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PubMedDate not supplied

A practical approach to coma diagnosis in the unresponsive patient.

Diagnosis of coma in the unresponsive patient can be done in a relatively short time by making key observations that will confirm disease of either the brain stem or the hemispheres, the two locations in which coma originates. Determining the location of the lesion is the primary goal in early assessment of the unresponsive patient. Examination of the patient's eyes is the single most important step in understanding coma.

Brain Stem↗
PubMed1976

[Prolonged traumatic and vascular coma: prognostic and therapeutic indications based on hemodynamic and metabolic studies].

From haemodynamic and metabolic investigation of 65 comatose subjects following cranial traumatism or cerebral vascular accident, the following prognostic and therapeutic indications emerged: The isolated increase in oxygen pressure in the jugular vein to above 50 mm Hg, the simultaneous decrease in circulation of the brain to below of 30 ml/100g/min., and of the brain consumption of oxygen to below 1.5 ml/100g/min., combined with a loss of autoregulation and a decrease in carbon dioxide reactivity indicate that prognosis is very poor. Induced arterial hypertension, associated with hyperventilation, partially corrects brain hypoperfusion in coma from bulbo-pontine lesions. Sodium penthiobarbital and sodium gamma hydroxybutyrate and have the effect of reducing oxygen metabolism which might have some therapeutic value during the acute phase of coma. Clomipramine which has a stimulating effect on oxygen metabolism should be kept in reserve for the chronic phase of prolonged coma.

Blood Gas Analysis↗
PubMed1979

[Diabetic ketoacidosis and hyperosmolar diabetic coma in childhood. Low-dose continuous intravenous infusion of insulin (author's transl)].

Continuous intravenous infusion of low doses of insulin has been successfully used since 1972 in the treatment of "diabetic coma". The achieved levels of plasma insulin satisfy the transport of glucose and the inhibition of lipolysis. We are to report upon 8 children (mean age: 8.5 years), 6 with diabetic ketoacidosis and 2 with hyperosmolar diabetic coma. Blood sugar levels of 300 mg/dl or less were reached after averagely 8 hours of therapy and an average consumption of 0.8 U insulin/kg. Sodium and potassium levels, osmolality and acid base parameters for the first 24 hours are described. Low-dose continuous intravenous insulin infusion was effective, simple and safe in all cases. The presently recommended dosage of 0.1 insulin/kg x hour is to be used flexibly (range: 0.05--0.2 U/kg x hour). The administration of bicarbonate should be cautiously used for patients with severe acidosis. Infusion of hypotonic solutions as part of the treatment of the hyperosmolar diabetic coma can be dangerous. A new therapeutic regime based on our results is proposed.

Adolescent↗
PubMedDate not supplied

[Peculiarities of changes in the EEG in the development of coma in patients with a focal injury of the brain].

A number of new electrographic variants reflecting the specifity distinguishing the evolution of coma in focal affections of the brain and clearly correlating with its clinical manifestations were elicited. The comatose status, apart from a fall of the level and frequency of the brain biopotentials, is shown to be characterized by an imbalance of spatial and temporal relations in the cortex of the large hemispheres, a correlation between the degree of disrupted inter-central relations and the stage marking the development of the comatose process having been disclosed. Some EEG findings were obtained that may be taken advantage of in judging about the prognosis as to the evolution of coma. An electroencephalographic investigation of the comatose states in focal lesions of the brain opens up the possibilities for a differential approach to the study of coma.

Adult↗
PubMed2001

[A case of carbamazepine intoxication with alpha coma and status epilepticus].

We report a 14-year-old girl with carbamazepine intoxication who developed alpha coma and status epilepticus. She fell into deep coma and developed frequent generalized convulsions. The EEG during coma showed diffuse alpha activity predominantly in the frontal area. Serum carbamazepine concentration was 42.8 micrograms/ml. The convulsions were suppressed by diazepam only transiently, and by midazolam completely. Although half a day had passed since carbamazepine ingestion, we could wash out much of drug remnants by gastric lavage. Thereafter, the serum concentration of carbamazepine decreased efficiently and the patient recovered dramatically without complication. Early diagnosis and appropriate treatments should improve the prognosis of carbamazepine intoxication.

Adolescent↗
PubMed2002

Coma and apnea in a dog with hydroxyzine toxicosis.

Hydroxyzine is a commonly prescribed H1-receptor antagonist in small animal practice. The most common adverse effect reported after therapeutic dosing is mild sedation; severe reactions resulting in coma have occasionally been reported in children. We present a case of large po hydroxyzine exposure causing in coma and apnea in a dog. Exposure was confirmed with gas chromatography/mass spectrometry analysis of urine. Extensive therapeutic measures to enhance drug elimination and assist ventilation were required for 11 d. The positive outcome justifies critical care of similarly exposed animals. Veterinarians should be aware of the potential for coma and apnea secondary to hydroxyzine exposure.

Animals↗
PubMed2002

Value of MR imaging of the brain in children with hypoxic coma.

BACKGROUND AND PURPOSE: The contribution of MR imaging to identify hypoxic-ischemic injuries has been studied mostly in neonates or adults. The purpose of this study was to describe the MR imaging findings of toddlers and older children with hypoxic coma and to analyze the prognostic value of an MR imaging scoring system. METHODS: The conditions of 40 children with hypoxic coma (age range, 6 weeks to 18 years) were clinically graded according to the pediatric risk of mortality score, and MR imaging studies were performed. Sixty-four MR imaging studies were distributed in five categories according to their timing relative to the hypoxic event: days 1 through 3, 4-7, 8-15, 16-50, and after day 50. These were evaluated retrospectively by using an eight-point scoring system based on two lesion categories assessing watershed areas and basal ganglia involvement, including signal intensity and morphologic features with respect to maturation-related norms. Two age groups (< or =1 year and >1 year) were considered. The surviving children were grouped according to neurologic outcome. RESULTS: The occurrence of watershed areas or basal ganglia involvement was not significantly different in association with age. Sixteen children died. Twelve children had moderate to severe sequelae resulting from neurodevelopmental disabilities, and 12 had good neurologic outcomes. There was no correlation between pediatric risk of mortality score and neurologic evolution. There was a strong correlation between first MR imaging score (P <.001) and neurologic outcome. The sensitivity of the first MR imaging score was high (96%), even when obtained during the first 3 days, with a specificity of 50% and a positive predictive value of 82%. Six patients with definite abnormal MR imaging findings experienced good neurologic outcomes. CONCLUSION: The MR imaging scoring system proposed in this study can be used to establish an early prognosis in a significant proportion of children with hypoxic coma. It is helpful, even during the first 3 days after the event. However, some patients with definite abnormal MR imaging findings may experience good neurologic evolution.

Adolescent↗
PubMed2002

Role of semantic control of action in the comprehensive rehabilitation of patients recovering from prolonged post-traumatic coma.

BACKGROUND: Apraxia, broadly understood as the acquired inability to perform learned, skilled movements not caused by paresis or incomprehension, occurs with greater frequency among patients recovering from prolonged post-traumatic coma than has previously been reported. The present article prevents an evaluation of the effectiveness of a rehabilitation program called Semantic Priming, aimed at rebuilding praxis in these patients. MATERIAL/METHODS: Out of a consecutive series of 51 patients with post-traumatic coma lasting longer than 4 weeks treated at the centers represented by the authors, 24 were found to have pathological scores on the Boston Test of Praxis. These patients were divided into two matched groups, of whom the experimental group received the Semantic Priming program (involving the systematic use of verbal cues to prime movement activation patterns), and the control group did not. Progress was measured by the Boston Test of Praxis and a test developed by the authors on the basis of Luria's procedure for testing praxis. RESULTS: After 5 weeks of therapy the patients in the experimental group showed significantly greater improvement in all measured parameters (p<0.001). CONCLUSIONS: Apraxia in the broader sense is a more common problem among post-coma patients than heretofore recognized, and causes concrete problems in rehabilitation and adjustment to daily living. Our program based on the use of semantic priming of activation proved to be highly successful in remediating apraxia in these patients.

Activities of Daily Living↗
PubMedDate not supplied

[Blood lactate semiautomatic estimation during acidotic diabetic coma (author's transl)].

Blood lactate levels were determined by Lactate Analyzer 640 Kontron during the course of 7 cases of hyperglycemic hyperosmolar diabetic coma, with severe acidosis and more or less marked ketosis. In 5 cases lactate values were found in normal range; slight increases around 2 mmol/l were rapidly corrected following standard coma treatment. One of these cases presented with extreme acidosis and relatively mild hyperglycemia, with differential problems in regard to lactic acidosis. In 2 cases, the former with alcoholic cirrhosis, the latter with myocardial infarction, blood lactate was markedly increased; in the second case, full clinical recovery was accompanied by normalization of lactate levels. A previous biguanide treatment could be ruled out as a cause of lactic acidosis. Thus the association of lactic acidosis and diabetic ketoacidosis seems to be unusual in the absence of concurrent serious conditions. The semiautomatic determination of blood lactate, because of its remarkable prognostic importance, should be included among the routine procedures for the emergency treatment of diabetic coma.

Adult↗
PubMed1975

[Diabetic coma as a task for intensive therapy].

On the basis of 763 cases with diabetic coma from 1960 to 1973 is referred to the advantages of the foundation of a coma ward as department of intensive observation. It is reported on some successful changes of therapy in recent years. The introduction of methods of intensive therapy has led to a significant decrease of lethality. A sufficient administration of potassium (not less than 200 mval/die) and the prevention of a cerebral oedema are actual demands for the improvement of the prognosis of diabetic coma.

Berlin↗
PubMed1976

[Non-ketosic hyperosmolar hyperglycemic coma. Case reports and therapeutic consideration].

Non-ketonic hyperosmolar hyperglycaemic coma (N.K.H.H.C.) is by no means uncommon in diabetes. Its picture includes sensorial depression, hyperglycaemia, hyperazotemia, marked dehydration and plasma hyperosmolarity. It is mostly found in elderly subjects with non-serious diabetes. Reference is made to 6 personal cases observed during a period of 14 months. The incidence of N.K.H.H.C. noted during this period was 2.2%; this was higher than that of ketoacidotic coma. Two patients died from hypovolaemic shock and one from septic complications. Three survived the episode. Treatment was based on three main points: high doses of insulin, though less than those employed for equal blood sugar levels in cases of ketoacidotic coma, hypotonic saline solutions, and correction of electrolyte imbalance. It is hoped that improved knowledge of the syndrome and, more particularly, earlier diagnosis and treatment, with lead to a reduction in the ta 50% mortality present associated with the disease.

Adult↗
PubMedDate not supplied

[Coma in type 2 diabete mellitus on metformin treatment].

Non traumatic coma in diabete mellitus has two origins : hypo- or hyperglycemia. Coma with hyperglycemia can be due to ketoacidosis, hyperosmolar state or lactic acidosis. The present observation reports on a type 2 diabete mellitus patient presenting with a coma while the patient was on metformin and glibenclamide treatment. On admission, biologicals tests showed major acidosis, hyperglycemia and hyperosmolarity. No metformine accumulation was demonstrated by analytical measure. In this case, the association of hyperosmolar state and metabolic acidosis prove the difficulty of the differential diagnosis.

Aged↗
PubMed1976

When seizures are complicated by coma.

Convulsions in elderly patients result from systemic biochemical or focal structural processes. These patients require a thorough evaluation, because idiopathic seizures are virtually unknown in this age group. Marginal circulatory and pulmonary function compromises central nervous system function, which can result in prolonged postictal coma. Furthermore, the patient's fragility can coma. Furthermore, the patient's fragility can complicate anticonvulsant therapy. The physician must be prepared to support the patient in prolonged postictal coma, since many patients can recover the preictal level of function.

Aged↗
PubMed2003

[Coma caused by hypermagnesemia in a pregnant woman complicated with HELLP syndrome].

This case report describes a pregnant woman with acute renal failure, caused by aggravation of HELLP syndrome, who developed coma induced by overdose of continuous magnesium sulfate administration for eclampsia. Before examination of serum concentration of magnesium, coma was suspected to be the result of brain vascular problem or brain infarction. Patient was treated in ICU and hemodialysis was started, and she recovered fully from abnormal neurological symptoms. This case illustrate that hypermagnesemia should be considered in the pregnant woman with coma at ER and ICU. Furthermore, the accurate information about the continuous administration of magnesium by previous clinician helped us to make correct diagnosis and to treat the patient successfully.

Adult↗
PubMed2003

[Acute coma in children: etiology, morbidity and mortality].

OBJECTIVE: An analysis was conducted on the etiology and the morbi-mortality of pediatric patients in acute coma, hospitalized at the Intensive Care Unit of Hospital Infantil Pequeno Príncipe (UTI-HIPP). METHOD: One hundred and four control sheets of children hospitalized at the UTI-HIPP and diagnosed as being in acute coma were analyzed. The Glasgow coma scale duly modified for children was used, with a score count equal to or lower than 8 points. The observation period was from March/98 to January/2001. All the supplementary exams as well as the neurological conditions of the patients when discharged were analyzed. RESULTS: The study comprised 104 children whose ages varied from 2 months to 13 years, with 57 (54.8%) of them being males. Hospital - stay time varied from 1 to 114 days, plus 3 cases in a persistent vegetative condition. As regards to etiology, 31 (29.8%) of the cases were due to meningo-encephalitis, 24 (23.1%) to an epileptic condition, 19 (18.3%) were toxic-metabolic, 16 (15.4%) to intra-cranial hypertension, 7 (6.7%) to shock/anoxia, 4 (3.8%) to an indeterminate etiology and 3(2.9%) were miscellaneous. Insofar as the clinical evolution of the children is concerned, 23 (22.1%) died, 32 (30.8%) evolved without any sequelae, 39 (37.5%) were discharged with neurological sequelae and for 10 (9.6%), no information is available. CONCLUSION: According to this study, one third of the children has died, one third presented neurological sequelae, and one third presented no further complications.

Adolescent↗
PubMed2003

Post-cardiorespiratory arrest beta-alpha coma: an unusual electroencephalographic phenomenon.

The presence of frontally-dominant alpha pattern in the EEG is common in patients with coma due to trauma, toxic-metabolic causes and following cardiorespiratory arrest. Diffuse beta activity following resuscitation after a cardiac arrest is not well recognized. We report a case of coma in a 3-year-old girl who had a cardiac arrest from which she was revived. Initial EEG showed diffuse beta activity, which later evolved to predominantly alpha activity. The possible mechanisms involved in the generation of such rhythms are discussed. Transition of EEG activity from faster to slower frequencies is suggested as an adverse prognostic factor in post-cardiorespiratory arrest coma.

Alpha Rhythm↗
PubMed2003

Correlation of regional metabolic rates of glucose with glasgow coma scale after traumatic brain injury.

UNLABELLED: After traumatic brain injury (TBI), subcortical white matter damage may induce a functional disconnection leading to a dissociation of regional cerebral metabolic rate of glucose (CMRglc) between the cerebral cortex and deeper brain regions. Therefore, thalamic and brain stem CMRglc may have a closer correlation than does the cerebral cortex with depth of coma after TBI. METHODS: Eleven adult healthy volunteers and 23 adult patients with TBI (median initial Glasgow Coma Scale score [GCSini], 8) underwent (18)F-FDG PET within 5 d after injury. The CMRglc of cortical areas (remote from hemorrhagic lesions), striatum, thalamus, brain stem, cerebellar cortex, and whole brain was compared with severity of injury and the level of consciousness evaluated using GCSini and the Glasgow Coma Scale score at the time of PET (GCSpet). RESULTS: The regional CMRglc of the brain stem is relatively unaffected by the TBI. Compared with healthy volunteers, TBI patients exhibited significantly depressed CMRglc in the striatum (3.9 +/- 1.3 vs. 5.1 +/- 0.9 mg/100 g/min, P < 0.05) and thalamus (3.1 +/- 1.0 vs. 4.3 +/- 0.9 mg/100 g/min, P < 0.05). CMRglc levels were not statistically lower in the cerebellum (2.9 +/- 0.8 vs. 3.5 +/- 0.8 mg/100 g/min, P = NS) and brain stem (2.5 +/- 0.5 vs. 2.6 +/- 0.5 mg/100 g/min, P = NS). However, compared between comatose and noncomatose patients, CMRglc values in the thalamus (2.7 +/- 0.7 vs. 3.6 +/- 1.2 mg/100 g/min, P < 0.05), brain stem (2.2 +/- 0.4 vs. 2.8 +/- 0.5 mg/100 g/min, P < 0.01), and cerebellar cortex (2.6 +/- 0.5 vs. 3.4 +/- 1.0 mg/100 g/min, P < 0.05) were significantly lower in comatose patients. When individual values of regional CMRglc were plotted against posttraumatic level of consciousness, CMRglc values for the thalamus, brain stem, and cerebellum significantly correlated with the level of consciousness at the time of PET (r = 0.58, P < 0.01; r = 0.66, P < 0.01; r = 0.64, P < 0.01, respectively). CT or MRI findings were normal for the analyzed structures except for 3 patients with diffuse axonal injury of the brain stem. The presence of shear injury was associated with poor GCSini (P < 0.05.) but was not related to GCSpet and brain stem CMRglc. CONCLUSION: A PET investigation using (18)F FDG demonstrated a significant difference in glucose metabolism in the thalamus, brain stem, and cerebellum between comatose and noncomatose patients acutely after TBI. The metabolic rate of glucose in these regions significantly correlated with the level of consciousness at the time of PET.

Adolescent↗
PubMedDate not supplied

[Role of calcium and magnesium ions in cerebrospinal fluid in alcoholic-traumatic coma].

The goal of investigation was to determine the role of calcium and magnesium ions in the cerebrospinal fluid in ethylic-traumatic coma. We measured the level of calcium in the cerebrospinal fluid within simple photometric test and the magnesium level within xylidyl blue photometric test. We found a high mortality in patients with high level of calcium in cerebrospinal fluid and low level of magnesium in cerebrospinal fluid. At patients with ethylic-traumatic coma high levels of calcium in cerebrospinal fluid are caused by the excitatory amino acids cascade and increased of hematoencephalic barrier permeability. Decreased levels of magnesium in cerebrospinal fluid are associated with convulsions and a poor prognosis of the patients. These analyses are very important for establishment of prognosis in patients with ethylic-traumatic coma.

Adult↗