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PubMed1992

Coma of vascular aetiology: evaluation and prognosis.

The authors have done a revision of 450 patients admitted during the last 3 years to the emergency service of the Hospital de S. José with the diagnosis of CVA. In this retrospective study were included the patients of greater than or equal to 3 degree of the RLS/85 coma scale, the diagnostic being confirmed by CAT, angiography and/or autopsy, and simultaneously evaluated by the Glasgow coma scale. The studied population was grouped into: SAH; ICH with or without ventricular drowning, cerebellar haematoma, brainstem haematoma, ischaemic CVA. The factors of vascular risk: diabetes and hypertension, the age of the patients and coma level were correlated with the degree of cerebral disability of discharge in all patients. The following factors are clearly related with bad prognosis: coma of degree greater than or equal to 4 in the RLS/85 scale; ischaemic aetiology; intraventricular haemorrhage.

Adult↗
PubMed1997

Childhood non-traumatic coma in Kuala Lumpur, Malaysia.

All post-neonatal children with acute non-traumatic coma admitted over an 8-month period were analysed and followed up for 18-24 months to determine the aetiology and outcome of their coma. One hundred and sixteen children, 72 boys and 44 girls, were recruited. Half the children were under 1 year of age and only 16 (14%) were more than 6 years of age. Eighty cases (69%) were due to infection, 15 (13%) to toxic metabolic causes, six (5%) to hypoxic ischaemic insults, four (3.5%) had intracranial haemorrhage, nine (7.8%) were due to miscellaneous causes and in two (1.7%) the cause was unknown. Seven cases were lost to follow-up. Of the remainder, 39 (35.7%) died, 32 (29.3%) developed permanent neurological deficit, and 38 (35%) were discharged well. The outcome was worst in the infectious group. Age of onset and sex did not significantly affect outcome. Our findings are similar to experience in Japan, where infection accounts for 74% of non-traumatic coma, but differ considerably from Western data on childhood coma where only a third of cases are due to infection.

Acute Disease↗
PubMed1996

Prediction of outcome in patients with anoxic coma: a clinical and electrophysiologic study.

OBJECTIVE: To evaluate and compare the predictive powers of clinical examination, electroencephalography (EEG), and studies of short-latency somatosensory evoked potentials in determining the prognosis in anoxic coma. DESIGN: Prospective case series of patients in anoxic coma, whose prognoses were uncertain based on previously established clinical criteria. The clinical features, EEG, and somatosensory evoked potentials results were correlated with outcome. SETTING: A 40-bed intensive care unit in a university teaching hospital. PATIENTS: Thirty-four consecutive patients admitted over a 2-yr period with anoxic coma as the principal diagnosis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Twenty-seven (79%) patients never recovered consciousness and seven (21%) patients made a good recovery. One of six patients whose pupillary reflexes were present but whose other cranial nerve reflexes were absent on day 1 recovered, but none of the seven patients with these features still present on day 3 survived. None of the patients with motor responses of extension to painful stimuli or worse on days 1 or 3 recovered. The EEGs were classified into benign, uncertain, and malignant categories. The results of both EEG and somatosensory evoked potentials studies were strongly associated with outcome. With malignant EEG, the sensitivity was 74%, the specificity was 71%, and the positive predictive value was 90% [corrected] for the prediction of no recovery (death or persistent vegetative state). However, two patients with an initially malignant EEG eventually made a good recovery. The sensitivity for low amplitude or absent somatosensory evoked potentials for prediction of no recovery was 66%. There were no falsely pessimistic predictions with somatosensory evoked potentials, as all 18 patients with absent or low-amplitude responses had no recovery (specificity and positive predictive value were 100%). EEG and somatosensory evoked potentials studies were complementary to clinical examination in the determination of prognosis. Using a combined clinical and electrophysiologic approach, 63% of patients who had no recovery could be identified by day 3. Repeat EEG and somatosensory evoked potentials studies were of value in patients whose prognoses were uncertain, as their evolution invariably correlated with outcome. CONCLUSIONS: Based on the present data and a literature review, we propose that clinical examination combined with the results of EEG and somatosensory evoked potentials can be used to establish an early, definitive prognosis in a significant proportion of patients in anoxic coma. On day 3 or thereafter, patients with motor response of extension to pain or worse and malignant EEG, or those patients with flexor posturing or worse and bilaterally absent cortical somatosensory evoked potentials invariably have poor outcome. However, some patients with initially malignant EEG and normal somatosensory evoked potentials may recover and should be supported until their prognoses become more definitive.

Adolescent↗
PubMed1998

Mortality prediction in head trauma patients: performance of Glasgow Coma Score and general severity systems.

OBJECTIVE: To assess the performance of general severity systems (Acute Physiology and Chronic Health Evaluation [APACHE] II, Simplified Acute Physiology Score [SAPS] II, and Mortality Probability Models [MPM] II) for head trauma patients and to compare these systems with the Glasgow Coma Score, in order to obtain a good estimate of severity of illness and probability of hospital mortality. DESIGN: Inception cohort. SETTING: Adult medical and surgical intensive care units in 12 European and North American countries. PATIENTS: Patients (n = 401) who were diagnosed with head trauma (with/without multiple trauma), leading to intensive care unit admission, and who were not brain dead at the time of arrival. INTERVENTIONS: Statistical analysis to assess the performance of general severity systems. MEASUREMENTS AND MAIN RESULTS: Vital status at the time of hospital discharge was the outcome measure. Performance of the severity systems (SAPS II, MPM II0 [MPM at admission], MPM II24 [MPM at 24 hrs], and APACHE II) was assessed by evaluating calibration and discrimination. Logistic regression was used to convert the Glasgow Coma Score into a probability of death. The MPM II system (either MPM II0 or MPM 1124) provided an adequate estimation of the mortality experience in patients with head trauma. SAPS II and APACHE II systems did not calibrate well, although they showed high discrimination (area under the receiver operating characteristic curve 0.95 for SAPS II, 0.94 for APACHE II, and 0.90 for MPM II0 and MPM II24). The logistic regression model containing the Glasgow Coma Score as an independent variable and developed in this group of patients was not as well calibrated as MPM II. The discrimination of this model was very high, in the range observed for the APACHE II, SAPS II, and MPM II systems. CONCLUSIONS: The MPM II system performs better than APACHE II, SAPS II, and Glasgow Coma Score for head trauma patients. If our results are supported by other studies, MPM II would be an appropriate tool to assess severity of illness in head trauma patients, with applications to clinical practice and clinical research.

APACHE↗
PubMed2000

Alteration of cyclic adenosine monophosphate response element binding protein in rat brain after hypoglycemic coma.

In the current study, the temporal and regional changes of the transcription factor cyclic adenosine monophosphate response element binding protein (CREB) were investigated in rat brains subjected to 30 minutes of hypoglycemic coma followed by varied periods of recovery using Western blot and confocal microscopy. The total amount of CREB was not altered in any area examined after coma. The level of the phosphorylated form of CREB decreased during coma but rebounded after recovery. In the relatively resistant areas, such as the inner layers of the neocortex and the inner and outer blades of the dentate gyms (DG), phospho-CREB increased greater than the control level after 30 minutes of recovery and continued to increase up to 3 hours of recovery. In contrast, little or no increase of phospho-CREB was observed during the recovery period in the outer layers of the neocortex and at the tip of the DG, that is, regions that are selectively vulnerable to hypoglycemic insults. The current findings suggest that a neuroprotective signaling pathway may be more activated in the resistant regions than in the vulnerable ones after hypoglycemic coma.

Animals↗
PubMed2001

Hyperosmolar diabetic non-ketotic coma, hyperkalaemia and an unusual near death experience.

Generally, cardiac arrest due to pulseless electrical activity has a poor outcome, except when reversible factors such as acute hyperkalaemia are identified and managed early. Hyperosmolar diabetic non-ketotic coma may lead to acute hyperkalaemia. Hyperosmolar diabetic non-ketotic coma is a metabolic emergency usually seen in elderly non-insulin dependent diabetics, characterized by severe hyperglycaemia, volume depletion, altered consciousness, confusion and less frequently neurological deficit. Cerebrovascular accident or transient ischaemic attack may be mistakenly diagnosed, particularly if the patient has no history of diabetes mellitus. Delays in diagnosis and management of glycaemic emergencies presenting as a constellation of neurological abnormalities can be avoided by routine early measurement of blood glucose. Hyperosmolar diabetic non-ketotic coma should be considered in any patient with altered consciousness or neurologic deficit in conjunction with hyperglycaemia. As hyperosmolar diabetic non-ketotic coma results in severe fluid depletion, electrolyte disturbance, profound hyperglycaemia and an altered mental state, the guiding principles of therapy include aggressive rehydration, insulin therapy, correction of electrolyte abnormalities and treatment of any underlying illnesses. Treatment of acute hyperkalaemia includes calcium ions, insulin with dextrose, salbutamol and haemodialysis.

Cardiac Output, Low↗
PubMed2006

Improved prediction of awakening or nonawakening from severe anoxic coma using tree-based classification analysis.

OBJECTIVE: To evaluate the utility of sensory and event-related evoked potentials for the prediction of awakening/nonawakening in severe anoxic coma and to design a decision tree helping decision for any patient in this condition. DESIGN: Prospective cohort study. SETTING: Clinical neurophysiology unit and intensive care unit of a French university hospital. PATIENTS: Sixty-two consecutive severe comatose patients after out-of-hospital cardiac arrest. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We gathered clinical variables and recorded the somatosensory, auditory, and cognitive evoked potentials within an average period of 8 days after cardiac arrest. The patients were followed for 12 months and classified as awake or nonawake (permanent vegetative state or death). The statistical study included measurements of specificity, sensitivity, and positive and negative predictive value for each clinical and electrophysiologic variable recorded at the early stage of coma. Furthermore, a tree-based classification analysis was performed.All patients in whom somatosensory evoked potentials or middle-latency auditory evoked potentials were abolished did not awaken (100% specificity). All patients in whom mismatch negativity (MMN) was present awakened (100% specificity). MMN was superior to somatosensory evoked potentials for the prediction of awakening and had the best specificity and positive predictive value for awakening. On the decision tree, the awakening/nonawakening explicative variables were, by order of importance, MMN, pupillary reactivity, and somatosensory evoked potentials. CONCLUSIONS: There is a need to predict early and accurately awakening or nonawakening in postanoxic comas. Using sensory and cognitive evoked potentials to assess the functional condition of the brain, a prognostic tree for the prediction of awakening/nonawakening in severe anoxic coma has been designed. It is applicable to any patient in this condition and offers the possibility to predict with very high probability awakening when MMN, the earliest component of event-related potentials, is present and nonawakening when MMN and pupillary light reflex are absent or cortical components of somatosensory evoked potentials are abolished.

Adolescent↗
PubMed2005

Atropine coma: a historical note.

Insulin coma and various types of convulsive therapies were the major biologic treatment modalities in psychiatry before the psychopharmacological era. Except for electroconvulsive therapy (ECT), these methods disappeared from the psychiatric armamentarium after the introduction of psychotropic drugs. Atropine coma therapy (ACT) was one variety of nonconvulsive coma therapy used from the 1950s in a few state mental hospitals in the United States and in several Middle- and Eastern European countries until the late 1970s. In ACT, a coma of 6-10 hours' duration was induced with doses of parenteral atropine sulfate that were hundreds of times greater than the therapeutic dose administered in internal medicine. Although ACT was given to thousands of patients with a variety of diagnoses for nearly 3 decades, it is rarely mentioned, even in papers on the history of psychiatry. The method, indications, contraindications and adverse effects of ACT are summarized together with patients' personal accounts. Hypotheses concerning its mode of action are briefly mentioned. The reasons why ACT never gained wider acceptance are explored in the context of both contemporary psychiatric practice and the broader sociocultural climate of the era.

Atropine↗
PubMed1994

Early intervention: coma stimulation in the intensive care unit.

Coma stimulation is a technique that has traditionally been reserved for patients in a rehabilitation setting. Information regarding the use of coma stimulation in the intensive care setting is limited. An individualized coma stimulation program in the early stages of recovery from brain injury is paramount in stimulating the reticular activating system and promoting brain reorganization. Coma stimulation program development within the intensive care setting includes the appropriate selection of patients and the utilization of the entire rehabilitation team in devising an approach specific to each patient's needs. Planning should include the family, with consideration to the prior interests of the patient. Ongoing evaluation of the patient's responses should be considered, as well as the ease of performing stimulation within the intensive care environment.

Adolescent↗
PubMed1978

Thyrotrophin, prolactin and growth hormone responses to TRH in barbiturate coma and in depression.

The effects of 200 microgram thyrotrophin-releasing hormone (TRH) i.v. on thyrotrophin (TSH), prolactin (PRL), growth hormone (GH) and triiodothyronine (T3) were studied in eight patients with barbiturate coma due to attempted suicide, in the same patients after recovery, in eight depressive patients and in eight normal controls. The patients with barbiturate coma presented normal basal TSH and PRL, elevated basal GH and normal PRL but blunted TSH responses to TRH; their GH concentrations varied widely without consistent relation to TRH administration. The same patients after recovery from coma presented normal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a clear-cut rise in GH (i.e. more than 10 ng/ml) occurred after TRH administration. The depressive patients presented normal basal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a moderated rise in GH (less than 10 ng/ml) occurred after TRH administration. The increment in T3 concentrations 120 min after TRH was found reduced in the comatose patients only. Basal cortisol was measured in all the subjects and found elevated in the comatose patients only. It is concluded that the abnormal TSH and GH responses to TRH observed in patients with barbiturate coma are more likely related to depressive illness than to an effect of barbiturates at the pituitary level. Barbiturates might affect thyroid secretion.

Adolescent↗
PubMed1983

Non-traumatic coma in childhood: clinical variables in prediction of outcome.

One hundred and four children suffering from non-traumatic coma were referred to the Pediatric Neurology Service, Children's Hospital, Winnipeg, between February 1976 and December 1978. Stepwise discriminant analysis was used to obtain a classification function of outcome, based on clinical variables determined at two separate time-periods of examination: (1) the time of admission and (2) about 24 hours after onset of coma. 12 clinical variables were included in the stepwise procedure. Seven of these: coma severity, extra-ocular movements, pupils, motor patterns, blood pressure, temperature and seizure type, entered the classification function for the first time-period, data being available for 102 children. 75 per cent of these cases were correctly classified into one of five outcome groups and 8 per cent were seriously misclassified. Similarly, 67 per cent of the 66 children evaluated in the second time-period were correctly classified and 3 per cent seriously misclassified. The variables that entered the classification function in this second time-period were age, coma severity, motor patterns, blood pressure and seizure type. The data suggest that the analysis of clinical variables recorded early in the comatose state can provide predictive information, and stepwise discriminant analysis may be one method of determining the most likely outcome for individual cases.

Adolescent↗
PubMed1991

Recurrent prolonged coma due to basilar artery migraine. A case report.

A 25 year old patient presented with recurrent prolonged episodes of life-threatening coma varying from 3 to 10 days. The clinical recovery was slow. The history and technical examinations led to the diagnosis of basilar artery migraine (BAM). The etiology of the coma episodes is thought to be related to ischemic dysfunction of the rostral part of the brainstem due to severe spasm of the basilar artery demonstrated by arteriography. Exceptional are the recurrent prolonged coma episodes of sudden onset, the severe spasm of the basilar artery, and the suppression-burst and FIRDA pattern on the EEG examinations during the coma episodes.

Adult↗
PubMed1990

Diagnostic utility of flumazenil in coma with suspected poisoning: a double blind, randomised controlled study.

OBJECTIVE: To assess the diagnostic value and safety of the benzodiazepine antagonist flumazenil in patients with coma of unclear origin with suspected poisoning. DESIGN: Double blind, placebo controlled, randomised study. SETTING: Intensive care unit at a major teaching hospital. PATIENTS: 105 Unconscious adults admitted consecutively with suspected drug overdosage during 18 months from a total of 362 cases of poisoning. Exclusion criteria were pregnancy, epilepsy, obvious poisoning with drugs identified unequivocally from information from relatives or others as other than benzodiazepines, and coma score greater than 10 on a scale graded from 4 to 20. Patients were allocated randomly to receive flumazenil (21 men and 32 women) or placebo (25 men and 27 women). INTERVENTIONS: Intravenous injection of flumazenil (10 ml, 0.1 mg/ml) or placebo (10 ml vehicle alone) given double blind over three minutes. MAIN OUTCOME MEASURES: Serum and urine concentrations of benzodiazepines, antidepressants, and several other agents; blood gas tensions; standardised evaluation on admission and five minutes after the injection by means of coma scale score and urgent diagnostic or therapeutic interventions indicated according to the history and clinical examination; standardised interview after the injection to try to ascertain further information; and adverse reactions. RESULTS: Benzodiazepines were found in the serum in 36 of the 53 patients in the flumazenil group and in 37 of the 52 who received placebo. The average coma scale score increased significantly after injection in the flumazenil group (6.4 v 12.1, p less than 0.001) but not in the placebo group. In the flumazenil group several interventions were rendered unnecessary by the injection: gastric lavage and urinary catheterisation (19 patients each), intubation (21), artificial ventilation and computed tomography of the brain (three patients each), blood culture and lumbar puncture (one patient each), and electroencephalography (two). In the placebo group the indications for these procedures did not change in any patient after injection. The 95% confidence interval for the difference in reduction of the frequency of indications for gastric lavage after injection between the two groups was 21% to 51%, that for intubation 25% to 55%, and that for urinary catheterisation 21% to 51%. In the flumazenil group 21 patients gave valuable information on their drug ingestion within 10 minutes after injection compared with only one in the placebo group (p less than 0.001). Nine adverse reactions were recorded in the flumazenil group, eight of which were graded as mild and one severe. The safety of the antagonist was acceptable, even though 60% of the patients in the flumazenil group had multiple drug poisoning including benzodiazepine. No epileptic seizures or arrhythmias were recorded. CONCLUSION: Flumazenil is a valuable and safe differential diagnostic tool in unclear cases of multiple drug poisoning.

Adolescent↗
PubMed2005

Epidemiology and prognosis of coma in daytime television dramas.

OBJECTIVE: To determine how soap operas portray, and possibly misrepresent, the likelihood of recovery for patients in coma. DESIGN: Retrospective cohort study. SETTING: Nine soap operas in the United States reviewed between 1 January 1995 and 15 May 2005. SUBJECTS: 64 characters who experienced a period of unconsciousness lasting at least 24 hours. Their final status at the end of the follow-up period was compared with pooled data from a meta-analysis. RESULTS: Comas lasted a median of 13 days (interquartile range 7-25 days). Fifty seven (89%) patients recovered fully, five (8%) died, and two (3%) remained in a vegetative state. Mortality for non-traumatic and traumatic coma was significantly lower than would be predicted from the meta-analysis data (non-traumatic 4% v 53%; traumatic 6% v 67%; Fisher's exact test both P < 0.001). On the day that patients regained consciousness, most (49/57; 86%) had no evidence of limited function, cognitive deficit, or residual disability needing rehabilitation. Compared with meta-analysis data, patients in this sample had a much better than expected chance of returning to normal function (non-traumatic 91% v 1%; traumatic 89% v 7%; both P < 0.001). CONCLUSIONS: The portrayal of coma in soap operas is overly optimistic. Although these programmes are presented as fiction, they may contribute to unrealistic expectations of recovery.

Cohort Studies↗
PubMed1984

Blood and brain concentrations of mercaptans in hepatic and methanethiol induced coma.

It has been suggested that mercaptans are important factors in the pathogenesis of hepatic encephalopathy. Using a gas liquid chromatographic technique which uses propanethiol as internal standard and a sulphur specific detector, blood methanethiol concentration was found to be significantly risen in encephalopathic patients with liver disease (13.2 +/- 1.0 nmol/ml; n = 47) compared with control subjects (5.7 +/- 0.3, n = 29; p less than 0.05) and non-encephalopathic patients with liver disease (7.7 +/- 1.1, n = 35; p less than 0.05) but ethanethiol and dimethylsulphide concentrations were similar in the three groups. Blood methanethiol, however, was not clearly related to coma grade, similar values being found in deeply comatosed patients to those showing only mild cerebral dysfunction. When rats were injected with 40-120 mumol methanethiol a range of responses was obtained which varied between normal consciousness and coma. The minimum blood concentration of methanethiol associated with coma (200 nmol/ml) was at least 10-fold greater than in patients with hepatic encephalopathy but brain concentrations were similar in comatose rats and those which remained awake. Blood methanethiol concentrations were similar in control and germ free rats and did not rise in cirrhotics or controls after ingestion of 2 g methionine. It is concluded that while methanethiol may accumulate in hepatic coma, it is unlikely to be of major pathogenetic importance. Endogenous mercaptans are unlikely to originate from bacterial metabolism in the gut.

Ammonia↗
PubMed1974

Cerebral blood flow and oxygen uptake, and cerebrospinal fluid biochemistry in severe coma.

Thirty-eight patients in coma due to head trauma, cerebrovascular accidents, hypoxia, hypoglycaemia, or barbiturate intoxication, and 15 cases of brain death were studied. Cerebral metabolic rate of oxygen (CMRO(2)) was obtained from the arteriovenous oxygen difference and cerebral blood flow (CBF) measured by intra-arterial (133)Xenon method. If hypothermia and CNS depressants were excluded, CMRO(2) below one-third of normal was incompatible with regaining of consciousness, but this was seen in only three comatose patients. Irrespective of the clinical outcome (death, vegetative survival, or recovery), CMRO(2) values of one-third to two-thirds of normal were seen in the majority of coma patients. CMRO(2) measurements were of no practical value to predict the prognosis in coma, even when the effect of temperature and sedatives were considered. In brain death the CBF studies gave indirect evidence of cerebral circulatory arrest. The cerebrospinal fluid (CSF) was obtained for analysis of lactate, pyruvate, and bicarbonate in 29 cases. Increased CSF lactate levels were found in all groups except barbiturate intoxication. The finding of a negative correlation between CSF bicarbonate and log CBF suggests that the CSFpH determines the wide range of CBF in coma.

Adult↗
PubMed1979

Blink reflexes in severe traumatic coma.

Blink reflexes were studied in 21 patients in coma after severe head injury. Our observations suggest that blink reflexes are a simple, objective, neurophysiological test to evaluate brainstem function. Correlations between these reflexes and the anatomoclinical stanges of coma and the Glasgow coma scale have been established. Presence of the early R1 component shows the integrity of at least a part of the pontine structures. The appearance of the late R2 component is correlated with a better chance of recovery from coma.

Acute Disease↗
PubMed1996

Early prognosis in coma after cardiac arrest: a prospective clinical, electrophysiological, and biochemical study of 60 patients.

BACKGROUND: The univariate study of clinical, electrophysiological, or biochemical variables has been shown to predict the outcome in postanoxic coma in about 50% of patients for each type of variable. Previous studies did not, however, consider the prognostic accuracy of a multivariate approach. METHODS: Sixty patients in coma for more than six hours after cardiac arrest were prospectively examined by means of repeated clinical examinations (including Glasgow coma score (GCS)), EEG, and medianus nerve somatosensory evoked potentials (SEPs). In 16 patients, the early concentrations of serum neuron specific enolase and ionised calcium were also measured. RESULTS: Within the first year after cardiac arrest, 20% of patients made a good neurological recovery; 80% remained in a vegetative state or died. Clinical examination correctly predicted outcome in 58% of patients, SEP in 59%, and EEG in 41%. The combination of clinical examination, SEP, and EEG raised the percentage of correct predictions to 82%, without false pessimistic predictions. Concentrations of serum neuron specific enolase and ionised calcium were of no additional prognostic help. Multivariate regression analysis identified the association of GCS < 8 at 48 hours with abnormal or absent early cortical SEPs as highly predictive of a bad outcome (risk = 97%, 95% confidence interval = 86-99%). CONCLUSION: The combination of GCS at 48 hours, SEP, and if these are non-conclusive, EEG, permits a more reliable prediction of outcome in postanoxic coma than clinical examination alone.

Adult↗