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PubMed2004

Effect of arousal methods for 175 cases of prolonged coma after severe traumatic brain injury and its related factors.

OBJECTIVE: To determine the effect of arousal methods for prolonged coma of 175 patients with severe traumatic brain injury and related factors. METHODS: There were 175 cases with persistent coma longer than 1 month after severe traumatic brain injury. Coma lasted 1-12 months. Arousal procedures included hyperbaric oxygen, physical therapy and arousal drugs. RESULTS: In the 175 prolonged coma patients 110 got recovery of consciousness; in 118 cases with coma of 1-3 months, 86 cases recovered consciousness (72.9%); in 42 cases with coma of 4-6 months, 20 cases recovered consciousness (47.6); and in 15 cases with coma of longer than 6 months, only 4 cases recovered consciousness (26.7%). The recovery of consciousness depended on patient's primary brain stem damage, cerebral hernia, GCS score, and age. CONCLUSIONS: Application of appropriate arousal procedures improves recovery of consciousness in patients with prolonged coma.

Adolescent↗
PubMed2005

Evaluation of coma patients after cardiopulmonary resuscitation.

BACKGROUND: Coma after cardiopulmonary resuscitation (CPR) is commonly seen in daily clinical practice. How to objectively evaluate brain function after CPR is essential to the following treatment. Coma patients after CPR had been studied prospectively at the Neuro-Intensive Care Unit of Xuanwu Hospital since 2002. In this study, we focused on the topic of how to evaluate the severity of coma after CPR. METHODS: From April 2002 to November 2004, patients in coma 24 hours after CPR were monitored, the evaluation methods included Glasgow coma score (GCS), brain stem reflection, and spinal reflection. Laboratory evaluation included electroencephalography (EEG), brainstem auditory evoked potential (BAEP), short latency somatosensory evoked potential (SLSEP), and transcranial Doppler (TCD). RESULTS: Twenty-four of 35 patients (68.57%) were in deep coma. The GCS was 3 except for 2 patients; EEG was evaluated not less than grade IV except for 4 patients, BAEP was evaluated as grade III except for 3 patients, and SLSEP was evaluated as grade III except for 1 patient. Twenty-four patients died within 1 month and 11 of them (45.83%) were determined as brain death. Glasgow outcome score (GOS) was evaluated as grade I. Eleven of the 35 patients survived and their consciousness changed from deep coma to coma vigil. EEG was evaluated as gradeIin 5 patients, BAEP and SLSEP were evaluated as grade I in 3 patients, and GOS was all evaluated as grade II among the 11 patients. Two patients (18.18%) regained consciousness in 35 and 90 days after cardiopulmonary resuscitation and GOS was evaluated as grade IV and III, respectively. CONCLUSION: Combined or continuous evaluation of clinical examinations and laboratory tests can accurately and objectively determine brain function after CPR.

Adolescent↗
PubMedDate not supplied

[Significance of epileptic seizures occurring during the first week of traumatic coma (author's transl)].

Clinically evident epileptic seizures were observed in 145 patients during the first week of traumatic coma. They frequently occurred during the first day in young subjects in reactive coma, and were often isolated attacks. When ssen at a later stage they are more common in adults with non-reactive coma. The partial or generalised nature of the seizures, the depth of the coma, and the chronological order in which the seizures appear have no bearing on the etiology; the only positive finding was that recurrent seizures were more frequent in patients with intracranial hematoma (18,6% of the patients). The early appearance of seizures does not worsen the prognosis of reactive coma or non-reactive coma in young people. Critical discharges without clinical manifestations were present in 37 patients with traumatic coma during the first week. The average age of these injured patients was higher, and the prognosis for non-reactive coma worse in this group. The comatous state does not modify the clinical aspects or the etiological significance of these early post-traumatic discharges.

Adolescent↗
PubMed1996

Histopathology of cutaneous changes in non-drug-induced coma.

To compare the histological features of non-drug-induced and drug-induced coma blister, we performed histopathological and immunopathological studies of four biopsy specimens from three patients with non-drug-induced coma. These results were compared with the previously well-documented histology of drug-induced coma. The findings of the present study of non-drug-induced coma included (a) a variable degree of epidermal cell degeneration, including vacuolation of basal cells, intraepidermal blister formation with pale cytoplasm, and extensive coagulation necrosis with pale nuclei; (b) alteration of the outer root sheath of telogen follicles, ranging from focal necrosis to total coagulation necrosis, and degeneration of sebaceous gland with disappearance of the germinative cell layer; (c) secretory eccrine cells with pyknotic nuclei, vacuolation of the cytoplasm, and intercellular edema, resulting in poorly defined cytoplasm, although the nuclei of the outer basal layer were partially preserved; (d) from slight edema of the vessel wall of the venules to fibrinoid, thrombosis and/or fibrinoid necrotic degeneration of arterioles and venules; and (e) deposits of immunoglobulins or complement as detected by direct immunofluorescent technique in all the three cases. One significant difference between non-drug-induced and drug-induced coma blister was the presence of fibrinoid thrombi in the lumina of non-drug-induced coma blisters. Since one of the three cases of non-drug-induced coma studied in the present report did not show thrombi in the lumina, this feature may not always be available for the differential diagnosis of these two conditions. However, fibrinoid thrombi may be a good marker for the differentiation of these two conditions, when the depth and duration of non-drug-induced coma are severe enough to induce these lesions.

Aged↗
PubMed1991

Acute physiology and chronic health evaluation (APACHE II) and Glasgow coma scores as predictors of outcome from intensive care after cardiac arrest.

OBJECTIVES: a) To examine the accuracy of the Acute Physiology and Chronic Health Evaluation (APACHE II) and the Glasgow Coma Scores as predictors of the outcome of patients following resuscitation from cardiac arrest; b) to study the impact of the components of APACHE II on the prediction. DESIGN: A nationwide study in Finland with prospectively collected data on all patients admitted to intensive care after cardiac arrest during a 14-month period. Two thirds of the cardiac arrest patients included in the study were randomly selected to derive predictive models, and the remaining one third constituted the validation sample. SETTING: A total of 25 medical and surgical ICUs in Finland (13 in tertiary referral centers). PATIENTS: Six-hundred nineteen consecutive cardiac arrest patients. Fifteen patients less than 16 yrs were excluded. MAIN OUTCOME MEASURES: Variables included in the APACHE II or Glasgow Coma Scores were collected at the time of ICU admission and then three times after admission, at 24-hr intervals. ICU- and hospital-mortality rates and a 6-month mortality rate after ICU admission were studied. RESULTS: Of 604 study patients, 370 (61.3%) patients died in the hospital. The most accurate prediction of hospital outcome was based on data collected after the first day of ICU care, not on the admission values. Twenty-one (21.9%) of 96 patients with a low APACHE II score (less than or equal to 9) died compared with 66 (84.6%) of 78 patients with a high APACHE II score (greater than or equal to 25) (p less than .001). Of 160 patients with a normal Glasgow Coma Score (14 to 15), 45 (28.1%) died, whereas there were 114 (81.4%) nonsurvivors among 140 patients with a low Glasgow Coma Score of 3 (p less than .001). The performance of predictive models, including age, the Chronic Health Evaluation, and either the Acute Physiology Score (Acute Physiology Score model) or the Glasgow Coma Score (Glasgow Coma Score model) were compared with the prediction according to the APACHE II in the validation sample. When using 80% probability of death as a decision rule, the Acute Physiology Score model determined 35 of 153 patients to have high risk of death, 29 of whom died (the positive predictive value being 82.9%). The Glasgow Coma Score model predicted 34 patients to die, 26 of whom died (positive predictive value 76.5%), and the APACHE II score predicted seven deaths, five of whom actually died (positive predictive value 71.4%). CONCLUSIONS: The APACHE II scoring system cannot be recommended as a prognostic tool to support clinical judgement in cardiac arrest patients, but by modifying it, a more accurate prediction of poor outcome could be achieved. The Glasgow Coma Score explained to a great extent the predictive power of the APACHE II.

Adult↗
PubMed1993

Use of flumazenil in the diagnosis and treatment of patients with coma of unknown etiology.

OBJECTIVES: To evaluate the use of single-dose flumazenil in the diagnosis of coma of unknown etiology, and of continuous flumazenil infusion in the treatment of benzodiazepine-induced coma. DESIGN: Prospective study. SETTING: Emergency room and general medicine ward of a teaching hospital. PATIENTS: A total of 42 comatose adults in whom metabolic, neurologic, or traumatic causes of coma were excluded. INTERVENTIONS: a) Intravenous bolus injections of 0.25 mg flumazenil were given at 1-min intervals, either until improvement by two coma grades or a total dose of 2.0 mg was reached. b) Loading doses as in (a) followed by a maintenance infusion administered as long as indicated by repeated coma grade evaluation. MEASUREMENTS AND MAIN RESULTS: a) Of 34 patients, 28 received only the flumazenil loading dose responded promptly. Twenty-one of 25 available urine samples of the responding patients contained only benzodiazepine metabolites. Four urine samples contained benzodiazepines in combination with other drugs. Six patients did not respond to the flumazenil loading dose. The urine of three patients contained a combination of benzodiazepines and another coma-exerting drug; the remaining three were negative. A total of 24 patients, who initially responded to flumazenil loading, deteriorated to their previous coma state and were admitted to the general medical ward. Six (25%) patients developed complications related to hospitalization and their bedridden state. b) Eight other patients, who deteriorated after an initial loading dose, received a second iv bolus of flumazenil, followed by maintenance infusions over 5 to 24 hrs. Their hospital course was uneventful. CONCLUSIONS: These findings indicate that flumazenil is safe and effective in the diagnosis of benzodiazepine-induced coma. Furthermore, the use of continuous flumazenil maintenance infusion is of considerable therapeutic value in patients who exhibit deterioration after initial response to the single loading dose.

Adolescent↗
PubMed1983

Physiologic and prognostic significance of "alpha coma".

A patient with posthypoxic "alpha coma" is described whose EEGs were recorded before coma, within two hours following the onset of coma and after recovery. The differences observed between the alpha activity during coma and that seen before and after suggest that the alpha activity during coma and the physiologic alpha rhythm are different phenomena. This case, as well as others reported, also suggests that "alpha coma" resolving in the first 24 hours following hypoxia may have a better prognosis than "alpha coma" detected after the first day, and stresses the need for EEG monitoring begun in the immediate period following hypoxia in order to assess accurately the prognostic significance of this EEG pattern in the early stages of postanoxic encephalopathy. The aetiology of "alpha coma" also affects outcome. The survival rate appears higher in patients with respiratory arrest than in those with combined cardiopulmonary arrest.

Alpha Rhythm↗
PubMed1991

Increasing incidence of hypoglycemic coma in children with IDDM.

OBJECTIVE: To examine the incidence of hypoglycemic coma in children with insulin-dependent diabetes mellitus (IDDM) over 8 yr from 1981 to 1988 and to investigate the importance of residual beta-cell function of HbA1 levels and other variables as risk factors for hypoglycemic coma. RESEARCH DESIGN AND METHODS: The study consisted of 155 children with IDDM aged less than 16 yr at study entry. Mean age at onset of diabetes was 7.9 yr (range 1.1-15.6 yr). We made a prospective assessment of hypoglycemic coma episodes, with a standardized questionnaire, over a total observation time of 816.6 person-yr. Three monthly clinical and laboratory examinations, which included determinations of C-peptide and HbA1 levels, were conducted. We compared children with hypoglycemic coma (cases) with children without hypoglycemic coma (controls) in a case-control analysis matched for diabetes duration. Yearly incidence of hypoglycemic coma, calculated as the number of subjects having an attack in 1 yr divided by the cumulative number of person-years for that year, was measured. Univariate and multivariate odds ratios were calculated from logistic regression. RESULTS: Over the first 4 yr, the average yearly incidence was 4.4/100 person-yr compared with 7.4/100 person-yr during the later 4 yr (P less than 0.0001). This tendency was accompanied by intensification of insulin treatment with an increase in the mean number of daily injections and a decrease in mean HbA1 levels. In the case-control analysis, absent residual beta-cell function was the most important risk factor for hypoglycemic coma (adjusted odds ratio 7.8, 95% confidence intervals 2.0-31.2), followed by near-normal HbA1 levels (adjusted odds ratio 4.5, 95% confidence intervals 1.9-10.5). CONCLUSIONS: In this group of children, improvement of glycemic control apparently led to an increase in the incidence of severe hypoglycemia. In children with recurrent hypoglycemic coma and undetectable C-peptide levels, it may be safer to aim for somewhat less tight glycemic control.

Adolescent↗
PubMed2000

Immediate coma following inertial brain injury dependent on axonal damage in the brainstem.

OBJECT: Immediate and prolonged coma following brain trauma has been shown to result from diffuse axonal injury (DAI). However, the relationship between the distribution of axonal damage and posttraumatic coma has not been examined. In the present study, the authors examine that relationship. METHODS: To explore potential anatomical origins of posttraumatic coma, the authors used a model of inertial brain injury in the pig. Anesthetized miniature swine were subjected to a nonimpact-induced head rotational acceleration along either the coronal or axial plane (six pigs in each group). Immediate prolonged coma was consistently produced by head axial plane rotation, but not by head coronal plane rotation. Immunohistochemical examination of the injured brains revealed that DAI was produced by head rotation along both planes in all animals. However, extensive axonal damage in the brainstem was found in the pigs injured via head axial plane rotation. In these animals, the severity of coma was found to correlate with both the extent of axonal damage in the brainstem (p < 0.01) and the applied kinetic loading conditions (p < 0.001). No relationship was found between coma and the extent of axonal damage in other brain regions. CONCLUSIONS: These results suggest that injury to axons in the brainstem plays a major role in induction of immediate posttraumatic coma and that DAI can occur without coma.

Animals↗
PubMed2006

Coverage of coma in headlines of US newspapers from 2001 through 2005.

OBJECTIVE: To review journalists' preferences and accuracy in reporting comatose states. METHODS: Using the Lexis-Nexis database, we selected newspaper headlines from January 1, 2001, through December 31, 2005, that included the words coma, comatose, unconsciousness, vegetative state, awakening, and brain dead. RESULTS: We identified 340 stories by headlines. The median age of persons in coma was 26 years. Coma cases in men were twice as common as those in women. In 71% of coma cases, the cause of coma was associated with motor vehicle crashes or violence. Persistent vegetative state was reported in 25 articles (7%), frequently when a family or physician conflict emerged. In 33 stories (10%), coma was medically induced but not mentioned in the headline. Three "miracle" recoveries involved resumption of speech in patients in a minimally conscious state. CONCLUSION: Few news reports had gross inaccuracies or misrepresentations; however, definitional difficulties of unconscious states with the reporters remain. The reporting of coma may be biased toward violence and trauma. Medically induced coma was present in 1 of 10 reports but rarely mentioned in the headline.

Coma↗
PubMed1987

"Theta pattern coma" occurring in younger adults.

Since our previous report, where "theta pattern coma" was described in 2 elderly patients as an EEG pattern with a grave prognosis, we have had the opportunity to see another 9 affected patients. In this article, 3 men with a mean age of 36 years who died after cardiorespiratory arrest presented a "theta coma pattern." The EEG activity was initially reactive to and attenuated by external stimulation in 2, but prior to death the pattern became arreactive. This article shows that "theta pattern coma" is not an age related phenomenon as previously considered. So far, 11 patients with this type of EEG abnormality have been seen in our department; all have died, and all were over 30 years of age. An expanded definition of "theta pattern coma" is given in the discussion. The pathophysiological mechanisms involved in generation of this abnormality are not known. This abnormality, when seen in the unconscious patient, should be classified as a grade 4 abnormality on the EEG coma scale and should be differentiated from rather diffuse theta activity in coma. The prognostic significance of "theta pattern coma" appears to be similar to that of "alpha pattern coma."

Adult↗
PubMed1978

[Differences in plasma aminograms in hepatic and diabetic coma].

In hepatic coma as well as diabetic coma severe disturbances occur in the amino acid metabolism. The defect lies in completely different levels which result two different plasma aminograms (PAG). In 24 patients with hepatic encephalopathy stage III-IV (7 patients with acute and 17 with chronic liver failure) the PAG were evaluated. The determination of the plasma amino acids (PAA) was carried out on Multichrom B (Beckmann, Munich). In hepatic coma high concentrations of Met, Tyr, Ala, Lys and Arg are found. The deviations of PAA from normal controls show between acute and chronic hepatic failure no qualitative but only quantitative differences. In diabetic coma the three branches chain AA (Val, Leu and Ile) were elevated upon 3--5 times of normal. Near normal concentrations are found for the AA Thr, Ser, Gly, Ala, Met and the aromatic AA (Phe and Tyr). The quotient between the branched chain and aromatic AA lies for hepatic coma at a mean of 1.18 and by diabetic coma at 7.18 (p less than 0.001). In hepatic coma a correlation exists between the level of the AA-quotient improvement and the decrease with a deterioriation of the metabolic encephalopathy. The high level of the AA-quotient in the patients of diabetic "coma" gives therefore a good explanation for the rare unconscious state of these patients.

Adult↗
PubMed1996

Therapeutic Intervention Scoring System used in the care of patients in pentobarbital-induced coma to determine nurse-patient ratios.

BACKGROUND: Critical care patients generally require extensive interventions, thereby consuming a large percentage of healthcare resources. Induced pentobarbital coma for the management of increased intracranial pressure is one such intervention, required to maintain patient stability. Quantification of these interventions, as well as the amount of nursing work required, has not been addressed in the literature. OBJECTIVE: To use the Therapeutic Intervention Scoring System to analyze and quantify how interventions affect nurse-patient ratios in the management of patients in pentobarbital coma for refractory increased intracranial pressure. METHODS: The medical records of patients with subarachnoid hemorrhage from aneurysmal rupture and subsequent increased intracranial pressure, in whom pentobarbital coma was salvage therapy, were reviewed retrospectively. The Therapeutic Intervention Scoring System was used to quantify the number of interventions required before, during, and after coma induction. The data were analyzed and daily Therapeutic Intervention Scoring System scores correlated with serum pentobarbital levels. Typically, a critical care nurse can manage a patient caseload of 40 to 50 Therapeutic Intervention Scoring System points. By quantifying the interventions, the score reflected the amount of care required to manage the patient in barbiturate coma. RESULTS: The intensity of interventions correlated with the level of coma, length of time in coma, and associated complications. CONCLUSIONS: The scores indicated the intensity of interventions used in pentobarbital coma and the use of resources. Nursing care and complications involved with this therapy were quantified and nurse-patient ratios were established.

Adult↗
PubMed1977

Clinical course and prognosis of one hundred and two patients with hepatic coma 1958 through 1975.

The clinical course and prognosis of hepatic coma were examined in 102 patients treated in the period from 1958 to 1975. The diagnoses included 9 fulminant hepatitis, 7 subacute hepatitis, 53 liver cirrhosis without liver carcinoma (40 cases of the acute type, 10 cases of the chronic type and 3 cases of another type, according to Sherlock's classification of hepatic coma) and 33 liver cirrhosis with primary liver carcinoma. Four of 9 fulminant hepatitis patients gained consciousness within 1 week and recovered completely. Seven subacute hepatitis patients died within 2 weeks after onset of hepatic coma. In the period from 1958 to 1969, 20% of liver cirrhosis patients with the acute type of coma recovered from coma, and in the period from 1970 to 1975, 45% of patients recovered. Seven of 10 patients with the chronic type of coma died between 4 months and 9 years after the onset of coma. Three other patients are presently still alive. The median survival time was 2.5 years. Nine primary liver carcinoma patients with coma were hospitalized from 1958 to 1969 and 24 from 1970 to 1975. Hepatorenal syndrome was present in 31 of 71 examined patients. Twenty-three patients with hepatorenal syndrome were in the period from 1970 to 1975.

Adolescent↗
PubMedDate not supplied

[Neurophysiological diagnosis of the patient in coma].

INTRODUCTION: In coma one loses both the ability to waken and consciousness. Patients in coma lie with their eyes shut and absence of psychologically understandable response to external stimuli or internal needs. Currently the most widely used scale for evaluation of coma is the Glasgow Coma Score. From the neurophysiological point of view different graduations of coma have been made based on the electroencephalographic changes found in patients in coma. DEVELOPMENT: Neurophysiological examination should be based on a study protocol which includes the following techniques: EEG lasting 30 minutes, cochlear-brainstem auditory evoked potentials and somatosensory evoked potentials. To obtain a satisfactory result it is advisable to use the three techniques jointly. Four degrees of severity are established for the neurophysiological diagnosis of coma. CONCLUSION: EEG reactivity to noxious stimuli is shown to be a sign of good prognosis, with marked statistical significance.

Cochlea↗
PubMed2005

[Evaluation of coma after cardiopulmonary resuscitation].

OBJECTIVE: To investigate the accurate and objective methods of evaluating coma after cardiopulmonary resuscitation. METHODS: Cases that were still in coma 24 hours after cardiopulmonary resuscitation were continuously observed and evaluated between April 2002 and November 2004. The methods of evaluation included various clinical examinations, for instance conscious state, Glasgow coma score (GCS), brain stem inflection, spinal reflexes and so on. Other methods of evaluation included laboratory examinations, such as electroencephalography (EEG), brain auditory evoked potential (BAEP), short latent somatosensory evoked potential (SLSEP) and transcranial doppler (TCD). RESULTS: 24 of a series of 35 cases (68.6%) were in deep coma. The GCS is score 3. EEG evaluated was not less than grade IV in all except 4; BAEP evaluated was grade III in all except 3; SLSEP evaluated was grade III in all except 1. 24 cases died within 1 month and 11 of them (45.8%) were evaluated as having brain death and Glasgow outcome score (GOS) was grade I. 11 of the 35 cases survived and their state of consciousness changed from deep coma to coma vigil, EEG evaluated was grade I in 5 cases. BAEP and SLSEP were grade I in the 3 cases evaluated and GOS is grade II. 2 cases (18.2%) regain consciousness at the time of 35 and 90 days after cardiopulmonary resuscitation and their GOS was grade IV and grade III respectively. CONCLUSION: Combined and continuous observation of clinical manifestations and laboratory parameters can accurately and objectively evaluate coma after cardiopulmonary resuscitation.

Adolescent↗
PubMed1981

[Pancreatic cancer revealed by hyperosmolar coma: report on two cases (author's transl)].

Hyperosmolar diabetic coma revealed the presence of a pancreatic cancer in two patients. The first case was a 59-year-old man, without a history of diabetes, treated with prednisone for jaundice and marked weight loss over the last month, and admitted in hyperosmolar coma (346 m0sm/l). After recovery from the acute episode, a diagnosis of adenocarcinoma of the head of the pancreas was established following operation. The patient died six months later. The second case, a 71-year-old man also without a history of diabetes, was admitted in hyperosmolar coma (315 m0sm/l) during the course of a pulmonary infection. Rapidly fatal cholostatic jaundice appeared one year later. An adenocarcinoma of the head of the pancreas was demonstrated at autopsy. The diagnostic criteria in both cases were those of hyperosmolar diabetic coma. Though cases of combined diabetes and pancreatic cancer are well documented, only one case of hyperosmolar coma and cancer of the pancreas has been reported in the published literature. The pathogenesis of hyperosmolar diabetic coma is discussed. The fact that it developed during the course of a pancreatic affection could be explained by a functional reduction in insulin secretion, associated with a triggering factor such as dehydration, infection, hypoglycemic agent administration, etc... The onset of hyperosmolar diabetic coma in an elderly patient without a history of diabetes, especially with associated marked weight loss, should lead to investigation for a possible pancreatic cancer.

Adenocarcinoma↗
PubMed2005

Non traumatic coma.

OBJECTIVE: To study the etiology and clinical profile of non-traumatic coma in children and to determine the clinical signs predictive of outcome. METHODS: 100 consecutive cases of non-traumatic coma between 2 months to 12 years. Clinical signs studied were temperature, pulse, heart rate, blood pressure, coma severity by Glasgow coma scale (GCS), respiratory pattern, pupillary and corneal reflex, extra ocular movements, motor patterns, seizure types and fundus picture. These were recoded at admission and after 48 hours of hospital stay. Etiology of coma was determined on basis of clinical history, examination and relevant laboratory investigations by the treating physician. The outcome was recorded as survived or died, and among those who survived as normal, mild, moderate, or severe disability. Chi-square test and logistic regression analysis were done to determine predictors of outcome. RESULTS: Etiology of coma in 60% cases was CNS infection (tubercular meningitis-19, encephalitis-18, bacterial meningitis-16, others-7); other causes were toxic-metabolic conditions (19%), status epilepticus (10%), intracranial bleed (7%), and miscellaneous (4%). 65 children survived, 11 were normal, 14 had mild disability, 21 had moderate disability and 14 were severely disabled and dependent. Survival was significantly better in patients with CNS infection (63%) as compared to those with toxic-metabolic causes (27%) and intracranial bleed (43%, P < 0.05). On bivariate analysis age < or = 3 years, poor pulse volume, abnormal respiratory pattern and apnoea, abnormal pupillary size and reaction, abnormal extra ocular movements, absent corneal reflex, abnormal motor muscle tone at admission or 48 hours correlated significantly with mortality. Survival was better with increasing GCS (Spearman rho = .32, P < 0.001). On logistic regression age < 3 years, poor pulse volume, absent extraocular movements and papilloedema at admission and 48 hours after admission were independent significant predictors of death. CONCLUSION: CNS infections were the most common cause of non-traumatic coma in childhood. Simple clinical signs were good predictors of outcome.

Child↗