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

The present report describes a rare of a 77-year-old woman who developed encephalopathy and metabolic acidosis associated with hyperammonemia, at the introduction of hemodialysis by chronic renal failure. With the intravenous infusion of HCO3-, levels of acidosis and hyperammonemia decreased rapidly. Concomitantly the disturbance of consciousness was improved. Results of plasma amino acid patterns of pre and post infusion of HCO3- showed improvement of the metabolism of the urea cycle, increased urea synthesis and decreased plasma ammonium levels. The role of the hepatic urea cycle has been considered to be exclusively the elimination of potentially toxic ammonia. In the conventional view, the acid base balance of the body obtains stabilized homeostasis by the function of the principal organs, lungs and kidneys. But, it has been recently shown that urea cycle is an important factor in the maintenance of pH homeostasis, due to regulated metabolism of HCO3-. Both HCO3- and NH4+ are converted to urea indicating the urea cycle's involvement in acid base homeostasis. 2HCO3- + 2NH4+-->urea+CO2+3H2O In this case, with the infusion of HCO3, the metabolism of the urea-cycle was improved and plasma ammonium levels were decreased. This indicates that HCO3- is an important factor for the metabolism of ammonia.
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PMID:[A case of hyperammonemia in chronic renal failure successfully treated with the infusion of NaHCO3]. 841 69

A wide range of toxic effects of aluminum (Al) have been demonstrated in plants and aquatic animals in nature, in experimental animals by several routes of exposure, and under different clinical conditions in humans. Aluminum toxicity is a major problem in agriculture, affecting perhaps as much as 40% of arable soils in the world. In fresh waters acidified by acid rain, Al toxicity has led to fish extinction. Aluminum is a very potent neurotoxicant. In humans with chronic renal failure on dialysis, Al causes encephalopathy, osteomalacia, and anemia. There are also reports of such effects in certain patient groups without renal failure. Subtle neurocognitive and psychomotor effects and electroencephalograph (EEG) abnormalities have been reported at plasma Al levels as low as 50 micrograms/L. Infants could be particularly susceptible to Al accumulation and toxicity, reduced renal function being one contributory cause. Recent reports clearly show that Al accumulation occurs in the tissues of workers with long-term occupational exposure to Al dusts or fumes, and also indicate that such exposure may cause subtle neurological effects. Increased efforts should be directed toward defining the full range of potentially harmful effects in humans. To this end, multidisciplinary collaborative research efforts are encouraged, involving scientists from many different specialties. Emphasis should be placed on increasing our understanding of the chemistry of Al in biological systems, and on determining the cellular and molecular mechanisms of Al toxicity.
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PMID:Status and future concerns of clinical and environmental aluminum toxicology. 877 97

To study the causes, diagnosis and treatment of aluminum toxicity in patients with chronic renal failure, the serum aluminum concentration was determined in 27 normal subjects, 28 patients of various kinds of diseases with normal renal function and 81 patients of chronic renal failure with hemodialysis in 65 and without in 16, of whom 41 patients were determined the aluminum concentration in the bone tissue. Clinical symptoms were carefully observed in all patients and desferrioxamine (DFO) test was performed in 17 patients, of whom 10 were treated with DFO. The results showed that treatment with improperly processed water and administration of aluminum compound were the major causes of aluminum toxicity in uremic patients. Aluminum toxicity may induce anemia, encephalopathy and bone disease, but its clinical features were nonspecific and the diagnosis may require several serum aluminum determinations or DFO test. DFO can chelate aluminum in a variety of tissues so that the latter may be released into the blood circulation. The DFO test may be used to assess the actual aluminum load in the bone tissue. The changes in serum aluminum concentration after intravenous infusion of DFO correlated closely with bone aluminum level, suggesting that the DFO test may be useful for the diagnosis of aluminum toxicity. The DFO therapy may be indicated for, 1, patients with uremia having hyperaluminumnemia due to treatment with improperly processed water and intake of aluminum-containing agents. 2. those who had serum aluminum concentration of higher than 200 micrograms/L and positive DFO test and 3. patients whose aluminum concentration in the bone tissue was 10 times greater than normal values. In this study, DFO was given intravenously in a dose of 20-40 mg/kg, twice a week. Satisfactory results were obtained in 3 to 6 months and there were no severe side effects when the agent was administered slowly.
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PMID:[The causes, diagnosis and treatment of aluminum toxicity in patients with chronic renal failure undergoing dialysis]. 927 45

Human recombinant erythropoietin is used to treat chronic anemia in patients with end-stage renal failure. Erythropoietin causes hypertension, and hypertensive encephalopathy has been associated with its use. We describe six dialysis-dependent, chronic renal failure patients who developed hypertension, headache, and seizures while on erythropoietin. Four of the six patients had posterior white matter changes on neuroimaging. The encephalopathy was managed by prompt antihypertensive and anticonvulsant treatment and by discontinuation of erythropoietin. Hypertensive posterior leukoencephalopathy is associated with erythropoietin use.
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PMID:Erythropoietin-associated hypertensive posterior leukoencephalopathy. 971 75

We report 81 of 107 cases of hemolytic uremic syndrome (HUS), admitted between July 1994 and February 1996, following an outbreak of Shigella dysenteriae type 1 dysentery in Kwazulu/Natal. All patients, excluding 1, were black with a mean age of 38 months (range 1-121); 50 (61.7%) were males. The mean duration of dysentery was 11.3 days (range 1-41) and HUS 15 days (range 1-91). Most patients had acute oliguric renal failure (90.1%), 42 (51.6%) required peritoneal dialysis. Complications included encephalopathy 30 (37.0%), convulsions 12 (14.8%) and hemiplegia 2 (2.3%), gastrointestinal perforation 8 (9.9%), protein losing enteropathy 26 (32.1%), toxic megacolon 4 (4.9%), rectal prolapse 5 (6.2%), hepatitis 11 (13.6%), myocarditis 5 (6.2%), congestive cardiac failure 3 (3.7%), cardiomyopathy 3 (3.7%), infective endocarditis 1 (1.2%), septicemia 15 (18.5%), disseminated intravascular coagulation 17 (21%). Leukemoid reactions were found in 74 (91.3%) patients, hyponatremia in 56 (69.1%), and hypoalbuminemia in 67 (82.7%). Stool culture for Shigella dysenteriae type I was positive in only 7 (8.6%) patients; Shiga toxin assays were not performed. Outcome was as follows: recovery 32 (39.5%), impaired renal function 8 (9.9%), chronic renal failure 26 (32.1%), end-stage renal disease 1 (1.2%), and death 14 (17.3%) patients.
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PMID:Post-dysenteric hemolytic uremic syndrome in children during an epidemic of Shigella dysentery in Kwazulu/Natal. 932 80

A 70-year-old man with advanced obstructive nephropathy began to hemorrhage from the bladder after decompression with a Foley catheter. Manifestations of encephalopathy appeared after continuous irrigation with 1% alum for 2 days and were associated with elevated serum aluminum concentrations. Repeated treatments with deferoxamine and hemodialysis accomplished some aluminum removal, but the patient succumbed to bronchopneumonia. Brain aluminum content was not excessive at autopsy. A literature review suggests that intact renal function is essential to rapid disposal of a parenteral aluminum load and indicates that most reported instances of encephalopathy after alum irrigation have occurred in patients with compromised renal function. We conclude that alum should not be employed as a bladder irrigant in patients with acute or chronic renal failure.
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PMID:Encephalopathy after bladder irrigation with alum: case report and literature review. 1048 8

Developmental disturbances and encephalopathy have been observed in children with chronic renal failure (CRF). The aim of this study was to investigate the efficiency of the cerebral circulation in uremic children. The study group consisted of 10 children with CRF on conservative treatment, 8 children on continuous ambulatory peritoneal dialysis (CAPD), and 8 children on maintenance hemodialysis (HD). Examination was performed using a TC2-64B, EME Doppler flowmeter machine and capnograph Datex, Normocap. Blood flow velocity in both middle cerebral arteries (MCA), at rest and after spontaneous hyperventilation for 30 s, was analyzed. The vascular reactivity coefficient was calculated as the percentage ratio of decline of blood flow velocity in MCA to PCO2 decrease. Baseline mean blood flow velocities of MCA in euvolemic children under conservative treatment and on CAPD were significantly higher than those in children on HD and healthy control children. The highest value of the vascular reactivity coefficient was significantly higher in the group of children with CRF on conservative and CAPD treatment, than in children on HD and healthy controls. We suggest that hyperreactivity of the cerebral circulation could be the result of impaired autoregulation of blood flow. Evaluation of cerebrovascular reactivity in uremic children requires further examination.
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PMID:Evaluation of cerebrovascular reactivity in children [corrected] with chronic renal failure. 1097 14

We report the case of a 59-year-old female aluminum encephalopathy patient who had chronic renal failure and took 3.0 g hydroxy-aluminum gel per day for the control of serum phosphorus level during a 15-year period. Nine months before her death she developed disorientation, memory disturbance, emotional incontinence, general convulsions and consciousness disturbance. Neuropathologically, the brain showed nerve cell atrophy and mild loss with stromal spongiosis, proliferation of astrocytes and microglia in the cerebral cortex, basal ganglia and thalamus. Some nerve cells were stained immunohistochemically by phosphorylated neurofilament, but apparent neurofibrillary tangles were not observed. Aluminum was detected in the nerve cells of the cerebral cortex by X-ray microanalysis. Despite the long-term intake of aluminum, there were no neuropathological findings of Alzheimer's disease. The findings in our case suggested that aluminum alone might not develop Alzheimer's disease.
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PMID:Autopsy case of aluminum encephalopathy. 1241 61

Vascular and neurologic impairment remain an important source of morbidity in patients with chronic renal failure (CRF). A portion of CRF patients still suffers from uremic encephalopathy or other signs of nervous system impairment. Several reports demonstrate increased incidence of cardiac infarction and cerebrovascular accidents in CRF patients, even in those with otherwise adequate dialysis treatment [1]. Premature vascular disease, including myocardial infarction, stroke, and peripheral vascular disorder, are the leading causes of death in this population. Although several traditional risk factors for vascular disease and endothelial dysfunction, including smoking, diabetes, dyslipidemia, and hypertension, are often increased in CRF, these factors can only partly explain the high vasculopathy-related morbidity and mortality. Several authors have postulated that CRF-associated atherosclerosis and endothelial dysfunction result from accumulation of certain 'uremic factors,' the identities of which are still a matter of debate. These factors include a variety of guanidino compounds (GCs), which have been shown to be nitric oxide synthase (NOS) modulators both in vitro and in vivo. However, other effects of accumulated uremic GCs have been identified.
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PMID:Nitric oxide in uremia: effects of several potentially toxic guanidino compounds. 1269 2

Acute pancreatitis, developing in a patient with chronic renal failure, was complicated by a fatal neurological illness during which MRI showed pontine and extrapontine changes consistent with pontine and extrapontine myelinolysis. At post mortem, acute pancreatitis was confirmed but the neuropathological findings were more in keeping with an unusual presentation of acute haemorrhagic leucoencephalitis, perhaps even representing a form of 'pancreatic encephalopathy'. Although the development of CT and MRI scanning has greatly increased the resolution of neuroimaging and facilitated diagnosis during life, the value of autopsy examination is confirmed in cases such as this. Sometimes the findings may raise more questions than may have been answered - this too is an important function!
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PMID:Fatal brain stem event complicating acute pancreatitis. 1276 45


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