Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Coma”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,459 records · Page 81Linked to original sources

[Coma in myxedema--a rare complication of hypothyroidism. Possible iatrogenic factors should be taken into account].

Myxedema coma is the most severe form of hypothyroidism and is characterized by extreme hypothermia, bradycardia, central hypoventilation and hypoxia. Common causes are intercurrent diseases, interruption of thyroid hormone treatment, or an overdose of sleeping pills or sedatives. The diagnosis is usually readily established on the basis of very high serum TSH and low T4 levels. Consideration must also be given to an extra-thyroidal influence on the hormone levels. Intensive care treatment involving intravenous high-dose L-thyroxine and the reversal of hypoxia improve the prognosis of the serious disease.

Coma↗

[Diagnostic and prognostic value of the brain stem reflexes in severe post-traumatic coma].

Authors study the neurological evolution of 50 cases of traumatic coma and recognize 5 misfunction levels corresponding to five steps of rostrocaudal deterioration. The level 1 (cortico-sub-cortical) is defined by the persistence of the mimic and flexion response to painful stimulation. The level 2 (diencephalic) is characterized by stereotypic responses to pain and lack of mimic. At these two levels, the fronto-orbicular and vertical oculo-vestibular reflexes are persistent. These reflexes disappear when the status impair caudodal to the level 3 (meso-diencephalix junction). The photomotor reflex disappear at the level 4 (mesencephalic), where the motor response to pain may be very poor, or may be a bilateral extension. The horizontal oculo-vestibular reflex is always persistent, except for the level 5 corresponding to a pontine lesion. The meso-diencephalic level 3 appears to be a critical impairment point: as long as the level is not overpassed, the half of the patients do improve and 10% only die. More than 75% of those who improve from this level have an excellent recovery. The restructuration probability is diminished by the half when the level of mesencephalic misfunction is reached.

Brain↗

Sudden death due to diabetic coma in insulin-department diabetes mellitus: an autopsy report.

Sudden death caused by the acute onset of diabetic coma is reported. A 15-year-old female had been suffering from insulin-dependent diabetes mellitus for the prior 8 years and had a fever and vomiting for the past few days. On the 4th day, after the onset of fever and vomiting, she died suddenly, and was autopsied to clarify the cause of death. Macroscopic examination revealed that the pancreas was atrophic (40 g) whereas the liver was markedly enlarged (2,740 g). Histological findings were: 1) The islets of Langerhans were decreased in size and number. They were not positive for aldehyde-fuchsin staining, 2) There were severe fatty changes in the liver cells. The retained blood in the left ventricle was analyzed: glucose, 1,016 mg/dl; acetone, 345 mg/l; acetoacetate, 5.91 mmol/l: D-3-hydroxybutyrate, 4.17 mmol/l; hemoglobin A1c, 10.2%; fructosamine, 416 mumol/l; total serum cholesterol, 220 mg/dl; triglycerides, 205 mg/dl; free fatty acid, 8.0 mEq/l; urea nitrogen, 40 mg/dl. Although the biochemical estimation of the glucose and ketone levels in post-mortem body fluids was recognized as being unreliable, many of these values were far elevated in comparison with those of normal individuals. Thus, we concluded that the cause of death was diabetic ketoacidosis. We also discuss the diagnostic problems of postmortem blood chemistry.

Adolescent↗

[Automatic movements of extremities induced in primary massive brain lesion with apneic coma].

In three cases of primary massive brain lesion with apneic coma, various automatic movements of the extremities were elicited by physical or sensory stimulation. In each case, these movements appeared after a period of cessation of spontaneous respiration followed by flaccid tetraplegia. Brainstem reflexes were absent throughout in all cases. The movements were induced mainly by ventroflexion of the neck, and each case showed movements as described below: in the first case, the patient flexed her elbows and raised both arms slowly, a typical Lazarus sign; in the second case, the patient raised both arms and showed myoclonic movements; and the third case showed abduction of both legs and extension in the upper extremities. Pathology in the first case showed ischemic changes in the entire brain and brainstem. Although ischemic change was also found in the anterior horn cells and white matter of the spinal cord of C1-C4 and of T4 and below, the spinal cord of C5-T3 was relatively well-preserved. These movements appear to have essentially originated in spinal neurons; however, it is assumed that they must have recovered from spinal shock which occurred due to upper level transection. These movements were induced by ventroflexion of the neck, so mechanical extension of the spinal roots, mechanical compression of the spinal cord, and various modalities of the sensation afferent might have some relation to these movements. As tonic neck reflex might also be a cause of these, movements, association with the lower medulla could not be ruled out completely. These movements appeared nearing or after brain death. Although in each case of brain death the spinal cord may have been affected by specific conditions, such as impaired circulation of whole central nervous sysytem, it might have been transversed at upper level, which then causes spinal automatism. These movements might appear even in the state of brainstem death. In each case, the distribution and severity of hypoxic changes in the spinal cord may have resulted in variations in the type and characteristics of these movements.

Aged↗

[Mechanisms of acute respiratory insufficiency in patients with hyperglycemic coma].

Basic parameters of pulmonary gas exchange, central and pulmonary hemodynamics, and colloid osmotic pressure were investigated in 31 patients in diabetic hyperglycemic coma over the course of intensive care. Pulmonary gas exchange disorders were observed in all patients in the presence of increased shunting of the blood in the lungs and disorders of transcapillary liquid exchange. On the other hand, we failed to obtain data indicative of an increase in the volume of extravascular water in the lungs. However, it does not rule out the possibility of iatrogenic disorders of gas exchange during noncontrolled rehydration.

Acute Disease↗

Modified Glasgow Coma Scale to predict mortality in children with acute infections of the central nervous system.

BACKGROUND: This study aimed to identify the predictors of hospital mortality in children with acute infective disorders of the central nervous system using an aggregate Modified Glasgow Coma Scale (MGCS) score and other clinical variables assessed within 24 hours of hospitalization. METHODS: We did a prospective cohort study in a teaching and referral hospital in Lucknow, North India. Consecutive children aged 1 month to 12 years of age admitted with acute infective disorders of the central nervous system were included in the study. The diagnosis was based on the presence of symptoms of fever, headache or irritability with or without vomiting, and either altered sensorium or first episode of seizures or both. The main outcome measure was hospital-based mortality. RESULTS: Of the 230 patients included in the study, 42.2% had pyogenic meningitis, 36.9% had tuberculous basal meningitis and 20.9% had meningo-encephalitis. There were 43 (18.7%) deaths of which 44.2% were within 3 days of admission. Death was associated with the day 1 aggregate MGCS score only. The area under the curve of four strata of aggregate MGCS was 0.63 (SE 0.05). The likelihood ratio for discharge with an aggregate MGCS score of < 5 was 0.52 (95% CI:0.29-0.95) and > 10 was 5.52 (9% CI:1.02-31.96). CONCLUSION: The MGCS can be used to predict discharge in patients with acute infective disorders of the central nervous system within 24 hours of hospitalization. The scale is simple, can be applied at the bedside and does not depend on any investigations. In developing countries with limited investigative facilities it can be used for identification and selective referral of patients with a higher risk of death to specialized centres. This study validates the predictive value of the MGCS.

Child↗

Spindle coma and alternating pattern in the course of measles encephalitis.

Acute disseminated encephalomyelitis (ADEM) is a well known complication of measles infection. Electroencephalographic abnormalities may occur frequently, in the form of moderate to severe diffuse high voltage theta-delta activity. We report a case of measles encephalitis with rapid benign outcome, that showed peculiar EEG features both of a "spindle coma" pattern and of an "alternating pattern." Possible physiological explanations of the EEG findings are discussed.

Adolescent↗

[Non-invasive nasal ventilation in a a case of hypercapnic coma].

Noninvasive positive pressure ventilation (NPPV) via nasal mask is well known to be effective in the treatment of acute respiratory failure (ARF) secondary to chronic obstructive pulmonary disease (COPD). A case of ARF with hypercapnic coma due to exacerbation of COPD is described. Six hours of conservative therapy with oxygen and medical treatment did not show any result. As endotracheal intubation (ET) was avoided on the basis of advanced age, poor life expectancy of the patient and family wish, NPPV was set up using a pressure triggered ventilator. After 61 hours of uninterrupted NPPV, the acid-base alteration and the lethargic status was fully reversed. The conclusions is drawn that NPPV may be useful also in the treatment of patients affected by severe decompensated hypercapnic respiratory failure in whom ET is not indicated.

Aged↗

[The hemispheric relationships of the human brain during the recovery of consciousness after a long-term coma: an EEG analysis].

Analysis of the intra- and interhemispheric EEG coherence in the dynamics of coma regress and its comparison with the clinical stages of postcomatose recovery period revealed both specific interhemispheric rearrangements of the structure of intercentral functional relations, which developed in parallel with the recovery at first of the visual, and then speech functions, and the adaptive-compensatory changes in activity of the regulatory systems, which provide the recovery of mental functions. It is emphasized that the interhemispheric EEG coherence asymmetry, its character and dynamics are significant for formation of neurophysiological mechanisms of consciousness and the course of compensatory processes under the extreme conditions.

Brain↗

Abdominal lymphomas, convulsive seizure and coma: a case of successfully treated, advanced Whipple's disease with cerebral involvement.

Whipple's disease is a rare, generalized inflammatory disorder due to the recently described bacterium Tropheryma whippelii. We report an unusual, successfully treated case of a 32-year-old woman, who presented with a 25 month history of large abdominal lymphomas, polyserositis and cachexia. The diagnosis of Whipple's disease was confirmed by duodenoscopy, lymph node and duodenal histology and polymerase chain reaction analysis of biopsy material and cerebrospinal fluid. A prolonged convulsive seizure with a subsequent 5 day period of coma were interpreted as signs of cerebral involvement. Under antibiotic treatment with trimethoprim-sulfamethoxazole (co-trimoxazole) the patient recovered completely, CT scans showed a complete regression of abdominal lymphomas. The therapy was continued over 18 months without the occurrence of a relapse.

Abdominal Neoplasms↗

Flumazenil for hepatic coma in patients with liver cirrhosis: an Italian multicentre double-blind, placebo-controlled, crossover study.

Several factors suggest that endogenous benzodiazepines and gamma-amino-butyric acid may be involved in pathophysiology of hepatic encephalopathy (HE). Contrasting opinions exist on the therapeutic efficacy of flumazenil in the treatment of HE. This study was planned to assess the efficacy of flumazenil by a double-blind, placebo-controlled, crossover design in a large and selected population of cirrhotic patients in stage 4a HE admitted to intensive care units over a 4-year period. Out of 236 patients selected for the study, 132 received flumazenil, whereas 131 patients received placebo. Improvement of the neurological score was documented in 31 patients (23%) of flumazenil group and in two patients (1.5%) of placebo group (p < 0.001) during the first study period, whereas during the crossover period, improvement of the neurological score was documented in seven patients (5.3%) of the flumazenil group and in none of the placebo group (p = 0.022). Improvements in EEG tracings were observed in 44 patients (33.3%) of flumazenil group and in five patients (3.8%) of placebo group (p < 0.001) during the first study period; during the crossover period, improvements in EEG tracings were observed in 10 patients (7.5%) of the flumazenil group and in two patients (1.5%) of the placebo group (p = 0.040). The presence of benzodiazepines was detected in the serum of three responders and in two non-responders. The presence of diazepam and NN-desmethyl diazepam was documented in two responders; prior intake of synthetic diazepam was later confirmed in these patients. The results of our study suggest that flumazenil is beneficial only in a selected subset of cirrhotic patients with severe HE; the applicability of this treatment to unselected patients with hepatic coma or to cirrhotic patients with less severe HE still remains to be determined.

Adult↗

Hepatic coma resulting from diaphragmatic rupture and hepatic herniation.

We treated a unique case of blunt rupture of the right hemidiaphragm that produced acute hepatic failure with jaundice and coma. Laparotomy showed total eventration of the liver into the chest. The hepatic failure was caused by strangulation of the extrahepatic biliary and venous structures. Surgical repair was followed by recovery and normalization of hepatic function. This case stresses the need to diagnose and treat diaphragmatic ruptures promptly to prevent such threatening complications. The diagnosis of right diaphragmatic rupture must be suspected in instances of blunt injury, with an awareness of misleading presentations.

Diaphragm↗

Ammonia inhibits insulin stimulation of the Krebs cycle: further insight into mechanism of hepatic coma.

Oxidation of [2,3-14C]succinate in the intramitochondrial Krebs cycle was used as a probe to investigate the effect of ammonia on protein incorporation and Krebs cycle oxidation of succinate carbons in isolated rat hepatocytes. At low concentrations of ammonium chloride (0.1 to 0.5 mM) a slight increase in 14CO2 formation from [2,3-14C]succinate was observed, however, the stimulatory effect of insulin was significantly reduced. Insulin failed to cause any stimulation of succinate carbons incorporation into hepatocyte protein in the presence of ammonium chloride. Addition of ammonium chloride also depressed the movement of tracer carbons into the gluconeogenesis pathway. The activity of the amphibolic amino acid pool was significantly enhanced by ammonia. The data presented in this paper lend strong support to the Krebs-cycle depletion theory of hepatic coma. They also suggest that reduced mitochondrial Krebs cycle activity caused by increased amphibolic depletion of substrates results in loss of insulin sensitivity in ammonia toxicity.

Ammonium Chloride↗

Beta-hydroxybutyrate reverses insulin-induced hypoglycemic coma in suckling-weanling mice despite low blood and brain glucose levels.

In normal suckling-weanling mice, DL-beta-hydroxybutyrate (30 mmol/kg ip) stimulated insulin secretion and reduced plasma glucose levels. In the brains of these animals, glucose levels were tripled due to a reduced rate of glucose utilization (determined by deoxyglucose phosphorylation). Other metabolite changes were compatible with inhibition of hexokinase, phosphofructokinase, glyceraldehyde-P-dehydrogenase, and pyruvate dehydrogenase activities. In contrast to the decrease in cerebral glycolysis, metabolite changes were compatible with an increase in the Krebs citric acid metabolic flux. The brain energy charge was also elevated. While it is generally believed that ketone bodies cannot sustain normal brain metabolism and function in the absence of glucose, DL-beta-hydroxybutyrate (20 or 30 mmol/kg ip) reversed insulin (100 U/kg sc)-induced hypoglycemia despite the persistence of a critically reduced plasma glucose concentration and near-zero brain glucose levels. Metabolic correlates of possible significance in the behavioral recovery from coma were reductions of the elevated levels of brain aspartate to below normal and ammonia levels to normal. Levels of acetyl CoA were unchanged both before and after treatment with beta-hydroxybutyrate.

3-Hydroxybutyric Acid↗

[A rare cause of hepatic coma].

CASE REPORT: A 65-year-old female patient was admitted to the hospital in somnolent state. During physical examination, she had an increase in blood pressure and a positive bilateral Babinski's sign. Laboratory findings showed elevated liver enzymes, metabolic alkalosis and slightly elevated kidney values. 3 h hours later she lapsed into a hepatic coma (ammonia > 400 micrograms/dl). Subsequently, indirect anamnesis revealed the following affections: ureterosigmoidostomy in 1942, cystectomy in 1943, and right-sided nephrectomy in 1950. DISCUSSION: This case presents with an uncommon origin of the hepatic encephalopathy: in the operated colon, bacterial overgrowth (bacteriogenic ureapoiesis) developed, which led to a hyperammonemia. Furthermore, in mild alcoholic liver disease--as in this case--ammonia cannot be metabolized to urea and leads to hepatic encephalopathy. We considered making this part of the colon poor in bacteria (by consequent administration of antibiotics), thus reducing the formation of ammonia.

Aged↗

Ultrastructure of the spermatozoon of the anoplocephalid cestode Gallegoides arfaai (Mobedi and Ghadirian, 1977) Tenora and Mas-Coma, 1978, an intestinal parasite of the wood mouse (Apodemus sylvaticus Linnaeus, 1758).

The present work involves an ultrastructural study of the mature spermatozoon of the anoplocephalid cestode Gallegoides arfaai (Mobedi and Ghadirian, 1977) Tenora and Mas-Coma, 1978, obtained from the small intestine of naturally infected wood mice, Apodemus sylvaticus Linnaeus, 1758 (Rodentia, Muridae). The mature spermatozoon of G. arfaai is a filiform cell, tapered at both ends and lacking mitochondria. It is characterized by the presence of a 1,000-nm-long apical cone and two 140-nm-thick crest-like bodies in its anterior extremity. The axoneme, of the 9 + '1' trepaxonematan pattern, lacks a periaxonemal sheath, and disorganization occurs at the level of the nuclear region of the sperm cell. The cortical microtubules form two to four fields according to the different regions of the male gamete. They are twisted at an angle of about 35 degrees , becoming parallel towards the posterior extremity of spermatozoon. The nucleus, spiralled around the axoneme, shows an irregular shape in both longitudinal and cross-sections. Numerous electron-dense granules were observed, which transform into an electron-dense material in the posterior extremity of the cell. Moreover, we describe for the first time the total length of the anterior region of sperm containing the helical crest-like bodies. This anterior extremity measures around 15 mum and presents two helical crest-like bodies of different lengths that describe 13-14 turns around the sperm body. Our ultrastructural results on the G. arfaai spermatozoon are compared with the ultrastructural organization of the spermatozoa of other previously studied species, with particular emphasis on the anoplocephalids.

Animals↗

Extracranial insults and outcome in patients with acute head injury--relationship to the Glasgow Coma Scale.

Hypoxia and hypotension are extracranial insults known to have an adverse effect on the outcome of patients with acute head injury. Arterial oxygen tension, blood pressure and the Glasgow Coma Score on admission of 67 patients seen over a 6-month period were correlated with the outcome at 6 months. With a given level of consciousness the presence of an extracranial insult resulted in a worse outcome than would be predicted. The combination of hypoxia and hypotension was uniformly fatal as was the presence of severe respiratory dysfunction.

Adolescent↗