma and the good prognosis indicate that the vascular aetiology, even if prevalent, could not be the only one. The role of institutionalization of the patient during the development of the syndrome has also been discussed.

Diabetes Mellitus, Type 2↗
PubMed1993

[Diabetic coma and bases of proper treatment].

Hyperglycaemic, hyperosmolar coma developing in diabetes mellitus-with or without ketoacidosis-is a perilous metabolic catastrophe, preserving its clinical importance even nowadays. The features of the two basic forms of diabetic coma, the development and characteristics of clinical symptoms and laboratory alterations caused by absolute or relative lack of insulin are reported by the author. The importance of early diagnosis and up-to-date intensive treatment is emphasized, regarding the need of decreasing of the still now considerable mortality rate. Fundamental principles of the therapeutic interventions are the following: improvement of the microcirculation through appropriate compensation of fluid and elektrolytes, intravenous or intramuscular administration of low-dose insulin, prevention of hypokalemic condition, and correction of acidosis under pH 7,1 value. Moreover, the well-planned supportive treatment is also essential: prevention of thromboembolism, averting the occasional development of shock caused usually by infections, and prophylaxis of the often fatal cerebral oedema. The estimation and follow-up of osmolality and the prevention of rapid changes in serum glucose and electrolyte levels are of particular importance in every cases. Careful observation of the patients regarding the cardiorespiratory and renal functions is of great significance in both (first and second) phases of the treatment. Improvement of patients' education, controlled care of diabetic patients, reduction of the number of recidive cases and increasing knowledge regarding diabetes among the general practitioners are determined by the author as the future possibilities for the prevention of this severe metabolic disorder.

Adolescent↗
PubMed1995

[Nonketotic hyperglycemic coma induced by somatostatin in an AIDS patient].

A 33-year-old woman with AIDS was treated with somatostatin (continuous infusion 6 mg/day) for intractable diarrhoea. Improvement was insufficient and the dose was increased to 12 mg/day 5 days later. Hyperosmolar non-ketotic coma occurred two days later (blood glucose 53 mmol/l, bicarbonate 8 mmol/l, pH of arterial blood 7.2). Search for urinary ketones was negative. Klebsiella pneumonia was isolated in the urine sample. Somatostatin was withdrawn and the patient improved with parenteral nutrition and intravenous insulin. Glucose tolerance was verified after recovery and was normal. Somatostatin is known to impair glucose tolerance and as shown in this case should also be recognized as a cause of hyperosmolar non-ketotic coma. Increasing use of somatostatin, particularly in HIV patients often given other hyperglycaemia inducing drugs such as didanosine, pentamidine, dapsone, and phenytoin should be accompanied with careful monitoring of blood glucose levels.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

[Complete recovery from transient coma in bilateral paramedian thalamic infarctions].

Bilateral paramedian thalamic infarcts (BPTI) can begin clinically with transient coma, after which symptoms of fluctuating hypersomnolence, irrational behaviour, or amnesic states may be observed. We present two patients with BPTI who began with coma, recovering spontaneously in under eight hours, with no accompanying symptoms.

Aged↗
PubMed1995

[Intensive care of patients in a coma following severe craniocerebral injury].

During last 14 years 748 patients in coma according to the Glasgow Coma Scale (scores less than 8) were treated at Neurosurgical intensive care unit. All the patients were mechanically ventilated. In 354 patients intracranial pressure (ICP) was monitored using Leeds boult. From 1990 arterial pressure was monitored invasively in all patients. According to ICP and cerebral perfusion pressure (CPP) we used mannitol and/or thipental, trying to keep ICP below 20 mmHg, and CPP at least near 65 mmHG. From 1992 we started also with arteriojugular oxygen saturation monitoring. According to narrow, normal or wide cerebral extraction of oxygen range so called optimized hyperventilation can be achieved. Despite mortality rate in patients with severe head injury is still high, aggressive intensive management can reduce it.

Brain Injuries↗
PubMed1997

[Correlation of carbamazepine levels in blood with clinical poisoning states, evaluated with the help of the APACHE II system and the Matthew coma scale].

Acute carbamazepine (CBZ) poisoning occurs recently quite often. Symptomatology of poisoning is variable but usually various degrees of consciousness impairment prevail. 77 patients (36 women and 41 man, mean age 31.5) were hospitalized last two years in this Centre. Clinical condition was evaluated in a regular descriptive way, classifying the degree of coma according to the Matthew scale but also by calculating the scores according to APACHE II and TOXSCORE. Serum CBZ was measured. A slight falling trend was found of the relation of the serum CBZ in the range 6-37.8 micrograms/ml (38 micrograms/ml = median) to APACHE II score and the TOXSCORE and slight rising trend of the relation of the serum CBZ to the degree of coma. The significance of this trend rose essentially at the serum CBZ levels of more than the median 38 micrograms/ml. The causes of the non significant correlation of serum CBZ (in particularly range) to the clinical condition is discussed. The individuals factors of the patient and possible effect of other, unknown drugs taken together with CBZ seem to play a minor role at the concentrations above 38 micrograms/ml. A very precise correlation has been found at the serum concentrations exceeding 40 micrograms/ml.

APACHE↗
PubMed1976

[Hyperglycemic, hyperosmolar nonketotic diabetic coma in the pediatric age].

A case of non-ketotic hyperglycaemic-hyperosmolar diabetic coma in a 8 yr. old boy after a severe mental trauma is reported. This joins the 18 similar cases of paediatric age published up to now. On the basis of the results of virological and immunological investigations, insulinogenic function and psychodiagnosis, the diagnosis, aetiopathogenesis and therapy of this unusual event are discussed. The desirability of measuring plasma osmolarity in children diabetic coma is stressed.

Age Factors↗
PubMed1997

Coma from long-term overingestion of isoniazid.

Overingestion of isoniazid can cause confusion, slurred speech, seizures, coma, and death. Most cases of a central nervous system toxic reaction due to isoniazid use result from sudden intentional or accidental overdose. We describe a patient taking 1200 mg of isoniazid daily for 6 weeks who presented to the hospital with confusion and lethargy that progressed to coma. Within 30 minutes of receiving 1 g of intravenous pyridoxine hydrochloride, the patient was fully alert and lucid. The diagnosis of a toxic reaction to isoniazid was delayed by the possibility of concurrent active neurosyphilis and the failure to initially consider isoniazid poisoning in a patient without a history of sudden isoniazid overdose.

Antitubercular Agents↗