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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bradycardia and hypotension were the first major signs of toxicity from a 250 mg bupivacaine axillary brachial plexus block experienced by a patient with chronic renal failure, who had an anion gap acidosis and hyperkalaemia. Without these metabolic abnormalities, this patient received four similar blocks: three were without incident and one was complicated by seizure. Acidosis and/or hyperkalaemia in man appears to increase the myocardial susceptibility to bupivacaine toxicity into the range of arterial concentrations of the drug normally produced by plexus blocks, even in the absence of drug-induced cerebral toxicity, seizures and hypoxia.
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PMID:Bupivacaine cardiotoxicity in a patient with renal failure. 683 32

After an upper respiratory tract infection an eight months old infant developed a severe hemolytic uremic syndrome with anemia, thrombocytopenia and anuria. Remarkable was a lesion of the erythrocytes by neuraminidase producing microorganisms. By early hemodialysis, blood transfusions and accurate fluid therapy the acute stage could be managed. The proceeding course was complicated by hypertension, seizures, coma, abdominal pain attacks and a fibrinous hemorrhagic pericarditis, which made an incomplete pericardectomy necessary. Although it came again to diuresis a severe chronic renal failure with its concluding effects as anemia, acidosis, hypertension and inanition resulted. After a four months period the patient died of biventricular congestive heart failure.
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PMID:[Severe course of a hemolytic-uremic syndrome]. 715 51

The examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
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PMID:Encephalopathy in infants and children with chronic renal disease. 729 12

Twenty-one patients with nephronophthisis are described with a follow-up of one to 16 years (mean 9.3 years). In 10 patients, there was a familial incidence. Autosomal recessive appears the likely mode of inheritance with a 20 per cent incidence noted (seven of 35) following correction for the bias of ascertainment by removing the probands. Seven patients had an associated and characteristic retinal degeneration from infancy. Associated neurologic problems, including mental retardation, seizures and cerebellar ataxis, were also seen in some patients. Previously described skeletal abnormalities and hepatic fibrosis were not seen in any of our patients. All presented at an advanced stage of chronic renal failure, usually associated with a history of polydipsia and polyuria from infancy. Renal cysts were noted in only one of the nine patients in whom tissue was obtained by needle biopsy. In seven patients in whom tissue was available at nephrectomy or autopsy, cysts were noted in six although only in two were they localized to the medulla. Eighteen patients have undergone dialysis, and 12 patients have received a renal transplant with no evidence of recurrence of the original disease. Sixteen patients are still alive. Many synonyms for nephronophthisis have appeared, with medullary cystic disease being the most common. Our experience suggests that nephronophthisis is a common cause of chronic renal failure and has commonly associated nonrenal abnormalities.
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PMID:Nephronophthisis. 736 32

We studied three boys who had a similar encephalopathy develop during moderate chronic renal failure. The features included cerebellar system dysfunction, seizures, and intellectual and motor retardation. Extensive laboratory investigation failed to disclose an etiology other than chronic azotemia. These cases suggest that the developing nervous system is particularly sensitive to the effects of chronic azotemia. Early dialysis and/or transplantation should be considered in such children in an attempt to modify the serious nervous system abnormalities.
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PMID:Encephalopathy in young children with moderate chronic renal failure. 738 32

The cranial computerized axial tomography (CAT) findings in groups of patients with epilepsy, migraine, hypertension, and other general medical disorders have been reviewed to assess the frequency and patterns of focal and diffuse brain damage. In addition to demonstrating focal lesions in a proportion of patients with seizures and in patients presenting with a stroke, the CAT scan showed a premature degree of cerebral atrophy in an appreciable proportion of patients with long-standing epilepsy, hypertension and diabetes, and in some patients with migraine, valvular and ischaemic, heart disease, chronic obstructive airways disease, and chronic renal failure. The value of CAT as a means of screening for brain damage in groups of individuals at risk is discussed.
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PMID:Computerized axial tomography in the detection of brain damage. 2. Epilepsy, migraine, and general medical disorders. 746 20

Progressive encephalopathy, developmental delay, microcephaly, electroencephalogram (EEG) and computed tomographic (CT) scan abnormalities have been reported in 80% of children with chronic renal failure (CRF) in infancy. Malnutrition, aluminium intoxication and psychosocial deprivation are proposed as causes. In 15 children with CRF from infancy we evaluated the effect of no aluminium salts and early vigorous nutritional and psychosocial support, in addition to the standard therapy, on neurological development. Six patients underwent dialysis (2 at birth) and 3 received transplants. None of our patients were given aluminium therapy. The nutritional status of the patients in the first 2 years of life was assessed with the waterlow classification. At the end of the follow-up period (mean 50 months range 14-148 months), patients underwent neurodevelopmental assessment, head CT scan, EEG, nerve conduction velocity (NCV) and auditory brain stem evoked response (ABER). None of our patients developed progressive encephalopathy or recurrent seizures. All have a normal neurological examination apart from hypotonia. Microcephaly was present in 5 patients. There was a good correlation between malnutrition in the first 2 years of life and microcephaly. Developmental delay was present in 3 patients; all 3 were microcephalic. There was evidence of brain atrophy on CT scan in only 3 patients. EEG was abnormal in 6 patients, but only severe in 1 patient. Only 1 patient had diminished NCV; all patients had a normal ABER. We conclude that a policy of no oral aluminium therapy and early nutritional support leads to better neurological outcome in children with CRF from infancy.
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PMID:Improved neurological outcome in children with chronic renal disease from infancy. 801

Seizures occurred in two adolescents approximately six hours after sedation with propofol for bone marrow biopsy. Case #1 was a patient with chronic renal failure, hypertension, and anaemia. Case #2 had just been diagnosed with acute lymphocytic leukaemia. Neither child had experienced seizures before, and both recovered without neurological sequelae. Although other factors may have caused the seizures, the episodes have raised concerns about the safety of propofol for patients travelling home after out-patient surgery. Further study is required to explain the cause of this complication or, at least, to identify risk factors.
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PMID:Delayed seizures following sedation with propofol. 840 71

The cytokines tumor necrosis factor-alpha (TNF-alpha) and its soluble TNF receptors 55 and 75 (sTNFR55, sTNFR75), interleukin-1 beta (IL-1BETA) and interleukin-6 (IL-6) were measured in plasma from 13 patients with the hemolytic uremic syndrome (HUS) on admission. No significant changes in the plasma levels of TNF-alpha and IL-1beta were detected in the HUS patients as compared to the plasma levels of the control groups. Levels of IL-6 were significantly elevated in the plasma of those HUS patients who had external manifestations, consisting of seizures, loss of consciousness, coma and pancreatic necrosis. Although the exact function of IL-6 in the plasma of HUS patients is still unknown and the group of HUS patients is small, plasma IL-6 is associated with the the severity and outcome of the disease. Plasma levels of sTNR55 and sTNFR75 were significantly elevated in all HUS patients compared to the healthy controls, but they were also elevated in the children with chronic renal failure. This indicates that elevated levels of circulating sTNFR should be carefully interpreted when kidney failure exists.
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PMID:Plasma cytokine levels in hemolytic uremic syndrome. 856 80

The clinical course as well as the effects of the treatment in 27 children suffering from IgA nephropathy were followed in this study. The observation period lasted from 1.5 to 15.5 years, mean 9.1. The clinical picture according to changes in urine was the criterion of classification into 4 groups, and was related to the WHO classification of pathomorphological types. Hypertension as well as acute renal failure were observed in each clinical group except the group of children with erythrocyturia and/or haematuria. Depending on the pathomorphological changes in kidneys, different groups of drugs were used, e.g. anticoagulants, corticosteroids and also alkylating agents. In 9 children no treatment was prescribed. Only 6 children showed regression of urine changes: 2 of them with steroid-sensitive nephrotic syndrome and 1 with steroid-resistant nephrotic syndrome. In 12 children, erythrocyturia and proteinuria decreased and the intervals between successive seizures of haematuria became longer. In 3 of 8 children with nephrotic syndrome, chronic renal failure as well as end-stage renal disease were observed. In 2 of them hypertension was present during the entire observation period and it was difficult to achieve control using hypotensive drugs. In the remaining 2 children, regression of nephrotic syndrome was found, but slight proteinuria and hypertension are observed.
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PMID:[Clinical course and treatment results of IgA nephropathy in children]. 897 18


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