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At least 919 records · Page 51Linked to original sources
PubMed1981

[Hepatic coma - experimental study with swine (part 1)].

An acute coma hepaticum was produced in 8 pigs by means of one intraperitoneal dose of thioacetamide. Distinct changes in the behaviour of the animals, changes of the biochemical parameters inclusively the enzyme pattern with a typical lesion pattern of the liver parenchyma and a displacement of the plasma amino acids were shown. All pathological changes in comparison with the normal animal characterize the liver insufficiency after 24 hours as a comatose state. This acute toxic model serves as the base for investigations within the physiology of nutrition about parenteral feeding of L-amino acid mixtures in coma hepaticum. The nearly exclusive hepatotropic lesion degree of thioacetamide is suitable as an experimental model for this purpose.

Acetamides↗
PubMed1980

[Experience in treating hepatic coma by extracorporal liver perfusion (author's transl)].

19 extracorporeal liver perfusions have been performed for treating hepatic coma in 11 patients. No improvement was found in 3 patients, improvement in 8.5 of these 8 patients recovered full consciousness. All 7 patients with pre-existent liver disease died. Of 4 patients without pre-existent liver disease, 2 were discharged and are still alive. At present, extracorporeal liver perfusion seems to be the most promising treatment for hepatic coma. It should be undertaken at Stage IV and at Stage III with increasing prothrombin time. Pre-existent liver disease should be excluded before by laparoscopy.

Adult↗
PubMed1996

[Hypothalamic-adenohypophysial function of corticotropin releasing hormone (CRH)-ACTH system in hypoxic coma].

To evaluate the hypothalamic-adenohypophysial function of corticotropin releasing hormone (CRH)-ACTH system in severe hypoxic coma, basal serum values of ACTH and cortisol was measured, and insulin-tolerance test (ITT) and CRH stimulation test was performed in 15 cases. They were divided into two groups according to their prognosis: brain death (group A, 7 cases) and persistent vegetative state (group B, 8 cases). Basal values were within normal range in most cases apart from those measured in few days after the brain death, however, stimulation tests were negative in many cases. In group A, basal values in impending stage were significantly higher han those after the brain death (p < 0.05), however, both stimulation tests were negative regardless of the stage. In group B, basal values in acute stage, which was measured within a week after the hypoxia, were slightly higher (without significance) than those in chronic stage, which was measured more than a months after the hypoxia. CRH test and ITT were positive in 0/4 and 2/5 in acute stage, and in 4/8 and 3/8 in chronic stage, respectively. In early stage of group A, the impending stage, showed slightly higher basal values than those in acute stage of group B (without significance). ITT was negative in the former whereas positive in some cases (2/5) of the latter, however, CRH test was negative in both groups. These results suggest that endocrinological evaluation of the hypothalamic-adenohypophysial function may help to predict outcome in early stage of hypoxic coma.

Adolescent↗
PubMed1993

Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank.

The outcome from severe head injury (GCS < or = 8 mmHg) was prospectively studied in patients from the Traumatic Coma Data Bank. We investigated the impact on outcome of hypotension (SBP < 90 mmHg) occurring from injury through resuscitation (early hypotension; N = 717) or in the Intensive Care Unit [ICU] (late hypotension; N = 493). Early hypotension occurred in 248 patients (34.6%) and was associated with a doubling of mortality (55% vs. 27%). If shock was present on admission, the mortality was 65%. These effects were independent of age, admission GCS motor score, presence of hypoxia, or associated severe extracranial trauma, suggesting that the influence of multiple system trauma in head injured patients is primarily due to associated hypotension. Late hypotension occurred in 156 of 493 patients (32%) and was the only hypotensive episode in 117 (24%). For 117 patients whose only hypotensive episode occurred in the ICU, 66% either died or were vegetative survivors, compared to 17% of patients who never suffered an hypotensive episode. Logistic regression modelling suggested that early and late shock were the most powerful independent predictors of mortality in this group of patients. These data demonstrate that hypotension is a common and devastating secondary brain insult in severe head injury patients, occurring not only during transport and resuscitation but also "right under our noses" in the ICU. We suggest that vigorous attention to eliminate or minimize such insults has the potential of markedly improving outcome from severe head injury.

Adolescent↗
PubMed1991

Head injuries in infants and young children: the value of the Paediatric Coma Scale. Review of literature and report on a study.

The normal verbal and motor responses embodied in the standard Glasgow Coma Scale (GCS) are not achievable during the first few years of life. The recent literature contains numerous reports of attempts to devise scales of responses quantitating the conscious level in infants and young children, both for research purposes and as clinical guides; some of these scales incorporate items, e.g. brainstem reflexes, that are not included in the GCS. We have reported on a simple paediatric version of the GCS, which uses the standard scale with minor modifications in the verbal component, and sets realistic age-related normal responses. This has been tested prospectively in a series of 60 head-injured infants and children (age range 0-72 months). Of 6 cases recorded as comatose 6 h after injury, 4 have confirmed or suspected residual disabilities. Of 35 cases considered to be fully conscious at 6 h, 31 have made good recoveries and only 1 has suspected residual disabilities. The study suggests that the scale accords with the realities of neurological immaturity, and confirms that it can be used in routine paediatric practice. For comparative therapeutic trials, the conscious level in infants has limited value as an index of brain injury, and should be complemented by other indices, such as brainstem reflexes.

Brain↗
PubMed1981

Hyperosmolar nonketotic diabetic coma.

The authors report the case of a 12-year-old boy with hyperosmolar nonketotic diabetic coma. Pathogenetic aspects and the HLA genotype are discussed. To reduce the hyperglycaemia, a continuous intravenous infusion of regular insulin at a low rate was used. The too rapidly infused sodium-bicarbonate overloaded tha body with sodium and caused intracellular sodium accumulation with edema. This could explain the disorientation after regaining consciousness. Much more important than the sodium-bicarbonate infusion is an accurate rehydration regimen.

Bicarbonates↗
PubMedDate not supplied

C-peptide blood levels in keto-acidosis and in hyperosmolar non-ketotic diabetic coma.

For further evaluation of B-cell secretion in diabetic keto-acidosis (KA) and in non-ketotic hyperosmolar coma (NKHC), basal and post-i.v. tolbutamide blood CPR and IRI values were measured in 34 patients (22 KA and 12 NKHC). FFA, cortisol and HGH measurements were also performed. IRI was low in both KA and NKHC (0.07 +/- 0.01 and 0.082 +/- 0.01 nmol/l) as opposed to CPR which was significantly higher in NKHC (1.14 +/- 0.1 nmol/l) than in KA (0.21 +/- 0.03 nmol/l). After tolbutamide injection, CPR and IRI levels did not change in any of the KA cases, whereas they significantly increased in half of the NKHC cases. Cortisol and FFA values were similarly increased in both situations, as opposed to HGH which was significantly higher (6.1 +/- 1.2 ng/ml) in KA than in NKHC (1.9 +/- 0.2 ng/ml). These results suggest that B-cell function is less deficient in NKHC than in KA. Residual insulin amounts reaching the liver via the portal vein could partly account for the absence of ketosis in NKHC.

Adult↗
PubMed1993

The Glasgow Coma Scale: a mathematical critique.

The Glasgow Coma Scale permits 120 possible mathematical combinations of eye, verbal and motor scores. Out of these only about 15 are clinically valid and useful in the assessment of altered consciousness. A mathematical analysis of this pruned scale shows a predominant skew towards the motor response. Without clinically altering the scale. The numerical values can be modified to produce a more equitable dominance by each of the factors and greater precision. This is also necessary as the value of a unit is the same in the sum score, whether contributed by the eye, verbal or motor elements.

Coma↗
PubMed1987

Poor oxygenation in the lungs of patients with hyperosmolar hyperglycemic non-ketotic diabetic coma after cardiac surgery.

The ratio of PaO2 to FiO2 was often low (300 or less) in four patients with complications of hyperosmolar hyperglycemic non-ketotic diabetic coma (HHNKDC) following open heart surgery. Four of our patients had poor oxygenation and subsequent spontaneous recovery from in the immediate post-operative period, although HHNKDC occurred only in one during this period. In the 3 others, poor oxygenation without accompanying HHNKDC lasted for 1-6 days and HHNKDC developed about 2 weeks after open heart surgery at time when poor oxygenation reoccurred. If a working diagnosis of congestive heart failure was made only on the basis of the most common probability, and the fluid supply was restricted, HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced. It is thus concluded that HHNKDC should be included in diagnoses for pulmonary dysfunction.

Blood Glucose↗
PubMed2001

Modified Glasgow Coma Scale to predict mortality in febrile unconscious children.

A prospective hospital based study was conducted in the Department of Pediatrics of the Kasturba Hospital, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha to predict the mortality in children admitted with fever and unconsciousness using the Modified Glasgow Coma Scale (MGCS) score. Forty eight children were admitted with fever and unconsciousness; cases of febrile convulsions, epilepsy and cerebral palsy were excluded. MGCS scores were assessed on admission and repeated at 12 hours, 24 hours, 48 hours and 72 hours after admission in each case. Diagnosis in each case was confirmed by history, examinations and investigations. All the cases were regularly followed up till death/discharge. The overall mortality was 29.1% (14/48) out of which 85% (12/14) died within the first 24 hours. Mortality was highest in the toddler age group and in patients with pyogenic meningitis. There was a significant association between death and MGCS scores on admission with a post test probability for discharge being only 10% with a score of less than 5 and 99% with a score of more than 10 respectively. MGCS scores on admission can be used to predict mortality in patients hospitalized with fever and unconsciousness. The scale is simple, easy, can be applied at bed side and does not need any investigations. Its application in developing countries with limited investigative and intensive care facilities can help the treating physician decide regarding referral and counseling the parents regarding the probable clinical outcome.

Analysis of Variance↗
PubMed2002

Serum neuron-specific enolase predicts outcome in post-anoxic coma: a prospective cohort study.

OBJECTIVE: The aim of this study was to investigate whether serial serum neuron-specific enolase (NSE) can be used to predict neurological prognosis in patients remaining comatose after cardiopulmonary resuscitation (CPR). DESIGN. Observational cohort study. Clinicians were blinded to NSE results. SETTING: Eighteen-bed general ICU. PATIENTS: Comatose patients admitted to the ICU after CPR. INTERVENTIONS: Serum NSE was measured at admission and daily for 5 days. MEASUREMENTS AND RESULTS: Patients received full intensive treatment until recovery or until absence of cortical response to somatosensory evoked potentials more than 48 h after CPR proved irreversible coma. Of the 110 patients included (mean GCS at ICU admission 3, range 3--9), 34 regained consciousness, five of whom died in hospital. Seventy-six patients did not regain consciousness, 72 of whom died in hospital. Serum NSE at 24 h and at 48 h after CPR was significantly higher in patients who did not regain consciousness than in patients who regained consciousness (at 24 h: median NSE 29.9 microg/l, range 1.8-250 vs 9.9 microg/l, range 4.5-21.5, P<0.001; at 48 h: median 37.8 microg/l, range 4.4-411 vs 9.5 microg/l, range 6.2-22.4, P= 0.001). No patient with a serum NSE level >25.0 microg/l at any time regained consciousness. Addition of NSE to GCS and somatosensory evoked potentials increased predictability of poor neurological outcome from 64% to 76%. CONCLUSIONS: High serum NSE levels in comatose patients at 24 h and 48 h after CPR predict a poor neurological outcome. Addition of NSE to GCS and somatosensory evoked potentials increases predictability of neurological outcome.

Aged↗
PubMed2005

Mortality prediction in critical care for acute stroke: Severity of illness-score or coma-scale?

BACKGROUND AND PURPOSE: The use of early prognostic data provided by various scores in critically ill stroke patients remains unclear. We tested the performance of the Simplified Acute Physiology Score (SAPS) II in prediction of mortality of acute stroke patients in the NeuroCriticalCareUnit (NCCU). METHODS: During one year every patient admitted to the NCCUs at 2 University hospitals for cerebral ischemia (CI) or intracerebral hemorrhage (ICH) and intubated was included in this study. Data for SAPS (I)/II and the Glasgow Coma Scale (GCS) were collected, and mortality at 10 days, 90 days and 1 year was determined. Prognostic performance of all scores was tested by calculation of receiver operating curve (ROC) and by Cox regression analysis. RESULTS: 90 patients were included in the study, 49 with ICH and 41 with CI. Mortality after 10 days was 32.2%, after 3 months 58.9% and after 1 year 67.8%. Compared by their area under curve the predictive values were overall quite good for both SAPS (I) (0.77) and SAPS II (0.77) as well as GCS. Motor subscore was equal to total GCS (0.75 vs. 0.73). In Cox regression models all three scores were independent predictors of fatal outcome. CONCLUSION: SAPS II and SAPS (I) but also the GCS are valuable tools for prediction of short and long-term mortality in acute stroke patients treated in NCCU. The GCS as a predictor for mortality in stroke patients could be further simplified by using its subscore "best motor response" alone.

Acute Disease↗
PubMed1993

Coma reversal with cerebral dysfunction recovery after repetitive hyperbaric oxygen therapy for severe carbon monoxide poisoning.

The accepted beneficial effects of hyperbaric oxygen (HBO) include a greatly diminished carboxyhemoglobin (COHgb) half-life, enhanced tissue clearance of residual carbon monoxide (CO), reduced cerebral edema, and reversal of cytochrome oxidase inhibition, and prevention of central nervous system lipid peroxidation. Debate regarding the criteria for selection of HBO versus 100% normobaric oxygen therapy continues, and frequently is based solely on the level of COHgb saturation. Patients who manifest signs of serious CO intoxication (unconsciousness, neuropsychiatric symptoms, cardiac or hemodynamic instability) warrant immediate HBO therapy. An unresponsive 33-year-old woman was found in a closed garage, inside her automobile with the ignition on. Her husband admitted to seeing her 6 hours before discovery. 100% normobaric oxygen was administered in the prehospital and emergency department settings. The patient had an initial COHgb saturation of 46.7%, a Glasgow coma score of 3, and was transferred for HBO therapy. Before HBO therapy, the patient remained unresponsive and demonstrated decerebrate posturing and a positive doll's eyes (negative oculocephalic reflex). The electroencephalogram pattern suggested bilateral cerebral dysfunction consistent with a toxic metabolic or hypoxic encephalopathy. The patient underwent HBO therapy at 2.4 ATA for 90 minutes twice a day for 3 consecutive days. On day 7, the patient began to awaken, was weaned from ventilatory support, and was not soon verbalizing appropriately. A Folstein mental status examination showed a score of 26 of 30. Neurological examination demonstrated mild residual left upper extremity weakness and a normal gait. There was no evidence of significant neurological sequelae at 1 month follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2007

Predicting coma and other low responsive patients outcome using event-related brain potentials: a meta-analysis.

OBJECTIVE: A meta-analysis was performed to estimate the predictive power (odd ratio, OR) for awakening of auditory event-related potential (ERP) components in low responsive patients with stroke or hemorrhage, trauma, anoxic, post-operative, and metabolic encephalopathy etiologies. METHODS: We reviewed MEDLINE and analyzed citations for retrieved articles. Logistic regressions were applied on patient samples (Glasgow Coma Scale <12) across and for separate etiologies. RESULTS: For stroke and hemorrhage the ORs with 95% confidence intervals were: 2.05 [1.12-3.75] (N100), 4.47 [1.92-10.44] (MMN), 10.29 [2.00-52.79] (P300), for trauma: 1.63 [0.70-3.80] (N100), 4.72 [1.35-16.44] (MMN), 12.89 [4.82-34.43] (P300), anoxic: 8.03 [2.83-22.75] (N100), 15.50 [4.27-56.26] (MMN), 5.93 [2.38-14.77] (P300), post-operative: 10.66 [1.98-57.50] (N100), metabolic encephalopathy: 2.12 [0.34-13.13] (N100), 3.60 [0.28-46.36] (MMN), 7.71 [0.75-79.77] (P300), and all etiologies: 2.85 [1.91-4.27] (N100), 6.53 [3.55-12.01] (MMN), and 8.79 [4.88-15.83] (P300). Based on six N100 studies (N=548 patients), five MMN studies (N=470), and six P300 studies (N=313), the N100, MMN, or P300, when present, significantly predicted awakening, P300 and MMN being significantly better predictors than N100. CONCLUSIONS: The MMN and P300 appear to be reliable predictors of awakening. SIGNIFICANCE: The prognostic assessment of low responsive patients with auditory ERP should take into account both MMN and P300.

Coma↗
PubMed1988

Diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma.

Diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma are two of the most common acute complications of diabetes. The pathophysiologic changes that occur in both disease states represent an extreme example of the super-fasted state. The physiology of the fed and fasted state, evaluation, therapeutic issues, recommendations for therapy, immediate follow up care, and complications of therapy are reviewed for both syndromes.

Diabetic Coma↗
PubMed1990

Concepts of fluid therapy in diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma.

Despite many advances in the overall treatment of type I diabetes mellitus during the last few years, no major advance has been made in decreasing the mortality rate of diabetic ketoacidosis or hyperosmolar hyperglycemic nonketotic coma. A major concern in both of these disease states is the development of cerebral edema during treatment. The guiding principles of therapy in both disease states are rehydration, electrolyte replacement, insulin therapy, and treatment of any underlying illnesses. If the patient is hypotensive, therapy begins with colloid or normal saline administration to support blood pressure. Fluid and electrolyte deficits should be calculated and replaced during 48 hours. Low-dose insulin therapy is employed for treatment of hyperglycemia. Neurologic function should be carefully monitored and mannitol administered if a change in neurologic function occurs.

Child↗