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

Inorganic lead, added to the diet of suckling rat in high doses, produces an encephalopathy similar to that seen in the immature human. Pathologic changes of edema and hemorrhage are seen earliest and are most prominent in the cerebellum. In this study, we measured respiration in cerebral hemisphere and cerebellar mitochondria isolated from led-fed and age-matched normal rat pups. Lactating mothers were begun on ad libitum feedins containing 4% lead carbonate when their pups were 2 weeks old. Mitochondria were isolated by differential centrifugation. Oxygen consumption was measured polarographically, NAD-linked respiration was measured with oxidation of the substrate pair, glutamate and malate. Cytochrome oxidase (cytochrome c oxidase, EC. 1.9.3.1) activity was measured in the presence of tetramethyl-p-phenylenediamine dihydrochloride (TMPD) and ascorbate. Within 2 days of starting lead feedings, rat pups showed a significant loss in body weight (P less than 0.02) and, after 1 week, a significant loss in cerebral hemisphere wet weight (P less than 0.01) compared with controls. Overt encephalopathy appeared in pups from two of nine litters receiving lead feedings for 1 week and in half of the litters after 2 weeks of feedings. None of the lead-fed mothers developed encephalopathic signs. With oxidation of the NAD-linked substrate pair, there was a progressive decrease, relative to controls, in ADP/O ratios in both cerebellar and cerebral mitochondria from lead-fed animals. After 2 weeks these differences were significant in mitochondria from both regions (cerebellum, P less than 0.02; cerebrum, P less than 0.005). Respiratory control ratios were significantly lower in cerebellar mitochondria from lead-fed rats within 2 days of beginning feedings (P less than 0.02) and in mitochondria from both regions after 2 weeks of lead feedings (cerebellum, P less than 0.01; cerebrum, P less than 0.05). The decrease in control ratios in cerebellar mitochondria from animals receivint lead feedings for 1 week or less was due to a small decrease in state 3 respiration and a large, but inconsistent, increase in state 4 respiration. The decrease in control ratios in both cerebellar and cerebral hemisphere mitochondria after 2 weeks of lead feedings was due to a marked inhibition of state 3 respiration, relative to controls (cerebellum, P less than 0.01; cerebral hemisphers, P less than 0.05). In cerebellar mitochondria from lead-fed animals, cytochrome oxidase activity showed similar changes compared with controls: a highly significant (P less than 0.001) increase within 2 days of beginning feedings and a significant (P less than 0.01) decrease after 2 weeks of feedings.
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PMID:Early effects of inorganic lead on immature rat brain mitochondrial respiration. 17 53

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

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

Secondary metabolic encephalopathy is a diffuse disorder of the brain caused by an extracerebral process. Underlying causes include oxygen deprivation, systemic metabolic disease, and drug intoxication. Symptoms and signs usually suggest a generalized disturbance of brain function: alterations in the level of consciousness; diffuse and, occasionally, focal motor abnormalities; and seizures. Electroencephalography in most instances gives evidence of generalized neuronal disturbance. Early diagnosis is important because encephalopathy secondary to an extracerebral process is potentially reversible. Treatment is directed toward reversal or control of the underlying process, supportive care, and prevention of complications such as infection, electrolyte imbalance, and cerebral edema.
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PMID:Secondary metabolic encephalopathy. Diagnosis and treatment. 77 43

In a series of 106 patients with fulminant hepatic failure and grade 4 encephalopathy, cardiac arrhythmias and other abnormalities occurred in 92 per cent. The most common was sinus tachycardia (75%) and this was the only abnormality in 22 per cent of the patients. Sudden cardiac arrest occurred in 25 per cent, various ectopic beats in 20 per cent, and heart block or bradycardia in 18 per cent. Other electrocardiographic abnormalities, mostly of the T wave and ST segment, were found in 31 per cent. Cardiac and respiratory arrests were usually unrelated to each other and both frequently occurred without warning. Only 7 out of 71 patients with arrhythmias other than sinus tachycardia survived, compared with 15 out of 31 patients without them (P less than 0-005). During the latter part of the series when an arrhythmia computer was used to monitor 38 patients, it was shown that significantly lower arterial oxygen levels occurred in those with arrhythmias, other than sinus tachycardia, than in those without. They were also found to be more acidotic and hyperkalaemic, and a higher number required dialysis and ventilation. Macroscopical cardiac abnormalities including scattered petechial haemorrhages, small pericardial effusions, and fatty, pale, and flabby ventricles, were found at necropsy in 64 per cent of the patients examined. Combinations of these macroscopical abnormalities occurred, particularly in the paracetamol overdose group. Another necropsy finding of possible significance in the pathogenesis of arrhythmias was cerebral oedema, present in 48 per cent of the patients examined, and often associated with coning of the brain stem. However, 7 of the 16 patients who suffered asystolic cardiac arrests had no macroscopical abnormality of either heart or brain. In the management of patients with fulminant hepatic failure continuous cardiac monitoring is essential. Correction of the biochemical and coagulation defects may decrease the frequency of arrhythmias but studies of the mechanism and control of cerebral oedema and its relation to cardiovascular function are urgently needed.
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PMID:Frequency of arrhythmias and other cardiac abnormalities in fulminant hepatic failure. 100 59

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

The developing nervous systems is subject to damage from lack of vital substances necessary for normal maturation and function as well as from trauma or a variety of toxins and infectious agents. By far, the most important of these is inadequate oxygen delivery to the fetus in utero, and/or during the intrapartum and/or early neonatal period. Many types of lesions have been described under the rubric of hypoxic-ischemic encephalopathy, a major proportion of which are found only in the immature nervous system and essentially are never seen later in life. Moreover, a large number are primarily hemorrhagic rather than ischemic in character. The unique character and distribution of these lesions results from a collision of the changing anatomy of the developing nervous system and pathophysiological factors afflicting the immature organism. Whereas the majority of hypoxic-ischemic lesions in the fetus/neonate fall into this group, abnormalities characteristically found in the mature nervous system are also seen. Recognition of the anatomic and physiological features peculiar to the developing nervous system will assist in diagnosis of hypoxic-ischemic damage peculiar to the fetus and neonate.
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PMID:Anatomical features of the developing brain implicated in pathogenesis of hypoxic-ischemic injury. 134 36

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

The clinical status and the computed and positron tomographic findings were compared in 10 patients with sequelae of hypoxic-ischemic encephalopathy after cardiopulmonary arrest and successful resuscitation. Conscious patients with moderate neuropsychiatric deficits had no significant computed tomography (CT) scan changes and normal values of regional cerebral blood flow and oxygen consumption, while patients in vegetative state had definite cerebral atrophy on CT scan and a severe and widespread decrease of regional cerebral blood flow and oxygen consumption. This decrease was even more pronounced in vegetative patients with the worst neurological score and with CT scans demonstrating additional diffuse white matter lucencies and hypodensities in the basal ganglia. In this group of patients increased regional oxygen extraction rates mainly in the white matter indicated the occurrence of delayed ischemic changes. The positron emission tomography and CT findings correlated well with the degree of posthypoxic-ischemic damage and the clinical status of the studied subjects.
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PMID:Significance of white matter lucencies in posthypoxic-ischemic encephalopathy: comparison of clinical status and of computed and positron emission tomographic findings. 149 May 1

A 63 year old male underwent 6,900 rads of external radiation for a squamous cell carcinoma of the left main bronchus. Recurrence of the tumor 8 months later was treated with 6,618 joules and patency of the left main bronchus was restored. Four months later, he developed complete atelectasis of the left lung requiring repeat laser. During the procedure he became hypotensive, bradycardic, and hypoxic due to a tension pneumothorax. Although treated promptly with thoracostomy tube drainage, the patient never awakened. CT scan of the brain demonstrated anoxic encephalopathy with air present in the right frontal lobe. Brain death was confirmed by an EEG and cerebral angiogram. Air embolism has been reported in conjunction with diagnostic procedures including therapeutic pneumothorax for tuberculosis, transthoracic needle biopsy of the lung, and positive pressure ventilation with or without pneumothorax. The only reported case of air embolism associated with laser was a small middle cerebral artery cerebro-vascular accident which was self limited. Its mechanism is unclear, but it is suspected to be due to a communication between a pulmonary vein and the atmosphere. A greater volume of air will enter the damaged vessel in the setting of positive pressure ventilation and/or a tension pneumothorax. When neurologic manifestations are present, hyperbaric oxygen therapy is the treatment of choice. Prompt institution in hemodynamically stable patients can minimize neurologic sequelae.
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PMID:Massive air embolism complicating Nd-YAG laser endobronchial photoresection. 150 30


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