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At least 685 records · Page 38Linked to original sources
PubMed1990

Nonsteroidal anti-inflammatory drugs and coma: a case report of fenoprofen overdose.

We present the case of a 17-year-old girl who ingested 24 to 36 g fenoprofen as a suicidal gesture. She presented with coma, hypotension, metabolic acidosis, and respiratory depression within four hours of ingestion. The most common adverse effects of the nonsteroidal anti-inflammatory drugs occur in both therapeutic and toxic doses and include gastrointestinal upset, blood dyscrasias, and analgesic nephropathy. The propionic acid derivatives of nonsteroidal anti-inflammatory drugs, including fenoprofen and ibuprofen, are rarely associated with severe toxic effects. This is the first report of pure fenoprofen overdose presenting as coma and metabolic acidosis.

Acidosis↗
PubMed1983

[Myxedema coma. Apropos of 8 cases].

Eight cases of hypothyroid coma observed between 1971 and 1981 are reported, and their main clinical, biological and therapeutic features described. Three out of the 8 patients died. Physiopathological and therapeutic comments are made with reference to these cases and previous reports, concerning the hypothermia, cardiac and respiratory function, hyponatraemia and the endocrine disturbances observed in hypothyroid coma.

Aged↗
PubMedDate not supplied

[Value of electroencephalographic serveillance in the framework of resuscitation in coma caused by acute drug intoxication].

The authors carried out long-term clinical and E.E.G. studies on 100 cases of acute drug poisoning. They made the following conclusions: - in unexplained coma, the E.E.G. can indicate toxic aetiology and may sometimes even suggest which drug is responsible, especially for certain chemical groups (barbiturates, phenothiasines, benzodiazepines); - the E.E.G. picture contributes a valuable indication of the depth of coma; the way in which it evolves affects the prognosis; - the effectiveness of therapy may be judged by monitoring cerebral electrical activity.

Acute Disease↗
PubMedDate not supplied

[Anatomical findings in 30 cases of acute severe traumatic coma (author's transl)].

A variety of lesions of varying complexity were noted during pathological examinations of the brain in 30 cases of acute severe traumatic coma, of whom 27 survived for less than 10 days. "Diffuse brain damage" were present in all cases and contusions were frequently noted (83 p. 100). The lesions appear immediately after, and are directly related to the injury. Ischemic lesions were present in 66 p. 100 of cases and their mechanisms of production are various and interwoven. The frequency of respiratory difficulties associated with brain injuries is stressed. Two thirds of the cases with brain stem lesions (80 p. 100) were secondary to phenomena related to trans-tentorial herniation. Clinical examinations of these patients with acute severe coma demonstrates the difficulties encountered in assessing prognosis based on clinical findings within the first 48 hours.

Brain↗
PubMedDate not supplied

[Deep alpha frequency coma after hanging not followed by immediate death. A report of two cases (author's transl)].

Two cases of deep alpha frequency coma after unsuccessful hanging attempts are reported. Studies were conducted after similar cases in which vascular or traumatic brain stem lesions were at the origin of the coma, and in those secondary to cardiorespiratory arrest. A review of the EEG findings in cases reported in the published literature showed that these were more similar to cases with cardiorespiratory arrest than to those following brain stem lesions, in spite of the existence of angiographic anomalies observed in the vertebral arteries. The differential diagnosis and the prognostic value of the electroclinical picture are discussed, as well as the physiopathogenicity, which remains obscure.

Adult↗
PubMed1984

[Brain stem AEP in toxic comas. Correlation with brain stem reflexes].

24 deep toxic comas with respiratory assistance were studied by brain-stem reflex and BAEP. Laboratory analysis showed several simultaneous toxics (phenobarbital, benzodiazepines, tricyclic antidepressants...). Three groups of patients were defined: Twelve patients with normal BAEP and with relatively preserved brain-stem reflex (oculocephalic and oculovestibular are often disturbed but photomotor is present). Eleven patients with delayed BAEP and with more disturbed brain-stem reflex (photomotor is missing 3 times). In 2 cases (one of which is mentioned above in group B) brain-stem reflex and BAEP disappear and these patients die. Cerebral anoxia is associated here with toxics. Causes of delayed latencies (group B) are discussed (hypothermia, toxics). BAEP seems important in diagnosis and prognosis of toxic coma.

Adult↗
PubMed2002

Miller Fisher syndrome with transient coma: comparison with Bickerstaff brainstem encephalitis.

We herein report a 4-year-old boy with Miller Fisher syndrome (MFS) who presented with transient coma in addition to the typical triad of internal and external ophthalmoplegia, cerebellar ataxia and areflexia after an influenza type B infection. The electroencephalogram findings revealed intermittently generalized slow wave bursts. The cerebrospinal fluid revealed high protein and a lack of any cellular response. The serum anti-GQ1b IgG antibody was elevated in the acute phase and disappeared in the convalescent phase. The transient coma with the triad of MFS in this patient indicated an extended brainstem lesion including a reticular formation, which is also the responsible lesion of Bickerstaff brainstem encephalitis (BBE), but the magnetic resonance imaging repeatedly showed no abnormal finding. Our patient suggested the involvement of central nervous system in addition to the peripheral nerve injury in MFS. He also suggested that MFS and BBE may belong to the same group of disorders as syndrome of ophthalmoplegia, ataxia and areflexia (SOAA).

Brain Stem↗
PubMed2006

[Coma following chemotherapy: is 5FU implicated? Discussion about on case-report].

5FU is one of the most frequently used antioncogenic and cytostatic drug in digestive oncology. It may cause severe adverse events, such as encephalopathy, possibly based on hyperammoniemia, and may lead to coma. We report here the case of a coma with a favorable outcome following 5FU chemotherapy. As any other etiologic findings came to light, hyperammoniemia was discussed as a credible cause.

Adenocarcinoma↗
PubMed1998

Coma and confusional states: emergency diagnosis and management.

Coma and confusion signal a failure of brain function with many possible causes. Since many of the potential causes may quickly lead to death or severe disability, it is important to develop a focused and ordered approach to facilitate the rapid diagnosis and early institution of proper therapies. This requires an understanding of the localizing features of the neurologic examination and of the syndromes likely to cause coma and confusion, a predetermined plan for empiric therapies in certain cases of doubt when diagnostic confirmation will be delayed, and a careful consideration of cases when the diagnosis is not revealed by the initial neuroimaging, lumbar puncture, or EEG.

Brain Diseases↗
PubMed1990

[Study of cerebral energy metabolism and development of postanoxia coma].

An open prospective study of brain energy metabolism was carried out in 20 consecutive cases of coma occurring after cardiopulmonary arrest (CPA) of various causes. Mean age was 54 years and mean duration of CPA 2.75 min, with a mean of 11 min for resuscitation. Brain energy metabolism was compared with clinical course, electroencephalogram (EEG), and neurological outcome. All the patients were given the usual intensive care: intermittent positive pressure ventilation, haemodynamic control, sedation with benzodiazepines, neuromuscular paralysis, anticonvulsants, mannitol. A clinical examination and an EEG were carried out daily, 4 h after all drugs which might interfere with these investigations or brain energy metabolism had been stopped (except for anticonvulsants). Successive measurements of the cerebral arteriovenous oxygen (C (a - v) O2) and glucose (C (a - v)gluc) contents were made. The oxygen glucose index (OGI) was calculated according to Cohen's formula. The first set of measurements were carried out within the first 30 h after CPA. The last measurements were made a few hours before death or recovery, or stabilization of the coma. Patients were assigned to 2 groups according to their neurological outcome: group R (n = 8), patients who recovered consciousness; group D (n = 12), patients who developed brain death or a vegetative state - Safar's cerebral performance category 4. During the first 30 h, there was no relationship between clinical course, EEG and cerebral outcome. Half of the patients died or recovered within 72 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Treatment of diabetic ketoacidosis and non-ketotic hyperosmolar diabetic coma.

Although mortality of diabetic ketoacidosis (KA) has decreased during the past 20 yr to 1-2%, hyperosmolar non-ketotic coma (HNC) is still lethal in 20-30% of cases due to severe underlying conditions or to complications. The most frequent causes of death are infections and thromboembolic disorders. The strategies of initial treatment of KA and HNC are similar; in KA, insulin, fluid and electrolyte replacement have first priority. In HNC, rehydration and electrolyte administration are of primary importance. It is now generally recognized that insulin therapy is best performed using low doses (4-8 units/h); after institution of insulin treatment and rehydration there are rapid changes of fluid and electrolytes from the extra- into the intravascular space. In this situation it is a major therapeutic challenge to avoid complications due to hypokalaemia, hypophosphataemia, hypomagnesaemia and hypovolaemia. These complications should be avoided by adequate replacement, and particularly by regular clinical and laboratory monitoring. When blood glucose concentrations decrease below 14 mmols/l, blood glucose concentrations should initially be maintained at this level because rapid lowering below this level may increase the risk of brain oedema. Too-vigorous fluid replacement with crystalline solutions also increases the risk that brain oedema or complications like the adult respiratory distress syndrome will develop. If hypovolaemia persists in spite of adequate crystalloid solutions, colloid-containing fluids such as albumin should be administered. It is not established whether replacements of phosphate and magnesium have clinical benefits. Nevertheless, it is probably justified to administer phosphate and magnesium when their serum concentrations are below the normal range, particularly if the clinical situation is critical. Mortality from diabetic coma in industrialized countries may only be decreased by prophylaxis, i.e. by education of all diabetic patients and physicians to detect metabolic decompensation early.

Diabetic Coma↗
PubMed1998

[Prediction by means of endogenous and exogenous evoked potentials of the favorable evolution of a prolonged coma].

A neurophysiological follow-up (EEG, exogenous and endogenous evoked potentials--EP) was performed over a 4-month period in a patient who presented a long-lasting coma following a cardiac arrest and an amniotic embolism. A pure anoxic aetiology was ruled out starting from the second day on the basis of a dissociation between mildly altered flash visual EP and markedly altered somatosensory EP, indicating focal brain-stem pathology. Endogenous EP reappeared after 12 days. This patient recovered consciousness after 51 days. Despite the absence of MRI abnormalities, we put forward the hypothesis that a brain-stem embolism had, in fact, worsened the clinical picture of an actually moderate anoxia. This case exemplifies the interest of an integrated neurophysiological approach (EEG, exogenous three-modality EP and endogenous EP) in the early evaluation of coma. It also illustrates the complement between structural imaging and functional assessment of the nervous system.

Adult↗
PubMed2001

Interrater reliability of the Glasgow Coma Scale scoring among nurses in sub-specialties of critical care.

The Glasgow Coma Scale (GCS) is used as an assessment tool to measure the levels of consciousness and coma in patients. This research investigated the reliability of scoring the GCS among registered nurses (RNs) working in five different sub-specialty clinical areas of critical care; general intensive care, neurosurgical intensive care, coronary care, emergency room and post anaesthetic recovery room. Seven video recordings were made of six patients (one patient was recorded twice) having their level of neurological response assessed utilising the GCS. Seventy five RNs (15 from each sub-specialty) viewed each of the GCS assessments on the videotape and rated each patient on the scoring sheet provided. Analysis was performed for all RN subjects as a single group as well as separately for each of the five groups under investigation. The ratings for the first six videos were used to test interrater reliability and the scores from videotape four and seven (same patient) were used to calculate intrarater reliability. Based on comparison with expert scores, of the 75 participants, 38 responded correctly to eye opening responses; only 26 responded correctly to the motor response ratings. However, a better accuracy was achieved in the verbal response category with 67 participants responding correctly. Education qualifications and previous neurosurgical experience were statistically significant with regard to the nurses' accuracy of GCS assessment with p values of 0.004 and 0.043 respectively. The results were consistent with previously published studies demonstrating the motor response rating is most problematic in relation to rate accuracy.

Adult↗
PubMed1996

Recurrent coma.

Recurrent episodes of coma are usually associated with a metabolic disorder. A healthy 9-year-old boy of normal intellect and intact corpus callosum on neuroimaging had recurrent episodes of coma associated with profound spontaneous hypothermia. An evaluation, differential diagnosis and insights into the pathogenesis of this disorder are discussed.

Body Temperature Regulation↗
PubMed1999

Etiology, neurologic correlations, and prognosis in alpha coma.

OBJECTIVE: To determine the factors affecting prognosis in alpha coma (AC). METHODS: Retrospective review of 36 study patients, 36 control coma patients matched for age and etiology, and meta-analysis of 335 cases in the world literature. RESULTS: Principal causes were cardiorespiratory arrest (CRA) (21 patients); infection, metabolic dysfunction, head trauma (3 each); and drugs, stroke and hypoxia (2 each). Outcome was predicated by EEG reactivity to noxious stimuli. Fourteen of the 15 patients with reactive EEGs, had measurable outcome, 8 awoke - all but two had etiologies other than CRA. Fourteen of 19 patients without EEG reactivity died; two had support discontinued and 3 awoke. Following CRA, 16/21 patients died and 3 had support discontinued. Only 3 patients made a good recovery - all with toxic or metabolic etiologies. Literature meta-analysis of 335 cases showed that overall, AC carried a poor prognosis (76% died). CRA (226 cases) had an 88% mortality; strokes (29 cases), a 90% mortality; hypoxia without cardiac arrest (28 cases), a 61% mortality; drug-induced AC (25 cases), an 8% mortality. CONCLUSIONS: Although the cause of AC largely predicts outcome, EEG reactivity in AC predicted survival: most patients with reactivity awoke; most of those without, died. Few survivors had meaningful recovery.

Adult↗
PubMed2000

Postanoxic alpha (theta) coma: a reappraisal of its prognostic significance.

OBJECTIVES: To appraise the controversial prognostic significance of postanoxic alpha or theta coma (ATC). METHODS: We prospectively assessed 14 comatose patients with ATC after cardiac arrest by means of a protocol which included repeated clinical examinations, EEG, and median somatosensory evoked potentials (SEP). Good outcome was defined by the reappearance of cognition (Glasgow outcome scale 3-5) at any time during the 1 year follow-up. RESULTS: Nine of 14 patients had a monotonous, frontally accentuated and a reactive alpha (theta) EEG activity (complete ATC). In these patients ATC was recorded a mean of 47 h after resuscitation, the mean Glasgow coma scale (GCS) was 4 at 48 h, and early cortical SEPs were altered or absent in 5 of 7 patients. All nine patients died. In five of 14 patients the alpha (theta) EEG activity was either not monotonous, partially reactive or posteriorly dominant (incomplete ATC). In these patients ATC was recorded a mean of 43 h after resuscitation, the mean GCS was 8 at 48 h, and early cortical SEP were normal in 4 of 5 patients. Three of 5 patients regained cognition, two of them remained however dependent in activities of everyday life. CONCLUSIONS: This study and a review 283 cases of postanoxic ATC reported in the literature suggest the existence of incomplete and complete variants of postanoxic ATC. Whereas complete ATC is invariably associated with a poor outcome, full recovery is possible in patients with incomplete ATC. The combination of EEG, clinical, and SEP findings improves the prognostic accuracy of postanoxic ATC.

Adult↗
PubMed2003

Effect of sodium succinate on gas exchange in rats with barbiturate-induced coma.

Injection of sodium succinate in doses of 5 or 10 mmol/kg (but not 1 mmol/kg) intensified oxygen consumption in rats with sodium thiopental-induced coma. Injection of SDH inhibitor (sodium malonate) inhibited gas exchange and abolished the effect of sodium succinate. The effect of succinate on rat survival was positive, while that of malonate was negative, but manifested only as a trend. The critical role of succinate oxidation in preventing lethal complications of barbiturate-induced coma is proved.

Animals↗
PubMed2004

Metabolic correction of gas exchange disturbances in rats with barbiturate coma.

Krebs cycle intermediates normalized gas exchange and decreased the mortality rate in rats with barbiturate coma. Treatment with other substrates including glucose and products of glycolysis was ineffective. Oxygen inhalation had no effect on oxygen consumption and indexes of external respiration. Our results suggest that deficiency of endogenous intermediates of the Krebs cycle, but not disturbances in oxygen mass transfer, serves as a limiting factor for oxygen consumption in rats with barbiturate coma.

Animals↗