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PubMed1978

Tryptophan and hepatic coma.

To clarify the involvement of tryptophan in the pathogenesis of hepatic coma, plasma and cerebrospinal fluid (CSF) tryptophan was studied in three patient groups (hepatic coma, stable cirrhosis, and control). An assessment of free fatty acids, some of the amino acids reported to compete with tryptophan for brain uptake, and albumin was also made. The data demonstrated that, whereas the elevated CSF tryptophan levels in cirrhotic patients compared to controls may have been attributable to decreased plasma branched chain amino acids, the elevated CSF tryptophan levels in hepatic coma compared to stable cirrhotic patients were probably attributable to increased plasma free tryptophan concentrations. Associated with the elevated plasma free tryptophan in coma patients was an increase in plasma free fatty acids and a marked decrease in serum albumin levels. Of all the amino acids investigated in the CSF, only tryptophan was significantly increased in patients in hepatic coma compared to cirrhotic patients not in coma.

Amino Acids↗
PubMed1984

Cerebral abnormalities in hepatectomized rats with acute hepatic coma.

When hepatectomized rats develop hepatic coma, they are found to have cerebral edema, together with a failure of the blood-brain barrier to contain materials usually limited to the circulation. The present studies were carried out to characterize the associated ultrastructural changes in the barrier. Rats were allowed to develop hepatic coma after a two-stage hepatectomy. Electrocortical and behavior monitoring during this period indicated deterioration similar to that seen in man with acute liver injury; the water contents of the brains of the animals in hepatic coma were increased. Electron microscopic examination of the brains from control rats and animals with hepatic coma were carried out after perfusion fixation. The examination of the brains from the comatose animals showed the appearance of greatly increased numbers of vesicles in the capillary endothelium and a marked watery swelling of adjacent astrocytes, which seemed to begin in foot processes and then to spread through the cell. Intravenous peroxidase was given to most rats in the late stages of coma, and the tracer was found to be included within the capillary endothelial vesicles. Occasional accumulations of peroxidase in the underlying capillary basement membrane were found. No interendothelial cell distruption was found. Low molecular weight microperoxidase was used as well as horseradish peroxidase; the results were the same with both compounds. The findings indicate as association between capillary endothelial vesicle formation and the cerebral edema found in animals with hepatic coma following hepatectomy.

Animals↗
PubMed1993

Observation of lipid profile and lipoproteins in viral hepatitis and hepatic coma.

Lipid profile and lipoprotein levels were estimated in 35 patients of viral hepatitis, 15 patients of viral hepatitis with coma and in age and sex match 35 healthy controls. The values were compared in different groups. Levels of triglycerides were significantly raised (145.00 +/- 30.70 mg/dl) in viral hepatitis as compared to viral hepatitis with coma (111.40 +/- 16.80 mg/dl) which were similar to controls (110.8 +/- 20.6 mg/dl). Patients who recovered had higher levels of triglycerides (136.0 +/- 30.8 mg/dl) as compared to those who expired (110 +/- 15.72 mg/dl). Total serum cholesterol remained statistically unaltered in both groups. HDLc was significantly decreased in both groups, viral hepatitis (2.23 +/- 6.7 mg/dl) and viral hepatitis with coma (16.52 +/- 2.27 mg/dl) in comparison to controls (62.21 +/- 18.04 mg/dl). The levels were much lower in patients with coma than without coma. Furthermore the values were still lower in patients who expired (15.82 +/- 2.27 mg/dl) than in patients who recovered (24.13 +/- 7 mg/dl). The levels of LDLc were significantly raised in both groups, as compared with each other and in relation to mortality. VLDLc levels were significantly decreased in patients of viral hepatitis (22.13 +/- 5.8 mg/dl) as well as on viral hepatitis with coma (21.89 +/- 4.3 mg/dl). However, no significant difference was observed when compared with each other and in relation to mortality. Thus it may be concluded that isolated low value of HDLc in viral hepatitis may be used as a prognostic indicator.

Acute Disease↗
PubMed2002

Life-threatening hyperkalaemia following therapeutic barbiturate coma.

OBJECTIVE: To report the occurrence of life-threatening hyperkalaemia following treatment with therapeutic thiopentone coma. SETTING: The neurosurgical intensive care units of Royal North Shore Hospital and Liverpool Hospital, Sydney, Australia. PATIENTS: Three patients treated with theraputic thiopentone coma. One patient with raised intracranial pressure secondary to a severe traumatic brain injury and two patients with refractory vasospasm secondary to subarachnoid haemorrhage. Two of the three patients developed hypokalaemia on starting thiopentone, which was resistant to potassium supplementation. All three patients developed severe hyperkalaemia during the recovery phase of coma. This was life-threatening in all three patients and fatal in one. CONCLUSIONS: Severe hypokalaemia refractory to potassium therapy may occur during therapeutic thiopentone coma. Severe rebound hyperkalaemia may occur after cessation of thiopentone infusion. Protocols for the management of patients with therapeutic barbiturate coma should recognise this potentially serious complication.

Adult↗
PubMed1993

The prognostic value of three-modality evoked potentials (TMEPs) in anoxic and traumatic comas.

Three-modality evoked potentials (TMEPs) were recorded in 184 comatose patients (52 anoxic, 132 traumatic). Both types of comas were associated with different TMEP patterns. Anoxic comas were associated with prognostically relevant abnormalities of cortical (visual and somatosensory) evoked potentials (EPs), while brainstem (auditory and somatosensory) EPs were not specifically altered. The prognostic value of TMEPs in anoxic comas depended on the time elapsed from the acute episode: mildly altered EPs were associated with a better prognosis in the first 10 days; strongly altered TMEPs were associated with a poorer prognosis from the first day; no definite conclusion could be drawn from mildly altered EPs after the 10th day, or from strongly altered TMEPs in the first 24 h. By contrast, both the cortical and the brain-stem activities were altered in head trauma. The abnormalities were clustered into four patterns: hemispheric damage without brain-stem involvement (pattern 1), mesencephalic lesion (pattern 2), transtentorial herniation (pattern 3), and brain death (pattern 4). Patterns 3 and 4 were uniformly associated with death. The prognostic value of pattern 1 was similar to that observed in anoxic comas. The outcome of patients presenting pattern 2 depended on the extent of hemispheric damage associated with the mesencephalic lesion; we thus suggest to systematically perform magnetic resonance imaging (MRI) in patients presenting TMEP pattern 2. We finally demonstrated that a few patients presenting absent cortical activities in the very acute stage of coma can eventually recover a good neurological function.

Acoustic Stimulation↗
PubMed2002

Sleep organization pattern as a prognostic marker at the subacute stage of post-traumatic coma.

OBJECTIVES: The aim of this study is to identify the predictive indexes for post-traumatic coma prognosis, which is important to better direct acute and subacute treatments and rehabilitation efforts. The pattern of sleep organization is a potential prognostic marker, but its role has not been established yet in the context of modern critical care. In the present study, we used a new protocol to evaluate the prognostic value of the different levels of sleep-wake organization recorded at the subacute stage of post-traumatic coma. METHODS: Twenty-four head-injured comatose patients were monitored with 24h polysomnographic recordings. The predictivity of the different levels of sleep-wake organization on polysomnography was compared with other possible prognostic indexes (i.e. neuroradiological findings, age and Glasgow Coma Scores (GCS)). Main outcome measures were survival and the degree of disability after recovery from coma. RESULTS: The presence of organized sleep patterns, but not GCS, was highly predictive of better outcome (odds ratio=10.78, P=0.01), even after correction for potentially confounding variables with multivariate analysis. CONCLUSIONS: Our study demonstrates that the sleep-wake organization pattern based on 24h polysomnographic recordings at the subacute stages of post-traumatic coma is a reliable prognostic marker, both for survival and for functional recovery.

Adolescent↗
PubMed2002

Mechanism of respiratory insufficiency in pure or mixed drug-induced coma involving benzodiazepines.

OBJECTIVE: We tested the hypothesis that the mechanism of respiratory insufficiency in drug-induced coma involving benzodiazepines is an increase in upper airway resistance. METHODS: Eighteen nonintubated and seven intubated (control) patients were poisoned with hypnotic sedatives involving benzodiazepines. Neurological and respiratory parameters were measured by polysomnography before and after flumazenil. Flumazenil was administered as escalating bolus doses followed by a continuous infusion. RESULTS: Upon entry, Glasgow Coma Score was 7 +/- 1 in nonintubated and 5 +/- 1 in intubated patients. Snoring with flow limitation and obstructive apnea were recorded in 16 and 5 among the 18 nonintubated patients, respectively. Central apnea was not observed. Total pulmonary resistance was 2.5-fold higher in nonintubated patients than in intubated patients. Total and resistive work of breathing (WOB) was significantly greater in the nonintubated group. Flumazenil bolus administration was associated with an improvement in Glasgow Coma Score from 7 +/- 1 to 13 +/- 1 in the nonintubatedpatients, and from 5 +/- 1 to 11 +/- in the intubated patients. Mean effective bolus doses were 0.3 +/- 0.1 mg in nonintubated patients and 0.6 +/- 0.1 mg in intubated patients. Tidal and minute volumes increased significantly, and WOB decreased significantly in nonintubated patients. In nonintubated patients, the decrease in total WOB resulted from a significant decrease in resistive WOB. CONCLUSION: Drug-induced coma involving benzodiazepines is characterized by snoring with flow limitation and obstructive apnea. The mechanism of respiratory insufficiency in nonintubated patients with drug-induced coma involving benzodiazepines is an increase in upper airway resistance and WOB.

Adult↗
PubMed2003

Predictive value of somatosensory evoked potentials for awakening from coma.

OBJECTIVES: A systematic review of somatosensory evoked potentials performed early after onset of coma, to predict the likelihood of nonawakening. The pooled results were evaluated for rates of awakening, confidence intervals, and the possibility of rare exceptions. DATA SOURCES: Forty-one articles reporting somatosensory evoked potentials in comatose patients and subsequent outcomes, from 1983 to 2000. STUDY SELECTION: Studies were included if they reported coma etiology, age group, presence or absence of somatosensory evoked potentials, and coma outcomes. DATA EXTRACTION: We separated patients into four groups: adults with hypoxic-ischemic encephalopathy, adults with intracranial hemorrhage, adults and adolescents with traumatic brain injury, and children and adolescents with any etiologies. Somatosensory evoked potentials were categorized as normal, abnormal, or bilaterally absent. Outcomes were categorized as persistent vegetative state or death vs. awakening. DATA SYNTHESIS: For each somatosensory evoked potential result, rates of awakening (95% confidence interval) were calculated: adult hypoxic-ischemic encephalopathy: absent 0% (0%-1%), abnormal 22% (17%-26%), normal 52% (48%-56%); adult intracranial hemorrhage: absent 1% (0%-4%), present 38% (27%-48%); adult-teen traumatic brain injury: absent 5% (2%-7%), abnormal 70% (64%-75%), normal 89% (85%-92%); child-teen: absent 7% (4%-10%), abnormal 69% (61%-77%), normal 86% (80%-92%). CONCLUSIONS: Somatosensory evoked potential results predict the likelihood of nonawakening from coma with a high level of certainty. Adults in coma from hypoxic-ischemic encephalopathy with absent somatosensory evoked potential responses have <1% chance of awakening.

Adolescent↗
PubMed2001

Incidence, aetiology, and outcome of non-traumatic coma: a population based study.

AIM: To determine the incidence, presentation, aetiology, and outcome of non-traumatic coma in children aged between 1 month and 16 years. METHODS: In this prospective, population based, epidemiological study in the former Northern NHS region of the UK, cases were notified following any hospital admission or community death associated with non-traumatic coma. Coma was defined as a Glasgow Coma Score below 12 for more than six hours. RESULTS: The incidence of non-traumatic coma was 30.8 per 100 000 children under 16 per year (6.0 per 100 000 general population per year). The age specific incidence was notably higher in the first year of life (160 per 100 000 children per year). CNS specific presentations became commoner with increasing age. In infants, nearly two thirds of presentations were with non-specific, systemic signs. Infection was the commonest overall aetiology. Aetiology remained unknown in 14% despite extensive investigation and/or autopsy. Mortality was highly dependent on aetiology, with aetiology specific mortality rates varying from 3% to 84%. With follow up to approximately 12 months, overall series mortality was 46%.

Adolescent↗
PubMed1991

Head-injured patients who talk and deteriorate into coma. Analysis of 211 cases studied with computerized tomography.

Of 838 patients with severe head injuries admitted since the introduction of computerized tomography, 211 (25.1%) talked at some time between trauma and subsequent deterioration into coma. Of these 211 patients, 89 (42.2%) had brain contusion/hematoma, 46 (21.8%) an epidural hematoma, 35 (16.6%) a subdural hematoma, and 41 (19.4%) did not show focal mass lesions. Thus, four of every five patients who deteriorated into coma after suffering an apparently nonsevere head injury had a mass lesion potentially requiring surgery: the mass was intracerebral in 52.3% of the cases and extracerebral in 47.6%. Patients aged 20 years or less had a 39% chance of having a nonfocal mass lesion (diffuse brain damage), a 29% chance of having an epidural hematoma, and a 32% chance of having an intradural mass lesion; patients over 40 years had only a 3% chance of having a nonfocal mass lesion, an 18% chance of having an epidural hematoma, and a 79% chance of having a intradural mass lesion. Sixty-eight (32.2%) patients died and 143 (67.8%) survived. The following were independent outcome predictors (in order of significance): Glasgow Coma Scale score following deterioration into coma, the highest intracranial pressure during the patient's course, the degree of midline shift, the type of intracranial lesion, and the age of the patient. In contrast, the mechanism of injury, the verbal Glasgow Coma Scale score during the lucid interval, and the length of time until deterioration or until operative intervention did not influence the final result.

Adult↗
PubMedDate not supplied

Visual impairment in children with acute nontraumatic coma.

PURPOSE: To determine the incidence and severity of visual impairment in children following acute nontraumatic coma. METHODS: An 18-month prospective epidemiologic study of acute nontraumatic coma was undertaken in the former Northern NHS Region of England. Children aged >1 month and <16 years were included in the study if they had a Glasgow Coma Score of < or = 12 for >6 hours or if they died within 6 hours of the onset of decreased levels of consciousness. For survivors, ophthalmologic assessments were performed 6 weeks and 12 months after presentation. RESULTS: Two hundred eighty-seven children were included in the study, of whom 127 died. Of the 137 examined survivors, 35 had visual abnormalities suspected by the examining neurologist during the ophthalmic assessment. Of these, visual impairment was confirmed in 10 children at the 6-week assessment by the pediatric ophthalmologist. At the 1 2-month assessment, visual impairment remained stable in 9 children and improved in 1. CONCLUSION: In this study, 6.6% of children surviving acute nontraumatic coma had visual impairment that persisted at the 12-month follow-up examination. Incidence of visual impairment in acute nontraumatic coma is 0.97 per 100,000 children per year.

Acute Disease↗
PubMed1989

Deaths associated with diabetic ketoacidosis and hyperosmolar coma. 1973-1988.

We assessed the possibility of improvements in the management of the potentially fatal acute hyperglycaemic complications of diabetes by a review of all deaths in patients who presented to the Alfred Hospital, Melbourne, with diabetic ketoacidosis or hyperosmolar coma during the 16 years, 1973-1988. All late deaths of patients during hospitalization were included in the mortality data. In the 610 episodes of diabetic ketoacidosis (pH, 7.30 or lower) or hyperosmolar coma (osmolality, 350 mOsmol/kg or greater), only one death occurred as a result of the acute metabolic disturbance--in a patient who had suffered a cardiac arrest before admission to hospital. The over-all mortality rate was 6.2% (38 deaths). The mortality rate was 4.9% (26 deaths) for 528 episodes of diabetic ketoacidosis and 14.6% (12 deaths) for 82 episodes of hyperosmolar coma. Patients with diabetic ketoacidosis who died were older than were those who survived (64 +/- 13 years compared with 40 +/- 21 years, respectively; P less than 0.001). Mortality in patients with hyperosmolar coma did not relate to age, initial blood-glucose level or osmolality. Twelve deaths resulted from bacterial pneumonia and two deaths resulted from aspiration pneumonia. Other major causes of death were mesenteric and iliac thromboses (six cases), myocardial infarction (eight cases) and cerebral haemorrhage (two cases). Of the 26 deaths that were associated with diabetic ketoacidosis, only two deaths--as a result of aspiration pneumonia and bowel infarction, respectively--were assessed as potentially avoidable after the patient's admission to hospital. Eight of the 12 hyperosmolar-coma-associated deaths occurred in newly recognized diabetic patients in whom there were avoidable delays in diagnosis. We conclude that further improvements in outcome will be difficult to achieve, but that efforts should be directed towards the earlier diagnosis of diabetes and the earlier recognition and treatment of associated acute pulmonary and vascular complications.

Adult↗
PubMed1990

[Intersubjective approach of traumatic coma in a rehabilitation center].

Some clinical factors make coma a particullary significant time on human level: in so far as a receptivity to others exists during coma, could some residual marks of memory be found, and therefore possible desire? In other respects, after a coma why a statistical disproportion is noticed between psychotic states and depressive states? This questions expound why this research is based upon an intersubjective accompanying during the coma. Results introduces a reflection on coma, its libidinal mobilization and its signification.

Amnesia↗
PubMed1986

Clinical features of hyperosmolar hyperglycemic nonketotic diabetic coma associated with cardiac operations.

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.

Adult↗
PubMed1984

[Pathophysiology and therapy of diabetic ketoacidosis and of non-ketoacidotic hyperosmolar diabetic coma].

Metabolic derangements in diabetic coma are the sequelae of insulin deficiency. These defects are aggravated by the actions of insulin counteracting ("diabetogenic") hormones and hypertonic dehydration, which both impair insulin action. Conversely, it has been shown that hypo-osmolar rehydration of a hyperosmolar, severely hyperglycaemic diabetic patient reduces insulin resistance and restores biological responsiveness of previously dehydrated insulin-dependent tissues towards insulin. Thus treatment of diabetic coma requires appropriate fluid and electrolyte replacement as a life-saving emergency action alongside insulin replacement. The use of proper rehydration during the past decade might also explain the reported fall in the insulin requirement for the treatment of diabetic coma from approximately 1,000 units per coma to low-dose insulin therapy. In order to guarantee proper treatment of severe hyperglycaemia and normalization of the hyperosmolar state, we feel that hypo-osmolar rehydration has to be initiated in parallel with low-dose insulin therapy (5 to 6 U/h) to restore the physiological response of the respective target tissues to insulin action and to ameliorate glucose utilization. This approach probably avoids a too rapid fall in plasma osmolarity, minimizes the risk of cerebral oedema and hypokalaemia, and improves survival. The development of severe diabetic ketoacidosis or of hyperosmolar non-ketotic diabetic coma should be prevented by advice to patients on the importance of metabolic monitoring, which can be done by proper self-monitoring of blood glucose. In addition, information should be provided on the detrimental metabolic effects of both dehydration and stress.

Amino Acids↗
PubMed1980

Fatal coma in diabetes.

Analysis of causes of death in a population of 3,113 diabetics was carried out for a period of eight years and those patients dying of some form of diabetic coma identified. Of 1,274 deaths, only 22 (1.73%) were primarily due to coma; 7 hypoglycaemia, 8 ketoacidosis, 3 hyperosmolar coma and 4 lactic acidosis. Three of the ketoacidosis patients may have died from other causes. Most deaths occurred in patients with long-standing diabetes. In the hypoglycaemic group all were on insulin and several had been difficult to control for many years. Infection was an important precipitating factor for ketoacidosis and hyperosmolar coma. Phenformin was the cause of all cases of fatal lactic acidosis. It is reassuring that death from coma is a comparatively rare event in known treated diabetic patients.

Adult↗
PubMed1990

Coma scales in pediatric practice.

Interobserver variability for six coma scales was assessed prospectively on a sample of 15 comatose children, by two physicians, in a double-blind fashion. The six scales were the Glasgow Coma Scale, the Simpson and Reilly Scale, the Children's Coma Score, the Children's Orthopedic Hospital and Medical Center Scale, the Jacobi Scale, and the 0 to IV Scale. Interobserver variability was measured by using disagreement rate and the kappa statistic. The results from both methods were generally concordant. The disagreement rate for the various items in the different scales ranged from a high of 0.20 to a low of 0.03. The disagreement rate was greater than 0.10 for verbal responses in the Children's Coma Score and Glasgow Coma Scale and for both items in the Children's Orthopedic Hospital and Medical Center Scale. The disagreement rate was 0.10 or less for the 0 to IV Scale and for all items in the Simpson and Reilly and Jacobi scales. The relatively high interobserver agreement for these scales makes them more suitable for the pediatric setting than the other three scales, since good agreement is essential for interpreting data reliably, both in clinical practice and for research.

Adolescent↗
PubMed2002

Sensory stimulation for brain injured individuals in coma or vegetative state.

BACKGROUND: Coma and vegetative state follow traumatic brain injury in about one out of eight patients, and in patients with non traumatic injury the prognosis is worse. The use of sensory stimulation for coma and vegetative state has gained popularity during the 1980's but beliefs and opinions about its effectiveness vary substantially among health professionals. OBJECTIVES: To assess the effectiveness of sensory stimulation programmes in patients in coma or vegetative state. SEARCH STRATEGY: We searched the Injuries Group specialised register, the Cochrane Controlled trials register, EMBASE, MEDLINE, CINAHL and PSYCHLIT from 1966 to January 2002, without language restriction. Reference lists of articles were scanned and we contacted experts in the area to find other relevant studies. SELECTION CRITERIA: Randomised or controlled trials that compared sensory stimulation programmes with standard rehabilitation in patients in coma or vegetative state. DATA COLLECTION AND ANALYSIS: Abstracts and papers found were screened by one reviewer. Three reviewers independently identified relevant studies, extracted data and assessed study quality resolving disagreement by consensus. MAIN RESULTS: Three studies were identified with 68 patients in total. The overall methodological quality was poor and studies differed widely in terms of outcomes measures, study design and conduct. We therefore did not carry out any quantitative synthesis but reviewed results of available studies qualitatively. REVIEWER'S CONCLUSIONS: This systematic review indicates that there is no reliable evidence to support, or rule out, the effectiveness of multisensory programmes in patients in coma or vegetative state.

Brain Injuries↗