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PubMed1987

[Myxedema coma with hypervasopressinism. 2 cases].

Hyponatremia is usual during myxedema coma. Hereafter we report two cases with increased plasma arginine vasopressin (AVP). Patients were admitted because of hypothyroid coma. In each case, there was an hyponatremia with normal urine sodium and low serum osmolality. Renal function was normal. On hormonal results, primary hypothyroidism was evident. Plasma AVP was increased. The plasma cortisol of one patient was high. Immediate therapy associated: water restriction, hypertonic saline infusion, furosemide, oral thyroid hormones with low doses. On the fourth day, conscience improved obviously. Natremia and plasma AVP went back to normal state before returning to euthyroid state. Patients went on improving along with normalizing thyroid status. Hyponatremia can be a serious sign of hypothyroidism. In case of myxedema coma with hyponatremia, clinical improvement seems to be related to fast correction of water and electrolyte disturbances and we prefer to give low doses of thyroid hormones at first. The hyponatremia and increased plasma AVP mechanisms are complex. However, in each of these cases, plasma AVP come back to normal before returning to euthyroid state. In one case, high plasma cortisol level rules out adrenal insufficiency as causal mechanism of electrolyte disorders.

Aged↗
PubMed1987

Spindle coma in viral encephalitis.

Our patient's EEG evolved from the spindle coma pattern to normality in parallel with his clinical improvement. This clinical and EEG evolution has been described previously, and emphasizes the heterogeneity of the spindle pattern. The initial focal asymmetry implied focal cerebral abnormality, and was one of the clinical findings favoring HSV encephalitis in the absence of radiologic or pathologic support. The ability of partially-damaged cerebral cortex to express spindle activity is well-described with various cerebral lesions, as is the spindle coma pattern after intoxication. We are not aware of a previous report with HSV or other encephalitis, but an infectious etiology could be suspected in two patients of Hansotia et al. and is conceivable in the three comatose patients of Britt in whom no diagnosis could be established. In such cases, the pathophysiology of the spindle coma pattern is likely to involve an aberrant cortical response to normal reticular formation input and thalamic spindle pacemakers.

Adolescent↗
PubMed1984

[Clinical and prognostic evaluation of post-traumatic coma according to the level of brain stem injury].

On the grounds of studies carried out in the last ten years, the authors criticize the usual classification of comas and question the Glasgow scale (opening of eyes, verbal answer, motor response). Their description of brain stem injury by axial herniation and explanation of the role of diffuse encephalic lesions causing intracranial hypertension is based upon anatomo-clinical findings and results of investigations in comatose patients with head injury. For prognostic purposes, a simple and fairly reliable classification of post-traumatic comas is proposed. Comas are divided into five stages of rostro-caudal destructuration (cortico-sub-cortical, diencephalic, meso-diencephalic, mesencephalic and pontic) by studying the response to pain (unadapted, adapted, absent) and four brain stem reflexes (fronto-orbicular, vertical and horizontal oculocephalic, light reflexes).

Brain Injuries↗
PubMed1983

Alcoholic coma and some associated conditions.

The diagnosis of alcoholic coma is made only when there is a high blood alcohol level and signs of bilateral cortical dysfunction, without focal neurologic signs, and when all other metabolic and structural causes of coma have been ruled out. The ethanol-induced hypoglycemic coma of youth appears to result from the failure of gluconeogenesis to release glucose into the bloodstream. If the hypoglycemia is not immediately corrected, permanent and possibly lethal brain damage will result.

Alcoholic Intoxication↗
PubMed1983

[Course and outcome of severe traumatic coma].

This study will consider the course and final outcome of severe traumatic coma (Glasgow coma scale score 5-3 at admission). Intensive rehabilitation programs aimed at functional recovery must be undertaken from the very beginning. The importance of retraining of axial motricity is stressed. Successive stages of evolution and various neurological syndromes disclosed during the awakening period are described. Even in the case of these very severe brain injuries, a considerable amount of recovery is possible and leads to a normal socio-economic status in 62% of the cases. 22% however will remain bound to some type of sheltered life. Functional outcome is not related to the depth of initial coma but rather to the length of comatose period. It can be safely predicted only at the awakening phase, the neurological status reached at this time reflecting rather well the overall extent and severity of brain lesions. Neurophysiological mechanisms likely to support the functional recovery after this type of trauma are discussed.

Adult↗
PubMed1983

Long-term outcome of children with severe head trauma and prolonged coma.

Forty-six children with significant head trauma who remained in coma more than 24 hours were the subjects of this long-term outcome study. Twelve (38%) died. The average length of coma in the 34 survivors was 15.5 days. Follow-up ranged from 9 months to 4 years (mean 21 months). Twenty-nine percent of the survivors were normal at follow-up. An additional 53% had mild cognitive or behavioral problems, but 61% of these had evidence of similar problems prior to the injury. Nine percent of survivors had motor residua but normal intellect. Nine percent had severe intellectual and motor problems. Children less than 2 years of age had a worse outcome. Despite severe injury and prolonged coma after head trauma, most children do well. Intensive medical and surgical care increases the rate of survival and does not result in a large number of severely disabled survivors.

Adolescent↗
PubMed1981

Barbiturate-induced coma to protect against cerebral ischemia and increased intracranial pressure.

The use of barbiturates to induce coma as a means of extending the period of reversible cerebral ischemia is reviewed. Barbiturate use in patients who had had strokes or were undergoing aneurysm surgery was initially encouraging. In uncontrolled feasibility trials in patients with cardiopulmonary arrest or in deep coma, 40 patients received 10 mg/kg thiopental sodium by i.v. push followed by 20 mg/kg thiopental sodium i.v. over the next 30 minutes; 60% of these patients regained consciousness. In a subgroup of 22 patients who had ischemia normally associated with a 90% mortality rate, 14 recovered completely. In the largest clinical trial, 45 patients with severe head injury and elevated intracranial pressure received 3--5 mg/kg pentobarbital over 10--20 minutes. A serum barbiturate level of 2.5--4.0 mg/dl was maintained for 14 days, and 30% of these patients recovered but with neurologic deficits. Other results in stroke and drowning victims were not as encouraging. It is concluded that barbiturate therapy is beneficial in the lowering of intracranial pressure. Focal and global cerebral ischemia have been shown amenable to barbiturate therapy in isolated cases. The prophylactic use of barbiturates in surgical procedures requiring focal cerebral anoxia appears to be beneficial. Controlled trials of the use of barbiturate-induced coma are clearly indicated.

Animals↗
PubMed1993

[Can coma and awakening be evoked in infants?].

This question occurred to me when I had the opportunity to consult an hospitalized nursling in Neonate Unit. I felt him to look like oldest children considered as being in coma. Coma diagnosis has not been evoked neither for him nor for other babies I had to know during their neonate hospitalization. They were described as somnolent, sleepy, flaccid. It seems that coma state could not be considered during their first weeks of life. This difference of impression appeared to me as interesting to question. What possibilities of relations with the nursling does this imply?

Coma↗
PubMed1996

Partial central diabetes insipidus complicating nonketotic hyperglycemic hyperosmolar coma.

Nonketotic hyperglycemic hyperosmolar coma is an uncommon, but significant, complication of type II diabetes mellitus with a high overall mortality rate. Treatment of this entity is controversial but mandates aggressive fluid resuscitation and strict control of serum glucose levels. In the patient described, nonketotic hyperglycemic hyperosmolar coma complicated by diabetes insipidus was successfully treated with desmopressin acetate. To the authors' knowledge, this is the first reported case of nonketotic hyperglycemic hyperosmolar coma associated with partial central diabetes insipidus.

Aged↗
PubMed1996

[Evaluation of prognosis in purulent meningitis-myelitis based on the Glasgow Coma Scale].

We presented data from the investigation of the usefulness of the Glasgow Coma Scale in predicting the outcome of bacterial meningitis. Patients who aggregated high Glasgow Coma Scale scores had a good prognosis, whereas those patients with low scores had a very poor prognosis, inspite of this limitation the Glasgow Coma Scale seems to be a valuable supplement to the physical examination of patients with bacterial meningitis and may help in predicting the outcome of the disease.

Adult↗
PubMed1997

[The evaluation of a newborn in a coma].

Coma is differentiated from sleep by the absence of a normal arousal response and from death by the presence of heart beats and the absence of brain death criteria. Most causes of coma are readily diagnosed and treated. Others require a test whose results are not immediately available, transportation or a risky procedure and empirical treatment has to be considered. In addition to treating the cause of coma, treatment of the systemic and neurological causes of secondary brain damage is paramount.

Cerebral Hemorrhage↗
PubMed1998

Is use of mechanical ventilation a reasonable proxy indicator for coma among Medicare patients hospitalized for acute stroke?

OBJECTIVE: To ascertain whether use of mechanical ventilation on admission to the hospital is a proxy indicator of coma (i.e., very severe stroke) among acute stroke patients. METHODS: A secondary analysis of data from a medical record review on a nationally representative sample of 2,824 Medicare patients, ages 65 years or older, who were hospitalized for stroke in 1982-1983 or 1985-1986 in 297 acute care hospitals in 30 areas within five geographically dispersed states. RESULTS: Use of mechanical ventilation on the first day of hospitalization was significantly associated with level of consciousness on admission: < 2 percent of noncomatose patients versus 17.5 percent of comatose (p < .001). With a high specificity and high likelihood ratio for a positive test, use of mechanical ventilation on the first day of hospitalization ruled-in coma. It was also significantly associated with severity of illness, prognostic indicators (i.e., admission through the emergency room, admission to intensive care, and having a "do-not-resuscitate" order written during the hospital stay), and with in-hospital death. Adjusting for patient demographics, stroke type, comorbidity, and process of care, early initiation of mechanical ventilation remained significantly associated with both coma and in-hospital death. CONCLUSIONS: A stroke patient's use of mechanical ventilation on the first day of hospitalization is a valid proxy indicator of level of consciousness.

Aged↗
PubMed1997

[Hypothyroid coma and thyrotoxic crisis].

Two clinical cases of endocrinologic emergency are presented: myxedema coma and thyrotoxic crisis. These are very severe situations with a high mortality rate. In myxedema coma it reaches 50% and in thyrotoxic crisis the range is between 25 and 30%. These entities are not the always present in mind because of their rarity. Consequently, they may well be undiagnosed. In our cases, the myxedema coma was initially diagnosed as brainstem stroke, and the hyperthyroidism was taken for concealed malignant tumor. The management of both situations is briefly commented.

Aged↗
PubMed1976

[Semiologic, biochemical and electrophysiologic analysis of the stages of apopleptic coma].

The paper contains some results of a comprehensive clinical, biochemical and electrophysiological study of 120 patients with different stages of an apoplectic coma. The authors studied the gas content, acid-base balance of the cranial blood inflow and outflow in the CSF and changes of EEG and EMG. It was shown that there were different levels of CNS lesions (cortico-subcortical, meso-diencephalic, meso-pontile and bulbar level) which corresponded to certain correlations between clinical, biochemical, EEG and EMG findings. The authors describe a classificational scheme of 4 stages of an apopletic coma. Special significance in the pathogenesis of a coma along with structural lesions in the different areas of the CNS is attached to metabolic disturbances and extracerebral factors (respiratory and circulatory disorders).

Acid-Base Equilibrium↗
PubMed2005

Juan Comas's summary history of the American association of physical anthropologists (1928-1968).

This translation of Juan Comas's Summary History of the American Association of Physical Anthropologists was originally published in Spanish by the Instituto Nacional de Antropología e Historia, Mexico, in 1969 (Departamento de Investigaciones Antropológicas, Publication 22). Physical anthropologists from North America and members of the American Association of Physical Anthropologists owe Juan Comas a debt of gratitude for having labored to produce this Summary History of the AAPA. There is much useful and interesting material in this document: extensive endnotes that are helpful to the historian of the profession; an appendix of the Journal issues where the proceedings of annual meetings can be found; a detailed listing of contributors of papers to annual meetings from 1930-1968; a warm acknowledgment and history of the contributions of the Wenner-Gren Foundation to biological anthropology; a history of the Yearbook of Physical Anthropology; and comments on the short-lived PA Newsletter. In addition, there are appendices with the founding AAPA Constitution and By-Laws from 1930 and as they existed in 1968. All of this synoptic information saves the reader with interests in the history of the AAPA considerable effort, especially when few university and college libraries have the full (old and new) series of the AJPA on their shelves. We have tried to provide a translation of Comas's history that is faithful to the original Spanish-language publication. In a few cases, we shortened sentences and applied a slightly more modern usage than was popular in the late 1960s.

Anthropology, Physical↗
PubMed1987

Evidence for methane and ammonia in the coma of comet P/Halley.

Methane and ammonia abundances in the coma of Halley are derived from Giotto IMS data using an Eulerian model of chemical and physical processes inside the contact surface to simulate Giotto HIS ion mass spectral data for mass-to-charge ratios (m/q) from 15 to 19. The ratio m/q = 19/18 as a function of distance from the nucleus is not reproduced by a model for a pure water coma. It is necessary to include the presence of NH3, and uniquely NH3, in coma gases in order to explain the data. A ratio of production rates Q(NH3)/Q(H2O) = 0.01-0.02 results in model values approximating the Giotto data. Methane is identified as the most probable source of the distinct peak at m/q = 15. The observations are fit best with Q(CH4)/Q(H2O) = 0.02. The chemical composition of the comet nucleus implied by these production rate ratios is unlike that of the outer planets. On the other hand, there are also significant differences from observations of gas phase interstellar material.

Ammonia↗
PubMed1982

Branched-chain amino acids vs lactulose in the treatment of hepatic coma: a controlled study.

A controlled study was carried out in two groups of 20 patients with cirrhosis of the liver and deep coma in order to compare the efficacy of intravenous branched-chain amino acid solutions in 20% glucose (group A) vs lactulose plus glucose in isocaloric amount (group B). There were 3 drop-outs from each group. Plasma amino acids and ammonia were assayed at fixed intervals throughout the 10-day observation period. Routine tests were assayed daily. Complete mental recovery was obtained in 70% of patients in group A and in 47% in group B. The difference was not significant, likely due to the lack of placebo group. With the exception of free tryptophan/all competing amino acids ratio, the modifications in plasma amino acid levels showed no correlation with the clinical course under either treatment. Ammonia, like free tryptophan, decreased significantly upon mental recovery, paralleling the clinical course throughout the study. In conclusion, branched-chain amino acids are at least as effective as lactulose in deep hepatic coma. It is suggested that branched-chain amino acids may reverse coma either by competing with brain entry of the aromatic amino acid or by metabolically decreasing free tryptophan and ammonia.

Amino Acids↗
PubMed1985

Successful treatment of hepatic coma by a new artificial liver device in the pig.

In this study, we tested a new artificial liver device using liver pieces in 8-h hemoperfusion of comatous porcine blood and compared two alternative tissue preparations. Acute hepatic coma in the pigs was induced by complete devascularization of the liver. The animals were killed in stage IV coma (15-25 h after the operation), and 1 l blood was perfused over 200 g fresh or DMSO-preserved liver cubes. After the devascularization GOT, GPT, GLDH, AP, LDH, SDH, bilirubin, free fatty acid, and bile acid levels in serum increased progressively. Ammonia concentrations underwent a rapid increase in the first 9 h of coma development from 126.0 +/- 9.9 to 321.9 +/- 62.2 mumol/l. Most of the amino acids in serum were elevated and molar ratio of BCAA/AAA declined from 3.87 +/- 0.79 to 0.92 +/- 0.24. In the course of hemoperfusion ammonia was removed from the perfusate to 71% of the initial values using fresh and to 39% using preserved tissue. Correspondingly, there was an increase in urea concentrations. Amino acid metabolism was ameliorated during the perfusion; Fischer's quotient increased from 0.91 +/- 0.15 to 1.38 +/- 0.14 (fresh liver) and from 0.89 +/- 0.14 to 2.11 +/- 0.44 (preserved liver); neuroexcitatory amino acids Asp and Glu were markedly elevated. Energy charge of the liver cells increased and reached levels exceeding 0.5 in both experimental groups, a balanced energy metabolism was maintained and suggests active metabolization by the liver pieces. In comparison with fresh tissue, preserved liver cubes proved effective. We consider our artificial liver device capable of temporary hepatic support in acute necrosis of the liver and suppose that its efficiency can be potentiated by combining this system with other procedures.

Adenine Nucleotides↗