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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parenteral realimentation in the patient with severely impaired nutrition is sometimes associated with the development of a metabolic encephalopathy with coma. The onset of this complication is sudden. The coma is deep, accompanied by signs of neuromuscular hyperexcitability and very marked hyperventilation. It generally regresses rapidly, without sequellae. The onset of such a realimentation coma should be feared in the presence of a certain combination of conditions : severely impaired nutrition, parenteral alimentation with a high level of nitrogen and calories, transfer to the anabolic phase (perfect carbohydrate utilisation, fall in blood phosphate levels with hypophosphaturia, sometimes very marked positivisation of nitrogen balance) and, sometimes, mild premonitory clinical signs. The relationship between this type of complication and hypophosphoraemia is quite definite, but the fall in serum phosphates would not appear to be directly responsible for the coma. The exact mechanism is not known. In order to avoid such complications, great caution should be observed in both the quality as well as the quantity of the intake, as well as in the clinical and laboratory surveillance of the malnourished patient undergoing realimentation.
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PMID:[Comas of realimentation]. 2 97

Sepsis is a major catabolic insult resulting in modifications in carbohydrate and fat energy metabolism, and leading to increased muscle breakdown and nitrogen loss. Insulin resistance, which develops in sepsis, decreases glucose utilization, but plasma insulin levels are sufficiently elevated to prevent lipolysis, resulting in a further energy deficit. The availability of fuels in sepsis is therefore limited, and the body resorts to muscle breakdown, gluconeogenesis, and amino acid oxidation for energy supply. Previous work has not defined, however, the exact alterations in amino acid metabolism. Therefore, the following studies were undertaken. Blood samples were drawn from fifteen patients in whom the diagnosis of sepsis was clinically established; the samples were analyzed for amino acid, beta-hydroxyphenylethanolamines, glucose, insulin and glucagon concentrations. The plasma amino acid pattern observed was characterized by an increase in total amino acid content, due mainly to high levels of the aromatic amino acids (phenylalanine and tyrosine) and the sulfur-containing amino acids (taurine, cystine and methionine). Alanine, aspartic acid, glutamic acid and proline were also elevated, but to a lesser degree. The branched chain amino acids (valine, leucine and isoleucine) were within normal limits, as were glycine, serine, threonine, lysine, histidine and tryptophan. Those patients who did not survive sepsis had higher levels of aromatic and sulfur-containing amino acids as compared to those patients surviving sepsis. On the other hand, those patients surviving sepsis had higher levels of alanine and the branched chain amino acids. In a second group of five patients with overwhelming sepsis accompanied by a state of metabolic encephalopathy, a parenteral nutrition solution consisting of 23% dextrose, and an amino acid formulation enriched with branched chain amino acids was administered. In these five patients, normalization of the plasma amino acid pattern and reversal of encephalopathy was observed. The following sequence of events may be postulated: The septic patient develops insulin resistance in the peripheral tissues, primarily muscle, while the adipose tissue is much less affected. The insulin resistance and the inability to utilize fat leads to increased muscle proteolysis. Muscle breakdown results in release into the blood of enormous amounts of various amino acids; the muscle itself is able to oxidize the branched chain amino acids, supplying the muscles' own energy requirements and alanine for gluconeogenesis. The extensive muscle proteolysis coupled with relative hepatic insufficiency occurring early in sepsis results in the appearance in the plasma of high levels of most of the amino acids present in muscle, particularly the aromatic and the sulfur-containing amino acids. The outcome of patients with sepsis might be positively affected by combined therapy with glucose, insulin and branched chain amino acids.
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PMID:Amino acid derangements in patients with sepsis: treatment with branched chain amino acid rich infusions. 9 98

Enteral hyperalimentation in four patients with severe alcoholic hepatitis and anorexia increased spontaneous food intake, increased their nitrogen balance and the patients improved clinically. Seven patients with alcoholic hepatitis, who were clinically ill and able to eat only 410-1,100 calories per day, were given a 900 mosM/l. parenteral "hyperalimentation" solution by a peripheral vein (P-900). The intravenous nutrition provided daily 51.6-77.4 gm. amino acids in addition to oral intake. All patients improved. None developed detectable encephalopathy after 16-42 days of P-900 therapy. Five additional patients had ascites and alcoholic hepatitis. The daily infusion of 2,000 ml. P-900 was not associated with hyponatremia, renal failure or encephalopathy in four of these five patients who improved and continued their diuresis. P-900 therapy was discontinued in one because of progressive hyponatremia. The observations indicate that over and above the maximum tolerable oral nutrition, intravenous nutrition can be effectively utilized by clinically ill, jaundiced patients with alcoholic hepatitis without precipitating encephalopathy or interference with standard therapy of ascites.
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PMID:Hyperalimentation in alcoholic hepatitis. 11 34

Pulmonary function and oxygen transfer was studied in five patients with cirrhosis of the liver and different degrees of portasystemic encephalopathy. Four patients were restudied after a change in CNS function. The contribution of various parameters of pulmonary gas exchange to the unsaturation found was evaluated employing the graphic analysis described by King and Briscoe. The following results were obtained: (1) there was no inequality of ventilation as judged by a nitrogen washout study; (2) a large true venous admixture was found in all patients; (3) in four patients studied twice venous admixture was larger when mean EEG frequency was lower; (4) besides the true venous admixture a low overall D/Q ratio was an important factor contributing to unsaturation in most cases; (5) in some cases a decreased overall V/Q ratio contributed to the unsaturation. This decreased V/Q ratio appeared to be due to an increase in pulmonary perfusion without a concomitant rise in ventilation. Changes in pulmonary perfusion pathways are suggested as the most likely cause of the defect in oxygen transfer found in patients with cirrhosis.
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PMID:Pulmonary function studies and oxygen transfer in patients with liver cirrhosis and different degree of portasystemic encephalopathy. 23 51

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).
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PMID:Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. 50 43

A midline stereotaxic lesion in rats destroying the periventricular tissue (lamina terminalis and preoptic-anterior hypothalamic periventricular stratum) surrounding the anteroventral third ventricle (AV3V) produces adipsia without other marked behavioral changes. Although food consumption is reduced in animals rendered adipsic by the lesion, feeding continued and intake is comparable to that of water-deprived-sham-lesioned animals. About half the rats recover drinking after a period of adipsia, but the others never resume water intake and become moribund. An analysis of urinary output indicates that adipsic animals fail to reduce urine volume and continue to elaborate an inappropriately dilute urine. The periventricular lesion-induced adipsia without compensating antidiuresis produces a significant rise in plasma protein, sodium, osmolality, and urea nitrogen which if untreated often results in acute encephalopathy leading to death. These data suggest that preoptic-anterior hypothalamic periventricular tissue houses vital neural elements which function in the modulation of water ingestive and conservation mechanisms directed at the maintenance of body fluid homeostasis.
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PMID:Periventricular preoptic-hypothalamus is vital for thirst and normal water economy. 62 68

Blood substrate and hormone concentration were determined in 16 children with Reye syndrome prior to and following administration of hypertonic glucose. Baseline concentrations of lactate, pyruvate, alanine, glutamine, glutamate, proline, hydroxyproline, lysine, and aspartate were elevated (p less than 0.01), whereas citrulline and arginine were low. All substrate concentrations were below or within the normal range following 36 hours of therapy except those of lactate, pyruvate, and aspartate. Urea nitrogen excretion was reduced (p less than 0.05) on the second day of therapy. Plasma concentrations of insulin and growth hormone increased and glucagon decreased during the first day. Cortisol remained elevated throughout the study period. We conclude that the high circulating concentrations of substrates are the result of both increased mobilization and decreased clearance and that hypertonic glucose infusion suppresses substrate mobilization. A primary abnormality of the mitochondria could explain the metabolic perturbations that occurred. A possible relationship between the encephalopathy in this disorder and an insult to both brain and brain capillary mitochondria is discussed.
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PMID:Metabolic response to hypertonic glucose administration in Reye syndrome. 66 61

Forty-three patients with decompensated alcoholic liver disease and ascites of recent onset were randomized to salt and water restriction alone (control group) or to salt and water restriction plus diuretics (diuresis group). The two treatment groups were comparable in clinical findings and laboratory results. Seven patients in the control group and 5 patients in the diuresis group died during the acute illness. Weight loss was more marked and the disappearance of ascites more common in those given diuretics. A modest decrease in serum sodium and increase in serum potassium, and readily reversible elevations of blood urea nitrogen were noted in the diuresis group. Eight patients in each treatment group developed either the hepatorenal syndrome, marked electrolyte abnormalities, or encephalopathy. Diuresis can be accomplished in these critically ill patients without serious complications that can be attributed to the diuretic treatment.
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PMID:Complications of diuresis in the alcoholic patient with ascites: a controlled trial. 89 52

Two cases of methane asphyxia occurring in two boys (age 11 and 12 years) who were found at the bottom of a 37-ft (11.1-m)-deep sewer shaft are described. Attempted resuscitation of the first patient was unsuccessful and achieved only temporary stabilization of the second, who died 48 h after his discovery. Autopsies revealed relatively minor multifocal traumatic injuries, with evidence of hypoxic-ischemic encephalopathy in the patient who survived for 2 days. Subsequent analysis of gas in the shaft revealed 21% oxygen at the surface, 14.3% at a depth of 5 ft (1.5 m), and only 4.8% at depths of 10 ft (3 m) and below. Other gases detected at the lower levels were methane, nitrogen, and carbon dioxide (4.3%). These cases demonstrate the value of atmospheric gas analysis in cases of possible methane asphyxia in confirming the presence of methane and in demonstrating levels of oxygen below that necessary to support life.
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PMID:Death scene gas analysis in suspected methane asphyxia. 815 65

Hepatic encephalopathy is a neuropsychiatric syndrome, which can occur in the clinical course of acute (fulminant) or chronic hepatic failure of various aetiology; reversible metabolic abnormalities without neuronal structural changes are frequently found in this condition. High blood ammonia levels, an imbalance between plasma concentrations of branched-chain and aromatic amino acids, false neurotransmitters and neurotransmitters receptor changes in CNS are the commonly recognized pathogenetic mechanism of this syndrome. Protein malnutrition is a frequent occurrence in liver cirrhosis, especially of alcoholic aetiology. High protein diets may precipitate hepatic encephalopathy; protein restriction leads to malnutrition and enhances a negative nitrogen balance. Several clinical studies have shown that vegetable proteins are tolerated better than animal in patients with liver cirrhosis and chronic portal-systemic encephalopathy: encephalopathy index is usually lower after vegetable-protein than animal-protein diet. The favourable therapeutic effect of vegetable diets on nitrogen metabolism can be mainly accounted for by the increased intake of dietary fibers and increased incorporation and elimination of nitrogen in fecal bacteria. Mixture of amino acids enriched with branched-chain amino-acids may contribute to maintain a positive nitrogen balance and minimize muscle wasting in cirrhotics.
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PMID:[The dietary protein contribution and hepatic encephalopathy in cirrhosis]. 162 17


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