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At least 883 records · Page 49Linked to original sources
PubMed1984

Hypothermia and barbiturate coma for refractory status epilepticus.

Three pediatric patients with generalized status epilepticus unresponsive to therapy with conventional anticonvulsants were successfully treated with moderate hypothermia (30 degrees to 31 degrees C) and barbiturate coma with thiopental. All 3 patients were treated with thiopental at doses producing burst suppression or an isoelectric tracing on the EEG and thiopental and barbiturate levels were followed sequentially in the plasma. Continuous thiopental infusion rates of 5 to 55 mg/kg X h maintained burst suppression and correlated with plasma thiopental levels of 25 to 40 mg/dl. Total doses of thiopental used to obtain and maintain burst suppression ranged from 15 to 50 g over 48 to 120 h. In all 3 patients, control of the status epilepticus was obtained. Moderate hypothermia and thiopental barbiturate coma are indicated in patients with generalized tonic-clonic status epilepticus which cannot be controlled with standard anticonvulsant drug therapy. This regimen has the advantage that the patient can be managed in an ICU without the need for general anesthesia with volatile anesthetic agents.

Adolescent↗
PubMed1989

Detection of brain death in barbiturate coma: the dilemma of an intracranial pulse.

Patients treated with barbiturate coma for elevated intracranial pressure after head injury may suffer brain death. Since such patients have an iatrogenically induced absence of neurological function, brain death cannot be diagnosed clinically. Furthermore, as demonstrated by two of our patients, monitoring of intracranial pressure, even in the face of brain death, may show a low intracranial pressure and an intracranial pulse, suggesting the presence of adequate cerebral perfusion pressure and, therefore, brain viability. Under these circumstances, however, significant intracranial blood flow may be absent. Therefore, we suggest that a patient in barbiturate coma should undergo serial blood flow studies, even when the intracranial pressure is low and an intracranial pulse is present, to determine whether brain death has occurred.

Adult↗
PubMed1980

Hepatic coma after open heart surgery.

Fulminant hepatic failure has been reported in patients with chronic congestive heart failure. Two patients in whom jaundice and coma followed cardiac surgery were studied to find the possible etiology. Clinical, biochemical, and histologic evaluations revealed low cardiac output; elevated levels of bilirubin, lactic dehydrogenase, serum glutamic oxaloacetic transaminase, and alkaline phosphatase; prolonged prothrombin time; and centrizonal necrosis of hepatocytes with sinusoidal dilatation. No other possible causes of hapatic dysfunction and coma were identified. We conclude that acute postoperative congestive heart failure may cause fulminant hepatic failure and metabolic encephalopathy.

Acute Disease↗
PubMed2004

Successful treatment of a child with fulminant liver failure and coma caused by Amanita phalloides intoxication with albumin dialysis without liver transplantation.

FLF is a life-threatening disease. Hepatic coma exerts dramatic impact on patient survival. At present, LTx is the treatment modality of choice that provides significant improvement in outcome of most patients with FLF. Multiple attempts have been made to reduce mortality and improve the patient's condition. One of the new options is AD - MARS. We present the case of a 11-yr-old boy with FLF and hepatic coma who avoided the scheduled LTx because of rapid neurological and biochemical improvement immediately after three MARS sessions.

Amanita↗
PubMed1986

Hemodiafiltration treatment of deep hepatic coma by protein passing membrane: case report.

Based on the assumption that middle molecules that induce hepatic coma occur in the plasma of patients with fulminant hepatic failure (FHF), the authors have developed a hemodiafiltration (HDF) method using a large-pore poly(methylmethacrylate) (PMMA) membrane that allows proteins to pass through. PMMA HDF resulted in complete recovery of deep coma and long-term survival in a patient with severe FHF. Although a large-scale controlled trial is needed, PMMA HDF is believed to be promising as a future artificial liver support.

Adult↗
PubMed1976

In vitro polarographic studies of rat brain oxygen uptake in simulated uraemia and hepatic coma.

A polarographic technique has been used to study the oxygen uptake of rat brain homogenates incubated with metabolites known to accumulate in uraemia and hepatic coma. In general, results with individual metabolites were in agreement with those previously obtained with brain slices using the Warburg technique. Inhibition was induced at higher concentrations with urea, creatine, indoxysulphate, guanidine, dimethylamine hydrochloride, ammonium chloride, taurocholate, glycodeoxycholate, sodium deoxycholate, skalote and indole. Serum and ultrafiltrate from drowsy uraemic patients also caused inhibition, and this was reversed by renal dialysis. Similarly serum and ultrafiltrate from patients in hepatic coma inhibited oxygen uptake but in this instance reversal of the inhibition was not demonstrated following exchange blood transfusion to the patients.

Adenosine Diphosphate↗
PubMed1986

Brain cholecystokinin and vasoactive intestinal polypeptide: immunoreactivity in rabbits with hepatic coma.

Recent studies have suggested that decreased excitatory neurotransmission in the brain may contribute to the overall neural inhibition which characterizes the syndrome of hepatic encephalopathy (HE), and that vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK) may promote neural excitation in the brain. To determine if brain levels of these neuropeptides are altered in HE, measurements were made of the concentrations of immunoreactive VIP (iVIP) and immunoreactive CCK (iCCK) in cerebral cortex, cerebellum and hypothalamus isolated from normal rabbits and rabbits with galactosamin-induced hepatic coma. Hepatic coma was associated with reduced concentrations of iVIP, small molecular weight iCCK and large molecular weight iCCK in the cerebral cortex but not in the cerebellum or hypothalamus. These findings are compatible with decreased VIP- and CCK-mediated neural excitation occurring in the syndrome of HE.

Animals↗
PubMed1974

Alpha-ketoglutaramate: increased concentrations in the cerebrospinal fluid of patients in hepatic coma.

alpha-Ketoglutaramate, a deaminated metabolite of glutamine not previously identified in biological tissues, was measured in the cerebrospinal fluid of human subjects and found to be increased three- to tenfold in patients with hepatic coma. When perfused into the cerebral lateral ventricles of rats, alpha-ketoglutaramate (10 mM) depressed the animals' nocturnal locomotor activity, and at higher doses induced circling behavior and myoclonus. The concentration of alpha-ketoglutaramate in cerebrospinal fluid appears to be a reliable diagnostic indicator of hepatic coma, and its accumulation may contribute to the pathogenesis of this disease.

Amides↗
PubMed1997

Evidence for interacting gas flows and an extended volatile source distribution in the coma of comet C/1996 B2 (Hyakutake).

Images of comet C/1996 B2 (Hyakutake) taken during its close approach to Earth show differences in the distribution of gas and dust in the inner coma and reveal two arc-shaped molecular resonant emission features. The morphology of these features, as well as the apparent decoupling gas from dust in the inner coma, suggest that an extended region of icy grains surrounds the nucleus of Hyakutake and contributes substantially to the production of volatiles. Model simulations suggest the same conclusion and indicate that the brighter arc is explainable by the presence of a trailing condensation of ice-bearing granules with a rate of volatile production approximately 23 percent of that of the nucleus.

Cosmic Dust↗
PubMed1997

An inverse compton process for the excess diffuse EUV emission from the virgo and coma galaxy clusters

The excess extreme-ultraviolet (EUV) emission detected in the Virgo and Coma clusters is explained by inverse Compton scattering of cosmic microwave background photons, which are scattered by the relativistic electrons that account for the extended radio synchrotron emission of these clusters. The lower limits of the average magnetic fields of these clusters estimated from the EUV excess are close to the equipartition magnetic fields derived from radio observations, indicating that the electron energies and magnetic field energies might be close to equipartition. The excess emission suggests energy reservoirs of approximately 10(61) and approximately 10(60) ergs for the Coma and Virgo clusters, respectively.

Journal Article↗
PubMed1997

Radar detection of the nucleus and coma of comet hyakutake

Radar observations of comet Hyakutake (C/1996 B2) made at the Goldstone Deep Space Communications Complex in California have detected echoes from the nucleus and from large grains in the inner coma. The nucleus of this bright comet was estimated to be only 2 to 3 kilometers in diameter. Models of the coma echo indicate backscatter from porous, centimeter-size grains ejected anisotropically at velocities of tens of meters per second. The radar observations suggest that a comet's activity may be a poor indicator of its size and provide evidence that large grains constitute an important component of the mass loss from a typical active comet.

Journal Article↗
PubMed1992

Transcriptional regulation of Bacillus subtilis glucose starvation-inducible genes: control of gsiA by the ComP-ComA signal transduction system.

The Bacillus subtilis glucose starvation-inducible transcription units, gsiA and gsiB, were characterized by DNA sequencing, transcriptional mapping, mutational analysis, and expression in response to changes in environmental conditions. The gsiA operon was shown to consist of two genes, gsiAA and gsiAB, predicted to encode 44.9- and 4.8-kDa polypeptides, respectively. The gsiB locus contains a single cistron which encodes a protein of unusual structure; most of its amino acids are arranged in five highly conserved, tandemly repeated units of 20 amino acids. The 5' ends of gsiA and gsiB mRNAs were located by primer extension analysis; their locations suggest that both are transcribed by RNA polymerase containing sigma A. Expression of both gsiA and gsiB was induced by starvation for glucose or phosphate or by addition of decoyinine, but only gsiA was induced by exhaustion of nutrient broth or by amino acid starvation. Regulation of gsiA expression was shown to be dependent upon the two-component signal transduction system ComP-ComA, which also controls expression of genetic competence genes. Mutations in mecA bypassed the dependency of gsiA expression on ComA. Disruption of gsiA relieved glucose repression of sporulation but did not otherwise interfere with sporulation, development of competence, motility, or glucose starvation survival. We propose that gsiA and gsiB are members of an adaptive pathway of genes whose products are involved in responses to nutrient deprivation other than sporulation.

Amino Acid Sequence↗
PubMed1972

Acute hepatic coma successfully treated by extracorporeal baboon liver perfusions.

Two patients in deep hepatic coma due to fulminant viral hepatitis were treated by extracorporeal baboon liver perfusion after failing to respond to medical treatment and three consecutive exchange transfusions. Both patients recovered full consciousness after one liver perfusion, made a complete recovery, and were leading normal lives seven and eight months after treatment. Perfusions were maintained for 13(1/2) and 16(1/2) hours without complication, and neither clinical immunological reactions nor antibaboon serum antibodies developed as a result of treatment.Whereas normal consciousness could be restored only by liver perfusion, both exchange transfusion and liver perfusion were effective in clearing bilirubin and in raising the level of clotting factors. Extracorporeal baboon liver perfusion provides a safe and effective method for the treatment of acute hepatic coma.

Adolescent↗
PubMed1969

Management of hepatic coma complicating viral hepatitis.

The treatment is described of 17 patients with presumed viral hepatitis who developed hepatic coma unresponsive to standard conservative measures. Five patients were considered for treatment by exchange transfusion. Four were treated, with transient improvement in two, but all died. Nine patients were considered for treatment by heterologous liver perfusion. Six were treated, with transient improvement in two and complete recovery in one. The last patient remains well 12 months later. Dialysis in four patients had no effect on the coma; the addition of albumin to the dialysate did not increase the extraction of bilirubin. The clinical course in most cases was irregular. Complications were common, the most important being cerebral oedema with medullary coning, bleeding, bacterial infection, hypoglycaemia, and pancreatitis. Heterologous liver perfusion was the most efficient method of removing bilirubin. However, it is not yet clear whether it is more effective than exchange transfusion in the treatment of the patient.

Adolescent↗
PubMed1982

Hemoperfusion in diabetic coma.

Hemoperfusion on ionic exchange resins in the therapy of diabetic keto-acidosis (DKA) coma is proposed. Resins used are strong anionic resins in mixed form able to release bicarbonates and to trap ketoanions and organic anions in a stoichiometric manner. A series of trials in open circuit are performed in order to search for a suitable mixture of resins and to establish the amounts of HCO3- and ketoanions respectively released or entrapped. Therefore, ten simulated hemoperfusions in closed circuit systems were performed, utilizing cartridges containing 1,700 g of mixed resin (9% HCO3- form and 91% Cl- form). The results indicate that all side effects of bicarbonate i.v. therapy of DKA coma are avoided because of the smooth HCO3- administration to the patient. Furthermore, a good removal of ketoanions and organic acids is obtained without changing the blood osmolality.

Bicarbonates↗
PubMed2004

Compensation of corneal horizontal/vertical astigmatism, lateral coma, and spherical aberration by internal optics of the eye.

Both the anterior surface of the cornea and the internal optics (the posterior cornea, crystalline lens) contribute to the aberration of a wavefront passing through the eye. Artal, Guirao, Berrio, and Williams (2001) reported that the wavefront aberrations produced by the internal optics offset, or compensate for, the aberrations produced by the cornea to reduce ocular wavefront aberrations. We have investigated the wavefront aberrations of the cornea, internal optics, and complete eye on both the population and individual level to determine which aberrations are compensated and probable paths leading to that compensation. The corneal and ocular aberrations of 30 young subjects at relaxed accommodation were measured with the Topcon Wavefront Analyzer, which simultaneously measures refraction, corneal topography (videokeratoscope), and wavefront aberrations (Hartmann-Shack sensor). We found strong evidence for compensation of horizontal/vertical (H/V) astigmatism (Zernike term Z5) lateral coma (Z8) and spherical aberration (Z12). H/V astigmatism compensation is scaled for each individual, suggesting that it is actively determined by a fine-tuning process. Spherical aberration shows no individual compensation, suggesting that is a passive result of genetically determined physiology. Lateral coma shows individually scaled compensation, some of which may be attributable to eccentricity of the fovea.

Accommodation, Ocular↗
PubMed1983

A study of disseminated intravascular coagulopathy in hepatic coma complicating acute viral hepatitis.

Thirty cases of viral hepatitis with and without coma and 15 normal healthy age and sex matched controls were studied for disseminated intravascular coagulopathy (DIC). Cases of viral hepatitis with coma showed strong evidence of DIC in the form of increased plasma FDP (240 +/- 190.64 dilution), diminished fibrinogen half life (48.1 +/- 15.3 hours) and increased fractional catabolic rate (46.13 +/- 14.7% per day) with normal Euglobulin clot lysis time and reduced fibrinogen (147.33 +/- 43.5%) and platelet count (1.27 +/- 0.324 lakhs/cm.). The possible role of heparin in the reversal of coagulation abnormalities have been discussed.

Adult↗
PubMed1976

[Experience with the treatment of acute hepatic coma using extracorporeal perfusion of heterologous liver and exchange transfusion].

Extracorporeal pig liver perfusion was adopted in 2 patients with acute hepatic coma due to fulminant hepatitis. Exchange transfusion was used in a third patient, while a fourth was subjected to both procedures. A marked haematological improvement was noted in all cases. Yet, three patients died without showing any clinical benefit. In the fourth case, coma regressed and gradual improvement to the point of complete recovery was achieved. Liver perfusion and exchange transfusion in the same patient were attended by very different clinical effects, though each procedure produced a comparable improvement at the blood chemistry data. Careful analysis of the data suggests that the difference was attributable to discrepancies between the degree of tissue purification achieved.

Acute Disease↗