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PubMed1993

[Serum sodium as prognostic factor in hepatic coma].

UNLABELLED: Among 17,628 discharges from the Department of Medical Gastroenterology, Odense University Hospital during the period 1 April 1973 to 31 May 1992, 66 (3.74/1000) discharges in 55 patients were found with the EDP-code 573.00 coma hepaticum. The case records of these patients were examined, and the lowest serum sodium values were compared between the patients who survived hepatic coma and those who did not and were correlated to the total duration of hospitalisation and the serum creatinine value measured at the same time as the lowest serum sodium value. The case records of 54 patients could be found, but in one case there was no serum sodium value; thus, the final material included 53 patients with 53 cases of hepatic coma and 53 lowest serum sodium values, 25 from patients who survived hepatic coma and 28 from patients who died. 15/28 (53.6%) lowest serum sodium values during fatal coma admissions were 119 mmol/l or below, whereas 6/25 values during non-fatal coma admissions were 119 mmol/l or below (p < 0.05). There was a negative correlation between the lowest measured serum sodium value and the total duration of hospitalisation (p < 0.00004). Exponential regression analysis showed negative correlation between serum creatinine and serum sodium (p = 0.0144). CONCLUSION: The correlations mentioned above may raise the question whether serum sodium should be kept at 120 mmol/l or above in patients suffering from hepatic coma. It is not predictable whether such a measure will prevent or attenuate cerebral symptoms and improve survival rate.

Hepatic Encephalopathy↗
PubMed1996

Event-related potentials--neurophysiological tools for predicting emergence and early outcome from traumatic coma.

OBJECTIVE: To determine the prognostic value of multimodal evoked potentials (EPs) and event-related (ERPs) potentials in coma (Glasgow Coma Score <8), after severe traumatic brain injury (TBI). DESIGN: Prospective, longitudinal study of neurophysiological responses recorded during traumatic coma. SETTING: Intensive Care Unit, Frenchay Hospital, Bristol, UK. PARTICIPANTS: Fifty-four comatose TBI patients (age range 1-80 years, mean 36.4). METHODS: Neurophysiological responses were recorded from 11 scalp electrodes with earlobe reference. Conduction times were measured for brainstem auditory, flash visual and somatosensory, short-latency EPs. Peak latencies and amplitudes were determined for long-latency components of visual and auditory ERPs, generated by passive "oddball" paradigms. These neurophysiological and various clinical parameters were correlated with patient outcome using Pearson's coefficient. MAIN OUTCOME MEASURE: Three month Glasgow Outcome Scale (GOS). RESULTS AND CONCLUSION: Highly significant (P <0.001) correlations exist between long-latency ERP components and 3-month outcome. Short-latency EPs, brainstem (wave I-V) and somatosensory conduction times also correlate significantly with the GOS (P <0.01). Of the clinical measurements, pupillary response patterns, APACHE II and Glasgow Coma Scores (GCS) correlate significantly with outcome, as do the retrospective measures of duration of coma and post-traumatic amnesia (PTA) in survivors. Unfortunately, due to variance of long-latency responses, even in controls, absolute values cannot be relied upon as prognosticators. The presence of "mismatch negativity" predicted the return of consciousness (89.7% sensitivity and 100% specificity) and preceded changes in GCS. Its latency was the single best indicator of 90-day outcome from coma (r = -0.641).

Acoustic Stimulation↗
PubMed2007

Prediction of recovery from a post-traumatic coma state by diffusion-weighted imaging (DWI) in patients with diffuse axonal injury.

INTRODUCTION: To determine whether diffusion-weighted magnetic resonance (MR) imaging findings combined with initial clinical factors indicate the depth of shearing lesions in the brain structure and therefore relate to coma duration in diffuse axonal injury (DAI). METHODS: A total of 74 adult patients (48 male and 26 female) with DAI were examined with conventional MR imaging and diffusion-weighted MR imaging between 2 hours and 20 days after injury. Apparent diffusion coefficient (ADC) maps were obtained and the mean ADC values of each region of interest (ROI) were measured using MRI console software. The involvement of the brainstem, deep gray matter, and corpus callosum was determined for each sequence separately as well as for the combination of all sequences. The correlations between MR imaging findings indicating the presence of apparent brain injury combined with initial clinical factors were determined. RESULTS: Clinical characteristics, such as initial score on the Glasgow coma scale (GCS), age and number of all lesions, and ADC scores were predictive of the duration of coma. CONCLUSION: It was possible to predict post-traumatic coma duration in DAI from cerebral MR imaging findings combined with clinical prognostic factors in the acute to subacute stage after head injury. Age, ADC scores, GCS score and number of lesions were highly significant in predicting coma duration. The technique presented here might provide a tool for in vivo detection of DAI to allow the prediction of the coma duration during the early stages in patients with traumatic brain injury.

Accidents, Traffic↗
PubMed2002

[How can we define the modalities and clinical levels of coma to wakefulness?].

OBJECTIVE: The starting point of the French conference of consensus concerning arousal after coma was to answer the following question: "How can we define the ways of going from coma to arousal and their clinical levels? MATERIALS AND METHOD: A team of readers have picked up in the literature one hundred and fifty papers, out of which fifty six have been analysed. RESULTS: From this analysis, three points emerged: The concepts of coma and arousal; The conditions of evolution from coma to arousal; Various groups of patients depending on their expressing arousal. One could not find any consensual model concerning the different ways of going from coma to arousal. The variability of the technics and the changing validity of all scores did not allow the conditions of arousal to reach a satisfactory level of proof. The Glasgow Coma Scale (GCS) is the recognised standard for severe wakefulness' impairment, but it is not sensitive enough while patients' arousing. The Glasgow Outcome Scale (GOS) takes into account the patients' situations far later and does not include situations such as Minimally Conscious States (MCS). That's why we face multiple scores, either ordinal, or categorial, all tending to evaluate the slow levels of arousal. CONCLUSION: Clinical findings concerning arousal are to be completed by non-clinical data. This would be greatly helpful to define appropriate management concerning individualized groups of patients. At this stage, another challenge for clinicians is to make the difference between emerging wakefulness and growing conscious activity.

Coma↗
PubMed1994

Clinical recovery of consciousness after traumatic coma.

OBJECTIVE: To describe early clinical stages in the recovery of consciousness, using selected items from the Glasgow Coma Scale and the Liège Coma Scale. DESIGN: Validation cohort study, conducted in a tertiary care center. SETTING: Neurosurgical intensive therapy unit in a university teaching hospital. PATIENTS: Patients (n = 137) with traumatic coma who were selected according to the following criteria: a) coma due to blunt head trauma with an initial Glasgow Coma Score of < or = 7; b) admission to the neurosurgical intensive therapy unit within the first 24 hrs after trauma; c) patients > 14 yrs of age; requiring endotracheal intubation, mechanical ventilation, and the administration of drugs; and d) survival period allowing analysis of the recovery of consciousness. MEASUREMENTS AND MAIN RESULTS: Arousal, as expressed by stimulated opening of the eyes and recorded as a delay in days, was correlated with the appearance of the localized pain response, capacity to obey commands, blink reflex, and the cessation of drugs in three groups of patients. These groups were defined according to the time in which there was an appearance of the stimulated opening of the eyes: < 8 days (group 1); between 8 and 15 days (group 2); and after 15 days (group 3). When the three groups of patients were compared, significant differences existed between the mean delays of appearance of stimulated eye opening and the appearance of the blink reflex. Extubation coincided with the appearance of spontaneous eye opening, with a mean delay of 13.5 days. CONCLUSIONS: This study confirms the classical clinical sequence of arousal and recovery of consciousness, with the appearance of stimulated eye opening and the blink reflex first, followed by spontaneous eye opening, and the capacity to obey commands in intubated, traumatized, coma patients. A direct correlation existed between the delay of arousal and the complete recovery of consciousness. When groups of patients with various mean delays for the appearance of stimulated eye opening are considered, reappearance of the blink reflex did not always coincide with stimulated eye opening, suggesting differing structural and functional brain recovery processes.

Acute Disease↗
PubMed1982

Hyperosmolar non-ketotic coma in diabetic stroke patients.

Hyperosmolar non-ketotic coma in diabetes is a life-threatening condition. We describe three patients, aged 59-67 years, who developed hyperosmolar coma during the first ten days after admission for stroke. Common to all three were normal plasma osmolality and slightly elevated plasma creatinine levels on admission, treatment with diuretics, parenteral dextrose administration before and low urinary glucose output during the coma. In the five days preceding the coma, total fluid deficits were 3.8, 6.5 and 9.4 1, respectively. In one patient the rate of glucose delivery had clearly exceeded utilization during adequate insulinization, in another a marked reduction in urinary glucose output preceded extreme hyperglycaemia and coma. Two of the three patients died, both from extensive thrombus formation in cerebral arteries and multiple emboli to the lungs. We conclude that enhanced endogenous glucose production and reduced renal clearance of glucose may contribute to precipitate hyperosmolar non-ketotic coma. A close monitoring of fluid and dextrose administration seems mandatory in diabetic stroke patients, in particular if renal function is impaired or if diuretics are given. Insulin treatment should be considered in all diabetic patients during the first days after a stroke.

Aged↗
PubMed2002

Sensory stimulation of brain-injured individuals in coma or vegetative state: results of a Cochrane systematic review.

OBJECTIVES: To assess the effectiveness of sensory stimulation programmes in patients in coma or vegetative state. DESIGN: Systematic review of randomized control trials (RCT) and nonrandomized controlled clinical trials (CCT) comparing any type of stimulation programmes with standard rehabilitation in patients in coma or vegetative state. The Injuries Group specialized register, the Cochrane Controlled trial register, EMBASE, MEDLINE, CINAHL, PSYCHLIT from 1966 to January 2002 were searched without language restriction. Reference lists of articles were scanned and experts in the area contacted to find other relevant studies. Abstracts and papers found were initially screened by one reviewer. Three reviewers independently identified relevant studies, extracted data and assessed study quality, resolving disagreement by consensus. OUTCOME MEASURES: Duration of unconsciousness (including coma and vegetative state) defined as the time between trauma and objective recovery of the ability to respond to verbal commands; level of consciousness, as measured by the Glasgow Coma Scale (GCS); level of cognitive functioning (LCF); functional outcomes, as measured by Glasgow Outcome Scale (GOS) or by Disability Rating Scale; negative effects (e.g. increased intracranial pressure). RESULTS: Three studies (one RCT and two CCTs) with 68 traumatic brain-injured patients in total, most of whom were road accident victims, met the inclusion criteria. The overall methodological quality was poor and studies differed widely in terms of study design and conduct. Moreover, due to the diversity in reporting of outcome measures, a quantitative metanalysis was not possible. None of the three studies provided useful and valid results on outcomes of clinical relevance for coma patients. CONCLUSIONS: This systematic review indicates that there is no reliable evidence to support the effectiveness of multisensory stimulation programmes in patients in coma or the vegetative state.

Adult↗
PubMed2005

Noninvasive positive-pressure ventilation to treat hypercapnic coma secondary to respiratory failure.

INTRODUCTION: Hypercapnic coma secondary to acute respiratory failure (ARF) is considered to be a contraindication to the use of treatment with noninvasive positive-pressure ventilation (NPPV). However, intubation exposes these patients to the risk of complications such as nosocomial pneumonia, sepsis, and even death. PATIENTS AND METHODS: We performed a prospective, open, noncontrolled study to assess the outcomes of NPPV therapy in patients with a Glasgow coma scale (GCS) score of </= 8 points due to ARF. The primary goal of the study was to determine the success of NPPV therapy (defined as a response to therapy allowing the patient to avoid endotracheal intubation, and to survive a stay in the ICU and at least 24 h on a medical ward) in patients with hypercapnic coma, compared to those who started NPPV therapy while awake. The secondary goal of the study was to identify the variables that can predict a failure of NPPV therapy in these patients. RESULTS: A total of 76 coma patients (80%) responded to NPPV therapy, and 605 patients with GCS scores > 8 responded to therapy (70%; p = 0.04). A total of 25 coma patients died in the hospital (26.3%), and 287 noncoma patients died in the hospital (33.2%; p = 0.17). The variables related to the success of NPPV therapy were GCS score 1 h posttherapy (odds ratio [OR], 2.32; 95% confidence interval [CI], 1.53 to 3.53) and higher levels of multiorgan dysfunction, as measured by the maximum sequential organ failure assessment index score reached during NPPV therapy (OR, 0.72; 95% CI, 0.55 to 0.92). CONCLUSIONS: We concluded that selected patients with hypercapnic coma secondary to ARF can be treated as successfully with NPPV as awake patients with ARF.

APACHE↗
PubMedDate not supplied

Coma arousal procedure: a therapeutic intervention in the treatment of head injury.

This study reports on the efficacy of a 'coma arousal procedure'. This procedure involved a programme of vigorous sensory stimulation administered to comatose patients by relatives using Comakits. An experimental group of 12 severely head-injured patients received the coma arousal procedure while a matched control group did not. Total duration of coma and weekly Glasgow Coma Scale Scores were recorded for the two groups. Results indicate that the total duration of coma was significantly shorter and that coma lightened more rapidly for the experimental group.

Adolescent↗
PubMed1978

[Hormone and metabolic profile in diabetic hyperosomolar coma. Plasma insulin response to intravenous tolbutamide (author's transl)].

Fifteen patients with non-ketotic hyperosmolar diabetic coma were investigated and compared with ketoacidotic patients. Basal plasma insulin levels were low in all patients (14.8 +/- 1.0 micronU/ml in hyperosmolar coma, 11.0 +/- 1.3 in keto-acidosis), but insulin level increased after intravenous tolbutamide (between 30 and 105 micronU/ml) in eight hyperosmolar comas. Insulin showed no increase in seven hyperosmolar comas and in none of the ketoacidotic patients. In hyperosmolar coma plasma free fatty acids (1710 +/- 197 micronEq/1), triglycerides (3,4 +/- 0,4 g/1) and cortisol levels (49,7 +/- 9,0 microgram/100 ml) were increased, must as in keto-acidosis. Growth hormone (1,7 +/- 0,1 ng/ml) was normal, unlike the case in keto-acidosis. Plasma lactate concentrations were elevated and account for the frequent mild acidosis found in hyperosmolar coma. In spite of the low peripheral "insulin/glycemia ratio", the positive response to tolbutamide in half of the hyperosmolar cases suggests a less complete pancreatic deficiency than in keto-acidosis. The plasma high free fatty acid and triglyceride levels suggest that the lack of ketosis is not due to inhibition of lipolysis but could be a consequence of inhibition of hepatic ketogenesis.

Adult↗
PubMed1999

Drug-induced hypoglycemic coma in 102 diabetic patients.

BACKGROUND: Hypoglycemic coma is a continuous threat for diabetic patients treated with insulin and/or oral hypoglycemic agents; it may be associated with substantial morbidity and mortality. METHODS: We retrospectively reviewed our clinical experience with drug-induced hypoglycemic coma during a 7-year period. RESULTS: The study consisted of 102 patients and included 61 females and 41 males. The median age was 72 years. Ninety-two patients suffered from type 2 diabetes mellitus; 10 patients had type 1 diabetes mellitus. The median lowest blood glucose level was 1.77 mmol/L (32 mg/dL). Drug-induced hypoglycemic coma occurred in 99 patients out of the hospital, while 3 patients developed it during hospitalization. Drug-induced hypoglycemic coma occurred in patients undergoing treatment with insulin, glyburide, and combined therapy with insulin and glyburide, insulin and metformin, or glyburide and metformin. Ninety-three patients had at least 1 of the following risk factors: age older than 60 years, renal dysfunction, decreased intake of energy, and infection. Fourteen patients concomitantly received drugs that potentiated hypoglycemia. Forty patients responded to treatment within the first 12 hours, while 62 patients had protracted hypoglycemia of 12 to 72 hours' duration. Morbidity included physical injuries in 7 patients, myocardial ischemia in 2 patients, and stroke in 1 patient. Death occurred in 5 patients. CONCLUSIONS: Hypoglycemic coma is a serious and not an uncommon problem among elderly patients with diabetes mellitus and treated with insulin and/or oral hypoglycemic drugs. Risk factors contribute substantially to the morbidity and mortality of patients with drug-induced hypoglycemic coma. Enhanced therapeutic monitoring may be warranted when hypoglycemic drugs are administered to an elderly patient with the above predisposing factors and potentiating drugs for hypoglycemia.

Adolescent↗
PubMed1998

Influence of hypoglycemic coma on brain water and osmolality.

To study the effects of pronounced hypoglycemia on brain osmolality and brain edema formation, fasted rats were rendered hypoglycemic by injection of insulin, and subjected to 30 min of hypoglycemic coma. Recovery was accomplished by glucose administration. The change in water content in different brain regions was measured as a change in specific gravity after 30 min of hypoglycemic coma, or 30, 60, and 180 min after glucose administration. Plasma and brain tissue osmolality were measured in separate animals. The results show a significant decrease in specific gravity (increase in water content) in all structures measured (caudoputamen, neocortex, hippocampus, and cerebellum) at the end of the period of coma, as well as after 30 min and 60 min of recovery. At 180 min of recovery, brain water was normalized. The edema affected all structures to the same degree regardless of their vulnerability to hypoglycemic damage. Brain tissue osmolality showed a tendency to decrease with decreasing tissue glucose content. The decrease was significant (P<0.01) at 30 min of isoelectric coma. In the recovery phase, normal brain osmolality was restored within 30 min. Measurements of blood-brain barrier (BBB) permeability after 30 min of hypoglycemic coma showed no extravasation of Evan's blue, though a small but significant increase in the permeability for aminoisobutyric acid (AIB) in caudoputamen and in cerebellum was found. To analyze the importance of tissue acidosis for formation of edema, hypoglycemic animals were made acidotic by increasing the CO2 concentration in inspired air to produce an arterial plasma pH of 6.8-6.9. In these animals the edema was of a similar degree to the normocapnic animals, and the permeability for AIB was normal. We conclude that osmolytic mechanisms are not the primary cause of the selective neuronal vulnerability in hypoglycemic coma. Furthermore, the BBB is largely intact during a hypoglycemic insult.

Acidosis↗
PubMed1983

Central somatosensory conduction time and short latency somatosensory evoked potentials in post-traumatic coma.

Short latency evoked potentials (SEPs) were elicited by stimulation of the median nerve at the wrist and recorded simultaneously from the neck and the contralateral scalp in 44 comatose patients with signs of brain stem impairment due to head injury. Thirty-four patients were studied in acute coma on day 1 or 2 after brain injury. Twenty-three patients were studied in prolonged coma during days 3-12 after trauma. Six patients were examined in brain death. Brain stem involvement was divided clinically and by CT scan into secondary lesions due to supratentorial mass displacement and primary lesions due to direct violence to the brain stem. The central somatosensory conduction time (CCT) was measured by subtracting the peak latency of the major response from the neck (N14) from that of the primary scalp response (N20). The amplitude ratios (ARs) N20/N14 were calculated for each trace. Further asymmetries and absence of SEP over one or both hemispheres were noted. In cases in coma due to supratentorial lesions CCT and AR were close to normal in patients with good outcome. CCT increased and AR decreased with the worsening of outcome both in acute and prolonged coma. Asymmetries of SEPs indicated moderate or severe final disability. Patients with absent SEPs over one or both hemispheres due to supratentorial lesions died or survived severely disabled (1 case). In patients suffering from primary brain stem dysfunction, confirmed by a normal or slightly abnormal CT scan, prolonged CCT, asymmetric but also absent SEPs were also found in patients with good outcome both in acute and prolonged coma. AR was generally low in these cases. Early appearance of SEPs or early recovery of initially distorted SEPs and decrease of CCT in prolonged coma or during recovery was a favourable prognostic sign. Therefore even absent or severely distorted SEPs should be interpreted cautiously in patients who may suffer from primary brain stem involvement. Scalp SEPs were totally absent in patients with brain death.

Adolescent↗
PubMed1983

Incidence and prognostic value of spindles in post-traumatic coma.

One hundred and thirty-three EEGs were analysed from 80 comatose patients with signs of brain stem impairment due to head/brain injury. Seventy EEGs were taken in acute coma on day 1 or 2 after brain injury. Sixty-three EEGs were recorded in prolonged coma 3-12 days after brain injury. Brain stem involvement was divided by neurological signs and by CT scan into secondary lesions due to supratentorial mass displacement and primary lesions due do direct violence to the brain stem. Different EEG patterns were observed, but spindle activity was of special interest. Spindles were classified as typical (easily recognizable, well organized, 12-14 c/sec activity) or atypical (hardly recognizable, distorted form, 6-11 c/sec activity). Furthermore, asymmetries of spindles were noted. The spindles and their alterations were related to different stages of outcome. Spindles were seen in 91% of the EEGs in acute coma and in 30% in prolonged coma. In acute coma due to secondary brain stem involvement a good outcome was heralded by the occurrence of typical symmetrical spindles combined with early stages of secondary brain stem impairment at neurological examination. In cases of primary brain stem involvement typical spindles also suggested a good prognosis despite the observation of serious clinical signs (decerebrate posturing). The percentage of spindle activity decreased, and distortion and asymmetry of spindles increased with the worsening of outcome. Severe intracerebral lesions (confirmed by clinical and CT scan examinations) led to distortion, asymmetry and finally disappearance of spindles. In prolonged coma spindle activity was markedly reduced regardless of the final outcome. When spindles were present atypical and asymmetric forms significantly increased in patients with bad outcome. There were no significant differences in spindle activity in the different outcome categories, if primary and secondary brain stem lesions were compared.

Adolescent↗
PubMed1993

Brain calcium metabolism in hypoglycemic coma.

The present experiments were designed to provide information on brain calcium metabolism during hypoglycemic coma. We specifically wished to evaluate changes in extracellular calcium concentration (Ca2+e) during prolonged hypoglycemic coma and recovery and to assess whether Ca2+e falls to similar values during hypoglycemia and ischemia. To that end, Ca2+e and K+e in neocortical tissue were recorded by ion-sensitive microelectrodes during hypoglycemic coma of 30 min duration and during 15 min of recovery. Cardiac arrest ischemia was induced either at the end of the period of hypoglycemia or after 15 min of recovery. Hypoglycemic coma, as reflected by a DC potential shift and by cellular release of K+, was accompanied by a sustained decrease in Ca2+e from approximately 1.2 to approximately 0.02 mM, i.e., to approximately 1% of control. Infusion of glucose was followed by a biphasic recovery of Ca2+e, starting within 2 min of infusion. During the first phase, completed within the initial 3-4 min, Ca2+e rose to about 25% of control. During the second phase, Ca2+e slowly increased toward normal within 25-30 min. Ischemia, when induced at the end of the period of hypoglycemia, was accompanied by a rise in Ca2+e to about 0.1 mM, i.e., about 10% of control. A similar value was recorded when ischemia was induced after 15 min of recovery following a 30-min hypoglycemic coma. Although the present results do not give information on Ca2+i during hypoglycemic coma, it is tempting to conclude that partial preservation of the nucleoside triphosphate stores, and absence of acidosis, allow some binding and sequestration of the calcium entering the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Cost effectiveness of aggressive care for patients with nontraumatic coma.

OBJECTIVE: To estimate the cost effectiveness of aggressive care for patients with nontraumatic coma. DESIGN: Cost-effectiveness analysis. SETTING: Five academic medical centers. PATIENTS: Patients with nontraumatic coma enrolled in the Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments (SUPPORT). Patients with reversible metabolic causes of coma such as diabetic ketoacidosis or uremia were excluded. MEASUREMENTS: We calculated the incremental cost effectiveness of continuing aggressive care vs. withholding cardiopulmonary resuscitation and ventilatory support after day 3 of coma. We estimated life expectancy based on up to 4.6 yrs of follow-up. Utilities (quality-of-life weights) were estimated using time-tradeoff questions. Costs were based on hospital fiscal data and Medicare data. Separate analyses were conducted for two prognostic groups based on five risk factors assessed on day 3 of coma: age > or = 70 yrs, abnormal brainstem response, absent verbal response, absent withdrawal to pain, and serum creatinine > or = 132.6 micromol/L (1.5 mg/dL). RESULTS: For the 596 patients studied, the median (25th, 75th percentile) age was 67 yrs (range, 55-77), and 52% were female. By 2 months after enrollment, 69% had died, 19% were severely disabled, 7% had survived without severe disability, and 4% had survived with unknown functional status. The incremental cost effectiveness of the more aggressive care strategy was $140,000 (1998 dollars) per quality-adjusted life year (QALY) for high-risk patients (3-5 risk factors, 93% 2-month mortality) and $87,000/QALY for low-risk patients (0-2 risk factors, 49% mortality). In sensitivity analyses, the incremental cost per QALY did not fall below $50,000/QALY, even with wide variation in our baseline estimates. CONCLUSIONS: Continuing aggressive care after day 3 of nontraumatic coma is associated with a high cost per QALY gained, especially for patients at high risk for poor outcomes. Earlier decisions to withhold life-sustaining treatments for patients with very poor prognoses may yield considerable cost savings.

Activities of Daily Living↗
PubMed1993

Predictive value of P300 event-related potentials compared with EEG and somatosensory evoked potentials in non-traumatic coma.

Developments in ethical decision making are increasing demand for more accurate predictions of outcome in coma. New neurophysiologic tests are needed to improve the ability to predict awakening as well as poor outcome. We have recently reported that the P300 event-related potential (P300) correlates with awakening and depth of nontraumatic coma. In this companion study, the predictive value of the P300 was compared with median nerve somatosensory evoked potentials (SEP) and EEG in 20 patients in non-traumatic coma. We also evaluated the predictive value of a simplified grading scale for both the EEG and SEP (the USC SEP scale and USC EEG scale). The presence of a P300 was significantly associated with higher Glasgow coma scores (GCS) and awakening. Severe abnormalities of the somatosensory evoked potentials significantly correlated with the absence of awakening and a low GCS. Moderate abnormalities of the SEP were significantly associated with awakening and higher GCS scores. The EEG was significantly associated with GCS score and severe abnormalities of the EEG were predictive of the absence of awakening and very low GCS scores. The data indicates that the P300 and SEP are more effective than the EEG in predicting awakening, and that the SEP and EEG are more effective than the P300 in predicting poor outcome. We conclude that, in addition to EEG and SEP, the P300 should be considered in the prognostic evaluation of patients in nontraumatic coma. Further, simplified scales for the EEG and SEP are predictive of depth of coma and outcome.

Adult↗
PubMed2003

Pupillary evaluation for differential diagnosis of coma.

OBJECTIVES: To determine the usefulness of bedside evaluation of pupils in determining the aetiology of coma by adopting a probabilistic approach. PATIENTS AND METHODS: One hundred and fifteen consecutive patients presenting with coma were enrolled in this prospective cohort during the 12 month study period in the emergency room of a community teaching hospital. Patients underwent structured clinical examinations and laboratory and imaging tests. Assignment of aetiology of coma was based on strict adherence to predetermined criteria and achieved by consensus of the two physician investigators. One year follow up was obtained in all patients. RESULTS: Aetiology of coma was determined in 98% of the patients. It was metabolic in 69 patients (60%) and structural in 46 patients (40%). Metabolic causes included drug overdose, acute alcohol intoxication, hypoglycaemia, sepsis, and pneumonia. Structural causes included intracerebral haemorrhage, subarachnoid haemorrhage, cerebral infarction, subdural haematoma, and epidural haematoma. Multivariate logistic regression analysis showed light reflex loss (likelihood ratio for positive test result 3.59) and anisocoria (likelihood ratio for positive test result 9.0) as independent predictors of structural origin. CONCLUSIONS: In this prospective study of patients presenting to the emergency room of a community based teaching hospital with coma, in about 60% the coma is of metabolic origins and in about 40% of structural origins. Light reflex loss and anisocoria suggest a structural aetiology.

Adolescent↗