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At least 901 records · Page 50Linked to original sources
PubMed1998

Generation of third-order spherical and coma aberrations by use of radically symmetrical fourth-order lenses.

We have extended the method of Alvarez [J. Am. Optom. Assoc. 49, 24 (1978)] to generate a variable magnitude of third-order spherical and/or coma aberration by using a combination of fourth-order plates with a magnification system. The technique, based on the crossed-cylinder aberroscope, is used to measure the wave-front aberration generated by the plates. The method has been applied to correct the third-order spherical aberration generated by an artificial eye as well as the coma produced by a progressive addition ophthalmic lens. The simplicity of the method and its relatively low cost make it attractive for partial correction of the aberrations of the eye.

Humans↗
PubMed1987

Effects of polylactic acid microcapsules containing prostaglandin E2 on the survival rates of grade II coma galactosamine induced fulminant hepatic failure rats.

Prostaglandin E2 was successfully incorporated into low molecular weight polylactic acid microcapsules. The size distribution of the microcapsules ranges from 20 to 50 micron. The microcapsules released drug continuously up to three days in vitro. The galactosamine induced fulminant hepatic failure rats model was used. 36 hours after the injection of galactosamine, those rats in grade II coma were chosen and pairs were matched for comparable degree of coma. Then each of the pair was randomly selected as control or treated. Each rat in the treated group received an intraperitoneal injection of PGE2 microcapsules containing 0.55 mg of PGE2. The control received blank PLA microcapsules only. The survival rate of the treated group was 40% compared to 10% in the control group. There was a significant (P less than 0.05) increase in the survival rate in the treated group.

Animals↗
PubMed1990

Transference of hepatic coma to normal rats from galactosamine treated donors by reverse plasma exchange.

It was possible by exchange transfusion to induce the same grade of hepatic coma in normal recipients as had occurred in donors which had previously been treated with D(+) galactosamine hydrochloride (HCl). The exchange transfusion was carried out by carotid arterial and jugular venous cannulation in conscious and unrestrained recipient rats. Thus, the coma inducing compounds generated as a consequence of acute hepatic failure, appear to circulate in the plasma for a considerable time after galactosamine-HCl is cleared and these substances are able to affect the nervous system in the presence of an intact and functioning normal liver.

Animals↗
PubMedDate not supplied

[Ketoacidosis coma auguring diabetes in black adults].

A particular form revealing diabetes mellitus in the black race is described: adult's inaugural ketoacidosis requiring a temporary insulin treatment, followed by a variable remission stage. We present in this work the clinical and evolutive characters of this coma inaugurating diabetes mellitus from twenty seven (27) patients of the metabolic diseases departement (CHU-Brazzaville). Among adult patients presenting a ketoacidosis coma, the prevalence rate of inaugural form is forty two percent (42%). The evolution is marked by a remission stage varying between six months and seven years.

Adult↗
PubMedDate not supplied

Complete recovery from fulminant hepatic failure with severe coma by living donor liver transplantation.

In Japan, living donor liver transplantation has been established as a therapeutic strategy for the rescue of terminal liver disease, including fulminant hepatic failure that shows no signs of recovery. We performed living donor liver transplantation for a subacute type fulminant hepatic failure patient, who had developed a hepatic coma of grade V (no right reflex, no response to pain stimuli). The electroencephalogram indicated almost flat waves. However, cranial computed tomography revealed that brain edema was not severe in this case. The recipient did not have hepatitis virus and had not taken medication that had been determined to cause hepatitis. The recipient was a 12-year-old boy, 165.5 cm in height and 45.5 kg in weight. The donor was his mother, who was 42 years old; her blood type, type B, was identical to that of the boy. The mother's right hepatic lobe was transplanted to her son (the recipient). The post-transplantation condition of recipient was quite excellent. He recovered consciousness 3 days after liver transplantation, and rapidly attained normal hepatic function. The donor was discharged on the 20th postoperative day without any problems. The recipient was discharged on the 79th postoperative day without any neurological deficits. This case suggests that deep coma without electroencephalogram waves may not be a contraindication for living donor liver transplantation in fulminant hepatic failure patients, if the brain edema is not severe.

Adult↗
PubMed1992

Clinical effects of a sorbent suspension dialysis system in treatment of hepatic coma (the BioLogic-DT).

Fifteen patients with acute deterioration of liver function, high serum ammonium, and an average coma level of 3.9 were identified. Eleven of the patients were on respirator support, and eleven had kidney failure pursuant to the liver failure. The patients were treated for 8-12 hours daily with the BioLogic-DT system, in which membranes of a cellulosic plate dialyzer actively pump blood through a single access at over 200 ml/min, and the dialysate contains a suspension of powdered activated charcoal (300,000 square meters surface area) and cation exchanger (160 meq capacity). No anticoagulant was used. In spite of the declining condition of the patients prior to treatment, there was a statistically significant improvement in neurologic status during individual treatments, and a positive trend over 1-12 (average four) daily treatments. Four patients recovered liver function and another four improved enough to receive a liver transplant operation. The BioLogic-DT system appears to be safe in treatment of patients with hepatic insufficiency and coma. The neurologic improvement of these patients indicates that many toxins of hepatic failure are dialyzable across cellulosic membranes and bound by charcoal.

Acute Disease↗
PubMed1990

[Complications of hepatic coma in liver cirrhosis].

59 patients with exogenous liver coma in state III-IV were treated from 1980 to 1989 in our clinic. Incidence and complications in these patients were evaluated retrospectively. The most frequent eliciting factors were gastrointestinal bleeding, infections and acute alcohol excess, more than 2/3 of them having severe portal hypertension with ascites and esophageal varices at the time. Altogether 55 of the 59 liver coma patients died. The most important complications were, beside bleeding and infections, disturbances of the renal function and of the coagulation. Severe acute or chronic liver injury is often associated with multiorgan failure.

Blood Coagulation Tests↗
PubMed1985

Nutritional goals from COMA and NACNE: how can they be achieved?

A simple way of altering the average British diet to make it comply with the short-term NACNE nutritional goals was discovered by comparing the diet of a cross-section of Cambridge adults with that of a subgroup whose diet approached the desired objectives. Between 1977 and 1979, 105 men and 112 women aged 18-57 completed 7-day semi-weighed records of food consumption. Although no subject achieved all of the NACNE or COMA goals, seven men and three women had diets in which fat provided less than 35 per cent of energy, alcohol less than 10 percent, with fibre more than 20 g/day; total sugars provided 25 per cent of energy. When these diets were compared with those of the rest of the sample (excluding diets where alcohol provided more than 10 per cent of energy), it was seen that men and women in the low-fat, high-fibre group ate more white bread, high-fibre breakfast cereals, low-fat meat dishes, and vegetables, and less brown bread, biscuits, eggs, poultry and fried fish. Only small changes were needed to make the average Cambridge diet consistent with the short-term NACNE goals for fat and fibre. Achieving the COMA or long-term NACNE goals will require more radical change, based on strategies to provide the necessary foodstuffs and nutrition education to allow informed individual choice.

Adolescent↗
PubMed1987

[Effect of psychopharmacotherapy on the course of forced insulin-coma treatment of patients with paranoid schizophrenia].

The course of forced insulin-coma therapy in cases of preliminary employment of psychotropic drugs (mainly derivatives of phenothiazine or leponex) may be attended by variable forms of deviations including serious complications whereas they are not encountered in cases of treatment with haloperidol and pharmacologically similar long-acting drugs. These findings justify the employment, when necessary, of the above drugs in combination with forced insulin-coma therapy.

Adolescent↗
PubMed1977

[Changes in brain metabolism in hepatic coma].

After controlling the physiological parameters during 6 hours of experimental hepatic coma in Sprague-Dawley rats the results show 1. No shortage of brain energy supply of the four main cerebral energy reserves, the brain glycogen is significantly elevated, and the phosphocreatine, ATP and glucose unaltered. 2. No alterations in intermediates of the glycolytic pathway and the tricarboxylic acid cycle in brain tissue. 3. A highly significant decrease in the brain content of the "excitatory" transmitter amino acids glutamate and aspartate. These findings do not support the well-known hypothesis of BESSMAN and BESSMANN and later authors on the role of ammonia in the pathogenesis of hepatic coma.

Adenosine Triphosphate↗
PubMed1986

[Pathogenesis and therapy of hepatic coma].

Even today, there is a markedly high rate of lethality resulting from an acute or chronic failure of the liver function. The reason of this seems to be the still unknown pathogenesis of the hepatic coma. In general, therapeutical measures will involve medical treatment of single symptoms on the basis of empirically made experience. However, any success will primarily depend on an early recognition of the approaching lethal breakdown and on the corresponding therapeutical measures taken before the final stage has been reached. Studies on its pathogenesis have to focus mainly on changes affecting the structure of the amino acid in the serum, in particular as regards the differences of the molecular ratio between aromatic and ramified-chain amino acids. The increased amount of serum ammonia does not seem to have major influence on the genesis of hepatic encephalopathy as has previously been assumed for a long time. Any treatment has to set in early, preferably in the General Department, as approximately 60% of cerebral malfunctions can already be registered in a zero coma state. Measures will involve detoxification, parental nutrition as well as substitution of such liver-generated substances as are not sufficiently produced at that stage. Any worked-out therapeutical scheme ought to be handled in a most flexible way in order to allow for an immediate response to the sometimes fast-changing clinical symptoms.

Combined Modality Therapy↗
PubMed1975

[Cerebral manifestations in the hepatic coma syndrome (author's transl)].

The pathogenesis of hepatic encephalopathy has been investigated in a two-stage devascularization model in the rat with portavacal shunt and hepatic artery ligation. There is a significant increase in brain octopamine and phenylethanolamine and a decrease in brain norepinephrine (NE) 6 to 9 hours after hepatic artery ligation. The depletion of NE seems the sequel of diminished synthesis in the presence of an unaltered turnover rate, due to a blockade of tyrosine hydroxylase either by accumulation of false neurochemical transmitters or by phenylalanine. It is most marked in the cortex and midbrain. The high-energy phosphate compounds, ATP, phosphocreatine and glucose-6-phosphate are not diminished in hepatic coma, nor is glucose, indicating that other mechanism are involved in the pathogenesis of metabolic state by the increased ammonia level. "intestinal sterilization" and total colectomy have no significant effect on the ammonia level, but cause a decrease in the level or aromatic precursor amino acids in the plasma and brain, with normalization of the level of cerebral transmitters. These results permit the formulation of a unified concept of the hepatic coma syndrome and its clinical manifestations such as flapping tremor, the hyperdynamic cardiovascular state and the hepatorenal syndrome. Moreover, they form the basis for the introduction of a new therapeutic principle in the management of hepatic encephalopathy by L-dopa or modified amino acid solutions, which act by altering the central and peripheral neurotransmitters.

Animals↗
PubMed1977

[Effect of exchange transfusion on the plasma amino acid concentration in hepatic coma].

Exchange transfusion (ET) were made twice on a 22 year old patient with fulminant hepatitis and hepatic coma. The influence of the ET on the plasma amino acids (PAA) was examined. The 1. ET reduced the concentration of the total PAA from 10,023 to 7,152 mugmol/l (about 28.6%) and the 2. ET from 11,770 to 9,706 mugmol/l (about 17.5%). Three hours after the 1. ET the concentration of the total PAA has passed over the prevalue and after the 2. ET has nearly reached it. The influence of both ET on the concentration of the individual PAA was very different (- 47.9% to + 71.2% after the 1. ET and - 32.9% to + 41.8% after the 2. ET respectively). Therefor the ET seems to be not a suitable method to reduce the pathologic concentration of the PAA in the hepatic coma.

Adult↗
PubMed1979

[Activity of coagulation factors in liver coma caused by viral hepatitis].

Coagulation studies were performed on 8 patients with acute liver failure from viral hepatitis. Four died and four recovered. At the time of development of coma, levels of clotting factors resulted markedly reduced in all cases and were not of value as a prognostic index. Subsequent serial determinations (every 8 hours) during the evolution of coma showed that prothrombin activity and levels of factor I, II, V and X were not correlated with clinical conditions, most probably owing to the influence of the administration of blood and blood components. Of all coagulation tests, the assay of factor VII, which has the shortest half-life, appeared the most reliable index of hepatic synthetic function at a particular point in time.

Adolescent↗
PubMed1983

[Liver coma with fatal course in 2 children under long-term antiepileptic therapy].

This is a report of two non related children who died after antiepileptic therapy for years in hepatic coma. In both children no other cause for hepatic failure could be found than treatment with anticonvulsive drugs. In both cases family history was interesting. Unexplained deaths in early infancy in the family of the girl, a carbamyl phosphate synthetase deficiency in the family of the boy, whose grandfather could have been heterozygote for this disturbance. It is supposed that heterozygotes for inborn errors of ammonia metabolism tolerate antiepileptic therapy worse showing increased hepatodiagnostic parameters, even necrosis of hepar and hepatic coma. In future examinations of the concerned families are suggested if disturbances of liver function are observed.

Adult↗
PubMed1977

[Pathology of liver failure and hepatic coma (author's transl)].

Liver failure and hepatic coma present with various clinical and morphological counterparts. While fulminant viral hepatitis is the most common cause of acute liver failure, liver cirrhosis with vascular bypass most often is responsible for the hepatic coma in chronic diseases. Prognosis is mainly determined by the extent of liver cell necrosis and regeneration, provided extrahepatic complications do not cause death. Prognosis can best be judged by stereology of liver biopsies and determination of the alpha-fetoprotein.

Alcoholism↗
PubMed1982

[Disorders of kidney function in hepatic coma].

Renal function was evaluated in 80 patients with hepatic coma stage III-IV (24 patients had acute fulminant hepatic failure, 48 patients chronic hepatic failure, 8 patients had a mixed form). Urea, creatinine and electrolytes were measured in plasma and urine as well as creatinine clearance and sodium/potassium ratio in urine. Renal failure was defined as an increase of serum creatinine above 3 mg/dl. In 15 of the 24 patients with fulminant hepatic failure creatinine clearance was reduced; hyperaldosteronism was present in 13 cases; in 2 patients there was necrosis of the tubulus, in 9 patients overt renal failure. In patients with chronic hepatic failure creatinine clearance was pathological in 36 cases, hyperaldosteronism was diagnosed in 23 cases and necrosis of renal tubules in 3 cases; 8 patients had overt renal failure. In the group with the mixed form of hepatic coma creatinine clearance was pathological in 3 cases, in 6 cases hyperaldosteronism was diagnosed; necrosis of the tubules could not be found in this group; 4 patients had overt renal failure. It is suggested that for treatment of this condition dopamine should be given prophylactically as well as intravenous sodium and water substitution.

Acute Kidney Injury↗