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

From the analysis of the fatty acid spectrum of the individual lipid fractions of the cerebral white matter in cyanide induced encephalopathy would appear that essentially the phosphatidyl ethanolamine and plasmalogen fractions showed appreciable deviations from the control spectra. The observed changes in the cholesteryl ester composition did not correlate with the macrophage reaction, which is known to appear as late as 14 days after HCN intoxication when morphological signs of demyelination become apparent. Neither was there a correlation between the alterations of the phosphatide fatty acid composition and that of cholesteryl esters. It thus would appear that esterification of cholesterol in the myelin of rats occurring during early stages following cyanide intoxication constitutes one of the primary factors injuring the myelin sheath. The same conclusion seems to be applicable to the changes in fatty acid composition of the white matter phospholipids.
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PMID:Fatty acid pattern of cerebral lipids in cyanide encephalopathy. 123 9

The correlation among hyperammonemia, brain neutral amino acid, and encephalopathy induced by cyanide was investigated in mice. Subcutaneous injection of 10 mg/kg of potassium cyanide increased the levels of blood ammonia by 2.5-fold as compared to those of the corresponding controls and caused loss of consciousness in 100% of the treated mice. alpha-Ketoglutarate (500 mg/kg, ip) completely blocked the development of loss of consciousness and hyperammonemia induced by cyanide. Furthermore, the same doses of potassium cyanide increased by 50-150% the levels of brain neutral and aromatic amino acids such as leucine, isoleucine, tyrosine, and phenylalanine, while the levels of acidic amino acid such as taurine, glutamate, and aspartate did not change. alpha-Ketoglutarate also significantly inhibited the increase of the neutral and aromatic amino acid levels in brain. These findings suggest that the hyperammonemia and the increase of neutral and aromatic amino acids may play an important role in development of loss of consciousness induced by cyanide.
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PMID:Hyperammonemia, increased brain neutral and aromatic amino acid levels, and encephalopathy induced by cyanide in mice. 274 30

A study was performed to elucidate the significance of various physiological factors contributing to the pathogenesis of experimental cyanide encephalopathy, such as the systemic arterial blood pressure, venous pressure, common carotid blood flow and local blood flow of the cerebral grey and white matters, and blood gas including pH. The histology and topography of the brain damage was also analysed. Twenty-one cats were divided into four groups. The animals in groups 1, 2 and 3 were subjected to continuous infusion of 0.2% sodium cyanide solution and to the ensuing hypotension below 100 mm Hg by administering a ganglion-blocking drug and by respiratory arrest. Severe damage developed in the deep cerebral white matter, corpus callosum, pallidum and substantia nigra, but the damage of the cerebral cortex and hippocampus was not remarkable. The animals in group 4 that were subjected to cyanide infusion without significant hypotension (above 100 mm Hg), but to the same degree of acidosis as that of the other groups, had similar morphological changes, but to a lesser degree. On the basis of our physiological and morphological findings, we speculated that the pathophysiological factors of tissue hypoxia and subsequent hypotension operated in cyanide leucoencephalopathy. The topographic selectivity seemed to be related to the characteristic cerebral vascular system, and the severity of the white matter lesions was related to the intensity of both hypoxia and hypotension during cyanide infusion, but not to the extent of acidosis, total dose of cyanide or duration of its infusion per se.
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PMID:A study of experimental cyanide encephalopathy in the acute phase--physiological and neuropathological correlation. 647 4

Sodium nitroprusside (SNP) is frequently used as an hypotensive agent for clipping of intracranial aneurysms, repair of arteriovenous malformations and resection of vascular tumours. Cyanide (CN), which is its main metabolic product, has been recovered from the cerebrospinal fluid (CSF) of the rat after intravenous administration of CN, but recovery of CN from CSF after SNP has not been reported in man. Seven consenting adults were studied. Adequate premedication was provided with pentobarbitone 2 mg x kg-1 and atropine 0.4 mg one hour before operation. Anaesthesia was induced with thiopentone 8 mg x kg-1 and maintained with nitrous oxide 60 per cent with oxygen and supplemental fentanyl 0.05 mg and pancuronium 0.5-1 mg as needed. Lumbar subarachnoid, radial artery, central venous, and Foley urinary catheters were inserted. Arterial carbon dioxide tension (PaCO2) was maintained between 4.6-5.32 kPa (35-40 torr) with an Air Shields ventilator. Red cell, plasma and CSF cyanide were measured using a digital ionanalyzer before and at 30 minutes interval after infusing SNP at a rate sufficient to maintain the blood pressure at two thirds of the pre-operative level. Average total dose of SNP was 0.51 mg x kg-1. CN concentration in the red blood cells increased from 9.5 +/- 2.05 to 75.12 +/- 17.12. Plasma CN increased from 0.54 +/- 0.05 to 1.09 +/- 0.14 micrograms per cent. CSF CN increased from 0.11 +/- 0.04 to 0.72 +/- 0.07 micrograms per cent. Significant increase in red cell, plasma and CSF CN occurred five minutes after the start of SNP and returned to the preoperative level 19 hours later. Conclusion CN crosses the blood-brain barrier. Large doses of SNP in patients with neurovascular brain disorders warrants caution because cytotoxic cerebral oedema and CN encephalopathy have been described in rats after intravenous injection of sodium cyanide or exposure to hydrogen cyanide.
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PMID:Cerebrospinal fluid cyanide after nitroprusside infusion in man. 723 15

The authors reviewed the clinical manifestations, complications, and the prognosis affected by Lilly Cyanide Antidote in 21 victims of acute cyanide poisoning over a 10-year period. The clinical signs and symptoms in cyanide poisoning are variable. Among 21 cases, loss of consciousness (15), metabolic acidosis (14), and cardiopulmonary failure (9) were the three leading manifestations of cyanide intoxication. Anoxic encephalopathy (6) was not uncommon in the severely intoxicated victims. Diabetes insipidus (1) or clinical signs and symptoms mimicking diabetes insipidus (3) may be an ominous sign to encephalopathy victims. The major cause of fatal cyanide poisoning is the intentional ingestion of cyanide compounds as part of a suicide attempt. Decrease of arteriovenous difference of O2 partial pressure may be a clue for the suspicion of cyanide intoxication. Although the authors cannot show a statistically significant difference (P = .47) for the Lilly cyanide antidote kit in terms of improving the survival rate for victims of cyanide poisoning, the antidote kit was always mandatory in our study in the cases of severely intoxicated victims who survived. Early diagnosis, prompt, intensive therapy with antidote, and supportive care are still the golden rules for the treatment of acute cyanide poisoning, whether in the ED or on the scene.
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PMID:The clinical experience of acute cyanide poisoning. 766 55

Experience with organ procurement from poisoned donors in brain death status is still limited in comparison with other etiologies. From 1963 to 1993, 2769 grafts (heart 141, kidney 1922, liver 623, pancreas 43) were performed in our University Hospital. Since 1975, among 1174 patients admitted to the ICU for acute poisoning, 12 patients who developed brain death status were considered for organ donation. The toxics involved were: methaqualone (1), benzodiazepines (1), benzodiazepines plus tricyclic antidepressants (2), barbiturates (2), insulin (2), carbon monoxide (1), cyanide (1), methanol (1), and acetaminophen (1). Exclusion criteria for organ removal were applied according to the nature of the toxin and the general criteria used for organ donation. The organs removed were: heart 5, heart valves for graft bank 2, kidneys 22, liver 4, pancreas 2, pancrease islet cells 2. Pertinent follow-up was obtained in 23 of 32 recipients. Immediate outcome was favorable in 20/23 patients (85%). Three patients died either from stroke, heart failure or preexisting encephalopathy. Two patients died from either chronic hepatic or renal graft rejection. None of these events could be directly related to a toxic origin. The one year survival rate of 75% is similar to that observed in the population who received organs from nonpoisoned donors. Organ procurement can be considered in few selected cases of acute poisoning. The accuracy of the diagnosis of irreversible brain damage is essential in this setting.
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PMID:Outcome following organ removal from poisoned donors in brain death status: a report of 12 cases and review of the literature. 852 98

Aspirin, Neem oil, valproic, adipic, benzoic, isovaleric, 3-mercaptopropionic and 4-pentenoic acids are implicated in the pathogenesis of Reye's syndrome, Jamaican vomiting sickness, and related chemical toxicities. These disorders are characterized by hyperammonemia, hypoglycemia, microvesicular steatosis and encephalopathy. The goal of this study was to determine whether chemicals implicated in Reye's-related disorders induce the mitochondrial permeability translation (MPT). The MPT is induced by opening of a high-conductance, cyclosporin-sensitive pore in the mitochondrial inner membrane, causing swelling, depolarization and uncoupling of oxidative phosphorylation. In freshly isolated rat liver mitochondria, unhydrolyzed aspirin (300 microM) did not induce the MPT in the presence of 50 microM CaCl2. Salicylate, the hydrolysis product of aspirin and its active metabolite, was much more potent causing dose-dependent onset of the MPT in a therapeutic range of concentrations (37.5-300 microM). Similarly, Neem oil and valproic, adipic, benzoic, isovaleric, 3-mercaptopropionic and 4-pentenoic acids induced onset of the MPT. In all cases, cyclosporin A (200 nM), a specific inhibitor of the permeability transition pore, blocked the MPT caused by these inducers. Induction of the MPT by these agents was not caused by mitochondrial depolarization because concentrations of valproic acid and salicylate inducing the MPT had little effect on mitochondrial delta psi. Moreover, equivalent uncoupling caused by 5 nM carbonyl cyanide p-trifluoromethoxyphenylhydrazone did not induce an MPT. These data suggest that induction of the MPT is a common pathophysiological mechanism causing mitochondrial injury in Reye's syndrome and Reye's-related drug toxicities.
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PMID:The mitochondrial permeability transition: a new pathophysiological mechanism for Reye's syndrome and toxic liver injury. 881 78

Bilateral striatal necrosis in acute encephalopathy has been reported in a small number of adults with methanol or cyanide intoxication, hypoxic encephalopathy or haemolytic-uraemic syndrome. Acute encephalopathy with bilateral striatal necrosis has been reported in infants and children. However, the pathogenesis of the necrosis remains unclear. This is the first report of serial imaging from the very early to chronic stage in two acute encephalopathic adults with bilateral striatal necrosis. A clinicoradiological study is presented for clarification of the pathological process and pathogenesis. Striatal lesions were not detected in the very early stages, but only thereafter. Serial studies suggested that the lesions were caused by delayed neuronal death. These patients had severe lactic acidosis, near the limit for survival. There have been few reports of adults with acute encephalopathy and bilateral striatal necrosis in whom arterial pH was described; all these exhibited marked acidosis. The common pathophysiological condition among these encephalopathies with bilateral striatal necrosis could be lactic acidosis elicited by impairment of ATP generation through the Krebs cycle. The striatum might represent one of the target areas of Krebs-cycle blockade.
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PMID:Serial imaging of bilateral striatal necrosis associated with acidaemia in adults. 883 86

By experiments of acute carbon-monoxide intoxication, acute nitrogen hypoxia and histotoxic hypoxia using sodium cyanide in cats, and by hemodynamic studies using plastic branch models, the following was elucidated; (1) severe tissue hypoxia, regardless of the underlying cause, and subsequent slight ischemia of the brain due to mild hypotension induce selective involvement of the cerebral white matter and pallidum, these two conditions being necessary and sufficient and this encephalopathy should be separately categorized as "hypoxic-ischemic encephalopathy" in hypoxic brain injuries, (2) the background of the selective involvement of these structures is an enormous development of the cerebrum in the brain, which induces thick white matter resulting in proper and long medullary artery, and especially small diameter ratio of the pallidal perforators to the middle cerebral artery, (3) the long course of the medullary artery produces the blood pressure drop in the deep white matter according to Hagen-Poiseuille's low, and according to that the smaller the diameter ratio, the larger the branching-loss coefficient (energy-loss co-efficient), smaller diameter ratio of the pallidal perforator, as compared with that of the putaminal perforator, induces more severe loss of the local blood flow selectively to the pallidum. This state seems to be a failure of compromise between the cardiovascular system and the brain parenchyma.
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PMID:Concept and pathogenesis of "hypoxic-ischemic encephalopathy". 1475 93

This report describes the clinical history of a patient intoxicated with methyl isocyanate (MIC), a toxic agent first receiving attention in 1984 after a mass accident in a pesticide plant in Bhopal, India, and treated with the cyanide-specific antidote 4-DMAP. The numerous clinical conditions requiring 39-day intensive care treatment included ARDS, renal and hepatic failure, haemolysis, bone marrow depression, septic encephalopathy and critical illness polyneuropathy. The most outstanding condition, however, was a methaemoglobinemia of 86.7%, which was predominantly related to the use of 4-DMAP, although uptake of MIC may have been a significant contributing factor. Since significant cyanide intoxication could be excluded clinically and by laboratory testing in the initial phase of emergency treatment, most of the clinical effects were due to the side-effects of the antidote therapy. Due to intensive therapy, the patient survived without any neurological or organ deficit. This case shows that antidotes should be used cautiously in cases where uncertainties about the nature of the underlying toxic agent exist. This may prevent severe side-effects associated with antidote therapy, e.g. 4-DMAP, if there is-as in our case-a mismatch between the toxic agent and the antidote.
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PMID:Excessive methaemoglobinaemia and multi-organ failure following 4-DMAP antidote therapy. 1595 Mar 59


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