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

Numerous studies have shown that longterm oxygen therapy in hypoxaemic patients with chronic airflow obstruction (BPCO) is capable of improving the prognosis and decreasing the risk of cardio-respiratory decompensation; in addition sometimes physical capacity and intellectual capacity is improved. Another result often noted is a reduction in the mean hospital stay which corresponds to an improvement in the quality of life. A PaO2 constantly below 55 mmHg (7.3 kPa) is defined by the majority of authors as a precarious state. At this level even a small change in alveolar ventilation or disturbance of distribution would lead to an important fall in the oxygen content of the arterial blood. The stability of the PaO2 during the weeks of respiratory reeducation with specially controlled medical treatment, as well as the willing consent of the patient and his family, are indispensable conditions for the prescription of OLT. When hypoxaemia is of moderate severity (PaO2 between 50 and 60 mmHg (6.6-8 kPa), prolonged medical treatment (with abstention from tobacco) for at least two months is advised and a study of complementary criteria to further validate the indications for oxygen. Such features would include a worsening of the hypoxaemia during exercise of 30 to 40 watts (PaO2 less than 50 mmHg, 6.6 kPa), an elevated haematocrit (greater than 55%), a rise of the P (A-a)O2 (greater than 30 mmHg or 4 kPa), a nocturnal desaturation even in the absence of apnoea (oxyhaemoglobin saturation (SaO2) of less than 80% for more than 50% of the time asleep). Added to these criteria are the radiological, echographic and clinical signs of the effect of hypoxaemia on the pulmonary circulation. Frank pulmonary arterial hypertension observed in hypoxaemia of moderate severity when the PaO2 is in the region of 55 mmHg and is an argument for the prescription of OLT. Amongst the developing criteria, exacerbations of respiratory encephalopathy, intellectual deterioration, progressive wasting, permanent ventilatory embarrassment with tachypnoea, should be borne in mind as the occasion arises. A schedule of 18 hours per day (without stopping for more than 3 hours) is necessary to obtain an improved survival and places a great demand on patient co-operation and on their environment. A prolonged educational programme is required. To achieve such a schedule the use of portable oxygen may be justified so that patients can lead a normal social life.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Critical study of the indications for long-term oxygen therapy. Chronic obstructive bronchopneumopathies]. 314 Mar 16

Cerebral oxygen and glucose metabolism have been studied in 8 patients with biochemically defined mitochondrial myopathies and 7 normal control subjects using positron emission tomography. Four patients had myopathy alone and 4 had predominantly central nervous system (CNS) disease. Cerebral oxygen and glucose metabolism were measured concurrently in the two groups of patients with 15O, 11C and 18F labelled tracers and positron emission tomography (PET). Patients with major CNS disease showed an uncoupling of glucose and oxygen metabolism when compared with patients without cerebral disease and normal subjects. The mean ratio between oxygen and glucose utilization was 3.8 moles of oxygen per mole of glucose in patients with CNS disease, compared with 5.6 for controls and 6.4 for patients with myopathy alone. The altered stoichiometry in CNS cases indicates aerobic glycolysis to lactate and/or other intermediate metabolites. Patients with major CNS disease showed a 50% reduction in cerebral oxygen utilization compared with cerebrally unaffected patients and normal subjects. These findings indicate that in patients with a mitochondrial encephalopathy the defect identified in skeletal muscle is also expressed in the brain.
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PMID:The cerebral metabolism of glucose and oxygen measured with positron tomography in patients with mitochondrial diseases. 326 67

We examined the impact of pre-treatment with the calcium antagonist flunarizine on the development of hypoxic-ischemic brain injury in the immature rat. Unilateral carotid artery ligation and subsequent exposure to 2 hours of 8% oxygen in 7-day-old rats was used as a model for perinatal hypoxic-ischemic encephalopathy. This procedure leads to atrophy in the cerebral hemisphere ipsilateral to carotid occlusion, with prominent foci of neuronal infarction in the caudate-putamen (striatum). The morphologic injury develops after 1 1/2 hours of hypoxia; and there is an equivalent time threshold for duration of hypoxic exposure needed to acutely stimulate dopamine release in the ipsilateral striatum. Parenteral administration of 30 mg/kg of flunarizine before hypoxic exposure limited both the release of dopamine acutely and the extent of morphologic damage observed two weeks after the insult. Oral administration of 30 mg/kg of flunarizine in a different vehicle prevented morphologic damage but had no effect on stimulated dopamine release. The drug vehicle for the parenteral preparation also prevented tissue injury, but to a lesser degree than flunarizine. However the parenteral vehicle was equipotent with parenteral flunarizine in limiting acute stimulation of dopamine release. The results demonstrate that flunarizine has potent neuroprotective properties against morphologic brain injury from hypoxia-ischemia, acting by a mechanism which is independent of effects on dopamine release.
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PMID:Flunarizine limits hypoxia-ischemia induced morphologic injury in immature rat brain. 371 46

To evaluate the influence of necrotic liver tissue on the cerebral metabolism and cerebral function in acute liver failure, comparison was made between hepatectomy and total liver devascularization in pigs. In both groups the cerebral blood flow and glucose uptake were significantly decreased. The cerebral oxygen uptake was not reduced. The EEG frequency gradually fell from 12-14 Hz to 1-2 Hz, with intermittent and finally persistent flattening of cortical activity. The visual evoked potentials were unchanged throughout the observation period. The vascular autoregulation and the CO2-reactivity of cerebral circulation disappeared, indicating complete vasoparalysis. As no difference was found between the two groups, it is concluded that the encephalopathy was not due to intoxication from necrotic liver tissue in the abdominal cavity, but to deprivation of liver function.
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PMID:Cerebral flow and metabolism in experimental liver failure. A comparison between hepatectomy and total hepatic devascularization in pigs. 376 31

To obtain further evidence of tissue hypoxia in fulminant hepatic failure, we have measured the mixed venous lactate concentration and the acid-base status of 32 patients at the time of their admission, in grade III or IV encephalopathy. The mixed venous lactate was elevated in 26 of the 32 patients (median 5.0 mmol/l, range 0.8-21.1 mmol/l), and, in 17 patients, this was associated with evidence of a metabolic acidosis. Mixed venous lactate levels correlated inversely with the mean arterial pressure (r = 0.56, P less than 0.005), systemic vascular resistance (r = 0.62, P less than 0.001) and the oxygen extraction ratio (r = 0.44, P less than 0.02). The 17 patients with a raised mixed venous lactate and metabolic acidosis had a significantly reduced systemic vascular resistance and oxygen extraction ratio compared with the other 15 (median systemic vascular resistances 944 and 1710 dyne X s/cm5/m2, respectively, P less than 0.05, median oxygen extraction ratios 19 and 23%, respectively, P less than 0.05). Survival was markedly reduced in the patients with hyperlactataemia and a metabolic acidosis, and only one out of the 17 survived compared with 12 of the remaining 15, P = 0.0002. These results suggest that lactic acid accumulation may be in part the consequence of tissue hypoxia that develops as a result of arteriovenous shunting, reflected in the reduction in systemic vascular resistance. This tissue hypoxia may occur despite apparently adequate systemic blood pressure, flow and oxygenation.
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PMID:Lactic acidosis in fulminant hepatic failure. Some aspects of pathogenesis and prognosis. 393 11

To assess the adequacy of tissue oxygenation in fulminant hepatic failure, we measured arterial oxygen delivery, the affinity of hemoglobin for oxygen, mixed venous oxygen tension, and lactate concentration in 32 patients suffering grade IV encephalopathy. In the patients who died, median systemic vascular resistance and oxygen extraction ratio were significantly (p less than .005) lower than in those who survived (1268 vs. 1866 dyne . sec/cm5 . m2 and 20% vs. 25%, respectively) despite a significantly (p less than .01) greater oxygen delivery in the former group (716 vs. 570 ml/min . m2). Furthermore, nonsurvivors had significantly greater in vivo P50 and mixed venous lactate values (31 vs. 29.5 torr [p less than .02], and 5.1 vs 3.0 mmol/L [p less than .05], respectively). Only in survivors was the in vivo P50 related to the oxygen extraction ratio (r = 0.68 and p less than .01, compared with r = 0.03 in nonsurvivors). These results suggest that the fall in systemic vascular resistance is related to some form of arteriovenous shunting and that this is more severe in patients who die. The subsequent development of tissue hypoxia is an important prognostic factor in fulminant hepatic failure that may contribute to the occurrence of irreversible multiple organ failure.
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PMID:Tissue hypoxia during fulminant hepatic failure. 393 11

The effects of a period of anoxia 18-24 h after birth on bilirubin levels in rat brain were investigated during anoxia, recovery, and development. Postnatal anoxia induces a significant, temporary increase (up to 200% with respect to control values) in newborn rat brain bilirubin levels during anoxia and short-term recovery. Pretreatment of the newborn rats with a single dose of the drug sulfixosazole markedly enhances bilirubin accumulation in the brain of the anoxic rats. A second rise in brain bilirubin concentration is detected in a group of the newborn rats 3-6 days after oxygen deprivation. Autoradiographic localization of radiolabeled bilirubin following in vivo experiments suggests that this substance is preferentially accumulated in some areas of the newborn rat brain as a consequence of postnatal anoxia, and indicates, together with the effect of sulfixosazole, that as a result of anoxia, a displacement of unbound bilirubin from blood to the nervous tissue occurs. Our results confirm the importance of anoxia as a risk factor for the development of bilirubin-induced encephalopathy. The possible relevance of intracerebral hemorrhages caused by perinatal asphyxia producing delayed bilirubin accumulation in the newborn rat brain is suggested.
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PMID:Effect of postnatal anoxia on bilirubin levels in rat brain. 398 85

Cerebral blood flow and cerebral metabolism were studied in six patients with moderately severe portosystemic encephalopathy before and after a 10-day course of lactulose. As a result of therapy there was a mean increase in cerebral oxygen utilization but no changes in either mean glucose consumption or in mean cerebral blood flow. It appears therefore that the abnormalities in cerebral metabolism that have been previously described in patients with hepatic encephalopathy can be improved by the oral administration of lactulose.
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PMID:Effect of lactulose on cerebral metabolism in patients with chronic portosystemic encephalopathy. 509 25

In an attempt to determine whether hypoxic-ischemic encephalopathy in and of itself or its associated pathologic conditions lead to increased concentrations of plasma beta-endorphin (beta-ED), measurements were made in three groups of term infants. Group 1 (control) consisted of 8 infants with a mean gestation of 38.6 +/- (SE) 0.4 weeks, a mean birth weight of 3,420 +/- 150 g, and a mean postnatal age of 1.4 +/- 0.7 days. Group 2 consisted of 10 infants with a mean gestational age, birth weight and postnatal age of 40.1 +/- 0.5 weeks, 3,310 +/- 80 g and 3,9 +/- 1.1 days, and group 3 included 6 infants with a mean gestational age, birth weight and postnatal age of 40.4 +/- 1 weeks, 3,650 +/- 310 g, and 2.8 +/- 1 days, respectively. The group 2 and 3 infants suffered clinical and neurological evidence of hypoxic-ischemic brain injury from perinatal asphyxia; however, the infants in group 2 suffered additional problems such as meconium aspiration, persistent fetal circulation with ongoing hypoxemia as measured by transcutaneous or umbilical arterial oxygen monitoring. The group 3 infants were normoxemic after resuscitation. The mean plasma beta-ED concentrations were 19 +/- (SE) 2.7, 103 +/- 35.7 and 25 +/- 4.5 pg/ml in groups 1, 2 and 3, respectively. A significant elevation of plasma beta-ED concentration was observed in group 2 when compared to groups 1 and 3. The association of increased plasma beta-ED concentration in infants with hypoxic-ischemic encephalopathy associated with ongoing hypoxemia suggests that hypoxemia may act as a strong stimulus for plasma beta-ED release in term infants.
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PMID:Hypoxic-ischemic encephalopathy and plasma beta-endorphin. 609 23

Carbon monoxide (CO) remains the leading cause of death due to poisoning in the United States. CO produces toxicity by binding to hemoglobin, thereby reducing oxygen-carrying capacity, and by binding to myoglobin, which may impair cardiac output and result in cerebral ischemia. Severe CO poisoning results in coma or encephalopathy, but milder intoxication may occur with nonspecific symptoms suggestive of hysteria, hyperventilation, psychosis, or viral syndrome. Survivors of severe CO poisoning may have permanent neurologic or neuropsychiatric sequelae. Subtle memory deficits or personality changes may not be readily apparent to the examining physician. Administration of 100% oxygen at ambient pressure remains convenient, safe, and inexpensive. Hyperbaric oxygen can shorten the half-life of carboxyhemoglobin and can carry oxygen independent of hemoglobin. However, it is not known if either 100% oxygen or hyperbaric oxygen can actually alter mortality or improve neurologic outcome in survivors. Carefully controlled prospective studies should be carried out to assess the potential value of hyperbaric oxygen in CO poisoning.
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PMID:Carbon monoxide poisoning: mechanisms, presentation, and controversies in management. 649 Dec 41


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